PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
2481974-7	1989	CHOP therapy with bleomycin and methotrexate was performed.	Bleomycin	18-27	DNA damage inducible transcript 3	Homo sapiens	0-4
2481844-0	1988	[Modified CHOP-Bleo protocol in the treatment of malignant non-Hodgkin"s lymphoma of low cell differentiation].	Bleomycin	15-19	DNA damage inducible transcript 3	Homo sapiens	10-14
2601224-7	1989	Although 3 courses of combination chemotherapy with cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP) were given, no remission was obtained.	Prednisolone	99-111	DNA damage inducible transcript 3	Homo sapiens	113-117
2466548-12	1989	Thirteen of 22 patients received cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP/bleomycin as first chemotherapeutic regimen.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
2681883-4	1989	As to 14 patients treated with CHOP regimen, CR rate was 87% and RFS curve trend toward plateau at 67% after 2 years and 3 months from the initiation of chemotherapy.	Chromium	45-47	DNA damage inducible transcript 3	Homo sapiens	31-35
2681883-6	1989	The CHOP regimen was effective in the treatment of III-IV Hodgkin"s disease but an alternative multidrug chemotherapy with ADM, CPM, VCR, BLM, etoposide and procarbazine is recommended for achieving a higher CR rate and a better RFS.	Chromium	134-136	DNA damage inducible transcript 3	Homo sapiens	4-8
2523211-8	1989	of 4 months duration with CHOP-Bleomycin.	Bleomycin	31-40	DNA damage inducible transcript 3	Homo sapiens	26-30
3167803-6	1988	Employing CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) and consolidation radiation therapy in most cases, 80% achieved a complete remission and 59% survive failure-free at 5 years by actuarial calculation.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	10-14
3167803-6	1988	Employing CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) and consolidation radiation therapy in most cases, 80% achieved a complete remission and 59% survive failure-free at 5 years by actuarial calculation.	Doxorubicin	47-58	DNA damage inducible transcript 3	Homo sapiens	10-14
3167803-6	1988	Employing CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) and consolidation radiation therapy in most cases, 80% achieved a complete remission and 59% survive failure-free at 5 years by actuarial calculation.	Vincristine	60-71	DNA damage inducible transcript 3	Homo sapiens	10-14
3203011-0	1988	Treatment of diffuse histiocytic and diffuse mixed non-Hodgkin lymphomas with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	137-141
3060443-2	1988	We have investigated the relationship between RDI of the combination of cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) and the results of therapy in a group of 78 newly diagnosed patients with diffuse histiocytic and diffuse mixed non-Hodgkin"s lymphoma.	Prednisone	118-128	DNA damage inducible transcript 3	Homo sapiens	130-134
3203011-0	1988	Treatment of diffuse histiocytic and diffuse mixed non-Hodgkin lymphomas with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Prednisone	125-135	DNA damage inducible transcript 3	Homo sapiens	137-141
3203011-9	1988	The 5-year survival rate for stage I & II patients treated by CHOP plus radiotherapy was 70% as compared to 55% for those treated by CHOP only; this difference was not statistically significant.	Adenosine Monophosphate	38-41	DNA damage inducible transcript 3	Homo sapiens	66-70
3827258-7	1987	Despite the moderate to severe myelotoxicity, these results provide evidence that MEPP is an effective regimen for non-Hodgkin"s lymphoma resistant to CHOP or CHOP-bleo.	mepp	82-86	DNA damage inducible transcript 3	Homo sapiens	151-155
2464185-5	1988	Therapeutic trials of CHOP-BLEO merit further assessment and the results should be compared to the baseline treatment using platinum and prednisolone.	Platinum	124-132	DNA damage inducible transcript 3	Homo sapiens	22-26
2464185-5	1988	Therapeutic trials of CHOP-BLEO merit further assessment and the results should be compared to the baseline treatment using platinum and prednisolone.	Prednisolone	137-149	DNA damage inducible transcript 3	Homo sapiens	22-26
3581030-0	1987	Cyclophosphamide, vincristine, adriamycin, and prednisone (CHOP) with and without intermediate dose methotrexate for the treatment of non-Hodgkin"s lymphomas of diffuse histology.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	59-63
3581030-0	1987	Cyclophosphamide, vincristine, adriamycin, and prednisone (CHOP) with and without intermediate dose methotrexate for the treatment of non-Hodgkin"s lymphomas of diffuse histology.	Prednisone	47-57	DNA damage inducible transcript 3	Homo sapiens	59-63
3080220-2	1986	The authors report the case of a patient with malignant thymoma unresponsive to combination chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone [CHOP] and cisplatin/VP-16) who subsequently achieved clinical response to continuous daily prednisone.	Prednisone	154-164	DNA damage inducible transcript 3	Homo sapiens	166-170
2428947-1	1986	Long-term follow-up results of two studies using cyclophosphamide, doxorubicin, vincristine, and prednisone plus bleomycin (CHOP-Bleo) for the treatment of diffuse large-cell lymphoma are presented.	Bleomycin	113-122	DNA damage inducible transcript 3	Homo sapiens	124-128
3751969-2	1986	A 30-year-old woman with Stage IIIA diffuse non-Hodgkins lymphoma was treated with doxorubicin, cyclophosphamide, vincristine, and prednisone (CHOP) every 3 weeks.	Doxorubicin	83-94	DNA damage inducible transcript 3	Homo sapiens	143-147
3751969-2	1986	A 30-year-old woman with Stage IIIA diffuse non-Hodgkins lymphoma was treated with doxorubicin, cyclophosphamide, vincristine, and prednisone (CHOP) every 3 weeks.	Prednisone	131-141	DNA damage inducible transcript 3	Homo sapiens	143-147
3840280-2	1985	We have reported a case of diffuse, poorly differentiated lymphocytic lymphoma, stage IIIa, in a patient whose disease went into remission after she received six courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone).	Cyclophosphamide	187-203	DNA damage inducible transcript 3	Homo sapiens	173-177
3754070-2	1986	We describe a case of a 68-year-old man with an immunoblastic primary cerebral lymphoma first treated with surgery and radiotherapy and subsequently with chemotherapy consisting of cyclophosphamide, adriamycin, vincristine and prednisone (CHOP).	Cyclophosphamide	181-197	DNA damage inducible transcript 3	Homo sapiens	239-243
3840280-2	1985	We have reported a case of diffuse, poorly differentiated lymphocytic lymphoma, stage IIIa, in a patient whose disease went into remission after she received six courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone).	Doxorubicin	205-216	DNA damage inducible transcript 3	Homo sapiens	173-177
3840280-2	1985	We have reported a case of diffuse, poorly differentiated lymphocytic lymphoma, stage IIIa, in a patient whose disease went into remission after she received six courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone).	Vincristine	218-229	DNA damage inducible transcript 3	Homo sapiens	173-177
3840280-2	1985	We have reported a case of diffuse, poorly differentiated lymphocytic lymphoma, stage IIIa, in a patient whose disease went into remission after she received six courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone).	Prednisolone	235-247	DNA damage inducible transcript 3	Homo sapiens	173-177
6396563-2	1984	Chemotherapy with cyclophosphamide, vincristine and prednisone (COP) yielded partial response, but the addition of adriamycin (CHOP) a complete remission.	Doxorubicin	115-125	DNA damage inducible transcript 3	Homo sapiens	127-131
3897470-7	1985	CHOP appears preferable for diffuse large-cell categories, since it resulted in greater overall survival in patients with DH lymphoma; this was due to a significantly greater response rate, since patients with DH lymphoma who did respond to BCOP maintained their response and survived as long as did the CHOP responders.	BCVP protocol	241-245	DNA damage inducible transcript 3	Homo sapiens	0-4
6347997-1	1983	The combination of cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) alternating with total body irradiation (TBI) has been shown earlier to be effective therapy in patients with malignant lymphoma who have received prior chemotherapy and/or radiation therapy.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	78-82
6090736-6	1984	Complete remission was obtained by CHOP therapy (consisting of cyclophosphamide, adriamycin, vincristine, and prednisolone) combined with cervical irradiation.	Cyclophosphamide	63-79	DNA damage inducible transcript 3	Homo sapiens	35-39
6090736-6	1984	Complete remission was obtained by CHOP therapy (consisting of cyclophosphamide, adriamycin, vincristine, and prednisolone) combined with cervical irradiation.	Doxorubicin	81-91	DNA damage inducible transcript 3	Homo sapiens	35-39
6697295-4	1984	A few hours after initiation of chemotherapy with cyclophosphamide, Adriamycin (doxorubicin), vincristine, and prednisolone (CHOP regimen), the patient developed an acute ascending paralysis.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	125-129
6697295-4	1984	A few hours after initiation of chemotherapy with cyclophosphamide, Adriamycin (doxorubicin), vincristine, and prednisolone (CHOP regimen), the patient developed an acute ascending paralysis.	Doxorubicin	68-78	DNA damage inducible transcript 3	Homo sapiens	125-129
6697295-4	1984	A few hours after initiation of chemotherapy with cyclophosphamide, Adriamycin (doxorubicin), vincristine, and prednisolone (CHOP regimen), the patient developed an acute ascending paralysis.	Prednisolone	111-123	DNA damage inducible transcript 3	Homo sapiens	125-129
6347997-1	1983	The combination of cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) alternating with total body irradiation (TBI) has been shown earlier to be effective therapy in patients with malignant lymphoma who have received prior chemotherapy and/or radiation therapy.	Prednisone	66-76	DNA damage inducible transcript 3	Homo sapiens	78-82
6347997-4	1983	CHOP was given in the following manner: cyclophosphamide 400 mg/M2 IV day 1, adriamycin 40 mg/M2 IV day 1, vincristine 2 mg IV day 1, and Prednisone 100 mg po daily X 5.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	0-4
6347997-4	1983	CHOP was given in the following manner: cyclophosphamide 400 mg/M2 IV day 1, adriamycin 40 mg/M2 IV day 1, vincristine 2 mg IV day 1, and Prednisone 100 mg po daily X 5.	Vincristine	107-118	DNA damage inducible transcript 3	Homo sapiens	0-4
6347997-4	1983	CHOP was given in the following manner: cyclophosphamide 400 mg/M2 IV day 1, adriamycin 40 mg/M2 IV day 1, vincristine 2 mg IV day 1, and Prednisone 100 mg po daily X 5.	Prednisone	138-148	DNA damage inducible transcript 3	Homo sapiens	0-4
7233568-0	1980	Combination chemotherapy with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) for non-Hodgkin"s lymphomas with unfavorable histology: preliminary results.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	88-92
6191677-0	1983	[Cyclophosphamide, adriamycin, vincristine, bleomycin and prednisolone (CHOP-Bleo) combination chemotherapy for advanced non-Hodgkin"s lymphoma].	Cyclophosphamide	1-17	DNA damage inducible transcript 3	Homo sapiens	72-76
6191677-0	1983	[Cyclophosphamide, adriamycin, vincristine, bleomycin and prednisolone (CHOP-Bleo) combination chemotherapy for advanced non-Hodgkin"s lymphoma].	Prednisolone	58-70	DNA damage inducible transcript 3	Homo sapiens	72-76
6191677-6	1983	A major complication during CHOP-Bleo regimen was myelosuppression, and peripheral neuropathy and reversible interstitial pneumonitis (2 cases) were also observed.	Bleomycin	33-37	DNA damage inducible transcript 3	Homo sapiens	28-32
6185212-4	1983	CR rate for 65 patients with large cell lymphoma treated with CHOP-BCG was 68% compared to 48% in 61 patients treated with CHOP-bleomycin (P = 0.02) (two-tailed test) or 44% for 45 patients treated with COP-bleomycin (P = 0.02).	Chromium	0-2	DNA damage inducible transcript 3	Homo sapiens	62-66
6185212-5	1983	CR duration for both CHOP-based regimens was similar and superior to that produced by COP-bleomycin (P = 0.03).	Chromium	0-2	DNA damage inducible transcript 3	Homo sapiens	21-25
6189041-0	1983	Long-term results of patients with advanced diffuse, non-Hodgkin"s lymphoma treated with cyclophosphamide, doxorubicin, vincristine, prednisone and bleomycin (CHOP-Bleo).	Bleomycin	148-157	DNA damage inducible transcript 3	Homo sapiens	159-163
6186997-0	1982	[Results of treatment of the lymphoblastic and immunoblastic malignant lymphomas using the CHOP-bleo protocol (cyclophosphamide, doxorubicin, vincristine, bleomycin and prednisolone)].	Bleomycin	96-100	DNA damage inducible transcript 3	Homo sapiens	91-95
6950800-5	1982	Combination chemotherapy with cyclophosphamide, Doxorubicin, vincristine, and prednisone (CHOP) has produced impressive clinical responses in patients with PL.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	90-94
6950800-5	1982	Combination chemotherapy with cyclophosphamide, Doxorubicin, vincristine, and prednisone (CHOP) has produced impressive clinical responses in patients with PL.	Doxorubicin	48-59	DNA damage inducible transcript 3	Homo sapiens	90-94
6950800-5	1982	Combination chemotherapy with cyclophosphamide, Doxorubicin, vincristine, and prednisone (CHOP) has produced impressive clinical responses in patients with PL.	Prednisone	78-88	DNA damage inducible transcript 3	Homo sapiens	90-94
6688200-0	1983	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in patients with advanced Hodgkin"s disease: a Southwest Oncology Group Phase II Study.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
6688200-0	1983	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in patients with advanced Hodgkin"s disease: a Southwest Oncology Group Phase II Study.	Prednisone	48-58	DNA damage inducible transcript 3	Homo sapiens	60-64
6688970-1	1983	In a pilot study of cyclical chemotherapy in patients with poor-prognosis non-Hodgkin"s lymphoma (NHL), high-dose methotrexate (MTX) 1 g/m2 with folinic acid rescue was given as initial treatment and then between cycles of a single-arm CHOP combination administered every 4 weeks.	Methotrexate	114-126	DNA damage inducible transcript 3	Homo sapiens	236-240
7233568-0	1980	Combination chemotherapy with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) for non-Hodgkin"s lymphomas with unfavorable histology: preliminary results.	Prednisone	76-86	DNA damage inducible transcript 3	Homo sapiens	88-92
7000347-0	1980	Advanced diffuse histiocytic lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) without maintenance therapy.	Prednisone	99-109	DNA damage inducible transcript 3	Homo sapiens	111-115
364284-1	1978	The results of a chemotherapy regimen utilizing adriamycin in combination with vincristine, prednisone plus or minus cyclophosphamide (CHOP-HOP) for the treatment of non-Hodgkin lymphoma are compared to those of a non-adriamycin containing combination (COP).	Cyclophosphamide	117-133	DNA damage inducible transcript 3	Homo sapiens	135-139
84706-3	1979	Confirmed rates of CR for 443 evaluable patients were 59% for 286 patients receiving the CHOP regimens and 59% for 157 patients receiving COP-Bleo.	Chromium	19-21	DNA damage inducible transcript 3	Homo sapiens	89-93
84706-6	1979	For patients with diffuse lymphomas the CR rate was higher with the CHOP programs (58%) than with COP-Bleo (44%) (p = 0.10).	Chromium	40-42	DNA damage inducible transcript 3	Homo sapiens	68-72
33894420-8	2021	Meanwhile, CCT combined with taxol caused significant ER stress through improving phosphorylated PERK, eukaryotic translation initiation factor 2alpha (eIF2alpha), C/EBP homologous protein (CHOP) and glucose-regulated protein 78 (GRP78).	Paclitaxel	29-34	DNA damage inducible transcript 3	Homo sapiens	164-188
33894420-8	2021	Meanwhile, CCT combined with taxol caused significant ER stress through improving phosphorylated PERK, eukaryotic translation initiation factor 2alpha (eIF2alpha), C/EBP homologous protein (CHOP) and glucose-regulated protein 78 (GRP78).	Paclitaxel	29-34	DNA damage inducible transcript 3	Homo sapiens	190-194
33904834-5	2021	ER-stress induction using tunicamycin and brefeldin A resulted in increased CHOP (4.6-fold change; P <= 0.001), XBP1 expression (1.7- and 1.3-fold change, respectively; P <= 0.001 and P < 0.05) and XBP1 splicing (7.9- and 12.8-fold change, respectively; P <= 0.001).	Tunicamycin	26-37	DNA damage inducible transcript 3	Homo sapiens	76-80
33857568-4	2021	Increased DDIT3 in these Dox-treated cardiomyocytes at 24h suggested that increased MitoBax may have promoted ER stress related changes in DDIT3.	Doxorubicin	25-28	DNA damage inducible transcript 3	Homo sapiens	10-15
33857568-4	2021	Increased DDIT3 in these Dox-treated cardiomyocytes at 24h suggested that increased MitoBax may have promoted ER stress related changes in DDIT3.	Doxorubicin	25-28	DNA damage inducible transcript 3	Homo sapiens	139-144
33857568-6	2021	In contrast, breast cancer MCF7 cells showed an ER stress response to Dox with increased DDIT3 as early as 3h which may have triggered a positive feedback activation of ATF6 at 12 and 24h and promoted Calnexin.	Doxorubicin	70-73	DNA damage inducible transcript 3	Homo sapiens	89-94
33857568-8	2021	DDIT3 response in tumors was evoked by Dox, however this response was inversely correlated with increased Bip and Bax expression in hearts from tumor bearing animals.	Doxorubicin	39-42	DNA damage inducible transcript 3	Homo sapiens	0-5
33857568-9	2021	It is suggested that in Dox-induced cardiotoxicity both mitochondrial and ER stresses play an integral role through a mutual interaction where an inhibition of DDIT3 or Calnexin may also be crucial to achieve Dox resistance in cardiomyocytes.	Doxorubicin	24-27	DNA damage inducible transcript 3	Homo sapiens	160-165
33857568-9	2021	It is suggested that in Dox-induced cardiotoxicity both mitochondrial and ER stresses play an integral role through a mutual interaction where an inhibition of DDIT3 or Calnexin may also be crucial to achieve Dox resistance in cardiomyocytes.	Doxorubicin	209-212	DNA damage inducible transcript 3	Homo sapiens	160-165
33907586-9	2021	The role of the CHOP target gene in curcumin-induced ACC cell apoptosis was verified via lentiviral transfection experiments.	Curcumin	36-44	DNA damage inducible transcript 3	Homo sapiens	16-20
33713737-6	2021	Combination of ASCT2 inhibitor V9302 and proteasome inhibitor carfilzomib upregulates the intracellular levels of ROS and oxidative stress markers and triggers catastrophic UPR as shown by upregulated spliced Xbp1 mRNA, ATF3 and CHOP levels.	v9302	31-36	DNA damage inducible transcript 3	Homo sapiens	229-233
33713737-6	2021	Combination of ASCT2 inhibitor V9302 and proteasome inhibitor carfilzomib upregulates the intracellular levels of ROS and oxidative stress markers and triggers catastrophic UPR as shown by upregulated spliced Xbp1 mRNA, ATF3 and CHOP levels.	carfilzomib	62-73	DNA damage inducible transcript 3	Homo sapiens	229-233
33511665-0	2021	Poly(U)-specific endoribonuclease ENDOU promotes translation of human CHOP mRNA by releasing uORF element-mediated inhibition.	Poly U	0-7	DNA damage inducible transcript 3	Homo sapiens	70-74
33904834-5	2021	ER-stress induction using tunicamycin and brefeldin A resulted in increased CHOP (4.6-fold change; P <= 0.001), XBP1 expression (1.7- and 1.3-fold change, respectively; P <= 0.001 and P < 0.05) and XBP1 splicing (7.9- and 12.8-fold change, respectively; P <= 0.001).	Brefeldin A	42-53	DNA damage inducible transcript 3	Homo sapiens	76-80
33904834-7	2021	Although GRP78 protein remained unaffected, low oxygen (2.5% O2) increased IRE1alpha phosphorylation (+52%; P < 0.05) and XBP1 splicing (1.8-fold change; P <= 0.001) after 24h, while eIF2alpha protein and CHOP expression were downregulated (-28%; P < 0.05 and -24%; P <= 0.001; respectively).	Oxygen	48-54	DNA damage inducible transcript 3	Homo sapiens	205-209
34012033-7	2021	For CD5 + DLBCL patients, systemic treatment with high-dose methotrexate was associated with superior OS compared to R-CHOP-based immunochemotherapy alone.	Methotrexate	60-72	DNA damage inducible transcript 3	Homo sapiens	119-123
33269515-6	2021	As the mechanisms, 200 mug/ml Cu, N-doped CDs and CB NPs promoted endoplasmic reticulum (ER) stress proteins IRE1alpha and chop, leading to increased cleaved caspase 3/pro-caspase 3 ratio, but CB NPs were more effective.	Copper	30-32	DNA damage inducible transcript 3	Homo sapiens	123-127
34022150-2	2021	We aimed to establish the safety and efficacy of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in patients with DLBCL in Malawi.	Prednisone	112-122	DNA damage inducible transcript 3	Homo sapiens	126-130
33957011-8	2021	Moreover, 4-NP induced-apoptosis seemed to involve both an ER-stress response, with the appearance of high level of GRP78, CHOP and the spliced XBP1, and a dysregulation of mitochondrial physiology, characterized by an overexpression of main markers of mitochondrial dynamics.	4-nonylphenol	10-14	DNA damage inducible transcript 3	Homo sapiens	123-127
33667956-0	2021	Calcium mitigates fluoride-induced kallikrein 4 inhibition via PERK/eIF2alpha/ATF4/CHOP endoplasmic reticulum stress pathway in ameloblast-lineage cells.	Calcium	0-7	DNA damage inducible transcript 3	Homo sapiens	83-87
33667956-0	2021	Calcium mitigates fluoride-induced kallikrein 4 inhibition via PERK/eIF2alpha/ATF4/CHOP endoplasmic reticulum stress pathway in ameloblast-lineage cells.	Fluorides	18-26	DNA damage inducible transcript 3	Homo sapiens	83-87
33989279-2	2021	However, the addition of lenalidomide to rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in randomized clinical trials has shown equivocal benefit, despite phase 2 studies that suggested otherwise.	Lenalidomide	25-37	DNA damage inducible transcript 3	Homo sapiens	118-122
33989279-2	2021	However, the addition of lenalidomide to rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in randomized clinical trials has shown equivocal benefit, despite phase 2 studies that suggested otherwise.	Prednisone	104-114	DNA damage inducible transcript 3	Homo sapiens	118-122
34054558-14	2021	Accumulation of ROS caused ER stress through the PERK-eIF2alpha-CHOP and IRE1alpha-CHOP pathways.	Reactive Oxygen Species	16-19	DNA damage inducible transcript 3	Homo sapiens	64-68
34054558-14	2021	Accumulation of ROS caused ER stress through the PERK-eIF2alpha-CHOP and IRE1alpha-CHOP pathways.	Reactive Oxygen Species	16-19	DNA damage inducible transcript 3	Homo sapiens	83-87
33751936-0	2021	Berberine-photodynamic induced apoptosis by activating endoplasmic reticulum stress-autophagy pathway involving CHOP in human malignant melanoma cells.	Berberine	0-9	DNA damage inducible transcript 3	Homo sapiens	112-116
33269515-6	2021	As the mechanisms, 200 mug/ml Cu, N-doped CDs and CB NPs promoted endoplasmic reticulum (ER) stress proteins IRE1alpha and chop, leading to increased cleaved caspase 3/pro-caspase 3 ratio, but CB NPs were more effective.	n-doped	34-41	DNA damage inducible transcript 3	Homo sapiens	123-127
33269515-6	2021	As the mechanisms, 200 mug/ml Cu, N-doped CDs and CB NPs promoted endoplasmic reticulum (ER) stress proteins IRE1alpha and chop, leading to increased cleaved caspase 3/pro-caspase 3 ratio, but CB NPs were more effective.	cds	42-45	DNA damage inducible transcript 3	Homo sapiens	123-127
33952780-7	2021	Honokiol reversed the effect of HG/HF on promoting cell apoptosis, ROS and MDA contents, and the expressions of CHOP, GRP78, p-PERK, p-IRE1alpha and cleaved caspase-3, and also reversed the inhibitory effect of HG/HF on cell viability, SOD content and SIRT1 expression.	honokiol	0-8	DNA damage inducible transcript 3	Homo sapiens	112-116
33632872-3	2021	Searching for molecular mechanisms leading to such differences, we found that VPA treatment dysregulated choline metabolism and triggered a stronger ER stress in pancreatic cancer cells than TSA, up-regulating CHOP, and activated COX2, thus promoting the release of prostaglandin (PG) E2.	Valproic Acid	78-81	DNA damage inducible transcript 3	Homo sapiens	210-214
33453553-1	2021	This study was designed to evaluate changes in color following pork chop supplementation with porcine hemin, astaxanthin and paprika red in response to repeated freeze-thaw processes.	porcine hemin	94-107	DNA damage inducible transcript 3	Homo sapiens	68-72
33453553-6	2021	In conclusion, hemin may be a superior supplement for the large scale preparation of prepared pork chop.	Hemin	15-20	DNA damage inducible transcript 3	Homo sapiens	99-103
33555941-1	2021	PURPOSE: Lenalidomide combined with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) (R2CHOP) in untreated diffuse large B-cell lymphoma (DLBCL) has shown promising activity, particularly in the activated B-cell-like (ABC) subtype.	Lenalidomide	9-21	DNA damage inducible transcript 3	Homo sapiens	113-117
33906643-0	2021	Successful treatment by on-demand glecaprevir and pibrentasvir for hepatitis C flare during R-CHOP in patients with diffuse large B-cell lymphoma: a case report.	glecaprevir	34-45	DNA damage inducible transcript 3	Homo sapiens	94-98
33906643-0	2021	Successful treatment by on-demand glecaprevir and pibrentasvir for hepatitis C flare during R-CHOP in patients with diffuse large B-cell lymphoma: a case report.	pibrentasvir	50-62	DNA damage inducible transcript 3	Homo sapiens	94-98
33906643-3	2021	CASE PRESENTATION: We report the first case of effective and safe treatment with on-demand 8-week glecaprevir and pibrentasvir for hepatitis C flare during R-CHOP in a patient with diffuse large B-cell lymphoma (DLBCL).	glecaprevir	98-109	DNA damage inducible transcript 3	Homo sapiens	158-162
33906643-3	2021	CASE PRESENTATION: We report the first case of effective and safe treatment with on-demand 8-week glecaprevir and pibrentasvir for hepatitis C flare during R-CHOP in a patient with diffuse large B-cell lymphoma (DLBCL).	pibrentasvir	114-126	DNA damage inducible transcript 3	Homo sapiens	158-162
33968299-4	2021	Our results showed that emodin-induced ROS activated ER stress and the UPR via the BiP/IRE1alpha/CHOP signaling pathway, followed by ER Ca2+ release and cytoplasmic Ca2+ overloading.	Emodin	24-30	DNA damage inducible transcript 3	Homo sapiens	97-101
33968299-9	2021	Thus, all the results indicated that emodin-induced excessive ROS generation and redox imbalance promoted apoptosis, which was mainly associated with BiP/IRE1alpha/CHOP signaling-mediated ER stress and would be enhanced by oxidative stress-mediated mitochondrial dysfunction.	Emodin	37-43	DNA damage inducible transcript 3	Homo sapiens	164-168
33621109-2	2021	Phase II studies demonstrated that adding the immunomodulatory agent lenalidomide to R-CHOP improved outcomes in ABC-type DLBCL.	Lenalidomide	69-81	DNA damage inducible transcript 3	Homo sapiens	87-91
33968299-0	2021	Emodin-Induced Oxidative Inhibition of Mitochondrial Function Assists BiP/IRE1alpha/CHOP Signaling-Mediated ER-Related Apoptosis.	Emodin	0-6	DNA damage inducible transcript 3	Homo sapiens	84-88
33555941-1	2021	PURPOSE: Lenalidomide combined with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) (R2CHOP) in untreated diffuse large B-cell lymphoma (DLBCL) has shown promising activity, particularly in the activated B-cell-like (ABC) subtype.	Doxorubicin	69-80	DNA damage inducible transcript 3	Homo sapiens	113-117
33924206-9	2021	Via regulation of expression/activity of pro- and anti-apoptotic Bcl-2 family members, and potentially also through the increase in ROS production, CHOP switches on the mitochondrial pathway of apoptosis induction.	ros	132-135	DNA damage inducible transcript 3	Homo sapiens	148-152
33665961-4	2021	Using transcriptome and metabolome analyses, we characterized a combinatorial response, mainly driven by the transcription factors CHOP and TFE3, which resulted in cell death through enhanced pyrimidine catabolism as well as reduced pyrimidine synthesis.	pyrimidine	192-202	DNA damage inducible transcript 3	Homo sapiens	131-135
33444079-3	2021	In combination with R-CHOP (R2-CHOP), lenalidomide has an acceptable level of toxicity and may mitigate the negative prognosis of the non-germinal center B-cell-like phenotype.	Lenalidomide	38-50	DNA damage inducible transcript 3	Homo sapiens	31-35
33837631-1	2021	Mitochondrial dysfunction mediated by CCCP (carbonyl cyanide m-chlorophenyl hydrazone), an inhibitor of mitochondrial oxidative phosphorylation, evokes the integrated stress response (ISR), which is analyzed here by eIF2alpha phosphorylation and expression profiles of ATF4 and CHOP proteins.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	38-42	DNA damage inducible transcript 3	Homo sapiens	278-282
33837631-1	2021	Mitochondrial dysfunction mediated by CCCP (carbonyl cyanide m-chlorophenyl hydrazone), an inhibitor of mitochondrial oxidative phosphorylation, evokes the integrated stress response (ISR), which is analyzed here by eIF2alpha phosphorylation and expression profiles of ATF4 and CHOP proteins.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	44-85	DNA damage inducible transcript 3	Homo sapiens	278-282
33665961-4	2021	Using transcriptome and metabolome analyses, we characterized a combinatorial response, mainly driven by the transcription factors CHOP and TFE3, which resulted in cell death through enhanced pyrimidine catabolism as well as reduced pyrimidine synthesis.	pyrimidine	233-243	DNA damage inducible transcript 3	Homo sapiens	131-135
33751401-0	2021	Efficacy and Safety of the Biosimilar IBI301 Plus Standard CHOP (I-CHOP) in Comparison With Rituximab Plus CHOP (R-CHOP) in Patients with Previously Untreated Diffuse Large B-Cell Lymphoma (DLBCL): A Randomized, Double-Blind, Parallel-Group, Phase 3 Trial.	ibi301	38-44	DNA damage inducible transcript 3	Homo sapiens	67-71
33837631-6	2021	ISRIB, an inhibitor of the ISR pathway, mitigates CCCP-induced expression of ATF4 and CHOP, activation of AKT, and autophagy, similar to NAC.	2-(4-chlorophenoxy)-N-(4-(2-(4-chlorophenoxy)acetamido)cyclohexyl)acetamide	0-5	DNA damage inducible transcript 3	Homo sapiens	86-90
33837631-6	2021	ISRIB, an inhibitor of the ISR pathway, mitigates CCCP-induced expression of ATF4 and CHOP, activation of AKT, and autophagy, similar to NAC.	Carbonyl Cyanide m-Chlorophenyl Hydrazone	50-54	DNA damage inducible transcript 3	Homo sapiens	86-90
33826840-4	2021	Our study found that after oxygen-glucose deprivation/reoxygenation (OGD/R) treatment, the levels of GPR4 and CHOP in SH-SY5Y cells were significantly increased, which was accompanied by a decrease in cell viability, and an increase in LDH release and apoptosis.	Glucose	34-41	DNA damage inducible transcript 3	Homo sapiens	110-114
33692867-9	2021	Miconazole-induced ER stress was associated with increases in binding immunoglobulin protein (BiP), inositol-requiring enzyme 1alpha (IRE1alpha) and CHOP expression, and phospho-eIF2alpha levels.	Miconazole	0-10	DNA damage inducible transcript 3	Homo sapiens	149-153
33875166-0	2021	Polyphyllin I promotes cell death via suppressing UPR-mediated CHOP ubiquitination and degradation in non-small cell lung cancer.	polyphyllin I	0-13	DNA damage inducible transcript 3	Homo sapiens	63-67
34007370-9	2021	Finally a leukemic DLBCL was diagnosed and immediately treatment with rituximab cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) was started.	Prednisone	127-137	DNA damage inducible transcript 3	Homo sapiens	141-145
33409875-4	2021	We observed that E2 treatment of HEMECs increased ERalpha expression and reduced the expression of GRP78, which led to reduction of Caspase 3 expression by the CHOP pathway.	Estradiol	17-19	DNA damage inducible transcript 3	Homo sapiens	160-164
33841136-13	2021	Moreover, alternol increased the level of CHOP, which is necessary for the enhancing effect of alternol on TRAIL-induced apoptosis, given that downregulation of CHOP abrogated the synergistic effect.	Alternol	10-18	DNA damage inducible transcript 3	Homo sapiens	42-46
33726556-8	2022	NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells.	Acetylcysteine	0-3	DNA damage inducible transcript 3	Homo sapiens	52-56
33841136-13	2021	Moreover, alternol increased the level of CHOP, which is necessary for the enhancing effect of alternol on TRAIL-induced apoptosis, given that downregulation of CHOP abrogated the synergistic effect.	Alternol	95-103	DNA damage inducible transcript 3	Homo sapiens	42-46
33841136-16	2021	Conclusion: Taken together, our research suggested that alternol increased TRAIL-mediated apoptosis via inhibiting antiapoptotic proteins and upregulating DR5 levels via ROS generation and the CHOP pathway.	Alternol	56-64	DNA damage inducible transcript 3	Homo sapiens	193-197
33734921-1	2021	BACKGROUND: Treatment with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is standard of care first line treatment for diffuse large B-cell lymphoma (DLBCL), though outcomes remain suboptimal.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	100-104
33734921-1	2021	BACKGROUND: Treatment with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is standard of care first line treatment for diffuse large B-cell lymphoma (DLBCL), though outcomes remain suboptimal.	Doxorubicin	56-67	DNA damage inducible transcript 3	Homo sapiens	100-104
33734921-1	2021	BACKGROUND: Treatment with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is standard of care first line treatment for diffuse large B-cell lymphoma (DLBCL), though outcomes remain suboptimal.	Prednisone	86-96	DNA damage inducible transcript 3	Homo sapiens	100-104
33782302-5	2021	After 6 cycles of CHOP-like chemotherapy, 18F-FDG PET/CT showed complete metabolic and morphologic resolution for follicular dendritic cell sarcoma.	Fluorodeoxyglucose F18	42-49	DNA damage inducible transcript 3	Homo sapiens	18-22
33726556-8	2022	NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells.	salubrinal	8-18	DNA damage inducible transcript 3	Homo sapiens	52-56
33726556-8	2022	NAC and salubrinal inhibited an increase in VEGF-A, CHOP and caspase-3 caused by ATRA in ARPE-19 cells.	Tretinoin	81-85	DNA damage inducible transcript 3	Homo sapiens	52-56
33714955-4	2021	In this study, we demonstrated that the eIF2-alpha/ATF4/CHOP branch of unfolded protein response (UPR) was activated in human trabecular meshwork cells (HTMCs) upon tert-butyl hydroperoxide (TBHP) exposure.	tert-Butylhydroperoxide	165-189	DNA damage inducible transcript 3	Homo sapiens	56-60
33714955-4	2021	In this study, we demonstrated that the eIF2-alpha/ATF4/CHOP branch of unfolded protein response (UPR) was activated in human trabecular meshwork cells (HTMCs) upon tert-butyl hydroperoxide (TBHP) exposure.	tert-Butylhydroperoxide	191-195	DNA damage inducible transcript 3	Homo sapiens	56-60
33675952-0	2021	NUPR1- CHOP experssion, autophagosome formation and apoptosis in the postmortem striatum of chronic methamphetamine user.	Methamphetamine	100-115	DNA damage inducible transcript 3	Homo sapiens	7-11
33688781-1	2021	Peripheral T-cell lymphoma (PTCL) is a group of aggressive lymphomas commonly treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Doxorubicin	109-120	DNA damage inducible transcript 3	Homo sapiens	151-155
33688781-1	2021	Peripheral T-cell lymphoma (PTCL) is a group of aggressive lymphomas commonly treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Prednisone	139-149	DNA damage inducible transcript 3	Homo sapiens	151-155
33688781-7	2021	These findings suggest that PFS24 is predictive of survival after CHOP treatment in Japanese patients with PTCL.	pfs24	28-33	DNA damage inducible transcript 3	Homo sapiens	66-70
33688781-1	2021	Peripheral T-cell lymphoma (PTCL) is a group of aggressive lymphomas commonly treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	151-155
33675952-3	2021	The current study aimed to assess the specific relationship between long-term Meth exposure and several endoplasmic reticulum stress-,autophagy-,and apoptosis-associated markers including C/EBP homologous protein (CHOP), Tribbles homolog 3(Trib3), Nuclear protein 1(NUPR1), and Beclin-1 expression in postmortem human striatum.	Methamphetamine	78-82	DNA damage inducible transcript 3	Homo sapiens	188-212
33675952-3	2021	The current study aimed to assess the specific relationship between long-term Meth exposure and several endoplasmic reticulum stress-,autophagy-,and apoptosis-associated markers including C/EBP homologous protein (CHOP), Tribbles homolog 3(Trib3), Nuclear protein 1(NUPR1), and Beclin-1 expression in postmortem human striatum.	Methamphetamine	78-82	DNA damage inducible transcript 3	Homo sapiens	214-218
33675952-7	2021	Based on our findings, the expression level of CHOP, Trib3, NUPR1, and Beclin-1 in the striatum of Meth group were significantly higher comparing the control group.	Methamphetamine	99-103	DNA damage inducible transcript 3	Homo sapiens	47-51
33675952-9	2021	Long-term presence of Meth in the brain can induce ER stress and overexpression of NUPR1 which is associated with the upregulation of CHOP, a pro-apoptotic transcription factor.	Methamphetamine	22-26	DNA damage inducible transcript 3	Homo sapiens	134-138
33675952-10	2021	Moreover, an increase in Trib3 expression is implicated in CHOP-dependent autophagic cell death during Meth-induced ER stress accompanied by an increase in neuronal cell death in the striatum of the postmortem human brains.	Methamphetamine	103-107	DNA damage inducible transcript 3	Homo sapiens	59-63
33651226-13	2021	4-PBA inhibits ER stress mainly through regulating PERK-ATF4-CHOP and IRE1-XBP1s branches.	4-phenylbutyric acid	0-5	DNA damage inducible transcript 3	Homo sapiens	61-65
32072190-9	2021	However, inhibition of NLPR3 and the ER stress maker CHOP restored the effect of PG on pyroptosis and cell metastasis, suggesting that the PG-induced antitumor effects on the HOS and the SAOS-2 cells were mediated by the ER stress-activated NLRP3 inflammasome.	physcione	81-83	DNA damage inducible transcript 3	Homo sapiens	53-57
33483276-0	2021	Impact of Omission/Reduction of Vincristine From R-CHOP in Treatment of DLBCL.	Vincristine	32-43	DNA damage inducible transcript 3	Homo sapiens	51-55
33483276-1	2021	BACKGROUND: The R-CHOP regimen (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) is the standard therapy for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	18-22
33483276-8	2021	CONCLUSIONS: Excessive dose omission/reduction of vincristine might lead to a substantial loss of efficacy of R-CHOP therapy.	Vincristine	50-61	DNA damage inducible transcript 3	Homo sapiens	112-116
33248829-7	2021	In conclusion, these findings indicate that excessive Cu could trigger ER stress via activation of the PERK/ATF4/CHOP signaling pathway and that ER stress might aggravate Cu-induced apoptosis in duck renal tubular epithelial cells.	Copper	54-56	DNA damage inducible transcript 3	Homo sapiens	113-117
33230565-5	2021	Combination of ADT with canavanine triggered catastrophic ER stress via the eIF2alpha-ATF4(GADD34)-CHOP pathway, thereby inducing apoptosis; the same signaling arm was irrelevant in ADT-related radiosensitization.	adt	15-18	DNA damage inducible transcript 3	Homo sapiens	99-103
33230565-5	2021	Combination of ADT with canavanine triggered catastrophic ER stress via the eIF2alpha-ATF4(GADD34)-CHOP pathway, thereby inducing apoptosis; the same signaling arm was irrelevant in ADT-related radiosensitization.	Canavanine	24-34	DNA damage inducible transcript 3	Homo sapiens	99-103
33248829-0	2021	Endoplasmic reticulum stress aggravates copper-induced apoptosis via the PERK/ATF4/CHOP signaling pathway in duck renal tubular epithelial cells.	Copper	40-46	DNA damage inducible transcript 3	Homo sapiens	83-87
33248829-5	2021	The results showed that excessive Cu could cause ER expansion and swelling, increase the expression levels of ER stress-associated genes (PERK, eIF2alpha, ATF4 and CHOP) and proteins (p-PERK and CHOP), induce intracellular Ca2+ overload, upregulate the expression levels of apoptosis-associated genes (Bax, Bak1, Caspase9 and Caspase3) and the cleaved-Caspase3 protein, downregulate Bcl-xl and Bcl2 mRNA levels and trigger apoptosis.	Copper	34-36	DNA damage inducible transcript 3	Homo sapiens	164-168
33248829-5	2021	The results showed that excessive Cu could cause ER expansion and swelling, increase the expression levels of ER stress-associated genes (PERK, eIF2alpha, ATF4 and CHOP) and proteins (p-PERK and CHOP), induce intracellular Ca2+ overload, upregulate the expression levels of apoptosis-associated genes (Bax, Bak1, Caspase9 and Caspase3) and the cleaved-Caspase3 protein, downregulate Bcl-xl and Bcl2 mRNA levels and trigger apoptosis.	Copper	34-36	DNA damage inducible transcript 3	Homo sapiens	195-199
32072190-9	2021	However, inhibition of NLPR3 and the ER stress maker CHOP restored the effect of PG on pyroptosis and cell metastasis, suggesting that the PG-induced antitumor effects on the HOS and the SAOS-2 cells were mediated by the ER stress-activated NLRP3 inflammasome.	physcione	139-141	DNA damage inducible transcript 3	Homo sapiens	53-57
33672735-6	2021	ATV treatment also caused the punctate appearance of CCAAT-enhancer-binding (C/EBP) protein homologous protein (CHOP), and altered expression of CHOP and GRP78/Bip, which are the representation of ER stress, only in differentiating adipocytes.	Atazanavir Sulfate	0-3	DNA damage inducible transcript 3	Homo sapiens	112-116
33629929-8	2021	Transcriptome analysis and other results demonstrated that ER stress and the ATF4-DDIT3-TRIB3-AKT-MTOR axis downstream of TRPV4 were involved in CBD-induced mitophagy in glioma cells.	Cannabidiol	145-148	DNA damage inducible transcript 3	Homo sapiens	82-87
33111362-10	2021	Simultaneously, Ligustilide effectively modulated ERS via inhibiting the over-activation of GRP78/PERK/CHOP signaling pathway.	ligustilide	16-27	DNA damage inducible transcript 3	Homo sapiens	103-107
33625586-1	2021	BACKGROUND: A combination of rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard first-line therapy for diffuse large B cell lymphoma (DLBCL), the most common aggressive lymphoma in adults.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	106-110
33625586-1	2021	BACKGROUND: A combination of rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard first-line therapy for diffuse large B cell lymphoma (DLBCL), the most common aggressive lymphoma in adults.	Doxorubicin	62-73	DNA damage inducible transcript 3	Homo sapiens	106-110
33625586-1	2021	BACKGROUND: A combination of rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard first-line therapy for diffuse large B cell lymphoma (DLBCL), the most common aggressive lymphoma in adults.	Prednisone	92-102	DNA damage inducible transcript 3	Homo sapiens	106-110
33625586-7	2021	CONCLUSION: Replacement of vincristine by vinorelbine due to neuropathy is effective and safe, and results in a significant improvement in neuropathy as compared to treatment with R-CHOP.	Vinorelbine	42-53	DNA damage inducible transcript 3	Homo sapiens	182-186
33758606-6	2021	Compared with erlotinib alone, beta-elemene plus erlotinib significantly promoted the apoptosis of NCI-H1975 cells, accompanied by the down-regulated expression of P-mTOR, P-EGFR, CHOP proteins and up-regulated expression of P-AMPKalpha and Bax proteins.	beta-elemene	31-43	DNA damage inducible transcript 3	Homo sapiens	180-184
33758606-6	2021	Compared with erlotinib alone, beta-elemene plus erlotinib significantly promoted the apoptosis of NCI-H1975 cells, accompanied by the down-regulated expression of P-mTOR, P-EGFR, CHOP proteins and up-regulated expression of P-AMPKalpha and Bax proteins.	Erlotinib Hydrochloride	49-58	DNA damage inducible transcript 3	Homo sapiens	180-184
33261869-8	2021	Arsenite promotes activation of the NRF2/BCL-2 signaling pathway inhibited CHOP increasing cellular resistance to apoptosis and further promoting malignant transformation.	arsenite	0-8	DNA damage inducible transcript 3	Homo sapiens	75-79
33672735-6	2021	ATV treatment also caused the punctate appearance of CCAAT-enhancer-binding (C/EBP) protein homologous protein (CHOP), and altered expression of CHOP and GRP78/Bip, which are the representation of ER stress, only in differentiating adipocytes.	Atazanavir Sulfate	0-3	DNA damage inducible transcript 3	Homo sapiens	145-149
33557839-0	2021	LiCl induces apoptosis via CHOP/NOXA/Mcl-1 axis in human choroidal melanoma cells.	Lithium Chloride	0-4	DNA damage inducible transcript 3	Homo sapiens	27-31
33602316-2	2021	The primary objective of this study was to determine the maximum tolerated dose (MTD) of belinostat combined with CHOP (Bel-CHOP).	belinostat	89-99	DNA damage inducible transcript 3	Homo sapiens	124-128
33573703-0	2021	5-Hydroxymethylcytosine profiles of cfDNA are highly predictive of R-CHOP treatment response in diffuse large B cell lymphoma patients.	5-hydroxymethylcytosine	0-23	DNA damage inducible transcript 3	Homo sapiens	69-73
33573703-1	2021	BACKGROUND: Although R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) remains the standard chemotherapy regimen for diffuse large B cell lymphoma (DLBCL) patients, not all patients are responsive to the scheme, and there is no effective method to predict treatment response.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	23-27
33573703-6	2021	CONCLUSIONS: Our findings suggest that the 5hmC modifications in cfDNA at the time before R-CHOP treatment are associated with treatment response and that 5hmC-Seal may potentially serve as a clinical-applicable, minimally invasive approach to predict R-CHOP treatment response for DLBCL patients.	5hmc	43-47	DNA damage inducible transcript 3	Homo sapiens	254-258
33560385-6	2021	Thus, synergy of the SAV combination may involve combined targeting of MCL1 and BCL2 via discrete, tolerable mechanisms, and cellular levels of MCL1 and DDIT3/CHOP may serve as biomarkers for action of artemisinins and SAV.	Artemisinins	202-214	DNA damage inducible transcript 3	Homo sapiens	153-158
33560385-6	2021	Thus, synergy of the SAV combination may involve combined targeting of MCL1 and BCL2 via discrete, tolerable mechanisms, and cellular levels of MCL1 and DDIT3/CHOP may serve as biomarkers for action of artemisinins and SAV.	Artemisinins	202-214	DNA damage inducible transcript 3	Homo sapiens	159-163
33560385-6	2021	Thus, synergy of the SAV combination may involve combined targeting of MCL1 and BCL2 via discrete, tolerable mechanisms, and cellular levels of MCL1 and DDIT3/CHOP may serve as biomarkers for action of artemisinins and SAV.	GW612286X	21-24	DNA damage inducible transcript 3	Homo sapiens	159-163
33728177-5	2021	Rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine sulfate, and prednisone (R-CHOP) with dexamethasone treatment resulted in significant radiographic regression of his intracranial lesions with dramatic symptomatic improvement.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	95-99
33557839-12	2021	Moreover, the protein expression of endoplasmic reticulum stress markers, including IRE1alpha, Bip, p-eIF2alpha, ATF4 and CHOP, were upregulated following treatment with LiCl.	Lithium Chloride	170-174	DNA damage inducible transcript 3	Homo sapiens	122-126
33728177-5	2021	Rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine sulfate, and prednisone (R-CHOP) with dexamethasone treatment resulted in significant radiographic regression of his intracranial lesions with dramatic symptomatic improvement.	Dexamethasone	106-119	DNA damage inducible transcript 3	Homo sapiens	95-99
33557839-13	2021	When CHOP expression was knocked down and cells were treated with LiCl, the protein level of NOXA was partially increased, and Mcl-1 expression was increased, while the cleavage of caspase8, caspase9, caspase3 and PARP that was induced by the LiCl was reduced compared with the vehicle treated group.	Lithium Chloride	66-70	DNA damage inducible transcript 3	Homo sapiens	5-9
33557839-13	2021	When CHOP expression was knocked down and cells were treated with LiCl, the protein level of NOXA was partially increased, and Mcl-1 expression was increased, while the cleavage of caspase8, caspase9, caspase3 and PARP that was induced by the LiCl was reduced compared with the vehicle treated group.	Lithium Chloride	243-247	DNA damage inducible transcript 3	Homo sapiens	5-9
33557839-16	2021	Furthermore, the CHOP/NOXA/Mcl-1 axis contributed to LiCl-induced apoptosis both in vitro and in vivo.	Lithium Chloride	53-57	DNA damage inducible transcript 3	Homo sapiens	17-21
33592897-8	2021	INTERVENTIONS: The patient was first treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	114-118
33562298-6	2021	Our results showed that TUDCA alleviated ER stress in TNC-treated chondrocytes, as demonstrated by reduced CHOP expression; however, it was not effective enough to prevent apoptosis of NHAC-kn cells in either normoxia nor hypoxia.	ursodoxicoltaurine	24-29	DNA damage inducible transcript 3	Homo sapiens	107-111
33592897-8	2021	INTERVENTIONS: The patient was first treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Doxorubicin	72-83	DNA damage inducible transcript 3	Homo sapiens	114-118
33592897-8	2021	INTERVENTIONS: The patient was first treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Prednisone	102-112	DNA damage inducible transcript 3	Homo sapiens	114-118
32747719-0	2021	LW-213 induces cell apoptosis in human cutaneous T-cell lymphomas by activating PERK-eIF2alpha-ATF4-CHOP axis.	CHEMBL4207919	0-6	DNA damage inducible transcript 3	Homo sapiens	100-104
33557248-9	2021	These results demonstrated that HEA treatments effectively protect against DCF- and MXC-induced ER stress damage in human proximal tubular cells through regulation of the GRP78/ATF6/PERK/IRE1alpha/CHOP pathway.	Diclofenac	75-78	DNA damage inducible transcript 3	Homo sapiens	197-201
33557248-9	2021	These results demonstrated that HEA treatments effectively protect against DCF- and MXC-induced ER stress damage in human proximal tubular cells through regulation of the GRP78/ATF6/PERK/IRE1alpha/CHOP pathway.	Meloxicam	84-87	DNA damage inducible transcript 3	Homo sapiens	197-201
33546433-6	2021	Differential array analysis revealed early modulation of stress response gene expression in both A375 melanoma and PANC-1 adenocarcinoma cells elicited by D2O (90%; <=6 h) (upregulated: CDKN1A, DDIT3, EGR1, GADD45A, HMOX1, NFKBIA, or SOD2 (up to 9-fold; p < 0.01)) confirmed by independent RT-qPCR analysis.	Deuterium Oxide	155-158	DNA damage inducible transcript 3	Homo sapiens	194-199
32747719-6	2021	LW-213 selectively activated CHOP and induced apoptosis in Hut-102 cells via activating PERK-eIF2alpha-ATF4 pathway.	CHEMBL4207919	0-6	DNA damage inducible transcript 3	Homo sapiens	29-33
32979141-7	2021	In conclusion, this study found that naringin combined with tunicamycin+BAY 11-7082 efficiently induced apoptotic cell death in HT29 colon cancer cells via oxidative stress and the PERK/eIF2alpha/ATF4/CHOP pathway, suggesting that naringin combined with tunicamycin plus BAY 11-7082 could be a new combination therapy strategy for effective colon cancer treatment with minimal side effects on healthy cells.	3-(4-methylphenylsulfonyl)-2-propenenitrile	72-83	DNA damage inducible transcript 3	Homo sapiens	201-205
33211168-13	2021	Dapagliflozin also significantly reduced ER stress-associated proteins including GRP78, PERK, eIF-2alpha, ATF-4, and CHOP.	dapagliflozin	0-13	DNA damage inducible transcript 3	Homo sapiens	117-121
32979141-0	2021	Naringin Combined with NF-kappaB Inhibition and Endoplasmic Reticulum Stress Induces Apoptotic Cell Death via Oxidative Stress and the PERK/eIF2alpha/ATF4/CHOP Axis in HT29 Colon Cancer Cells.	naringin	0-8	DNA damage inducible transcript 3	Homo sapiens	155-159
32979141-5	2021	Quantitative real-time PCR and western blot analysis demonstrated that drug combination-induced mitochondrial apoptosis was activated through the ROS-mediated PERK/eIF2alpha/ATF4/CHOP pathway.	ros	146-149	DNA damage inducible transcript 3	Homo sapiens	179-183
32979141-7	2021	In conclusion, this study found that naringin combined with tunicamycin+BAY 11-7082 efficiently induced apoptotic cell death in HT29 colon cancer cells via oxidative stress and the PERK/eIF2alpha/ATF4/CHOP pathway, suggesting that naringin combined with tunicamycin plus BAY 11-7082 could be a new combination therapy strategy for effective colon cancer treatment with minimal side effects on healthy cells.	naringin	37-45	DNA damage inducible transcript 3	Homo sapiens	201-205
32979141-7	2021	In conclusion, this study found that naringin combined with tunicamycin+BAY 11-7082 efficiently induced apoptotic cell death in HT29 colon cancer cells via oxidative stress and the PERK/eIF2alpha/ATF4/CHOP pathway, suggesting that naringin combined with tunicamycin plus BAY 11-7082 could be a new combination therapy strategy for effective colon cancer treatment with minimal side effects on healthy cells.	Tunicamycin	60-71	DNA damage inducible transcript 3	Homo sapiens	201-205
33348022-3	2021	This article reviews several chemical compounds that have been shown to regulate DOX-induced inflammation, apoptosis, and autophagy via inhibition of ER stress signaling pathways, such as the IRE1alpha/ASK1/JNK, IRE1alpha/JNK/Beclin-1, and CHOP pathways.	Doxorubicin	81-84	DNA damage inducible transcript 3	Homo sapiens	240-244
33288281-9	2021	TCDD exposure significantly affected gene expression in isolated islets: Glut2, Gck, Bcl-xL, MafA, Pdx1 FoxO1 and IRE1 gene expression was significantly decreased, whereas Puma, DP5, iNOS and Chop gene expression was significantly increased after 6 h exposure to TCDD.	Polychlorinated Dibenzodioxins	0-4	DNA damage inducible transcript 3	Homo sapiens	192-196
32648994-3	2021	Interestingly, fluorizoline treatment triggers the activation of the integrated stress response (ISR) in HeLa and HAP1 cells, with increased eIF2alpha phosphorylation, and induction of ATF3, ATF4 and CHOP.	Fluorizoline	15-27	DNA damage inducible transcript 3	Homo sapiens	200-204
33370716-10	2021	Next, we show that LHBs overexpression in conjunction with APOH leads to ER stress in 293 T cells, as evidenced by production of the binding immunoglobulin protein (BiP) and C/EBP homologous protein (CHOP), as well as increased splicing of X-box binding protein 1 (XBP1).	Luteinizing Hormone, beta Subunit	19-23	DNA damage inducible transcript 3	Homo sapiens	174-198
33370716-10	2021	Next, we show that LHBs overexpression in conjunction with APOH leads to ER stress in 293 T cells, as evidenced by production of the binding immunoglobulin protein (BiP) and C/EBP homologous protein (CHOP), as well as increased splicing of X-box binding protein 1 (XBP1).	Luteinizing Hormone, beta Subunit	19-23	DNA damage inducible transcript 3	Homo sapiens	200-204
33552253-11	2021	The baseline 18F-FDG PET/CT parameters and interim treatment response have important prognostic values in DLBCL patients who received R-CHOP chemotherapy.	Fluorodeoxyglucose F18	13-20	DNA damage inducible transcript 3	Homo sapiens	136-140
33796235-0	2021	Rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in diffuse large B-cell lymphoma.	Prednisone	78-88	DNA damage inducible transcript 3	Homo sapiens	92-96
33393595-0	2021	Omeprazole improves chemosensitivity of gastric cancer cells by m6A demethylase FTO-mediated activation of mTORC1 and DDIT3 upregulation.	Omeprazole	0-10	DNA damage inducible transcript 3	Homo sapiens	118-123
33393595-8	2021	Meanwhile, transcript level of DDIT3, which is an apoptosis-related tumor suppressor gene downstream of mTORC1 was regulated by omeprazole induced FTO silence through an m6A-dependent mechanism.	Omeprazole	128-138	DNA damage inducible transcript 3	Homo sapiens	31-36
33436910-2	2021	This study aimed to compare the area under the plasma concentration-time curves (AUCs) of vincristine (VCR), doxorubicin (DXR), and cyclophosphamide (CPA) between (R-)CHOP and (R-)miniCHOP regimens.	Cyclophosphamide	132-148	DNA damage inducible transcript 3	Homo sapiens	167-171
33436910-5	2021	The median AUCs of DXR and CPA were significantly smaller in the (R-)miniCHOP group than in the (R-)CHOP group (168.7 vs. 257.9 ng h/mL, P = 0.003, and 219.9 vs. 301.7 microg h/mL, P = 0.020, respectively).	Doxorubicin	19-22	DNA damage inducible transcript 3	Homo sapiens	73-77
33436910-5	2021	The median AUCs of DXR and CPA were significantly smaller in the (R-)miniCHOP group than in the (R-)CHOP group (168.7 vs. 257.9 ng h/mL, P = 0.003, and 219.9 vs. 301.7 microg h/mL, P = 0.020, respectively).	Cyclophosphamide	27-30	DNA damage inducible transcript 3	Homo sapiens	73-77
33436910-7	2021	It is possible that the AUCs of VCR, DXR, and CPA in patients aged 80 years and older receiving (R-)miniCHOP therapy may be lower than those in patients 65-79 years old receiving (R-)CHOP therapy.	Cyclophosphamide	46-49	DNA damage inducible transcript 3	Homo sapiens	104-108
33613969-9	2021	The LC3-II/LC3-I ratio was decreased after ERS inhibition with 4-PBA, but GRP78 and CHOP expressions were enhanced after autophagy inhibition with 3-MA.	3-methyladenine	147-151	DNA damage inducible transcript 3	Homo sapiens	84-88
32640963-9	2021	PPG up-regulated the protein levels of BIP, p-eIF2alpha and CHOP as well as IRE1alpha and p-JNK, and down-regulated the protein level of p-ASK1, all of which were reversed by N-acetylsysteine.	periplogenin	0-3	DNA damage inducible transcript 3	Homo sapiens	60-64
32446789-9	2021	Besides, DLBCL patients with higher total or bioavailable 25(OH)D levels were more sensitive to the R-CHOP regimen treatments.	25(oh)d	58-65	DNA damage inducible transcript 3	Homo sapiens	102-106
32640963-10	2021	Importantly, knockdown of CHOP or JNK protein level attenuated the PPG-elicited apoptosis.	periplogenin	67-70	DNA damage inducible transcript 3	Homo sapiens	26-30
32640963-11	2021	CONCLUSION: PPG-induced apoptosis was regulated via ROS-mediated BIP/eIF2alpha/CHOP and BIP/ASK1/JNK signaling pathway in colon cancer cells, providing that PPG as a promising therapeutic agent for the treatment of human colon cancer.	periplogenin	12-15	DNA damage inducible transcript 3	Homo sapiens	79-83
32640963-11	2021	CONCLUSION: PPG-induced apoptosis was regulated via ROS-mediated BIP/eIF2alpha/CHOP and BIP/ASK1/JNK signaling pathway in colon cancer cells, providing that PPG as a promising therapeutic agent for the treatment of human colon cancer.	ros	52-55	DNA damage inducible transcript 3	Homo sapiens	79-83
34033090-5	2021	In this chapter, we describe a quantitative PCR method to detect the upregulation of CHOP and XBP1s mRNA during Tunicamycin-induced UPR.	Tunicamycin	112-123	DNA damage inducible transcript 3	Homo sapiens	85-89
32504504-9	2021	BeWo cells cultured with high glucose and insulin showed decreased SDF2 expression, while high glucose increased CHOP and sXBP1 expression, which was then significantly reverted with insulin treatment.	Glucose	95-102	DNA damage inducible transcript 3	Homo sapiens	113-117
33384022-2	2020	Treatment in the front-line setting is most often cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens, which are effective in B cell lymphomas, but in TCL are associated with a high failure rate and frequent relapses.	Prednisone	98-108	DNA damage inducible transcript 3	Homo sapiens	110-114
33390989-7	2020	Interestingly, melatonin treatment significantly alleviates the high-glucose induced changes in cell growth, apoptosis, and calcium influx by inhibiting the PERK-eIF2alpha-ATF4-CHOP signaling pathway.	Melatonin	15-24	DNA damage inducible transcript 3	Homo sapiens	177-181
33225679-8	2020	Our mechanism of action studies further demonstrate that furosemide reduces LPS-induced upregulation of endoplasmic reticulum (ER) stress marker genes, including Grp78, Atf4, Chop, tXbp1, and sXbp1.	Furosemide	57-67	DNA damage inducible transcript 3	Homo sapiens	175-179
33390989-7	2020	Interestingly, melatonin treatment significantly alleviates the high-glucose induced changes in cell growth, apoptosis, and calcium influx by inhibiting the PERK-eIF2alpha-ATF4-CHOP signaling pathway.	Glucose	69-76	DNA damage inducible transcript 3	Homo sapiens	177-181
33390989-7	2020	Interestingly, melatonin treatment significantly alleviates the high-glucose induced changes in cell growth, apoptosis, and calcium influx by inhibiting the PERK-eIF2alpha-ATF4-CHOP signaling pathway.	Calcium	124-131	DNA damage inducible transcript 3	Homo sapiens	177-181
33327284-5	2020	INTERVENTIONS: The patient received 3 cycles of cyclophosphamide, epirubicin/ vinorelbine, and dexamethasone (CHOP) chemotherapy.	Dexamethasone	95-108	DNA damage inducible transcript 3	Homo sapiens	110-114
33317571-1	2020	As a widely recognized standard regimen, R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is able to cure two-thirds patients with diffuse large B cell lymphoma (DLBCL), and the remaining patients suffer from refractory or relapsed disease due to resistance to R-CHOP and fare poorly.	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	43-47
33317571-1	2020	As a widely recognized standard regimen, R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is able to cure two-thirds patients with diffuse large B cell lymphoma (DLBCL), and the remaining patients suffer from refractory or relapsed disease due to resistance to R-CHOP and fare poorly.	Doxorubicin	82-93	DNA damage inducible transcript 3	Homo sapiens	43-47
33317571-1	2020	As a widely recognized standard regimen, R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is able to cure two-thirds patients with diffuse large B cell lymphoma (DLBCL), and the remaining patients suffer from refractory or relapsed disease due to resistance to R-CHOP and fare poorly.	Vincristine	95-106	DNA damage inducible transcript 3	Homo sapiens	43-47
33317571-1	2020	As a widely recognized standard regimen, R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is able to cure two-thirds patients with diffuse large B cell lymphoma (DLBCL), and the remaining patients suffer from refractory or relapsed disease due to resistance to R-CHOP and fare poorly.	Prednisone	112-122	DNA damage inducible transcript 3	Homo sapiens	43-47
33311453-7	2020	In addition, tazemetostat promotes PUMA induction through the ROS/ER stress/CHOP axis.	tazemetostat	13-25	DNA damage inducible transcript 3	Homo sapiens	76-80
33275671-6	2020	Anthracycline-naive patients have the best outcomes if there is HT, and responses to R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) are similar to those of patients with de novo diffuse large B-cell lymphoma.	Anthracyclines	0-13	DNA damage inducible transcript 3	Homo sapiens	87-91
33302552-0	2020	Saturated Fatty Acids Promote GDF15 Expression in Human Macrophages through the PERK/eIF2/CHOP Signaling Pathway.	Fatty Acids	0-21	DNA damage inducible transcript 3	Homo sapiens	90-94
33323828-1	2020	Although the first-line rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone regimen (R-CHOP) substantially improved outcomes for patients with diffuse large B-cell lymphoma (DLBCL), 40% of the patients suffered from relapsed/refractory disease and had poor survival outcomes.	Doxorubicin	57-68	DNA damage inducible transcript 3	Homo sapiens	109-113
33323828-1	2020	Although the first-line rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone regimen (R-CHOP) substantially improved outcomes for patients with diffuse large B-cell lymphoma (DLBCL), 40% of the patients suffered from relapsed/refractory disease and had poor survival outcomes.	Prednisone	87-97	DNA damage inducible transcript 3	Homo sapiens	109-113
33229544-5	2020	Moreover, ATP13A2 knockdown induced an ATF4-CHOP-dependent stress response following rotenone exposure.	Rotenone	85-93	DNA damage inducible transcript 3	Homo sapiens	44-48
33229544-6	2020	MitoROS and ATF4-CHOP were blocked by MitoTEMPO, a mitochondrial antioxidant, suggesting that the impact of ATP13A2 on MitoROS may relate to the antioxidant properties of spermine.	Spermine	171-179	DNA damage inducible transcript 3	Homo sapiens	17-21
33007289-4	2020	AMC-04 upregulated the expression of activating transcription factor-4 (ATF4)-C/EBP homologous protein (CHOP) and death receptor 5 (DR5) in cancer cells, as revealed by microarray analysis, small-interference RNA assay, and western blotting.	7-amino-4-methylcoumarin	0-3	DNA damage inducible transcript 3	Homo sapiens	104-108
33095117-7	2020	In LOT1, relative to chlorambucil-administered patients, those prescribed fludarabine-based therapies had lower risk of disease progression (hazard ratio [HR] and 95% confidence interval [CI] 0.32 [0.19-0.54]), whereas C/CHOP-prescribed patients had higher risk (HR 95%CI 1.88 [1.17-3.04]).	fludarabine	74-85	DNA damage inducible transcript 3	Homo sapiens	221-225
33468831-8	2020	The patient started an immediate course of combination chemotherapy consisting of rituximab, cyclophosphamide, doxorubicin vincristine and prednisolone(R-CHOP)and no recurrence has been noted for 5 years and 10 months from first visit.	Prednisolone	139-151	DNA damage inducible transcript 3	Homo sapiens	154-158
32726164-8	2020	The treatment of UA232 could lead to an increase of CHOP expression rather than an increase in Bax or caspase-8, indicating that the apoptosis induced by UA232 was correlated with the endoplasmic reticulum stress (ER stress) pathway.	ua232	17-22	DNA damage inducible transcript 3	Homo sapiens	52-56
32200504-3	2020	Therefore, this study investigated the effects and mechanism of STF-083010 (an IRE1alpha inhibitor) on the cell growth/apoptosis of ovarian malignant cells via the XBP1-CHOP-Bim pathway following the induction of ER stress (ERS).	STF 083010	64-74	DNA damage inducible transcript 3	Homo sapiens	169-173
33169630-8	2020	Meanwhile, the expressions of activating transcription factor 6, inositol-requiring protein-1alpha, CCAAT/enhancer binding protein homologous protein, and glucose-regulated protein 78 were dramatically increased after Pb treatment, signifying the initiation of ER stress.	Lead	218-220	DNA damage inducible transcript 3	Homo sapiens	100-149
33269174-3	2020	Recent studies have demonstrated a potential benefit with combination of dose-adjusted rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-REPOCH) in comparison to standard combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in ABC DLBCL patients.	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	296-300
33247195-6	2020	Moreover, KUS121 markedly reduced the numbers of TUNEL-, CHOP-, MMP-13-, and ADAMTS-5-positive chondrocytes in the damaged knees.	4-amino-3-[2-[6-(4-fluoro-2-methylphenyl)-3-pyridinyl]diazenyl]-1-naphthalenesulfonic acid, monosodium salt	10-16	DNA damage inducible transcript 3	Homo sapiens	57-61
33269174-3	2020	Recent studies have demonstrated a potential benefit with combination of dose-adjusted rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-REPOCH) in comparison to standard combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in ABC DLBCL patients.	Cyclophosphamide	134-150	DNA damage inducible transcript 3	Homo sapiens	296-300
33269174-3	2020	Recent studies have demonstrated a potential benefit with combination of dose-adjusted rituximab, etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (DA-REPOCH) in comparison to standard combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in ABC DLBCL patients.	Doxorubicin	156-167	DNA damage inducible transcript 3	Homo sapiens	296-300
33230132-2	2020	The standard treatment is the CHOP chemotherapy protocols that include cyclophosphamide, doxorubicin, vincristine and prednisone, where the majority of dogs achieve complete/partial response; however, it is very important to predict non-responsive cases to improve treatment and to develop new targeted therapies.	Cyclophosphamide	71-87	DNA damage inducible transcript 3	Homo sapiens	30-34
33230132-2	2020	The standard treatment is the CHOP chemotherapy protocols that include cyclophosphamide, doxorubicin, vincristine and prednisone, where the majority of dogs achieve complete/partial response; however, it is very important to predict non-responsive cases to improve treatment and to develop new targeted therapies.	Doxorubicin	89-100	DNA damage inducible transcript 3	Homo sapiens	30-34
33230132-2	2020	The standard treatment is the CHOP chemotherapy protocols that include cyclophosphamide, doxorubicin, vincristine and prednisone, where the majority of dogs achieve complete/partial response; however, it is very important to predict non-responsive cases to improve treatment and to develop new targeted therapies.	Vincristine	102-113	DNA damage inducible transcript 3	Homo sapiens	30-34
33230132-2	2020	The standard treatment is the CHOP chemotherapy protocols that include cyclophosphamide, doxorubicin, vincristine and prednisone, where the majority of dogs achieve complete/partial response; however, it is very important to predict non-responsive cases to improve treatment and to develop new targeted therapies.	Prednisone	118-128	DNA damage inducible transcript 3	Homo sapiens	30-34
32811746-4	2020	Analysis of lipid reactive oxygen species (ROS), Bip, CHOP, p-IRE1alpha, GPX4, SLC7A11, alpha-SMA, and CTGF showed that chrysophanol attenuated HBx-repressed cell death.	chrysophanic acid	120-132	DNA damage inducible transcript 3	Homo sapiens	54-58
33266427-0	2020	Rubi Fructus Water Extract Alleviates LPS-Stimulated Macrophage Activation via an ER Stress-Induced Calcium/CHOP Signaling Pathway.	Water	13-18	DNA damage inducible transcript 3	Homo sapiens	108-112
33266427-8	2020	We concluded that RF demonstrated immunoregulatory activity on LPS-stimulated macrophages via an endoplasmic reticulum (ER) stress-induced calcium/CCAAT-enhancer-binding protein homologous protein (CHOP) pathway and the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway.	Calcium	139-146	DNA damage inducible transcript 3	Homo sapiens	198-202
33218059-9	2020	The combined effect of MEL and ABT-737 (0.2 muM) increased the expression of protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), leading to a decrease in the level of binding immunoglobulin protein (BIP) followed by an increase in the level of C/EBP homologous protein (CHOP).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	31-34	DNA damage inducible transcript 3	Homo sapiens	257-281
33218059-9	2020	The combined effect of MEL and ABT-737 (0.2 muM) increased the expression of protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK), leading to a decrease in the level of binding immunoglobulin protein (BIP) followed by an increase in the level of C/EBP homologous protein (CHOP).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	31-34	DNA damage inducible transcript 3	Homo sapiens	283-287
32885420-8	2020	Indeed, HO-1 induction with cobalt protoporphyrin (CoPP) treatment in arsenical-treated HEK293 cells afforded cytoprotection by attenuating CHOP-associated apoptosis and cytokine mRNA levels.	cobaltiprotoporphyrin	28-49	DNA damage inducible transcript 3	Homo sapiens	140-144
32885420-8	2020	Indeed, HO-1 induction with cobalt protoporphyrin (CoPP) treatment in arsenical-treated HEK293 cells afforded cytoprotection by attenuating CHOP-associated apoptosis and cytokine mRNA levels.	cobaltiprotoporphyrin	51-55	DNA damage inducible transcript 3	Homo sapiens	140-144
32885420-8	2020	Indeed, HO-1 induction with cobalt protoporphyrin (CoPP) treatment in arsenical-treated HEK293 cells afforded cytoprotection by attenuating CHOP-associated apoptosis and cytokine mRNA levels.	Arsenicals	70-79	DNA damage inducible transcript 3	Homo sapiens	140-144
33215449-11	2020	Parecoxib could also suppress CHOP caused by COX-2 upregulation and apoptosis in NP cells.	parecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	30-34
32716561-5	2020	KEY FINDINGS: Epigallocatechin gallate suppressed increases in p-PERK/p-eIF-2alpha/ATF-4/CHOP and p-IRE-1alpha/p-JNK1/2 expression levels in the cells treated with any of the ER stressors, leading to inhibition of apoptosis.	epigallocatechin gallate	14-38	DNA damage inducible transcript 3	Homo sapiens	89-93
32716561-7	2020	The potentiation effect of phyllanthin seen with the three ER stressors was related to suppression of survival p-Nrf-2/HO-1 expression, resulting in increased activation of the eIF-2alpha/ATF-4/CHOP pathway.	phyllanthin	27-38	DNA damage inducible transcript 3	Homo sapiens	194-198
33091357-1	2020	The integration of rituximab (R) into cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) by Coiffier and colleagues was the first, and last, successful modification of this backbone regimen, which has endured now for almost 20 years.	Doxorubicin	56-67	DNA damage inducible transcript 3	Homo sapiens	98-102
32639626-10	2020	Palmitate-induced ER stress led to PPARgamma expression through interactions between CHOP and FoxO6 corresponding to findings in vivo study.	Palmitates	0-9	DNA damage inducible transcript 3	Homo sapiens	85-89
33091357-1	2020	The integration of rituximab (R) into cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) by Coiffier and colleagues was the first, and last, successful modification of this backbone regimen, which has endured now for almost 20 years.	Prednisone	86-96	DNA damage inducible transcript 3	Homo sapiens	98-102
31730796-6	2020	Furthermore, palmitate induced mRNA levels of endoplasmic reticulum (ER) stress markers, including Chop, Grp78 and Bax/Bcl2, as well as C/ebp-beta, whereas SNP induced Bax/Bcl2 and C/ebp-beta.	Palmitates	13-22	DNA damage inducible transcript 3	Homo sapiens	99-103
33143349-6	2020	Moreover, as a consequence of ROS production, TBT-F increased the levels of glucose regulated protein 78 (Grp78) and C/EBP homologous protein (CHOP), two ER stress markers.	tbt-f	46-51	DNA damage inducible transcript 3	Homo sapiens	117-141
32814076-10	2020	Further investigations showed that Ghrelin significantly inhibited the endoplasmic reticulum stress PERK-eIF2alpha-ATF4-CHOP pathway.	Ghrelin	35-42	DNA damage inducible transcript 3	Homo sapiens	120-124
32901341-8	2020	Expression of the endoplasmic reticulum stress (ERS)-related factors activating transcription factor 6 (ATF6) and C/EBP-homologous protein (CHOP) in HepG2 cells increased with increasing ESP concentration and treatment time.	Oxydeprofos	187-190	DNA damage inducible transcript 3	Homo sapiens	114-138
32901341-8	2020	Expression of the endoplasmic reticulum stress (ERS)-related factors activating transcription factor 6 (ATF6) and C/EBP-homologous protein (CHOP) in HepG2 cells increased with increasing ESP concentration and treatment time.	Oxydeprofos	187-190	DNA damage inducible transcript 3	Homo sapiens	140-144
33143349-6	2020	Moreover, as a consequence of ROS production, TBT-F increased the levels of glucose regulated protein 78 (Grp78) and C/EBP homologous protein (CHOP), two ER stress markers.	tbt-f	46-51	DNA damage inducible transcript 3	Homo sapiens	143-147
33085744-8	2020	The levels of caspase-12 and CHOP were increased within 2 days of dihydroartemisinin treatment.	artenimol	66-84	DNA damage inducible transcript 3	Homo sapiens	29-33
32669378-9	2020	Interestingly, Carfilzomib sensitive transcriptomic profile did not show any association with the proteasome activity but strongly correlates with ATF4 and CHOP expression which are key markers of the unfolded protein response and critical to trigger the cell death program.	carfilzomib	15-26	DNA damage inducible transcript 3	Homo sapiens	156-160
32730183-1	2020	PURPOSE: Immunochemotherapy with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become standard of care for patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	66-77	DNA damage inducible transcript 3	Homo sapiens	110-114
33190441-6	2020	ATRA acted on the ERS-related PERK/eif2alpha signaling pathway and continued to increase the ERS of FLT3-ITD cells, resulting in an upregulation of apoptotic gene CHOP expression.	Tretinoin	0-4	DNA damage inducible transcript 3	Homo sapiens	163-167
32798562-10	2020	Capillarisin inhibited bupivacaine-induced oxidative stress, decrease of mitochondrial respiratory chain complex I, II, and III activities and ATP content, and increase of GRP78 and CHOP expression in SH-SY5Y cells.	capillarisin	0-12	DNA damage inducible transcript 3	Homo sapiens	182-186
32798562-10	2020	Capillarisin inhibited bupivacaine-induced oxidative stress, decrease of mitochondrial respiratory chain complex I, II, and III activities and ATP content, and increase of GRP78 and CHOP expression in SH-SY5Y cells.	Bupivacaine	23-34	DNA damage inducible transcript 3	Homo sapiens	182-186
33116611-8	2020	Western blots showed that delicaflavone overcame DDP resistance by increasing the expression of GRP78 and CHOP and the apoptosis-related protein cleaved caspase-3.	delicaflavone	26-39	DNA damage inducible transcript 3	Homo sapiens	106-110
33116611-9	2020	Conclusion: Delicaflavone can reverse DDP resistance in A549/DDP and PC9/DDP cells by inhibiting cell proliferation and migration and enhancing apoptosis and cleaved caspase-3 levels by increasing the expression of CHOP and GRP78 protein via the endoplasmic reticular stress pathway.	delicaflavone	12-25	DNA damage inducible transcript 3	Homo sapiens	215-219
32730183-1	2020	PURPOSE: Immunochemotherapy with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become standard of care for patients with diffuse large B-cell lymphoma (DLBCL).	Prednisone	96-106	DNA damage inducible transcript 3	Homo sapiens	110-114
32871086-6	2020	RESULTS: Melatonin improved the total antioxidant capacity (T-AOC) of the HK-2 cells, as evidenced by the dose-dependent reduction in apoptosis, ROS levels, and protein expression of ATF6, GRP78, DDIT3, p-PERK, p-IRE1, XBP1s, caspase-12, cleaved caspase-3 and cleaved caspase-9.	Melatonin	9-18	DNA damage inducible transcript 3	Homo sapiens	196-201
33116582-14	2020	The expressions of grp78 and chop were decreased after treatment by chaetomugilin J combined with low-dose cisplatin.	Chaetomugilin J	68-83	DNA damage inducible transcript 3	Homo sapiens	29-33
33116582-14	2020	The expressions of grp78 and chop were decreased after treatment by chaetomugilin J combined with low-dose cisplatin.	Cisplatin	107-116	DNA damage inducible transcript 3	Homo sapiens	29-33
33116822-6	2020	Subsequently, the patient was treated by six cycles of CHOP (cyclophosphamide + doxorubicin + vincristine + hydroprednisone) regimens.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	55-59
33116822-6	2020	Subsequently, the patient was treated by six cycles of CHOP (cyclophosphamide + doxorubicin + vincristine + hydroprednisone) regimens.	Doxorubicin	80-91	DNA damage inducible transcript 3	Homo sapiens	55-59
32506763-0	2020	ROS-mediated PERK-eIF2alpha-ATF4 pathway plays an important role in arsenite-induced L-02 cells apoptosis via regulating CHOP-DR5 signaling.	Reactive Oxygen Species	0-3	DNA damage inducible transcript 3	Homo sapiens	121-125
32673756-0	2020	Phosphorylation within the bipartite NLS alters the localization and toxicity of the ER stress response factor DDIT3/CHOP.	bipartite	27-36	DNA damage inducible transcript 3	Homo sapiens	111-116
32673756-0	2020	Phosphorylation within the bipartite NLS alters the localization and toxicity of the ER stress response factor DDIT3/CHOP.	bipartite	27-36	DNA damage inducible transcript 3	Homo sapiens	117-121
32673756-6	2020	And while co-stimulation with the SERCA inhibitor thapsigargin induced injury in cells expressing wild-type CHOP, the S107A point-mutant blocked this response.	Thapsigargin	50-62	DNA damage inducible transcript 3	Homo sapiens	108-112
32506763-0	2020	ROS-mediated PERK-eIF2alpha-ATF4 pathway plays an important role in arsenite-induced L-02 cells apoptosis via regulating CHOP-DR5 signaling.	arsenite	68-76	DNA damage inducible transcript 3	Homo sapiens	121-125
32506763-8	2020	PERK inhibitor and ATF4 siRNA significantly attenuated NaAsO2 -induced CHOP and DR5 expressions.	sodium arsenite	55-61	DNA damage inducible transcript 3	Homo sapiens	71-75
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	Reactive Oxygen Species	42-45	DNA damage inducible transcript 3	Homo sapiens	184-188
32506763-10	2020	Taken together, the results indicate that ROS-mediated PERK-eIF2alpha-ATF4 pathway activated by NaAsO2 is the critical upstream event for subsequent apoptosis induction via regulating CHOP-DR5 signaling in L-02 cells when chronic exposure to arsenic, and support that antioxidants might be potential therapeutic agents for preventing or delaying the onset and progress of arsenic-induced hepatotoxicity.	sodium arsenite	96-102	DNA damage inducible transcript 3	Homo sapiens	184-188
31933404-7	2020	In addition, Ru360 significantly attenuated seizure-induced endoplasmic reticulum (ER) stress, which is characterized by the expression of glucose-regulated protein 78 (GRP78) and C/-EBP homologous protein (CHOP), while spermine had the opposite effect.	Ru 360	13-18	DNA damage inducible transcript 3	Homo sapiens	180-205
32855694-0	2020	Hydrogen peroxide induces nucleus pulposus cell apoptosis by ATF4/CHOP signaling pathway.	Hydrogen Peroxide	0-17	DNA damage inducible transcript 3	Homo sapiens	66-70
32855694-2	2020	The present study explored the activating transcription factor 4 (ATF4)/C/EBP homologous protein (CHOP) signaling pathway in the H2O2-induced nucleus pulposus (NP) cell apoptosis.	Hydrogen Peroxide	129-133	DNA damage inducible transcript 3	Homo sapiens	98-102
32855694-10	2020	H2O2 induced NP cell apoptosis by upregulating expression of ATF4, CHOP and caspase-9.	Hydrogen Peroxide	0-4	DNA damage inducible transcript 3	Homo sapiens	67-71
32855694-13	2020	In this study, we found H2O2 could promote NP cell apoptosis by activating the ATF4/CHOP signaling pathway resulting in the upregulation of caspase-9.	Hydrogen Peroxide	24-28	DNA damage inducible transcript 3	Homo sapiens	84-88
32855694-14	2020	Interdict of ATF4, CHOP, or caspase-9 contributed to the reduction of apoptosis caused by H2O2.	Hydrogen Peroxide	90-94	DNA damage inducible transcript 3	Homo sapiens	19-23
33046822-7	2020	PPZ023 treatment causes cell death via the PERK-eIF2alpha-CHOP axis in both NSCLC cell lysates and exosomes, and PERK and CHOP knockdown significantly blocks ER stress-mediated apoptosis by reducing cleaved caspase-3.	ppz023	0-6	DNA damage inducible transcript 3	Homo sapiens	58-62
31933404-7	2020	In addition, Ru360 significantly attenuated seizure-induced endoplasmic reticulum (ER) stress, which is characterized by the expression of glucose-regulated protein 78 (GRP78) and C/-EBP homologous protein (CHOP), while spermine had the opposite effect.	Ru 360	13-18	DNA damage inducible transcript 3	Homo sapiens	207-211
31933404-8	2020	We also found that pre-treatment with the mitochondria-targeted antioxidant, mitoquinone, decreased GRP78 and CHOP expression.	mitoquinone	77-88	DNA damage inducible transcript 3	Homo sapiens	110-114
32042095-3	2020	In current study, we aimed to explore the association between gene networks and overall survival (OS) of DLBCL patients treated with CHOP-based chemotherapy (cyclophosphamide combination with doxorubicin, vincristine and prednisone).	Cyclophosphamide	158-174	DNA damage inducible transcript 3	Homo sapiens	133-137
32885410-8	2020	Finally, lycopene significantly ameliorated ER stress-induced activation and nuclear translocation of CHOP.	Lycopene	9-17	DNA damage inducible transcript 3	Homo sapiens	102-106
32885410-9	2020	Overexpression of CHOP markedly reversed the antiapoptotic effects of lycopene, indicating that it is essential for the latter"s protective effects.	Lycopene	70-78	DNA damage inducible transcript 3	Homo sapiens	18-22
32885410-10	2020	Taken together, lycopene protects neuroblastoma cells from oxidative stress and ER stress-induced damage by inhibiting the PERK-CHOP signaling pathway, which is a potential therapeutic target in neurodegenerative diseases.	Lycopene	16-24	DNA damage inducible transcript 3	Homo sapiens	128-132
32945482-2	2020	The present study aimed to investigate the protective effects of dexmedetomidine (Dex) on H/R injury and its association with the C/EBP-homologous protein (CHOP) signaling pathway.	Dexmedetomidine	65-80	DNA damage inducible transcript 3	Homo sapiens	156-160
32945482-2	2020	The present study aimed to investigate the protective effects of dexmedetomidine (Dex) on H/R injury and its association with the C/EBP-homologous protein (CHOP) signaling pathway.	Dexmedetomidine	82-85	DNA damage inducible transcript 3	Homo sapiens	156-160
32700751-7	2020	Additionally, AITC prompted induced cytosolic Ca2+ release and Ca2+-dependent ER stress-related signals, such as calpain 1, activating transcription factor 6alpha, glucose-regulated proteins 78 and 94, growth arrest- and DNA damage-inducible protein 153 (GADD153), and caspase-4.	allyl isothiocyanate	14-18	DNA damage inducible transcript 3	Homo sapiens	202-253
32700751-7	2020	Additionally, AITC prompted induced cytosolic Ca2+ release and Ca2+-dependent ER stress-related signals, such as calpain 1, activating transcription factor 6alpha, glucose-regulated proteins 78 and 94, growth arrest- and DNA damage-inducible protein 153 (GADD153), and caspase-4.	allyl isothiocyanate	14-18	DNA damage inducible transcript 3	Homo sapiens	255-262
32623836-6	2020	ABT-737 combined with a low dose of cyclophosphamide, a major component of the conventional CHOP chemotherapy regimen for BL patients, reduced tumor growth during treatment but failed to improve the overall survival of BL xenograft mice.	ABT-737	0-7	DNA damage inducible transcript 3	Homo sapiens	92-96
32623836-6	2020	ABT-737 combined with a low dose of cyclophosphamide, a major component of the conventional CHOP chemotherapy regimen for BL patients, reduced tumor growth during treatment but failed to improve the overall survival of BL xenograft mice.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	92-96
32990902-0	2020	VD3 and LXR agonist (T0901317) combination demonstrated greater potency in inhibiting cholesterol accumulation and inducing apoptosis via ABCA1-CHOP-BCL-2 cascade in MCF-7 breast cancer cells.	T0901317	21-29	DNA damage inducible transcript 3	Homo sapiens	144-148
32990902-7	2020	Importantly, VD3 + T0901317 combination showed higher effects in increasing apoptosis as measured by annexin apoptosis assay, cell viability and was associated with induction of CHOP protein and gene expression.	T0901317	19-27	DNA damage inducible transcript 3	Homo sapiens	178-182
32700751-8	2020	The level of reactive oxygen species (ROS) production was found to induce the hallmark of ER stress GADD153, proapoptotic marker caspase-3, and calpain activity after AITC treatment.	Reactive Oxygen Species	13-36	DNA damage inducible transcript 3	Homo sapiens	100-107
32700751-8	2020	The level of reactive oxygen species (ROS) production was found to induce the hallmark of ER stress GADD153, proapoptotic marker caspase-3, and calpain activity after AITC treatment.	Reactive Oxygen Species	38-41	DNA damage inducible transcript 3	Homo sapiens	100-107
32700751-8	2020	The level of reactive oxygen species (ROS) production was found to induce the hallmark of ER stress GADD153, proapoptotic marker caspase-3, and calpain activity after AITC treatment.	allyl isothiocyanate	167-171	DNA damage inducible transcript 3	Homo sapiens	100-107
32042095-3	2020	In current study, we aimed to explore the association between gene networks and overall survival (OS) of DLBCL patients treated with CHOP-based chemotherapy (cyclophosphamide combination with doxorubicin, vincristine and prednisone).	Doxorubicin	192-203	DNA damage inducible transcript 3	Homo sapiens	133-137
32042095-3	2020	In current study, we aimed to explore the association between gene networks and overall survival (OS) of DLBCL patients treated with CHOP-based chemotherapy (cyclophosphamide combination with doxorubicin, vincristine and prednisone).	Prednisone	221-231	DNA damage inducible transcript 3	Homo sapiens	133-137
32998376-8	2020	Moreover, 6-Shogaol also upregulated the expression and phosphorylation of GRP-78, eIF-2alpha, ATF4, and CHOP, known ER stress markers, in SW872 cells, illustrating the induction of ER stress.	shogaol	10-19	DNA damage inducible transcript 3	Homo sapiens	105-109
32915975-2	2020	Exposure to R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) is likely to increase the risk of fracture, but evidence is lacking to define fracture incidence in this group.	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	14-18
33061438-15	2020	Molecular mechanism analysis indicated that inhibition of P4HB by BAC treatment enhanced the anticancer effects of GEM through increasing cellular ROS content and promoting cell apoptosis and PERK/eIF2alpha/ATF4/CHOP signaling.	gemcitabine	115-118	DNA damage inducible transcript 3	Homo sapiens	212-216
32915975-2	2020	Exposure to R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) is likely to increase the risk of fracture, but evidence is lacking to define fracture incidence in this group.	Doxorubicin	49-60	DNA damage inducible transcript 3	Homo sapiens	14-18
32994268-5	2020	PBL is an extremely aggressive lymphoma and is usually treated using a CHOP-like regimen (cyclophosphamide, doxorubicin, vincristine and prednisone/dexamethasone), but with poor outcome.	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	71-75
32915975-2	2020	Exposure to R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) is likely to increase the risk of fracture, but evidence is lacking to define fracture incidence in this group.	Vincristine	62-73	DNA damage inducible transcript 3	Homo sapiens	14-18
32915975-2	2020	Exposure to R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) is likely to increase the risk of fracture, but evidence is lacking to define fracture incidence in this group.	Prednisolone	79-91	DNA damage inducible transcript 3	Homo sapiens	14-18
32967221-7	2020	Furthermore, TUDCA suppressed thapsigargin-induced ER stress in RPE cells, as demonstrated by decreased the expression of CCAAT-enhancer-binding protein homologous protein (CHOP) and apoptosis.	ursodoxicoltaurine	13-18	DNA damage inducible transcript 3	Homo sapiens	122-171
32967221-7	2020	Furthermore, TUDCA suppressed thapsigargin-induced ER stress in RPE cells, as demonstrated by decreased the expression of CCAAT-enhancer-binding protein homologous protein (CHOP) and apoptosis.	ursodoxicoltaurine	13-18	DNA damage inducible transcript 3	Homo sapiens	173-177
32967221-7	2020	Furthermore, TUDCA suppressed thapsigargin-induced ER stress in RPE cells, as demonstrated by decreased the expression of CCAAT-enhancer-binding protein homologous protein (CHOP) and apoptosis.	Thapsigargin	30-42	DNA damage inducible transcript 3	Homo sapiens	122-171
32967221-7	2020	Furthermore, TUDCA suppressed thapsigargin-induced ER stress in RPE cells, as demonstrated by decreased the expression of CCAAT-enhancer-binding protein homologous protein (CHOP) and apoptosis.	Thapsigargin	30-42	DNA damage inducible transcript 3	Homo sapiens	173-177
32723872-11	2020	In summary, CHOP and c-JUN up-regulate SERPINA1 transcription and play an important role in hepatic disease by increasing the burden of proteotoxic ATZ, particularly in the pediatric population.	Atazanavir Sulfate	148-151	DNA damage inducible transcript 3	Homo sapiens	12-16
33042407-9	2020	Intriguingly, Chlorin A-PDT promoted autophagy via activation of ROS-induced ERS-related PERK/p-eif2alpha/CHOP axis, and blocked the ensuing autophagy flux by lysosomal damage.	Reactive Oxygen Species	65-68	DNA damage inducible transcript 3	Homo sapiens	106-110
32953569-7	2020	Western blot and qRT-PCR revealed that levels of CHOP and BIP were elevated in a concentration-dependent pattern after the cells were incubated with ATRA (2.5-20 micromol/L).	Tretinoin	149-153	DNA damage inducible transcript 3	Homo sapiens	49-53
32953569-8	2020	The upregulation of VEGF-A and CHOP induced by ATRA could be inhibited by NAC (antioxidant) and Salubrinal (ERS inhibitor) in vitro.	Tretinoin	47-51	DNA damage inducible transcript 3	Homo sapiens	31-35
32953569-8	2020	The upregulation of VEGF-A and CHOP induced by ATRA could be inhibited by NAC (antioxidant) and Salubrinal (ERS inhibitor) in vitro.	Acetylcysteine	74-77	DNA damage inducible transcript 3	Homo sapiens	31-35
32953569-8	2020	The upregulation of VEGF-A and CHOP induced by ATRA could be inhibited by NAC (antioxidant) and Salubrinal (ERS inhibitor) in vitro.	salubrinal	96-106	DNA damage inducible transcript 3	Homo sapiens	31-35
33014875-9	2020	Mechanism studies demonstrated that VP activated ER stress by upregulating the expression of GRP78, CHOP, and Caspase-12, and VP-induced apoptosis can be alleviated when ER stress pathway was inhibited.	Verteporfin	36-38	DNA damage inducible transcript 3	Homo sapiens	100-104
32982432-13	2020	Subsequently, Western blotting analysis demonstrated that endoplasmic reticulum (ER) stress-related proteins (GRP78, phosphorylated-PERK, phosphorylated-eIF2alpha and CHOP) were up-regulated in Hep-2 and TU212 cells exposed to oridonin.	oridonin	227-235	DNA damage inducible transcript 3	Homo sapiens	167-171
32982432-14	2020	In addition, 4-PBA (an ER stress inhibitor) or knockdown of CHOP could antagonize oridonin-induced apoptosis.	oridonin	82-90	DNA damage inducible transcript 3	Homo sapiens	60-64
32658627-2	2020	The preferred treatment is abbreviated rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) and radiation therapy.	Prednisone	98-108	DNA damage inducible transcript 3	Homo sapiens	112-116
32529585-0	2020	Impact of prednisolone dosage in the CHOP regimen for follicular lymphoma: a retrospective study.	Prednisolone	10-22	DNA damage inducible transcript 3	Homo sapiens	37-41
32529585-1	2020	Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) is one of the standard regimens for indolent B-cell non-Hodgkin"s lymphoma (NHL).	Prednisolone	63-75	DNA damage inducible transcript 3	Homo sapiens	79-83
32705218-5	2020	CCB dose-dependently enhanced LC3-II and reduced p62 levels through AMPK activation and inhibition of the Akt/mTOR pathway and upregulated expression of ATF4/CHOP, leading to activation of endoplasmic reticulum (ER) stress-dependent autophagy.	Celecoxib	0-3	DNA damage inducible transcript 3	Homo sapiens	158-162
32923089-13	2020	CONCLUSION: M2 TAM could have a prognostic role for IPI >= 2 DLBCL patients receiving R-CHOP, which thus warrants further investigation.	tam	15-18	DNA damage inducible transcript 3	Homo sapiens	88-92
32736984-7	2020	CCAAT/enhancer-binding protein homologous protein (CHOP), an ER stress marker, was demonstrated to participate in PA-induced cytotoxicity.	Palmitic Acid	114-116	DNA damage inducible transcript 3	Homo sapiens	0-49
32736984-7	2020	CCAAT/enhancer-binding protein homologous protein (CHOP), an ER stress marker, was demonstrated to participate in PA-induced cytotoxicity.	Palmitic Acid	114-116	DNA damage inducible transcript 3	Homo sapiens	51-55
32717251-9	2020	However, inhibition of the ER stress response by pretreatment with 4-PBA included apparently and dose-dependently reduced levels of p-PERK, p-IRE1, CHOP, cleaved ATF6, p-ASK1, p-JNK, cleaved caspase-3, procaspase-12, and MMP depolarization in AgNP-treated ARPE-19 cells; it also led to significantly increased Mcl-1 protein levels in a dose-dependent manner in ARPE-19 cells.	4-phenylbutylamine	67-72	DNA damage inducible transcript 3	Homo sapiens	148-152
32878253-7	2020	These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions.	Reactive Oxygen Species	6-9	DNA damage inducible transcript 3	Homo sapiens	145-194
32878253-7	2020	These ROS-mediated responses induce caspase-dependent apoptosis via the activation of B-cell lymphoma 2 (Bcl2), Bcl2-associated X protein (Bax), CCAAT/enhancer-binding protein homologous protein (chop), and phosphoprotein p53 gene expressions.	Reactive Oxygen Species	6-9	DNA damage inducible transcript 3	Homo sapiens	196-200
32590070-11	2020	Scoulerine activated ER stress, as evidenced by the increased GRP78 and CHOP expression in CRC cells.	discretamine	0-10	DNA damage inducible transcript 3	Homo sapiens	72-76
32506039-6	2020	In human epidermal reconstructs a topical use-relevant DHA-dose regimen elicited a comparable stress response as revealed by gene expression array (HSPA1A, HSPA6, HSPD1, IL6, DDIT3, EGR1) and immunohistochemical analysis (CEL, HO-1, p-Hsp27-S78).	Dihydroxyacetone	55-58	DNA damage inducible transcript 3	Homo sapiens	175-180
32842538-9	2020	In addition, lack of the N-glycan on prM induced nuclear translocation of CCAAT-enhancer-binding protein homologous protein (CHOP), an ER stress marker.	n-glycan	25-33	DNA damage inducible transcript 3	Homo sapiens	74-123
32847118-6	2020	Biopsy revealed primary cutaneous PTCL-NOS, treated successfully with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus etoposide combination chemotherapy.	Prednisone	118-128	DNA damage inducible transcript 3	Homo sapiens	130-134
32842538-9	2020	In addition, lack of the N-glycan on prM induced nuclear translocation of CCAAT-enhancer-binding protein homologous protein (CHOP), an ER stress marker.	n-glycan	25-33	DNA damage inducible transcript 3	Homo sapiens	125-129
32871991-0	2020	Can early switch to rituximab-bendamustine in a patient with follicular non-Hodgkin lymphoma progressing during R-CHOP be considered frontline treatment?	Bendamustine Hydrochloride	30-42	DNA damage inducible transcript 3	Homo sapiens	114-118
32360360-6	2020	Our data demonstrated an increase in pERK, Bip/Grp78, IRE1alpha, Calnexin and CHOP/GADD153 within 6-24 hrs of PG545 treatment in EC cells.	PG 545	110-115	DNA damage inducible transcript 3	Homo sapiens	78-82
33093947-0	2020	ACCEPT - combining acalabrutinib with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) for Diffuse Large B-cell Lymphoma (DLBCL): study protocol for a Phase Ib/II open-label non-randomised clinical trial.	acalabrutinib	19-32	DNA damage inducible transcript 3	Homo sapiens	112-116
33093947-0	2020	ACCEPT - combining acalabrutinib with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) for Diffuse Large B-cell Lymphoma (DLBCL): study protocol for a Phase Ib/II open-label non-randomised clinical trial.	Prednisolone	96-108	DNA damage inducible transcript 3	Homo sapiens	112-116
33093947-3	2020	R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) is accepted as the international standard first-line regimen, but improvement in first line treatment is needed.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	2-6
33093947-3	2020	R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) is accepted as the international standard first-line regimen, but improvement in first line treatment is needed.	Doxorubicin	37-48	DNA damage inducible transcript 3	Homo sapiens	2-6
33093947-3	2020	R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) is accepted as the international standard first-line regimen, but improvement in first line treatment is needed.	Vincristine	50-61	DNA damage inducible transcript 3	Homo sapiens	2-6
33093947-3	2020	R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) is accepted as the international standard first-line regimen, but improvement in first line treatment is needed.	Prednisolone	63-75	DNA damage inducible transcript 3	Homo sapiens	2-6
32766857-1	2020	Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard treatment of diffuse large B-cell lymphoma (DLBCL).	Prednisone	59-69	DNA damage inducible transcript 3	Homo sapiens	73-77
32766857-4	2020	Herein, we report activity and safety of R-CHOP preceded by NGR-hTNF in patients with PCNSL relapsed/refractory to high-dose methotrexate-based chemotherapy enrolled in a phase 2 trial.	Methotrexate	125-137	DNA damage inducible transcript 3	Homo sapiens	43-47
32784851-5	2020	Nanosome honokiol also mitigated endoplasmic reticulum stress through down regulation of Bip-ATF4-CHOP signaling pathway.	honokiol	9-17	DNA damage inducible transcript 3	Homo sapiens	98-102
32577843-4	2020	Systemic high-dose methotrexate in combination with R-CHOP has been suggested as a potential prophylactic method, since methotrexate penetrates the blood-brain barrier and achieves high concentration in the CNS.	Methotrexate	120-132	DNA damage inducible transcript 3	Homo sapiens	54-58
32360360-6	2020	Our data demonstrated an increase in pERK, Bip/Grp78, IRE1alpha, Calnexin and CHOP/GADD153 within 6-24 hrs of PG545 treatment in EC cells.	PG 545	110-115	DNA damage inducible transcript 3	Homo sapiens	83-90
32798401-9	2020	CCK-8 showed that the proliferation activity of U266 cells could be inhibited by aspirin, which showed a time-and dose-dependent manner; at the same time, the expression level of Blimp1 in U266 cells were decreased with the increasing of aspirin concentration, while the expression level of ATF4 and CHOP was increased with the increasing of aspirin concentration.	Aspirin	81-88	DNA damage inducible transcript 3	Homo sapiens	300-304
32150297-0	2020	Bortezomib maintenance after R-CHOP, cytarabine and autologous stem cell transplantation in newly diagnosed patients with mantle cell lymphoma, results of a randomised phase II HOVON trial.	Bortezomib	0-10	DNA damage inducible transcript 3	Homo sapiens	31-35
32467994-7	2020	The results showed that HG treatment induced ER stress in ARPE-19 human adult retinal pigment epithelial cells by upregulating the expression levels of phosphorylated (p)-protein kinase R-like ER kinase, p-eukaryotic initiation factor 2alpha, activating transcription factor 4 and CCAAT/enhancer-binding protein homologous protein.	Mercury	24-26	DNA damage inducible transcript 3	Homo sapiens	281-330
32798401-10	2020	CONCLUSIONS: Blimp1 may display the anti-apoptosis of myeloma cells through interfering with ATF4/CHOP signaling pathway; low dose of aspirin may play anti-myeloma effect by inhibiting the expression of Blimp1 in myeloma cells.	Aspirin	134-141	DNA damage inducible transcript 3	Homo sapiens	98-102
32751169-4	2020	The gefitinib-resistant subline HCC827GR possesses lowered proapoptotic CHOP (CCAAT/enhancer-binding protein homologous protein) and elevated cytoprotective GRP78 (glucose regulated protein of a 78 kDa molecular weight) endoplasmic reticulum (ER) stress response elements, and it has elevated beta-catenin and cyclooxygenase-2 (COX-2) levels.	Gefitinib	4-13	DNA damage inducible transcript 3	Homo sapiens	72-76
32751169-4	2020	The gefitinib-resistant subline HCC827GR possesses lowered proapoptotic CHOP (CCAAT/enhancer-binding protein homologous protein) and elevated cytoprotective GRP78 (glucose regulated protein of a 78 kDa molecular weight) endoplasmic reticulum (ER) stress response elements, and it has elevated beta-catenin and cyclooxygenase-2 (COX-2) levels.	Gefitinib	4-13	DNA damage inducible transcript 3	Homo sapiens	78-127
32722779-2	2020	Conventional chemotherapies such cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) and hyperfractionated cyclophosphamide, vincristine, doxorubicin, dexamethasone alternating with high-dose cytarabine and methotrexate (CVAD) have been commonly used for the BPDCN treatment until a recent study showed promising outcomes in patients treated with SL-401 (Tagraxofusp).	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
32722598-7	2020	Treatment of cancer cell lines with the antioxidant N-acetylcysteine reduces the extent of membrane dysfunction and the expression of both CHOP-DR5 and miR-425-PTEN axes, attenuating PAM/TRAIL-induced cancer cell apoptosis.	Acetylcysteine	52-68	DNA damage inducible transcript 3	Homo sapiens	139-143
32774144-8	2020	Moreover, high T3 levels upregulate the ERS-related proteins PERK, IRE1, ATF6, and GRP78, as well as ERS-related apoptosis CHOP and caspase-12.	Triiodothyronine	15-17	DNA damage inducible transcript 3	Homo sapiens	123-127
32407927-5	2020	In hepatocyte-derived cells and primary hepatocytes, luteolin significantly decreased Tm- or thapsigargin-mediated C/EBP homologous protein (CHOP) expression.	Tunicamycin	86-88	DNA damage inducible transcript 3	Homo sapiens	115-139
32376267-10	2020	Through hemin administration, hepatocyte apoptosis was suppressed companied down-regulation of CHOP, caspase12 and up-regulation of BCL2.	Hemin	8-13	DNA damage inducible transcript 3	Homo sapiens	95-99
32407927-5	2020	In hepatocyte-derived cells and primary hepatocytes, luteolin significantly decreased Tm- or thapsigargin-mediated C/EBP homologous protein (CHOP) expression.	Tunicamycin	86-88	DNA damage inducible transcript 3	Homo sapiens	141-145
32407927-5	2020	In hepatocyte-derived cells and primary hepatocytes, luteolin significantly decreased Tm- or thapsigargin-mediated C/EBP homologous protein (CHOP) expression.	Thapsigargin	93-105	DNA damage inducible transcript 3	Homo sapiens	115-139
32407927-5	2020	In hepatocyte-derived cells and primary hepatocytes, luteolin significantly decreased Tm- or thapsigargin-mediated C/EBP homologous protein (CHOP) expression.	Thapsigargin	93-105	DNA damage inducible transcript 3	Homo sapiens	141-145
32651429-2	2020	Canine diffuse large B cell lymphoma shows a relatively good response to treatment with multi-agent cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy; however, the 2-year survival rate is as low as 20%.	Prednisone	148-158	DNA damage inducible transcript 3	Homo sapiens	160-164
32417940-2	2020	Progression or relapse of FL within 2 years (so-called POD24) after diagnosis is associated with a poor outcome for patients treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, prednisone) in clinical trials.	Cyclophosphamide	161-177	DNA damage inducible transcript 3	Homo sapiens	140-144
32439176-8	2020	Moreover, it was found salidroside induced ER stress and increased expression of p-PERK, eIF2a, p-eIF2a, ATF-6 and CHOP in HepG2 cells.	rhodioloside	23-34	DNA damage inducible transcript 3	Homo sapiens	115-119
32439176-9	2020	Interestingly, knockdown of CHOP impaired salidroside induced inhibitory effects on HepG2 cells, suggesting the important role of ER stress in cytotoxic effect of salidroside.	rhodioloside	42-53	DNA damage inducible transcript 3	Homo sapiens	28-32
32439176-9	2020	Interestingly, knockdown of CHOP impaired salidroside induced inhibitory effects on HepG2 cells, suggesting the important role of ER stress in cytotoxic effect of salidroside.	rhodioloside	163-174	DNA damage inducible transcript 3	Homo sapiens	28-32
32650488-5	2020	CuSO4 exposure up-regulated the activities and mRNA expression of caspases-9 and -3 as well as the expression of glucose-regulated protein 78 (GRP78), GRP94, DNA damage-inducible gene 153 (GADD153/CHOP), caspase-12 mRNAs in the kidney tissues.	Copper Sulfate	0-5	DNA damage inducible transcript 3	Homo sapiens	189-196
32650488-5	2020	CuSO4 exposure up-regulated the activities and mRNA expression of caspases-9 and -3 as well as the expression of glucose-regulated protein 78 (GRP78), GRP94, DNA damage-inducible gene 153 (GADD153/CHOP), caspase-12 mRNAs in the kidney tissues.	Copper Sulfate	0-5	DNA damage inducible transcript 3	Homo sapiens	197-201
32648457-1	2020	BACKGROUND: The CHOP regimen comprising cyclophosphamide, doxorubicin, vincristine, and prednisone is a basic chemotherapeutic regimen for diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	16-20
32648457-1	2020	BACKGROUND: The CHOP regimen comprising cyclophosphamide, doxorubicin, vincristine, and prednisone is a basic chemotherapeutic regimen for diffuse large B cell lymphoma (DLBCL).	Doxorubicin	58-69	DNA damage inducible transcript 3	Homo sapiens	16-20
32648457-1	2020	BACKGROUND: The CHOP regimen comprising cyclophosphamide, doxorubicin, vincristine, and prednisone is a basic chemotherapeutic regimen for diffuse large B cell lymphoma (DLBCL).	Vincristine	71-82	DNA damage inducible transcript 3	Homo sapiens	16-20
32648457-1	2020	BACKGROUND: The CHOP regimen comprising cyclophosphamide, doxorubicin, vincristine, and prednisone is a basic chemotherapeutic regimen for diffuse large B cell lymphoma (DLBCL).	Prednisone	88-98	DNA damage inducible transcript 3	Homo sapiens	16-20
32417940-2	2020	Progression or relapse of FL within 2 years (so-called POD24) after diagnosis is associated with a poor outcome for patients treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, prednisone) in clinical trials.	Doxorubicin	179-190	DNA damage inducible transcript 3	Homo sapiens	140-144
32417940-2	2020	Progression or relapse of FL within 2 years (so-called POD24) after diagnosis is associated with a poor outcome for patients treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, prednisone) in clinical trials.	Vincristine	192-203	DNA damage inducible transcript 3	Homo sapiens	140-144
32417940-2	2020	Progression or relapse of FL within 2 years (so-called POD24) after diagnosis is associated with a poor outcome for patients treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, prednisone) in clinical trials.	Prednisone	205-215	DNA damage inducible transcript 3	Homo sapiens	140-144
32604833-0	2020	TRPV1 Antagonist DWP05195 Induces ER Stress-Dependent Apoptosis through the ROS-p38-CHOP Pathway in Human Ovarian Cancer Cells.	dwp05195	17-25	DNA damage inducible transcript 3	Homo sapiens	84-88
32441887-0	2020	Lestaurtinib potentiates TRAIL-induced apoptosis in glioma via CHOP-dependent DR5 induction.	lestaurtinib	0-12	DNA damage inducible transcript 3	Homo sapiens	63-67
32441887-5	2020	While U87 and U251 cells showed resistance to TRAIL single treatment, they were sensitized to apoptosis induced by TRAIL in the presence of lestaurtinib because of increased death receptor 5 (DR5) levels through CHOP-dependent manner.	lestaurtinib	140-152	DNA damage inducible transcript 3	Homo sapiens	212-216
32643971-3	2020	For elderly patients, the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) regimen is well tolerated, but it is an insufficient induction therapy for this group.	Prednisolone	85-97	DNA damage inducible transcript 3	Homo sapiens	101-105
32604833-6	2020	Sodium phenylbutyrate (4-PBA), an ER-stress inhibitor, and CHOP knockdown significantly suppressed DWP5195-induced cell death.	dwp5195	99-106	DNA damage inducible transcript 3	Homo sapiens	59-63
32604833-9	2020	Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation.	Acetylcysteine	35-54	DNA damage inducible transcript 3	Homo sapiens	103-107
32604833-9	2020	Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation.	Acetylcysteine	56-59	DNA damage inducible transcript 3	Homo sapiens	103-107
31686395-7	2020	While inorganic arsenic may induce various glucose-related proteins, i.e., GRP78, GRP94 and CHOP, XBP1, and calpains, cadmium upregulates GRP78.	Arsenic	16-23	DNA damage inducible transcript 3	Homo sapiens	92-96
31686395-11	2020	Nickel, a carcinogenic element upregulates the expression of Bak, cytochrome C, caspase-3, caspase-9, caspase-12, and GADD 153.	Nickel	0-6	DNA damage inducible transcript 3	Homo sapiens	118-126
32515472-7	2020	Moreover, high glucose increased mRNA and protein expression of CHOP, ATF-6 and GRP78.	Glucose	15-22	DNA damage inducible transcript 3	Homo sapiens	64-68
32604833-0	2020	TRPV1 Antagonist DWP05195 Induces ER Stress-Dependent Apoptosis through the ROS-p38-CHOP Pathway in Human Ovarian Cancer Cells.	Reactive Oxygen Species	76-79	DNA damage inducible transcript 3	Homo sapiens	84-88
32604833-9	2020	Pre-treatment with the antioxidant N-acetyl-L-cysteine (NAC) significantly suppressed DWP05195-induced CHOP expression and p38 activation.	dwp05195	86-94	DNA damage inducible transcript 3	Homo sapiens	103-107
32604833-11	2020	Taken together, the findings indicate that DWP05195 induces ER stress-induced apoptosis via the ROS-p38-CHOP pathway in human ovarian cancer cells.	dwp05195	43-51	DNA damage inducible transcript 3	Homo sapiens	104-108
32608212-7	2020	In addition, H2O2 and TM could increase the levels of PGE2, GRP78, CHOP, caspase-12, and reactive oxygen species (ROS), resulting in the degeneration of CHs.	Hydrogen Peroxide	13-17	DNA damage inducible transcript 3	Homo sapiens	67-71
32608212-7	2020	In addition, H2O2 and TM could increase the levels of PGE2, GRP78, CHOP, caspase-12, and reactive oxygen species (ROS), resulting in the degeneration of CHs.	Tunicamycin	22-24	DNA damage inducible transcript 3	Homo sapiens	67-71
32505213-1	2020	BACKGROUND: Rituximab (R) plus cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) is the current standard therapy for diffuse large B cell lymphoma (DLBCL).	Doxorubicin	49-60	DNA damage inducible transcript 3	Homo sapiens	91-95
32500753-7	2021	Polatuzumab vedotin is currently being studied in a randomized trial in the front line setting in combination with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	vedotin	12-19	DNA damage inducible transcript 3	Homo sapiens	188-192
32555254-10	2020	SiO2NPs could induce the endoplasmic reticulum (ER) stress-related signals, including the increase in CHOP, XBP-1, and phospho-eIF2alpha protein expressions, and the decrease in pro-caspase-12 protein expression.	sio2nps	0-7	DNA damage inducible transcript 3	Homo sapiens	102-106
32655816-0	2020	Endoplasmic reticulum stress triggers delanzomib-induced apoptosis in HCC cells through the PERK/eIF2alpha/ATF4/CHOP pathway.	delanzomib	38-48	DNA damage inducible transcript 3	Homo sapiens	112-116
32655816-5	2020	In addition, delanzomib induced endoplasmic reticulum stress (ERS) in HCC cells by activating the PERK and ERS-associated proteins including p-eIF2alpha, ATF4 and CHOP.	delanzomib	13-23	DNA damage inducible transcript 3	Homo sapiens	163-167
32655816-9	2020	In conclusion, delanzomib could exhibit good pre-clinical antitumor effects against HCC cells by inducing ERS and activating the PERK/eIF2alpha/ATF4/CHOP pathway, as potential drug candidate on treatment of advanced HCC patients.	delanzomib	15-25	DNA damage inducible transcript 3	Homo sapiens	149-153
32521713-5	2020	Moreover, the LEP-treated groups showed suppression of ER stress-regulating factors, such as the C/EBP homologous protein (CHOP), eukaryotic translation initiation factor 2alpha (eIF2alpha), inositol-requiring protein 1 (IRE1)alpha, and Jun-N-terminal kinase (JNK) during anti-hepatic steatosis effects.	lep	14-17	DNA damage inducible transcript 3	Homo sapiens	97-121
32521713-5	2020	Moreover, the LEP-treated groups showed suppression of ER stress-regulating factors, such as the C/EBP homologous protein (CHOP), eukaryotic translation initiation factor 2alpha (eIF2alpha), inositol-requiring protein 1 (IRE1)alpha, and Jun-N-terminal kinase (JNK) during anti-hepatic steatosis effects.	lep	14-17	DNA damage inducible transcript 3	Homo sapiens	123-127
32505213-1	2020	BACKGROUND: Rituximab (R) plus cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) is the current standard therapy for diffuse large B cell lymphoma (DLBCL).	Prednisone	79-89	DNA damage inducible transcript 3	Homo sapiens	91-95
32581844-8	2020	EPA, DPA, and DHA co-treatment maintained cell viability, prevented PAL-induced apoptosis and attenuated PAL-induced increases in BiP, whereas only DPA prevented increases in CHOP.	Eicosapentaenoic Acid	0-3	DNA damage inducible transcript 3	Homo sapiens	175-179
32581844-8	2020	EPA, DPA, and DHA co-treatment maintained cell viability, prevented PAL-induced apoptosis and attenuated PAL-induced increases in BiP, whereas only DPA prevented increases in CHOP.	Docosahexaenoic Acids	14-17	DNA damage inducible transcript 3	Homo sapiens	175-179
32581844-8	2020	EPA, DPA, and DHA co-treatment maintained cell viability, prevented PAL-induced apoptosis and attenuated PAL-induced increases in BiP, whereas only DPA prevented increases in CHOP.	docosapentaenoic acid	148-151	DNA damage inducible transcript 3	Homo sapiens	175-179
32145589-5	2020	Protein of ER stress-mediated apoptosis, CHOP, was overexpressed in the cisplatin group.	Cisplatin	72-81	DNA damage inducible transcript 3	Homo sapiens	41-45
32066885-5	2020	Furthermore, exposure to low and median doses of CMR induced paraptosis but not apoptosis, which was presented as the formation of extensive cytoplasmic vacuolation with increased expression of endoplasmic reticulum stress markers, Bip and Chop, as well as activation of MAPK pathway in the lung cancer cells.	chalcomoracin	49-52	DNA damage inducible transcript 3	Homo sapiens	240-244
32416730-8	2020	PCDC4, CHOP and FBXO32) were induced by Pao extract in both two cell lines.	pao extract	40-51	DNA damage inducible transcript 3	Homo sapiens	7-11
32400851-0	2020	Homocysteine induces melanocytes apoptosis via PERK-eIF2alpha-CHOP pathway in vitiligo.	Homocysteine	0-12	DNA damage inducible transcript 3	Homo sapiens	62-66
32400851-6	2020	Notably, Hcy induced cell apoptosis in melanocytes via activating reactive oxygen species (ROS) and endoplasmic reticulum (ER) stress protein kinase RNA-like ER kinase (PERK)-eukaryotic translation initiation factor 2alpha (eIF2alpha)-C/EBP homologous protein (CHOP) pathway.	Homocysteine	9-12	DNA damage inducible transcript 3	Homo sapiens	261-265
32397857-4	2021	Using a wide range of biochemical and lipidomic analyses, we demonstrated that ABTL0812 increases cellular long-chain dihydroceramides by impairing DEGS1 (delta 4-desaturase, sphingolipid 1) activity, which resulted in sustained ER stress and activated unfolded protein response (UPR) via ATF4-DDIT3-TRIB3 that ultimately promotes cytotoxic autophagy in cancer cells.	ABTL-0812	79-87	DNA damage inducible transcript 3	Homo sapiens	294-299
32370057-0	2020	Curcumin Sensitizes Kidney Cancer Cells to TRAIL-Induced Apoptosis via ROS Mediated Activation of JNK-CHOP Pathway and Upregulation of DR4.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	102-106
32239921-11	2020	Additionally, combining UDCA with the proteasome inhibitor bortezomib (BTZ) achieved a synergistic effect through enhancing the PERK/ATF4/CHOP pathway and protracting ER stress.	Bortezomib	59-69	DNA damage inducible transcript 3	Homo sapiens	138-142
32239921-11	2020	Additionally, combining UDCA with the proteasome inhibitor bortezomib (BTZ) achieved a synergistic effect through enhancing the PERK/ATF4/CHOP pathway and protracting ER stress.	Bortezomib	71-74	DNA damage inducible transcript 3	Homo sapiens	138-142
32070879-0	2020	Aspirin exerts anti-tumor effect through inhibiting Blimp1 and activating ATF4/CHOP pathway in multiple myeloma.	Aspirin	0-7	DNA damage inducible transcript 3	Homo sapiens	79-83
32070879-5	2020	Therefore, we aim to explore whether Aspirin could induce AFT4/CHOP apoptosis pathway in MM by inhibiting Blimp1 expression, thereby promoting MM cell apoptosis and exerting anti-tumor effects.	Aspirin	37-44	DNA damage inducible transcript 3	Homo sapiens	63-67
32187361-11	2020	The identification of both good and poor risk subtypes in patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) clearly show the clinical value of the approach, confirming the need for a consensus classification.	Cyclophosphamide	99-115	DNA damage inducible transcript 3	Homo sapiens	82-86
32187361-11	2020	The identification of both good and poor risk subtypes in patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) clearly show the clinical value of the approach, confirming the need for a consensus classification.	Doxorubicin	117-128	DNA damage inducible transcript 3	Homo sapiens	82-86
32187361-11	2020	The identification of both good and poor risk subtypes in patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) clearly show the clinical value of the approach, confirming the need for a consensus classification.	Vincristine	130-141	DNA damage inducible transcript 3	Homo sapiens	82-86
32187361-11	2020	The identification of both good and poor risk subtypes in patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) clearly show the clinical value of the approach, confirming the need for a consensus classification.	Prednisone	147-157	DNA damage inducible transcript 3	Homo sapiens	82-86
32369565-6	2020	MK-2048 specifically activated the ER stress-related proapoptotic gene, DNA damage-inducible transcript 3 protein (DDIT3), also known as C/EBP homologous protein (CHOP), in HTLV-1-infected but not uninfected cells of HTLV-1-carrier PBMCs.	MK-2048	0-7	DNA damage inducible transcript 3	Homo sapiens	72-113
32369565-6	2020	MK-2048 specifically activated the ER stress-related proapoptotic gene, DNA damage-inducible transcript 3 protein (DDIT3), also known as C/EBP homologous protein (CHOP), in HTLV-1-infected but not uninfected cells of HTLV-1-carrier PBMCs.	MK-2048	0-7	DNA damage inducible transcript 3	Homo sapiens	115-120
32369565-6	2020	MK-2048 specifically activated the ER stress-related proapoptotic gene, DNA damage-inducible transcript 3 protein (DDIT3), also known as C/EBP homologous protein (CHOP), in HTLV-1-infected but not uninfected cells of HTLV-1-carrier PBMCs.	MK-2048	0-7	DNA damage inducible transcript 3	Homo sapiens	163-167
32397306-0	2020	L-Ascorbic Acid Inhibits Breast Cancer Growth by Inducing IRE/JNK/CHOP-Related Endoplasmic Reticulum Stress-Mediated p62/SQSTM1 Accumulation in the Nucleus.	Ascorbic Acid	0-15	DNA damage inducible transcript 3	Homo sapiens	66-70
32397306-9	2020	Furthermore, L-AA induced endoplasmic reticulum (ER) stress via the IRE-JNK-CHOP (inositol-requiring endonuclease-c-Jun N-terminal kinase-C/EBP homologous protein) signaling pathways, which increased the nuclear levels of p62/SQSTM1.	l-aa	13-17	DNA damage inducible transcript 3	Homo sapiens	76-80
32201213-0	2020	Activation of notch 3/c-MYC/CHOP axis regulates apoptosis and promotes sensitivity of lung cancer cells to mTOR inhibitor everolimus.	Everolimus	122-132	DNA damage inducible transcript 3	Homo sapiens	28-32
32370057-0	2020	Curcumin Sensitizes Kidney Cancer Cells to TRAIL-Induced Apoptosis via ROS Mediated Activation of JNK-CHOP Pathway and Upregulation of DR4.	ros	71-74	DNA damage inducible transcript 3	Homo sapiens	102-106
31829475-8	2020	Noteworthy, kaempferol enhances cell survival through C/EBP homologous protein (CHOP) suppression and GRP78 increment in noncancerous cells, while it enhances cell mortality through the induction of unfolding protein response and CHOP increment in cancer cells.	kaempferol	12-22	DNA damage inducible transcript 3	Homo sapiens	54-78
32250167-1	2020	While combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) cures most patients with diffuse large B-cell lymphoma (DLBCL), those with high-risk international prognostic index disease have inferior survival.	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	93-97
32250167-1	2020	While combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) cures most patients with diffuse large B-cell lymphoma (DLBCL), those with high-risk international prognostic index disease have inferior survival.	Doxorubicin	50-61	DNA damage inducible transcript 3	Homo sapiens	93-97
32250167-1	2020	While combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) cures most patients with diffuse large B-cell lymphoma (DLBCL), those with high-risk international prognostic index disease have inferior survival.	Prednisone	79-89	DNA damage inducible transcript 3	Homo sapiens	93-97
32009586-7	2020	LCC induced the protein expression of ER stress markers (GRP78 and CHOP) and phosphorylation JNK, c-Jun and p38.	licochalcone A	0-3	DNA damage inducible transcript 3	Homo sapiens	67-71
31829475-8	2020	Noteworthy, kaempferol enhances cell survival through C/EBP homologous protein (CHOP) suppression and GRP78 increment in noncancerous cells, while it enhances cell mortality through the induction of unfolding protein response and CHOP increment in cancer cells.	kaempferol	12-22	DNA damage inducible transcript 3	Homo sapiens	80-84
31829475-8	2020	Noteworthy, kaempferol enhances cell survival through C/EBP homologous protein (CHOP) suppression and GRP78 increment in noncancerous cells, while it enhances cell mortality through the induction of unfolding protein response and CHOP increment in cancer cells.	kaempferol	12-22	DNA damage inducible transcript 3	Homo sapiens	230-234
32113150-0	2020	beta-Elemonic acid inhibits the growth of human Osteosarcoma through endoplasmic reticulum (ER) stress-mediated PERK/eIF2alpha/ATF4/CHOP activation and Wnt/beta-catenin signal suppression.	beta-Elemonic acid	0-18	DNA damage inducible transcript 3	Homo sapiens	132-136
32343512-6	2020	Naringin increases the protein expression of ER stress sensors, phosphorylates eIF2alpha by and activates apoptosis-associated protein CHOP and other associated proapoptotic proteins (PARP1 and caspase-3).	naringin	0-8	DNA damage inducible transcript 3	Homo sapiens	135-139
32326583-8	2020	However, Sp1 overexpression reversed the observed cell-growth inhibition and PERK/CHOP signaling activation induced by BA.	betulinic acid	119-121	DNA damage inducible transcript 3	Homo sapiens	82-86
32326583-9	2020	Because temozolomide-resistant cells exhibited significantly increased Sp1 expression, we concluded that Sp1-mediated PERK/CHOP signaling inhibition protects glioblastoma against cancer therapies; hence, BA treatment targeting this pathway can be considered as an effective therapeutic strategy to overcome such chemoresistance and tumor relapse.	Temozolomide	8-20	DNA damage inducible transcript 3	Homo sapiens	123-127
32326583-9	2020	Because temozolomide-resistant cells exhibited significantly increased Sp1 expression, we concluded that Sp1-mediated PERK/CHOP signaling inhibition protects glioblastoma against cancer therapies; hence, BA treatment targeting this pathway can be considered as an effective therapeutic strategy to overcome such chemoresistance and tumor relapse.	betulinic acid	204-206	DNA damage inducible transcript 3	Homo sapiens	123-127
32035621-5	2020	Tunicamycin treatment upregulated the expression of ER stress markers (DNA damage inducible transcript 3, heat shock protein family A (Hsp70) member 5, and phosphorylated eukaryotic translation initiation factor 2 alpha kinase 3, eukaryotic translation initiation factor 2 subunit alpha, and endoplasmic reticulum to nucleus signaling 1); however, these were decreased in ULK1 and ATG13 KO cells.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	71-104
32245975-8	2020	Geranylgeranylacetone, a therapeutic that increases cell chaperone content, prevented mitochondrial H2O2 accumulation, preserved the CORE, reduced the burden of misfolded proteins and CHOP expression, and significantly improved survival in gentamicin-exposed cells.	geranylgeranylacetone	0-21	DNA damage inducible transcript 3	Homo sapiens	184-188
32245975-8	2020	Geranylgeranylacetone, a therapeutic that increases cell chaperone content, prevented mitochondrial H2O2 accumulation, preserved the CORE, reduced the burden of misfolded proteins and CHOP expression, and significantly improved survival in gentamicin-exposed cells.	Gentamicins	240-250	DNA damage inducible transcript 3	Homo sapiens	184-188
31972357-13	2020	Treatment with oleandrin also upregulated the expression of endoplasmic reticulum stress associated proteins, including eIF2alpha, ATF4, and CHOP, but not PERK.	oleandrin	15-24	DNA damage inducible transcript 3	Homo sapiens	141-145
31520549-5	2020	Palmitate led to cytotoxicity, TG accumulation, and apoptosis in HepG2 cells and also strongly induced ER stress indicated by increased GRP78, phosphorylation of eIF2alpha, ATF6, and CHOP.	Palmitates	0-9	DNA damage inducible transcript 3	Homo sapiens	183-187
32349779-1	2020	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy is widely used in peripheral T cell lymphoma (PTCL).	Cyclophosphamide	12-28	DNA damage inducible transcript 3	Homo sapiens	74-78
32349779-1	2020	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy is widely used in peripheral T cell lymphoma (PTCL).	Prednisolone	60-72	DNA damage inducible transcript 3	Homo sapiens	74-78
32349779-1	2020	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy is widely used in peripheral T cell lymphoma (PTCL).	Prednisolone	60-72	DNA damage inducible transcript 3	Homo sapiens	80-84
32112707-5	2020	In a small sample size, etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (EPOCH-R) achieved better outcomes than a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Etoposide	24-33	DNA damage inducible transcript 3	Homo sapiens	231-235
32112707-5	2020	In a small sample size, etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (EPOCH-R) achieved better outcomes than a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	35-45	DNA damage inducible transcript 3	Homo sapiens	231-235
32112707-5	2020	In a small sample size, etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (EPOCH-R) achieved better outcomes than a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Cyclophosphamide	60-76	DNA damage inducible transcript 3	Homo sapiens	231-235
32112707-5	2020	In a small sample size, etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, and rituximab (EPOCH-R) achieved better outcomes than a regimen of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Doxorubicin	78-89	DNA damage inducible transcript 3	Homo sapiens	231-235
32326583-0	2020	Betulinic Acid-Mediated Tuning of PERK/CHOP Signaling by Sp1 Inhibition as a Novel Therapeutic Strategy for Glioblastoma.	betulinic acid	0-14	DNA damage inducible transcript 3	Homo sapiens	39-43
32326583-7	2020	Moreover, BA treatment increased activation of the protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C/EBP homologous protein (CHOP) apoptotic pathway, and reduced specificity protein 1 (Sp1) expression.	betulinic acid	10-12	DNA damage inducible transcript 3	Homo sapiens	137-141
31702836-0	2020	Lenalidomide maintenance for diffuse large B-cell lymphoma patients responding to R-CHOP: quality of life, dosing, and safety results from the randomised controlled REMARC study.	Lenalidomide	0-12	DNA damage inducible transcript 3	Homo sapiens	84-88
31922618-8	2020	These three polyphenols suppressed Bax/Bcl-2 mRNA ratio, CHOP up-regulation and MMP disruption in NSAIDs-treated cells.	Polyphenols	12-23	DNA damage inducible transcript 3	Homo sapiens	57-61
31922618-11	2020	CONCLUSION: The cytoprotective activity of polyphenols against NSAIDs-induced toxicity stemmed from either suppression of CHOP-related ER and mitochondria stresses or other CHOP-independent pathways, but not from the intrinsic ROS scavenging capacity.	Polyphenols	43-54	DNA damage inducible transcript 3	Homo sapiens	122-126
31922618-11	2020	CONCLUSION: The cytoprotective activity of polyphenols against NSAIDs-induced toxicity stemmed from either suppression of CHOP-related ER and mitochondria stresses or other CHOP-independent pathways, but not from the intrinsic ROS scavenging capacity.	Polyphenols	43-54	DNA damage inducible transcript 3	Homo sapiens	173-177
32171071-2	2020	We aimed to ascertain the safety and activity of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) with high-dose methotrexate and intrathecal chemotherapy as CNS-oriented therapy for patients with previously untreated IVLBCL.	Methotrexate	145-157	DNA damage inducible transcript 3	Homo sapiens	51-55
31707450-11	2020	In addition, treatment with FLX increased the expression of the endoplasmic reticulum (ER) stress marker, CHOP.	Fluoxetine	28-31	DNA damage inducible transcript 3	Homo sapiens	106-110
32292717-8	2020	NiPT-induced autophagy is through either concomitant activation of AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) signaling, or eliciting endoplasmic reticulum (ER)-stress by activating activating transcription factor 4 (ATF4) and C/EBP-homologous protein (CHOP).	dichlorobis(azomycin)platinum II	0-4	DNA damage inducible transcript 3	Homo sapiens	277-301
32036399-6	2020	He was successfully treated with six cycles of R-CHOP chemotherapy, with discontinuation of MTX, resulting in a complete response.	methotrexate-alpha-phenylalanine	92-95	DNA damage inducible transcript 3	Homo sapiens	49-53
32292717-8	2020	NiPT-induced autophagy is through either concomitant activation of AMP-activated protein kinase (AMPK) and inhibition of mechanistic target of rapamycin (mTOR) signaling, or eliciting endoplasmic reticulum (ER)-stress by activating activating transcription factor 4 (ATF4) and C/EBP-homologous protein (CHOP).	dichlorobis(azomycin)platinum II	0-4	DNA damage inducible transcript 3	Homo sapiens	303-307
32218719-6	2020	Meanwhile, we found that NaHS reduced SD-exerted hippocampal endoplasmic reticulum (ER) Stress, including downregulations of GRP78, CHOP, and cleaved-caspase-12 expression.	sodium bisulfide	25-29	DNA damage inducible transcript 3	Homo sapiens	132-136
32026316-10	2020	Finally, the ER stress marker CHOP (CCAAT-enhancer binding protein homologous protein), which can cause transcriptional activation of genes involved in cell apoptosis, was markedly induced by both VER-155008 and bortezomib.	VER 155008	197-207	DNA damage inducible transcript 3	Homo sapiens	30-34
31700088-0	2020	Xanthatin induces glioma cell apoptosis and inhibits tumor growth via activating endoplasmic reticulum stress-dependent CHOP pathway.	xanthatin	0-9	DNA damage inducible transcript 3	Homo sapiens	120-124
31700088-6	2020	More importantly, xanthatin treatment markedly increased the expression levels of the endoplasmic reticulum (ER) stress-related markers in both the glioma cell lines as well as in C6 xenografts, including glucose-regulated protein 78, C/EBP-homologous protein (CHOP), activating factor 4, activating transcription factor 6, spliced X-box binding protein-1, phosphorylated protein kinase R-like endoplasmic reticulum kinase, and phosphorylated eukaryotic initiation factor 2a.	xanthatin	18-27	DNA damage inducible transcript 3	Homo sapiens	235-259
31700088-6	2020	More importantly, xanthatin treatment markedly increased the expression levels of the endoplasmic reticulum (ER) stress-related markers in both the glioma cell lines as well as in C6 xenografts, including glucose-regulated protein 78, C/EBP-homologous protein (CHOP), activating factor 4, activating transcription factor 6, spliced X-box binding protein-1, phosphorylated protein kinase R-like endoplasmic reticulum kinase, and phosphorylated eukaryotic initiation factor 2a.	xanthatin	18-27	DNA damage inducible transcript 3	Homo sapiens	261-265
31700088-7	2020	Pretreatment of C6 glioma cells with the ER stress inhibitor 4-phenylbutyric acid (4-PBA, 7 mM) or knockdown of CHOP using small interfering RNA significantly attenuated xanthatin-induced cell apoptosis and increase of proapoptotic caspase-3.	xanthatin	170-179	DNA damage inducible transcript 3	Homo sapiens	112-116
31700088-8	2020	These results demonstrate that xanthatin induces glioma cell apoptosis and inhibits tumor growth via activating the ER stress-related unfolded protein response pathway involving CHOP induction.	xanthatin	31-40	DNA damage inducible transcript 3	Homo sapiens	178-182
32125443-10	2020	The protein content of GRP78, AT6, CHOP, Calpain and Caspase-12 of neuronal cells treated with UCB for 24 h was at least twofold higher compared to controls.	ucb	95-98	DNA damage inducible transcript 3	Homo sapiens	35-39
32026316-10	2020	Finally, the ER stress marker CHOP (CCAAT-enhancer binding protein homologous protein), which can cause transcriptional activation of genes involved in cell apoptosis, was markedly induced by both VER-155008 and bortezomib.	VER 155008	197-207	DNA damage inducible transcript 3	Homo sapiens	36-85
32026316-10	2020	Finally, the ER stress marker CHOP (CCAAT-enhancer binding protein homologous protein), which can cause transcriptional activation of genes involved in cell apoptosis, was markedly induced by both VER-155008 and bortezomib.	bortezomib	212-222	DNA damage inducible transcript 3	Homo sapiens	30-34
32026316-10	2020	Finally, the ER stress marker CHOP (CCAAT-enhancer binding protein homologous protein), which can cause transcriptional activation of genes involved in cell apoptosis, was markedly induced by both VER-155008 and bortezomib.	bortezomib	212-222	DNA damage inducible transcript 3	Homo sapiens	36-85
31883977-0	2020	Fumarate and oxidative stress synergize to promote stability of C/EBP homologous protein in the adipocyte.	Fumarates	0-8	DNA damage inducible transcript 3	Homo sapiens	64-88
31924023-6	2020	The apoptotic signaling pathway of A549 cells induced by FAC and the protection mechanism of NITPh(OMe)2 were all discussed through the expression of three relating proteins, Bcl-2, Bax and DDIT3.	nitph(ome)2	93-104	DNA damage inducible transcript 3	Homo sapiens	190-195
31945549-14	2020	CONCLUSION: Our work showed that miR-7112-3p directly targeted PERK and further regulated PERK/ATF4/CHOP/caspase cascade pathway, resulting in enhanced apoptosis in CX-1 cells treated with DVDMS-PDT.	RG7112	37-44	DNA damage inducible transcript 3	Homo sapiens	100-104
32124960-13	2020	Overall, the present study provided evidence that ICA sensitized tumor cells to TRAIL-induced apoptosis via ROS-, ERK- and CHOP-mediated upregulation of DR5 and DR4.	icariin	50-53	DNA damage inducible transcript 3	Homo sapiens	123-127
31883977-3	2020	CHOP protein levels increase in parallel with protein succination, a fumarate derived cysteine modification, in the adipocyte during metabolic stress.	Fumarates	69-77	DNA damage inducible transcript 3	Homo sapiens	0-4
31883977-3	2020	CHOP protein levels increase in parallel with protein succination, a fumarate derived cysteine modification, in the adipocyte during metabolic stress.	Cysteine	86-94	DNA damage inducible transcript 3	Homo sapiens	0-4
31883977-4	2020	We investigated the factors contributing to sustained CHOP proteins levels in the adipocyte, with an emphasis on the regulation of CHOP protein turnover by metabolite-driven modification of Keap1 cysteines.	Cysteine	196-205	DNA damage inducible transcript 3	Homo sapiens	131-135
31883977-5	2020	CHOP protein stability was investigated in conditions of nutrient stress due to high glucose or elevated fumarate (fumarase knockdown model); where cysteine succination is specifically elevated.	Glucose	85-92	DNA damage inducible transcript 3	Homo sapiens	0-4
31883977-5	2020	CHOP protein stability was investigated in conditions of nutrient stress due to high glucose or elevated fumarate (fumarase knockdown model); where cysteine succination is specifically elevated.	Fumarates	105-113	DNA damage inducible transcript 3	Homo sapiens	0-4
31883977-5	2020	CHOP protein stability was investigated in conditions of nutrient stress due to high glucose or elevated fumarate (fumarase knockdown model); where cysteine succination is specifically elevated.	Cysteine	148-156	DNA damage inducible transcript 3	Homo sapiens	0-4
31883977-6	2020	CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation.	Glucose	69-76	DNA damage inducible transcript 3	Homo sapiens	0-4
31883977-6	2020	CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation.	Glucose	69-76	DNA damage inducible transcript 3	Homo sapiens	114-118
31883977-6	2020	CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation.	Glucose	69-76	DNA damage inducible transcript 3	Homo sapiens	114-118
31883977-6	2020	CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation.	Fumarates	81-89	DNA damage inducible transcript 3	Homo sapiens	0-4
31883977-6	2020	CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation.	Fumarates	81-89	DNA damage inducible transcript 3	Homo sapiens	114-118
31883977-6	2020	CHOP protein turnover is significantly reduced in models of elevated glucose and fumarate with a ~30% increase in CHOP stability (p > 0.01), in part due to decreased CHOP phosphorylation.	Fumarates	81-89	DNA damage inducible transcript 3	Homo sapiens	114-118
31883977-9	2020	Elevated fumarate indirectly regulates CHOP stability through the induction of oxidative stress.	Fumarates	9-17	DNA damage inducible transcript 3	Homo sapiens	39-43
31883977-10	2020	The antioxidant N-acetylcysteine (NAC) reduces fumarate levels, protein succination and CHOP levels in adipocytes matured in high glucose.	Acetylcysteine	16-32	DNA damage inducible transcript 3	Homo sapiens	88-92
31883977-10	2020	The antioxidant N-acetylcysteine (NAC) reduces fumarate levels, protein succination and CHOP levels in adipocytes matured in high glucose.	Acetylcysteine	34-37	DNA damage inducible transcript 3	Homo sapiens	88-92
31883977-13	2020	This study demonstrates that physiological increases in the metabolite fumarate during high glucose exposure contributes to the presence of oxidative stress and sustained CHOP levels in the adipocyte during diabetes.	Fumarates	71-79	DNA damage inducible transcript 3	Homo sapiens	171-175
31883977-13	2020	This study demonstrates that physiological increases in the metabolite fumarate during high glucose exposure contributes to the presence of oxidative stress and sustained CHOP levels in the adipocyte during diabetes.	Glucose	92-99	DNA damage inducible transcript 3	Homo sapiens	171-175
32042116-6	2020	The treatment of SCNT embryos with melatonin significantly reduced the level of ROS and H3K9me3, and the expression levels of IRE-1 and CHOP.	Melatonin	35-44	DNA damage inducible transcript 3	Homo sapiens	136-140
31735743-8	2020	In addition, melatonin markedly reduced reactive oxygen species (ROS) and the transcription of Caspase12 and Chop, which is vital in endoplasmic reticulum stress (ERS)-mediated apoptosis.	Melatonin	13-22	DNA damage inducible transcript 3	Homo sapiens	109-113
32079116-0	2020	Unique Distribution of Diacyl-, Alkylacyl-, and Alkenylacyl-Phosphatidylcholine Species Visualized in Pork Chop Tissues by Matrix-Assisted Laser Desorption/Ionization-Mass Spectrometry Imaging.	diacyl	23-29	DNA damage inducible transcript 3	Homo sapiens	107-111
32079116-0	2020	Unique Distribution of Diacyl-, Alkylacyl-, and Alkenylacyl-Phosphatidylcholine Species Visualized in Pork Chop Tissues by Matrix-Assisted Laser Desorption/Ionization-Mass Spectrometry Imaging.	, alkylacyl-, and alkenylacyl-phosphatidylcholine	30-79	DNA damage inducible transcript 3	Homo sapiens	107-111
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Thapsigargin	49-61	DNA damage inducible transcript 3	Homo sapiens	311-344
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Thapsigargin	49-61	DNA damage inducible transcript 3	Homo sapiens	346-351
31774307-11	2020	However, downstream signaling of eIF2alpha (activating transcription factor 4 and CCAAT/enhancer-binding protein homologous protein) was diminished in the heart but upregulated in the diaphragm with DOX.	Doxorubicin	199-202	DNA damage inducible transcript 3	Homo sapiens	82-131
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Thapsigargin	63-65	DNA damage inducible transcript 3	Homo sapiens	311-344
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Thapsigargin	63-65	DNA damage inducible transcript 3	Homo sapiens	346-351
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Tunicamycin	71-82	DNA damage inducible transcript 3	Homo sapiens	311-344
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Tunicamycin	71-82	DNA damage inducible transcript 3	Homo sapiens	346-351
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Tunicamycin	84-86	DNA damage inducible transcript 3	Homo sapiens	311-344
32040528-4	2020	Treatment with two different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), caused a dose-dependent induction of ER stress as evident from up-regulation of protein kinase RNA-like ER kinase (PERK), heat shock protein family A (Hsp70) member 5 (HSPA5), activating transcription factor (ATF4), ATF6, DNA damage inducible transcript 3 (DDIT3) and spliced X-box binding protein 1 (sXBP1) and impaired cell viability and decreased expression of vitamin D receptor (VDR) in MCF-7 cells (P &lt; 0.05).	Tunicamycin	84-86	DNA damage inducible transcript 3	Homo sapiens	346-351
32040528-5	2020	Treatment with 1,25D3 (100 nM) inhibited TG (10 nM)- and TM (1 mug/mL)-induced mRNA and/or protein levels of ATF4, ATF6, DDIT3 and HSPA5 in MCF-7 cells (P &lt; 0.05).	Thapsigargin	41-43	DNA damage inducible transcript 3	Homo sapiens	121-126
32040528-5	2020	Treatment with 1,25D3 (100 nM) inhibited TG (10 nM)- and TM (1 mug/mL)-induced mRNA and/or protein levels of ATF4, ATF6, DDIT3 and HSPA5 in MCF-7 cells (P &lt; 0.05).	Tunicamycin	57-59	DNA damage inducible transcript 3	Homo sapiens	121-126
32059099-2	2020	STUDY DESIGN: An economic model was developed using clinical and quality-of-life (QOL) data from the ECHELON-2 trial, in which A+CHP demonstrated significant improvement in progression-free survival (PFS) and overall survival (OS) versus cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	somatostatin, cyclic hexapeptide(Phe-Phe-Trp-Lys-Thr-Phe)-	129-132	DNA damage inducible transcript 3	Homo sapiens	298-302
32059099-8	2020	RESULTS: The model predicted that A+CHP extended PFS and OS by 2.92 and 3.38 years, respectively, over CHOP.	somatostatin, cyclic hexapeptide(Phe-Phe-Trp-Lys-Thr-Phe)-	36-39	DNA damage inducible transcript 3	Homo sapiens	103-107
31902733-4	2020	Our findings demonstrate good outcomes following induction treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), suggesting that these cases can be treated as DLBCL rather than primary central nervous system lymphoma, obviating the need for more aggressive and toxic approaches.	Cyclophosphamide	93-109	DNA damage inducible transcript 3	Homo sapiens	76-80
31902733-4	2020	Our findings demonstrate good outcomes following induction treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), suggesting that these cases can be treated as DLBCL rather than primary central nervous system lymphoma, obviating the need for more aggressive and toxic approaches.	Doxorubicin	111-122	DNA damage inducible transcript 3	Homo sapiens	76-80
31902733-4	2020	Our findings demonstrate good outcomes following induction treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), suggesting that these cases can be treated as DLBCL rather than primary central nervous system lymphoma, obviating the need for more aggressive and toxic approaches.	Vincristine	124-135	DNA damage inducible transcript 3	Homo sapiens	76-80
31902733-4	2020	Our findings demonstrate good outcomes following induction treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone), suggesting that these cases can be treated as DLBCL rather than primary central nervous system lymphoma, obviating the need for more aggressive and toxic approaches.	Prednisone	141-151	DNA damage inducible transcript 3	Homo sapiens	76-80
32020188-5	2020	Knockdown of the transcription factor C/EBP homologous protein (CHOP), an unfolded protein response factor activated by ER stress, inhibits testosterone-induced RAGE expression and AGE accumulation.	Testosterone	140-152	DNA damage inducible transcript 3	Homo sapiens	38-62
32020188-5	2020	Knockdown of the transcription factor C/EBP homologous protein (CHOP), an unfolded protein response factor activated by ER stress, inhibits testosterone-induced RAGE expression and AGE accumulation.	Testosterone	140-152	DNA damage inducible transcript 3	Homo sapiens	64-68
31698509-9	2020	Ecn induced ROS production and GRP78, CHOP, DR5 and DR4 expression as well as depolarized the mitochondria membrane potential.	ecn	0-3	DNA damage inducible transcript 3	Homo sapiens	38-42
31891755-9	2020	In the present study, we demonstrated that the ER stress-related PERK-CHOP signalling pathway is a novel mechanism for FB1-induced cytotoxicity and the gastrointestinal injury caused by FB1 should be concerned in the future.	fumonisin B1	119-122	DNA damage inducible transcript 3	Homo sapiens	70-74
31974624-5	2020	The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes.	Tunicamycin	45-56	DNA damage inducible transcript 3	Homo sapiens	258-282
31974624-5	2020	The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes.	Tunicamycin	45-56	DNA damage inducible transcript 3	Homo sapiens	284-288
31974624-5	2020	The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes.	Tunicamycin	58-60	DNA damage inducible transcript 3	Homo sapiens	258-282
31974624-5	2020	The present study demonstrated that 3 microM tunicamycin (TM) increased the expression of the ER stress-related proteins protein kinase RNA-like endoplasmic reticulum kinase (PERK), alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) and C/EBP homologous protein (CHOP) in human primary epidermal melanocytes.	Tunicamycin	58-60	DNA damage inducible transcript 3	Homo sapiens	284-288
31891755-0	2020	Involvement of PERK-CHOP pathway in fumonisin B1- induced cytotoxicity in human gastric epithelial cells.	fumonisin B1	36-48	DNA damage inducible transcript 3	Homo sapiens	20-24
32028388-7	2020	INTERVENTIONS: The patient was successfully treated by Poly-chemotherapy with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vindesine and prednisolone).	Cyclophosphamide	97-113	DNA damage inducible transcript 3	Homo sapiens	80-84
32027271-19	2020	After aspirin stimulation of different concentrations for 48 hours, the expression level of Blimp1 in U266 cells decreased with increasing of drug concentration, while the expression levels of ATF4 and CHOP increased with increasing of drug concentration.	Aspirin	6-13	DNA damage inducible transcript 3	Homo sapiens	202-206
32027271-21	2020	Aspirin can inhibit the proliferation activity of myeloma cells by down-regulating Blimp1 expression in myeloma cells and up-regulating ATF4 and CHOP expression, therefore plays an anti-tumor rote.	Aspirin	0-7	DNA damage inducible transcript 3	Homo sapiens	145-149
31987044-9	2020	PERK, ATF4 and CHOP were required for Tg-induced cell death, but surprisingly acted in parallel rather than as a linear pathway; ATF4 and CHOP were independently required for Tg-mediated upregulation of death receptor 5 and MAP1LC3B proteins, whereas PERK acted via other pathways.	Thapsigargin	38-40	DNA damage inducible transcript 3	Homo sapiens	15-19
31987044-9	2020	PERK, ATF4 and CHOP were required for Tg-induced cell death, but surprisingly acted in parallel rather than as a linear pathway; ATF4 and CHOP were independently required for Tg-mediated upregulation of death receptor 5 and MAP1LC3B proteins, whereas PERK acted via other pathways.	Thapsigargin	175-177	DNA damage inducible transcript 3	Homo sapiens	138-142
32021288-11	2020	Induction of apoptosis by Brv-A was found to be associated with ROS generation by targeting NOX2 and NOX3, mitochondrial dysfunction (MMP dissipation and Bcl-2 family proteins modulation), DNA fragmentation, JNK and p38 MAPK activation, endoplasmic reticulum (ER) stress by increasing Bip/GRP78, ATF4 and CHOP protein expressions and inhibition of STAT3 activation via decreased phosphorylation of JAK2 and SRC.	brevilin A	26-31	DNA damage inducible transcript 3	Homo sapiens	305-309
31629555-0	2020	Corrigendum to "Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP" [Gene 551 (2014) 230-235].	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	16-26	DNA damage inducible transcript 3	Homo sapiens	119-123
31940809-2	2020	Despite this, the standard therapeutic approach is still immunochemotherapy (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone-R-CHOP), which allows a 60% overall survival (OS) rate, but up to 40% of patients experience relapse or refractory (R/R) disease.	Prednisone	140-150	DNA damage inducible transcript 3	Homo sapiens	153-157
31629555-0	2020	Corrigendum to "Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP" [Gene 551 (2014) 230-235].	Tretinoin	36-40	DNA damage inducible transcript 3	Homo sapiens	119-123
32698734-0	2020	ATF4, DLX3, FRA1, MSX2, C/EBP-zeta, and C/EBP-alpha Shape the Molecular Basis of Therapeutic Effects of Zoledronic Acid in Bone Disorders.	Zoledronic Acid	104-119	DNA damage inducible transcript 3	Homo sapiens	24-34
31483910-9	2020	In addition, gene expression results showed that the expression levels of ATF4 (p&lt;0.05) and ATF6 (p&lt;0.001) significantly increased in resveratrol treatment group, while the expression levels of CHOP, GRP78, and XBP1 (p&lt;0.001 for all) significantly decreased.	Resveratrol	140-151	DNA damage inducible transcript 3	Homo sapiens	200-204
32698734-8	2020	RESULTS: Gene expression and promoter methylation level for DLX3, FRA1, ATF4, MSX2, C/EBPzeta, and C/EBPa was up or down-regulated in both ZA-treated and untreated cells during the osteodifferentiation process on days 0 to 21.	Zoledronic Acid	139-141	DNA damage inducible transcript 3	Homo sapiens	84-93
33164541-10	2020	It was found that propranolol treatment enhanced the activity of caspase-3 while the expression of bax, wee1, gadd153, grp78 and AIF decreased bcl-2 which is antiapoptotic protein in cSCC cell lines.	Propranolol	18-29	DNA damage inducible transcript 3	Homo sapiens	110-117
31666439-7	2020	We found that schizandrin B increased cell survival rate in dose-dependent and time-dependent manner, decreased cell apoptosis rate, and reduced protein and gene expression levels of GRP78, PERK, ATF4, CHOP, ATF6, ARMET and XBP-1.	schizandrin B	14-27	DNA damage inducible transcript 3	Homo sapiens	202-206
31573118-7	2020	In addition, beta-carotene decreased the activation of GRP78, CHOP, and JNK/p38 MAPK and the ratio of Bax/Bcl-2.	beta Carotene	13-26	DNA damage inducible transcript 3	Homo sapiens	62-66
31585902-2	2020	Here, we tested whether blockage of homocysteine (Hcy) induced ERS and subsequent apoptosis in vascular smooth muscle cells can be inhibited by  blockage of PERK/eIF2alpha/ATF4/CHOP signaling.	Homocysteine	36-48	DNA damage inducible transcript 3	Homo sapiens	177-181
31585902-2	2020	Here, we tested whether blockage of homocysteine (Hcy) induced ERS and subsequent apoptosis in vascular smooth muscle cells can be inhibited by  blockage of PERK/eIF2alpha/ATF4/CHOP signaling.	Homocysteine	50-53	DNA damage inducible transcript 3	Homo sapiens	177-181
31585902-4	2020	Long-term Hcy exposure, however, increased the expression of ATF-4 and CHOP and led to apoptosis.	Homocysteine	10-13	DNA damage inducible transcript 3	Homo sapiens	71-75
31573118-0	2020	beta-carotene attenuates weaning-induced apoptosis via inhibition of PERK-CHOP and IRE1-JNK/p38 MAPK signalling pathways in piglet jejunum.	beta Carotene	0-13	DNA damage inducible transcript 3	Homo sapiens	74-78
31573118-9	2020	In the present study, beta-carotene pre-treatment attenuated the ratio of Bax/Bcl-2 and prevented TG-induced increases in the level of PERK-CHOP and IRE1-JNK/p38 MAPK pathway activation in a dose-dependent manner.	beta Carotene	22-35	DNA damage inducible transcript 3	Homo sapiens	140-144
32897819-8	2020	In summary, the results of the present study indicate that miR-96-5p protects HK-2 cells from malathion-induced ER stress-dependent apoptosis by targeting DDIT3.	Malathion	94-103	DNA damage inducible transcript 3	Homo sapiens	155-160
31364909-10	2020	These results suggested that psoralen causes liver injury due to the induction of the ER stress-mediated apoptosis via PERK-eIF2alpha-ATF4-CHOP and ATF6-CHOP related pathways.	Ficusin	29-37	DNA damage inducible transcript 3	Homo sapiens	139-143
32897819-0	2020	miR-96-5p attenuates malathion-induced apoptosis of human kidney cells by targeting the ER stress marker DDIT3.	Malathion	21-30	DNA damage inducible transcript 3	Homo sapiens	105-110
31814016-6	2020	To test this hypothesis, we elucidate whether dienogest affects endometriotic stromal cell apoptosis, proliferation, and invasiveness by modulating ER stress-induced CCAAT/enhancer-binding protein homologous protein (CHOP) expression.	dienogest	46-55	DNA damage inducible transcript 3	Homo sapiens	166-215
31814016-6	2020	To test this hypothesis, we elucidate whether dienogest affects endometriotic stromal cell apoptosis, proliferation, and invasiveness by modulating ER stress-induced CCAAT/enhancer-binding protein homologous protein (CHOP) expression.	dienogest	46-55	DNA damage inducible transcript 3	Homo sapiens	217-221
31814016-12	2020	Furthermore, dienogest-induced ER stress increased CHOP expression through activation of both PERK/elf2alpha/ATF4 and IRE1/TRAF2/ASK1/JNK signaling.	dienogest	13-22	DNA damage inducible transcript 3	Homo sapiens	51-55
31814016-14	2020	Taken together, our findings indicate that dienogest enhances ER stress induction in endometriotic stromal cells, which affects apoptosis, proliferation, and invasiveness via CHOP upregulation.	dienogest	43-52	DNA damage inducible transcript 3	Homo sapiens	175-179
31364909-10	2020	These results suggested that psoralen causes liver injury due to the induction of the ER stress-mediated apoptosis via PERK-eIF2alpha-ATF4-CHOP and ATF6-CHOP related pathways.	Ficusin	29-37	DNA damage inducible transcript 3	Homo sapiens	153-157
31518729-8	2020	PA affected cellular proliferation, apoptosis and endoplasmic reticulum stress markers along with reducing the phosphor-AKT/AKT levels and increasing the expression levels of caspase-3 and CHOP in GCs.	Palmitic Acid	0-2	DNA damage inducible transcript 3	Homo sapiens	189-193
31861425-4	2019	ZEN increased GRP78 and CHOP, and eIF2alpha phosphorylation, indicating ER stress; elevated transcription of the autophagy-associated genes, beclin1 and LC3, and translation of LC3; and increased phase I metabolism by increasing PXR and CYP3A4.	Zearalenone	0-3	DNA damage inducible transcript 3	Homo sapiens	24-28
30649790-8	2020	And relapsed patients undergoing radiotherapy (RT) plus temozolomide chemotherapy after primary tumor removal induces C/EBP homologous protein (CHOP).	Temozolomide	56-68	DNA damage inducible transcript 3	Homo sapiens	118-142
30649790-8	2020	And relapsed patients undergoing radiotherapy (RT) plus temozolomide chemotherapy after primary tumor removal induces C/EBP homologous protein (CHOP).	Temozolomide	56-68	DNA damage inducible transcript 3	Homo sapiens	144-148
31868632-1	2019	BACKGROUND: Six cycles of R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) are the standard treatment for aggressive B-cell non-Hodgkin lymphoma.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	28-32
31868632-1	2019	BACKGROUND: Six cycles of R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) are the standard treatment for aggressive B-cell non-Hodgkin lymphoma.	Prednisone	97-107	DNA damage inducible transcript 3	Homo sapiens	28-32
31651708-5	2019	In addition, fusidic acid effectively attenuated SNP-induced endoplasmic reticulum (ER) stress markers, such as GRP78, IRE1, ATF6, PERK, XBP1s, eIF2alpha, CHOP, and caspase-12.	Fusidic Acid	13-25	DNA damage inducible transcript 3	Homo sapiens	155-159
31819768-5	2019	Defensin and cathelicidin LL37 activated tumor cell apoptosis, especially for the HT29, but also for A549 line, by increasing gene expression of CHOP and by lowering BCL2 gene expression.	Defensins	0-8	DNA damage inducible transcript 3	Homo sapiens	145-149
31818069-10	2019	Case 2 was treated with 4 cycles of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) therapy after surgery and attained partial remission, and was then treated with apatinib and ibrutinib, and remained stable 18 months after initial diagnosis.	Prednisone	94-104	DNA damage inducible transcript 3	Homo sapiens	108-112
30873870-5	2019	Shikonin significantly triggered ER stress-mediated apoptosis by upregulating the expression of p-eIF2alpha, CHOP, and cleaved caspase-3.	shikonin	0-8	DNA damage inducible transcript 3	Homo sapiens	109-113
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	Acetylcysteine	34-51	DNA damage inducible transcript 3	Homo sapiens	297-301
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	shikonin	53-61	DNA damage inducible transcript 3	Homo sapiens	297-301
31852157-11	2019	INTERVENTIONS: The current first-line treatment for diffuse large B-cell lymphoma is the cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) protocol.	Cyclophosphamide	89-105	DNA damage inducible transcript 3	Homo sapiens	144-148
30101679-1	2019	OBJECTIVES: Chemoimmunotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone combined with rituximab (R-CHOP) is currently the first-line therapy for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	124-128
31185769-2	2019	Among 65% of patients receiving treatment after diagnosis, R-CHOP (Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, Prednisone) was the most common frontline therapy, increasing with more recent treatment year: 51% (2001-2003) vs. 69% (2010-2014).	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	61-65
31185769-2	2019	Among 65% of patients receiving treatment after diagnosis, R-CHOP (Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, Prednisone) was the most common frontline therapy, increasing with more recent treatment year: 51% (2001-2003) vs. 69% (2010-2014).	Doxorubicin	96-107	DNA damage inducible transcript 3	Homo sapiens	61-65
31852157-11	2019	INTERVENTIONS: The current first-line treatment for diffuse large B-cell lymphoma is the cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) protocol.	Doxorubicin	107-117	DNA damage inducible transcript 3	Homo sapiens	144-148
31852157-11	2019	INTERVENTIONS: The current first-line treatment for diffuse large B-cell lymphoma is the cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) protocol.	Prednisone	132-142	DNA damage inducible transcript 3	Homo sapiens	144-148
31832222-11	2019	Conclusions: This study suggests that granisetron alone could be one treatment option in the management of CINV in patients with non-Hodgkin lymphoma receiving CHOP or R-CHOP regimen.	Granisetron	38-49	DNA damage inducible transcript 3	Homo sapiens	160-164
31801186-7	2019	Enhanced sensitivity to different BH3-mimetics after CHOP treatment was confirmed in specific cell lines, indicating heterogeneity of CHOP-induced resistance in DLBCL.	BH 3	34-37	DNA damage inducible transcript 3	Homo sapiens	53-57
31801186-7	2019	Enhanced sensitivity to different BH3-mimetics after CHOP treatment was confirmed in specific cell lines, indicating heterogeneity of CHOP-induced resistance in DLBCL.	BH 3	34-37	DNA damage inducible transcript 3	Homo sapiens	134-138
31801186-8	2019	Analysis of single CHOP compounds demonstrated that similar changes could also be induced by doxorubicin or vincristine, providing evidence for clinical combination therapies of doxorubicin or vincristine with BH3-mimetics in DLBCL.	Doxorubicin	93-104	DNA damage inducible transcript 3	Homo sapiens	19-23
31801186-8	2019	Analysis of single CHOP compounds demonstrated that similar changes could also be induced by doxorubicin or vincristine, providing evidence for clinical combination therapies of doxorubicin or vincristine with BH3-mimetics in DLBCL.	Vincristine	108-119	DNA damage inducible transcript 3	Homo sapiens	19-23
31801186-8	2019	Analysis of single CHOP compounds demonstrated that similar changes could also be induced by doxorubicin or vincristine, providing evidence for clinical combination therapies of doxorubicin or vincristine with BH3-mimetics in DLBCL.	Doxorubicin	178-189	DNA damage inducible transcript 3	Homo sapiens	19-23
31801186-8	2019	Analysis of single CHOP compounds demonstrated that similar changes could also be induced by doxorubicin or vincristine, providing evidence for clinical combination therapies of doxorubicin or vincristine with BH3-mimetics in DLBCL.	Vincristine	193-204	DNA damage inducible transcript 3	Homo sapiens	19-23
31801186-10	2019	These results provide new perspectives for the treatment of CHOP-resistant DLBCL and underline the potential of BH3 profiling in predicting therapy outcomes.	BH 3	112-115	DNA damage inducible transcript 3	Homo sapiens	60-64
31783518-8	2019	KEAP1, CPT1, and CHOP mRNA expressions were reduced by amoxicillin treatments.	Amoxicillin	55-66	DNA damage inducible transcript 3	Homo sapiens	17-21
31783518-13	2019	Based on evaluating alterations in KEAP1, CPT1, and CHOP mRNA expressions plus PPARalpha transactivation, we suggest that a reduced PPARalpha activation is a potential mechanism behind the observed amoxicillin effects on ApoA-I expression.	Amoxicillin	198-209	DNA damage inducible transcript 3	Homo sapiens	52-56
31832222-0	2019	Granisetron plus aprepitant versus granisetron in preventing nausea and vomiting during CHOP or R-CHOP regimen in malignant lymphoma: a retrospective study.	Granisetron	0-11	DNA damage inducible transcript 3	Homo sapiens	88-92
31832222-0	2019	Granisetron plus aprepitant versus granisetron in preventing nausea and vomiting during CHOP or R-CHOP regimen in malignant lymphoma: a retrospective study.	Granisetron	0-11	DNA damage inducible transcript 3	Homo sapiens	98-102
31832222-1	2019	Background: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen includes a high dose of prednisolone (100 mg/body), which exhibits an anticancer and antiemetic effect.	Cyclophosphamide	12-28	DNA damage inducible transcript 3	Homo sapiens	74-78
31832222-11	2019	Conclusions: This study suggests that granisetron alone could be one treatment option in the management of CINV in patients with non-Hodgkin lymphoma receiving CHOP or R-CHOP regimen.	Granisetron	38-49	DNA damage inducible transcript 3	Homo sapiens	170-174
31832222-1	2019	Background: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen includes a high dose of prednisolone (100 mg/body), which exhibits an anticancer and antiemetic effect.	Doxorubicin	30-41	DNA damage inducible transcript 3	Homo sapiens	74-78
31537387-0	2019	Artesunate activates the ATF4-CHOP-CHAC1 pathway and affects ferroptosis in Burkitt"s Lymphoma.	Artesunate	0-10	DNA damage inducible transcript 3	Homo sapiens	30-34
31832222-1	2019	Background: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen includes a high dose of prednisolone (100 mg/body), which exhibits an anticancer and antiemetic effect.	Prednisolone	60-72	DNA damage inducible transcript 3	Homo sapiens	74-78
31832222-1	2019	Background: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen includes a high dose of prednisolone (100 mg/body), which exhibits an anticancer and antiemetic effect.	Prednisolone	112-124	DNA damage inducible transcript 3	Homo sapiens	74-78
31537387-5	2019	Results showed that artesunate induced ferroptosis in DAUDI and CA-46 cells, as evidenced by the protective effect of liproxstatin-1, ferrostatin-1, and desferoxamine, resulting in an endoplasmic reticulum stress response, activation of the ATF4-CHOP-CHAC1 pathway enhanced ferroptosis in DAUDI and CA-46 cells.	Artesunate	20-30	DNA damage inducible transcript 3	Homo sapiens	246-250
31718641-10	2019	And the ER stress apoptotic molecule CHOP and ER stress related molecule HERPUD1 were both highly expressed in Ishikawa cells (PRB+) treated with MPA.	Medroxyprogesterone Acetate	146-149	DNA damage inducible transcript 3	Homo sapiens	37-41
31718641-11	2019	Co-expression analysis showed lnc-CETP-3 was highly correlated with CHOP and HERPUD1, suggesting it might participate in ER stress pathway-related EC cell apoptosis caused by MPA.	Medroxyprogesterone Acetate	175-178	DNA damage inducible transcript 3	Homo sapiens	68-72
31718641-12	2019	In addition, compared with untreated cells, lnc-CETP-3, CHOP and HERPUD1 were significantly up-regulated in Ishikawa cells (PRB+) treated with MPA, whereas they have no statistical significance in KLE cells (PRB-).	Medroxyprogesterone Acetate	143-146	DNA damage inducible transcript 3	Homo sapiens	56-60
31718641-13	2019	CONCLUSIONS: MPA may activate ER stress by progesterone-PRB pathway to up-regulate CHOP expression, which may be one of the molecular mechanisms underlying the inhibitory effect of MPA on EC cells with PRB+.	Medroxyprogesterone Acetate	13-16	DNA damage inducible transcript 3	Homo sapiens	83-87
31718641-13	2019	CONCLUSIONS: MPA may activate ER stress by progesterone-PRB pathway to up-regulate CHOP expression, which may be one of the molecular mechanisms underlying the inhibitory effect of MPA on EC cells with PRB+.	Progesterone	43-55	DNA damage inducible transcript 3	Homo sapiens	83-87
31251343-1	2019	We compared treatment outcomes between rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy alone with R-CHOP followed by consolidative radiation therapy (RT) in diffuse large B-cell lymphoma (DLBCL).	Prednisone	98-108	DNA damage inducible transcript 3	Homo sapiens	112-116
31718641-13	2019	CONCLUSIONS: MPA may activate ER stress by progesterone-PRB pathway to up-regulate CHOP expression, which may be one of the molecular mechanisms underlying the inhibitory effect of MPA on EC cells with PRB+.	prb	56-59	DNA damage inducible transcript 3	Homo sapiens	83-87
31718641-13	2019	CONCLUSIONS: MPA may activate ER stress by progesterone-PRB pathway to up-regulate CHOP expression, which may be one of the molecular mechanisms underlying the inhibitory effect of MPA on EC cells with PRB+.	Medroxyprogesterone Acetate	181-184	DNA damage inducible transcript 3	Homo sapiens	83-87
31512113-5	2019	Our results showed that VPA treatment could inhibit the increased expressions of ER stress proteins (GRP78 and CHOP), and significantly reduce neuronal apoptosis in the PTZ-induced experimental seizure model.	Valproic Acid	24-27	DNA damage inducible transcript 3	Homo sapiens	111-115
31314918-1	2019	OBJECTIVES: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is the standard therapy for patients with previously untreated diffuse large B-cell lymphomas (DLBCL).	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	14-18
31314918-1	2019	OBJECTIVES: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is the standard therapy for patients with previously untreated diffuse large B-cell lymphomas (DLBCL).	Doxorubicin	49-60	DNA damage inducible transcript 3	Homo sapiens	14-18
31314918-1	2019	OBJECTIVES: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is the standard therapy for patients with previously untreated diffuse large B-cell lymphomas (DLBCL).	Vincristine	62-73	DNA damage inducible transcript 3	Homo sapiens	14-18
31314918-1	2019	OBJECTIVES: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is the standard therapy for patients with previously untreated diffuse large B-cell lymphomas (DLBCL).	Prednisone	75-85	DNA damage inducible transcript 3	Homo sapiens	14-18
31018735-4	2019	In recent years, bendamustine-based therapy has been increasingly adopted for older MCL patients and more recently, vincristine has been replaced by bortezomib in the R-CHOP combination as VR-CAP for previously untreated patients.	Bortezomib	149-159	DNA damage inducible transcript 3	Homo sapiens	169-173
31055769-5	2019	This is demonstrated by a significant reduction in the expression levels of BiP, significantly reduced basal respiration, maximal respiration, and spare respiratory capacity as well as a significant increase in the expression levels of CHOP; however, these effects were significantly attenuated following pretreatment with rutin.	Rutin	323-328	DNA damage inducible transcript 3	Homo sapiens	236-240
31222719-1	2019	Central nervous system (CNS) relapse following R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) occurs in 2-5% of patents with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	66-82	DNA damage inducible transcript 3	Homo sapiens	49-53
31222719-1	2019	Central nervous system (CNS) relapse following R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) occurs in 2-5% of patents with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	84-95	DNA damage inducible transcript 3	Homo sapiens	49-53
31222719-1	2019	Central nervous system (CNS) relapse following R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) occurs in 2-5% of patents with diffuse large B-cell lymphoma (DLBCL).	Vincristine	97-108	DNA damage inducible transcript 3	Homo sapiens	49-53
31222719-1	2019	Central nervous system (CNS) relapse following R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) occurs in 2-5% of patents with diffuse large B-cell lymphoma (DLBCL).	Prednisolone	110-122	DNA damage inducible transcript 3	Homo sapiens	49-53
31222719-13	2019	CNS-IPI is valid in elderly R-CHOP-treated DLBCL patients, with the highest risk in those with CNS-IPI 6 and R/A involvement.	diprotin A	4-7	DNA damage inducible transcript 3	Homo sapiens	30-34
31452347-8	2019	After eight cycles of rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy, the lymphoma was cured clinically, and his interstitial lung disease (ILD) had improved.	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	94-98
31516571-10	2019	Furthermore, the acetylation levels of H4 in the promoter regions of GRP78, ATF4 and CHOP were significantly increased in HepG2 cells exposed to 6 microM SAHA for 36 h. Thus, SAHA induces apoptosis in HepG2 cells by activating the ER stress-mediated apoptotic signaling pathway, at least partially by enhancing the acetylation of histone H4 on the promoter regions of ER-stress associated genes, including GRP78, ATF4 and CHOP.	Vorinostat	154-158	DNA damage inducible transcript 3	Homo sapiens	422-426
31516571-10	2019	Furthermore, the acetylation levels of H4 in the promoter regions of GRP78, ATF4 and CHOP were significantly increased in HepG2 cells exposed to 6 microM SAHA for 36 h. Thus, SAHA induces apoptosis in HepG2 cells by activating the ER stress-mediated apoptotic signaling pathway, at least partially by enhancing the acetylation of histone H4 on the promoter regions of ER-stress associated genes, including GRP78, ATF4 and CHOP.	Vorinostat	175-179	DNA damage inducible transcript 3	Homo sapiens	85-89
31516571-10	2019	Furthermore, the acetylation levels of H4 in the promoter regions of GRP78, ATF4 and CHOP were significantly increased in HepG2 cells exposed to 6 microM SAHA for 36 h. Thus, SAHA induces apoptosis in HepG2 cells by activating the ER stress-mediated apoptotic signaling pathway, at least partially by enhancing the acetylation of histone H4 on the promoter regions of ER-stress associated genes, including GRP78, ATF4 and CHOP.	Vorinostat	175-179	DNA damage inducible transcript 3	Homo sapiens	422-426
31516571-6	2019	The effects of SAHA on the acetylation of H4 in the promoter regions of GRP78, ATF4 and CHOP were evaluated by chromatin immunoprecipitation assays.	Vorinostat	15-19	DNA damage inducible transcript 3	Homo sapiens	88-92
31516571-8	2019	SAHA induced dose-dependent apoptosis and increased both protein and mRNA expression levels of GRP78, ATF4 and CHOP in HepG2 cells.	Vorinostat	0-4	DNA damage inducible transcript 3	Homo sapiens	111-115
31516571-10	2019	Furthermore, the acetylation levels of H4 in the promoter regions of GRP78, ATF4 and CHOP were significantly increased in HepG2 cells exposed to 6 microM SAHA for 36 h. Thus, SAHA induces apoptosis in HepG2 cells by activating the ER stress-mediated apoptotic signaling pathway, at least partially by enhancing the acetylation of histone H4 on the promoter regions of ER-stress associated genes, including GRP78, ATF4 and CHOP.	Vorinostat	154-158	DNA damage inducible transcript 3	Homo sapiens	85-89
31534626-0	2019	Predictive value of interim FDG-PET/CT findings in patients with diffuse large B-cell lymphoma treated with R-CHOP.	Fluorodeoxyglucose F18	28-31	DNA damage inducible transcript 3	Homo sapiens	110-114
31546731-6	2019	Our results also showed that I3M enhanced transcription factor C/EBP homologous protein (CHOP) expression, resulted in endoplasmic reticulum (ER) stress-mediated DR5 expression, which was upregulated by ROS production in HCT116 p53+/+ cells.	indirubin-3'-monoxime	29-32	DNA damage inducible transcript 3	Homo sapiens	63-87
31546731-6	2019	Our results also showed that I3M enhanced transcription factor C/EBP homologous protein (CHOP) expression, resulted in endoplasmic reticulum (ER) stress-mediated DR5 expression, which was upregulated by ROS production in HCT116 p53+/+ cells.	indirubin-3'-monoxime	29-32	DNA damage inducible transcript 3	Homo sapiens	89-93
31325684-11	2019	Results indicated that benzoquinones exert their toxicity by triggering ER stress, as shown by increased expression of CHOP (mRNA and protein levels), intracellular reactive oxygen species, changes in calcium dynamics and caspase-4 activation.	Benzoquinones	23-36	DNA damage inducible transcript 3	Homo sapiens	119-123
31723484-12	2019	Chemotherapy with rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine (Oncovin ), and prednisolone (R-CHOP) was then resorted to which mitigated his symptoms.	Prednisolone	102-114	DNA damage inducible transcript 3	Homo sapiens	118-122
31295479-5	2019	The exposure of HeLa cells to these concentrations of fucoidan induced phosphorylation of ER stress sensors followed by upregulation of Bip/GRP78, CHOP expression which triggered a buildup of malfolded proteins in ER, therefore, initiating unfolded protein response (UPR) mechanism.	fucoidan	54-62	DNA damage inducible transcript 3	Homo sapiens	147-151
31548837-18	2019	In addition, pholidonone had pro-apoptotic effect on AGS and BGC-823 cells, and it upregulated the levels of proteins involved in ER stress, including BiP, PDI, Calnexin, Ero1-Lalpha, IRE1alpha, PERK, CHOP, and cleaved-caspase-3 in AGS and BGC-823 cells.	pholidonone	13-24	DNA damage inducible transcript 3	Homo sapiens	201-205
31322172-4	2019	By contrast, treatment with heparin, an inositol 1,4,5-triphosphate receptor inhibitor, remarkably attenuated cytotoxicity and decreased the intracellular level of Ca2+, the apoptosis rate and the expression levels of GRP78, CHOP and Caspases.	Heparin	28-35	DNA damage inducible transcript 3	Homo sapiens	225-229
31484321-5	2019	The increases observed in C/EBP homologous protein (CHOP), p-IRE, and p-JNK levels in PHMG-P-treated cells indicated the induction of endoplasmic reticulum stress.	polyhexamethyleneguanidine	86-92	DNA damage inducible transcript 3	Homo sapiens	26-50
31484321-5	2019	The increases observed in C/EBP homologous protein (CHOP), p-IRE, and p-JNK levels in PHMG-P-treated cells indicated the induction of endoplasmic reticulum stress.	polyhexamethyleneguanidine	86-92	DNA damage inducible transcript 3	Homo sapiens	52-56
31322172-3	2019	Treatment with the Ca2+-ATPase inhibitor thapsigargin significantly increased PQ-induced cytotoxicity, elevated the intracellular level of Ca2+, and increased the apoptosis rate, the protein expression of glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP), and the activities of caspase-7 and caspase-12 in PQ-treated cells.	Thapsigargin	41-53	DNA damage inducible transcript 3	Homo sapiens	246-270
31524237-0	2019	High glucose and bupivacaine-induced cytotoxicity is mediated by enhanced apoptosis and impaired autophagy via the PERK-ATF4-CHOP and IRE1-TRAF2 signaling pathways.	Glucose	5-12	DNA damage inducible transcript 3	Homo sapiens	125-129
31322172-3	2019	Treatment with the Ca2+-ATPase inhibitor thapsigargin significantly increased PQ-induced cytotoxicity, elevated the intracellular level of Ca2+, and increased the apoptosis rate, the protein expression of glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP), and the activities of caspase-7 and caspase-12 in PQ-treated cells.	Thapsigargin	41-53	DNA damage inducible transcript 3	Homo sapiens	272-276
31524237-0	2019	High glucose and bupivacaine-induced cytotoxicity is mediated by enhanced apoptosis and impaired autophagy via the PERK-ATF4-CHOP and IRE1-TRAF2 signaling pathways.	Bupivacaine	17-28	DNA damage inducible transcript 3	Homo sapiens	125-129
31524237-7	2019	Compared with the control group, high glucose and bupivacaine significantly increased ATF4, CHOP and caspase-12 expression, increased apoptosis, and decreased p-IRE1, TRAF2, LC3-II/LC3-I and Beclin1 expression.	Glucose	38-45	DNA damage inducible transcript 3	Homo sapiens	92-96
31524237-7	2019	Compared with the control group, high glucose and bupivacaine significantly increased ATF4, CHOP and caspase-12 expression, increased apoptosis, and decreased p-IRE1, TRAF2, LC3-II/LC3-I and Beclin1 expression.	Bupivacaine	50-61	DNA damage inducible transcript 3	Homo sapiens	92-96
31524237-8	2019	Promoting autophagy with RAPA partly reversed the high glucose and bupivacaine-induced changes in p-PERK, CHOP, TRAF2, Beclin1, caspase-12 and apoptosis, while inhibiting autophagy with 3-MA further enhanced the changes in ATF4, CHOP, p-IRE1, TRAF2 and apoptosis.	Bupivacaine	67-78	DNA damage inducible transcript 3	Homo sapiens	106-110
31524237-8	2019	Promoting autophagy with RAPA partly reversed the high glucose and bupivacaine-induced changes in p-PERK, CHOP, TRAF2, Beclin1, caspase-12 and apoptosis, while inhibiting autophagy with 3-MA further enhanced the changes in ATF4, CHOP, p-IRE1, TRAF2 and apoptosis.	Bupivacaine	67-78	DNA damage inducible transcript 3	Homo sapiens	229-233
31524237-9	2019	High glucose and bupivacaine induced cytotoxicity in SH-SY5Y cells, at least in part, through enhancing cell apoptosis and inhibiting autophagy via the PERK-ATF4-CHOP and IRE1-TRAF2 signaling pathways.	Glucose	5-12	DNA damage inducible transcript 3	Homo sapiens	162-166
31524237-9	2019	High glucose and bupivacaine induced cytotoxicity in SH-SY5Y cells, at least in part, through enhancing cell apoptosis and inhibiting autophagy via the PERK-ATF4-CHOP and IRE1-TRAF2 signaling pathways.	Bupivacaine	17-28	DNA damage inducible transcript 3	Homo sapiens	162-166
30850561-1	2019	BACKGROUND: About one third of patients with diffuse large B-cell lymphoma (DLBCL) relapse after receiving first-line (1L) treatment of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Doxorubicin	165-176	DNA damage inducible transcript 3	Homo sapiens	209-213
31398899-7	2019	NOB-induced apoptosis was also mediated by regulating endoplasmic reticulum stress via the PERK/elF2alpha/ATF4/CHOP pathway, and downregulating the PI3K/AKT/mTOR pathway.	nobiletin	0-3	DNA damage inducible transcript 3	Homo sapiens	111-115
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Acetylcysteine	25-41	DNA damage inducible transcript 3	Homo sapiens	110-114
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Acetylcysteine	43-46	DNA damage inducible transcript 3	Homo sapiens	110-114
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	tempol	52-58	DNA damage inducible transcript 3	Homo sapiens	110-114
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Reactive Oxygen Species	132-135	DNA damage inducible transcript 3	Homo sapiens	110-114
31054874-6	2019	Whereas the antioxidants N-acetylcysteine (NAC) and Tempol significantly suppressed the expression of BiP and CHOP, suggesting that ROS generation is an early trigger of Cd-activated ER stress.	Cadmium	170-172	DNA damage inducible transcript 3	Homo sapiens	110-114
31054874-11	2019	Additionally, inhibition of autophagy with si-Beclin 1 and 3-Methyladenine significantly ameliorated Cd-induced CHOP expression and cytotoxicity, indicating that autophagy was detrimental in Cd-accumulated ARPE-19 cells, and a positive feedback regulation mechanism may exist between Cd-triggered ER stress and autophagy.	Silicon	43-45	DNA damage inducible transcript 3	Homo sapiens	112-116
31054874-11	2019	Additionally, inhibition of autophagy with si-Beclin 1 and 3-Methyladenine significantly ameliorated Cd-induced CHOP expression and cytotoxicity, indicating that autophagy was detrimental in Cd-accumulated ARPE-19 cells, and a positive feedback regulation mechanism may exist between Cd-triggered ER stress and autophagy.	3-methyladenine	59-74	DNA damage inducible transcript 3	Homo sapiens	112-116
31054874-11	2019	Additionally, inhibition of autophagy with si-Beclin 1 and 3-Methyladenine significantly ameliorated Cd-induced CHOP expression and cytotoxicity, indicating that autophagy was detrimental in Cd-accumulated ARPE-19 cells, and a positive feedback regulation mechanism may exist between Cd-triggered ER stress and autophagy.	Cadmium	101-103	DNA damage inducible transcript 3	Homo sapiens	112-116
31054874-11	2019	Additionally, inhibition of autophagy with si-Beclin 1 and 3-Methyladenine significantly ameliorated Cd-induced CHOP expression and cytotoxicity, indicating that autophagy was detrimental in Cd-accumulated ARPE-19 cells, and a positive feedback regulation mechanism may exist between Cd-triggered ER stress and autophagy.	Cadmium	191-193	DNA damage inducible transcript 3	Homo sapiens	112-116
31054874-11	2019	Additionally, inhibition of autophagy with si-Beclin 1 and 3-Methyladenine significantly ameliorated Cd-induced CHOP expression and cytotoxicity, indicating that autophagy was detrimental in Cd-accumulated ARPE-19 cells, and a positive feedback regulation mechanism may exist between Cd-triggered ER stress and autophagy.	Cadmium	191-193	DNA damage inducible transcript 3	Homo sapiens	112-116
31335477-15	2019	Prolonged survival is obtainable with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP)-like in elderly Chinese patients in all age groups, indicating that the R-CHOP-like regimen should be considered for this population, even for those aged 70 years or older.	Prednisone	97-107	DNA damage inducible transcript 3	Homo sapiens	111-115
31335477-15	2019	Prolonged survival is obtainable with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP)-like in elderly Chinese patients in all age groups, indicating that the R-CHOP-like regimen should be considered for this population, even for those aged 70 years or older.	Prednisone	97-107	DNA damage inducible transcript 3	Homo sapiens	191-195
31390836-8	2019	In this light, we studied the effects of EA-100C red on the expression of CHOP and XBP1, that are implicated in ER-stress-mediated cell death.	ea-100c red	41-52	DNA damage inducible transcript 3	Homo sapiens	74-78
30707413-0	2019	Pollen Typhae Total Flavone Inhibits Endoplasmic Reticulum Stress-Induced Apoptosis in Human Aortic-Vascular Smooth Muscle Cells through Down-Regulating PERK-eIF2alpha-ATF4-CHOP Pathway.	flavone	20-27	DNA damage inducible transcript 3	Homo sapiens	173-177
31390836-9	2019	In summary, our findings revealed that EA-100C red induced ER stress-mediated apoptosis associated to autophagy in GBM cells through CHOP and Beclin1 up-regulation and activation of caspases 3, 9, JNK and NF-kappaB pathway.	ea-100c red	39-50	DNA damage inducible transcript 3	Homo sapiens	133-137
30689468-1	2019	Combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) is regarded as standard care for diffuse large B-cell lymphoma (DLBCL) and upfront intensification of therapy is still controversial.	Prednisone	73-83	DNA damage inducible transcript 3	Homo sapiens	87-91
31047947-5	2019	Differently from dox, HA-Lsdox delivered the drug within the endoplasmic reticulum (ER), inducing protein sulfhydration and ubiquitination, and activating a ER stress pro-apoptotic response mediated by CHOP.	Hyaluronic Acid	22-24	DNA damage inducible transcript 3	Homo sapiens	202-206
30667058-5	2019	This review exhibited the effects of arsenic on the metabolism and signaling pathways within adipose tissue (such as sirtuin 3 [SIRT3]- forkhead box O3 [FOXO3a], mitogen-activated protein kinase [MAPK], phosphoinositide-dependant kinase-1 [PDK-1], unfolded protein response, and C/EBP homologous protein [CHOP10]).	Arsenic	37-44	DNA damage inducible transcript 3	Homo sapiens	305-311
31073022-0	2019	Phase II Study of Bendamustine and Ofatumumab in Elderly Patients with Newly Diagnosed Diffuse Large B-Cell Lymphoma Who Are Poor Candidates for R-CHOP Chemotherapy.	Bendamustine Hydrochloride	18-30	DNA damage inducible transcript 3	Homo sapiens	147-151
31069753-13	2019	Additionally, PFT-alpha significantly attenuated Meth-induced CHOP expression.	pifithrin	14-23	DNA damage inducible transcript 3	Homo sapiens	62-66
31069753-13	2019	Additionally, PFT-alpha significantly attenuated Meth-induced CHOP expression.	Methamphetamine	49-53	DNA damage inducible transcript 3	Homo sapiens	62-66
31054322-3	2019	BeWo human trophoblast cells treated with Delta9-THC (3-30 muM) led to a dose-dependent increase in all ER stress markers and CHOP; these effects could be blocked with CB1R/CB2R antagonists.	Dronabinol	42-52	DNA damage inducible transcript 3	Homo sapiens	126-130
31543772-3	2019	We present a case of newly diagnosed Graves" thyrotoxicosis following a successful R-CHOP (Rituximab, Cyclophosphamide, Doxorubicine, Vincristine and Prednisone) treatment in a patient with concurrent abdominal and thyroid diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	120-132	DNA damage inducible transcript 3	Homo sapiens	85-89
31358006-8	2019	However, this endoplasmic reticulum (ER) pathway was activated in the Cd-exposed ovaries and the expression of GRP78, ATF4, CHOP, and p-JNK was upregulated, which was reversed by treatment with melatonin.	Cadmium	70-72	DNA damage inducible transcript 3	Homo sapiens	124-128
31543772-3	2019	We present a case of newly diagnosed Graves" thyrotoxicosis following a successful R-CHOP (Rituximab, Cyclophosphamide, Doxorubicine, Vincristine and Prednisone) treatment in a patient with concurrent abdominal and thyroid diffuse large B-cell lymphoma (DLBCL).	Prednisone	150-160	DNA damage inducible transcript 3	Homo sapiens	85-89
31329160-8	2019	Remarkably, human recipients of Abx treatment plus OLT (Abx-OLT), despite severe pretransplantation clinical acuity, had higher EP4 and LC3B levels but lower CHOP levels, which coincided with improved hepatocellular function (serum aspartate aminotransferase/serum aspartate aminotransferase [sALT/sAST]) and a decreased incidence of early allograft dysfunction (EAD).	CHEMBL369125	32-35	DNA damage inducible transcript 3	Homo sapiens	158-162
31084986-3	2019	We investigated whether high-glucose concentrations augment lipopolysaccharide-induced reduction in macrophage phagocytosis via the endoplasmic stress-C/EBP homologous protein (CHOP) pathway using animal and laboratory investigations.	Glucose	29-36	DNA damage inducible transcript 3	Homo sapiens	144-175
31118164-2	2019	The use of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) could overcome these difficulties, but blood-brain barrier (BBB) penetration of related drugs is poor.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	13-17
31118164-2	2019	The use of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) could overcome these difficulties, but blood-brain barrier (BBB) penetration of related drugs is poor.	Doxorubicin	48-59	DNA damage inducible transcript 3	Homo sapiens	13-17
31118164-2	2019	The use of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) could overcome these difficulties, but blood-brain barrier (BBB) penetration of related drugs is poor.	Vincristine	61-72	DNA damage inducible transcript 3	Homo sapiens	13-17
31118164-4	2019	We tested the hypothesis that NGR-hTNF can break the BBB, thereby improving penetration and activity of R-CHOP in patients with relapsed/refractory PCNSL (NCT03536039).	pcnsl	148-153	DNA damage inducible transcript 3	Homo sapiens	106-110
31337142-5	2019	Oxaliplatin and DHA also increased the expression of Sestrin 2 (SESN2) and endoplasmic reticulum (ER) stress related C/EBP homologous protein (CHOP).	Oxaliplatin	0-11	DNA damage inducible transcript 3	Homo sapiens	117-141
31337142-5	2019	Oxaliplatin and DHA also increased the expression of Sestrin 2 (SESN2) and endoplasmic reticulum (ER) stress related C/EBP homologous protein (CHOP).	Oxaliplatin	0-11	DNA damage inducible transcript 3	Homo sapiens	143-147
31337142-5	2019	Oxaliplatin and DHA also increased the expression of Sestrin 2 (SESN2) and endoplasmic reticulum (ER) stress related C/EBP homologous protein (CHOP).	Docosahexaenoic Acids	16-19	DNA damage inducible transcript 3	Homo sapiens	117-141
31337142-5	2019	Oxaliplatin and DHA also increased the expression of Sestrin 2 (SESN2) and endoplasmic reticulum (ER) stress related C/EBP homologous protein (CHOP).	Docosahexaenoic Acids	16-19	DNA damage inducible transcript 3	Homo sapiens	143-147
31337142-6	2019	Additionally, treatment with Oxaliplatin and DHA enhanced the binding of CHOP to the promotor region of SESN2, increasing SESN2 expression.	Oxaliplatin	29-40	DNA damage inducible transcript 3	Homo sapiens	73-77
31337142-6	2019	Additionally, treatment with Oxaliplatin and DHA enhanced the binding of CHOP to the promotor region of SESN2, increasing SESN2 expression.	Docosahexaenoic Acids	45-48	DNA damage inducible transcript 3	Homo sapiens	73-77
31084986-3	2019	We investigated whether high-glucose concentrations augment lipopolysaccharide-induced reduction in macrophage phagocytosis via the endoplasmic stress-C/EBP homologous protein (CHOP) pathway using animal and laboratory investigations.	Glucose	29-36	DNA damage inducible transcript 3	Homo sapiens	177-181
30488444-9	2019	The increased osteogenic differentiation ability and IDH1 expression, as induced by the DDIT3 knockdown, could be partially turned over by the addition of NF-kappaB inhibitor BAY 11-7082.	3-(4-methylphenylsulfonyl)-2-propenenitrile	175-186	DNA damage inducible transcript 3	Homo sapiens	88-93
31183612-6	2019	Resveratrol decreased protein expression of the ER stress markers, p-PERK, p-IRE1alpha, and CHOP, and increased the expression of the ER-associated degradation (ERAD) factors, SEL1L and HRD1, in tunicamycin-treated cells.	Resveratrol	0-11	DNA damage inducible transcript 3	Homo sapiens	92-96
31280230-7	2019	Among 125 patients receiving CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens, complete response and complete control were increased in patients receiving triple antiemetics, compared to those with double antiemetics.	Doxorubicin	35-46	DNA damage inducible transcript 3	Homo sapiens	29-33
31280230-7	2019	Among 125 patients receiving CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens, complete response and complete control were increased in patients receiving triple antiemetics, compared to those with double antiemetics.	Vincristine	66-77	DNA damage inducible transcript 3	Homo sapiens	29-33
31280230-7	2019	Among 125 patients receiving CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens, complete response and complete control were increased in patients receiving triple antiemetics, compared to those with double antiemetics.	Prednisone	79-89	DNA damage inducible transcript 3	Homo sapiens	29-33
31516154-4	2019	He was managed by the oncologist with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) regimen which alleviated his symptoms considerably after completion of three cycles and was under follow-up.	Cyclophosphamide	57-73	DNA damage inducible transcript 3	Homo sapiens	40-44
31516154-4	2019	He was managed by the oncologist with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) regimen which alleviated his symptoms considerably after completion of three cycles and was under follow-up.	Doxorubicin	75-86	DNA damage inducible transcript 3	Homo sapiens	40-44
31516154-4	2019	He was managed by the oncologist with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) regimen which alleviated his symptoms considerably after completion of three cycles and was under follow-up.	Prednisone	105-115	DNA damage inducible transcript 3	Homo sapiens	40-44
31206696-0	2019	Tissue-Specific Distribution of Sphingomyelin Species in Pork Chop Revealed by Matrix-Assisted Laser Desorption/Ionization-Imaging Mass Spectrometry.	Sphingomyelins	32-45	DNA damage inducible transcript 3	Homo sapiens	62-66
31305432-7	2019	INTERVENTION: The patient was treated with 6 courses of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	119-129	DNA damage inducible transcript 3	Homo sapiens	133-137
30976089-8	2019	Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP.	Phosphorylcholine	24-41	DNA damage inducible transcript 3	Homo sapiens	43-47
31180536-7	2019	In addition, treatment with metformin increased the expression of Bip, CHOP and caspase-12 in vitro, activating endoplasmic reticulum (ER) stress.	Metformin	28-37	DNA damage inducible transcript 3	Homo sapiens	71-75
31180536-10	2019	Finally, treatment with metformin inhibited thyroid cancer growth and increased the expression of Bip and CHOP in a TPC-1 cell xenograft model.	Metformin	24-33	DNA damage inducible transcript 3	Homo sapiens	106-110
30976089-8	2019	Lipopolysaccharide from phosphorylcholine (ChoP)-positive bacteria induced NLRP3 and caspase-1 proteins in human alveolar epithelial cells, however antagonism of PAFR prevented NLRP3 activation by ChoP.	Phosphorylcholine	24-41	DNA damage inducible transcript 3	Homo sapiens	197-201
31212679-5	2019	The C. turczaninowii extract attenuated the increased mRNA expression of IL-6, TNF-alpha, and CHOP in hASMCs under high glucose conditions.	Glucose	120-127	DNA damage inducible transcript 3	Homo sapiens	94-98
31357761-9	2019	SP600125 and SB203580 had inhibited oxidative stress and apoptosis induced by palmitic acid (including CYP2E1, MDA, Bax, Bcl-2, caspase3, CHOP) (P&lt; 0.05).	pyrazolanthrone	0-8	DNA damage inducible transcript 3	Homo sapiens	138-142
31357761-9	2019	SP600125 and SB203580 had inhibited oxidative stress and apoptosis induced by palmitic acid (including CYP2E1, MDA, Bax, Bcl-2, caspase3, CHOP) (P&lt; 0.05).	SB 203580	13-21	DNA damage inducible transcript 3	Homo sapiens	138-142
31316722-8	2019	Our results revealed that Ni2+ treatment significantly primed the Zn2+-induced ER stress response, especially expression of the CCAAT-enhancer-binding protein homologous protein (CHOP).	Nickel(2+)	26-30	DNA damage inducible transcript 3	Homo sapiens	128-177
31198003-13	2019	Furthermore, after 4-PBA inhibiting ERS, the expressions of GRP78, CHOP, IL-1beta, TNF-alpha, and P65 were significantly decreased ( P&lt;0.05), and flow cytometry results showed that cell apoptotic rate in smoking group was decreased, showing significant difference compared with the non-smoking group ( P&lt;0.05).	4-phenylbutylamine	19-24	DNA damage inducible transcript 3	Homo sapiens	67-71
31316722-8	2019	Our results revealed that Ni2+ treatment significantly primed the Zn2+-induced ER stress response, especially expression of the CCAAT-enhancer-binding protein homologous protein (CHOP).	Nickel(2+)	26-30	DNA damage inducible transcript 3	Homo sapiens	179-183
31316722-8	2019	Our results revealed that Ni2+ treatment significantly primed the Zn2+-induced ER stress response, especially expression of the CCAAT-enhancer-binding protein homologous protein (CHOP).	Zinc	66-70	DNA damage inducible transcript 3	Homo sapiens	128-177
31316722-8	2019	Our results revealed that Ni2+ treatment significantly primed the Zn2+-induced ER stress response, especially expression of the CCAAT-enhancer-binding protein homologous protein (CHOP).	Zinc	66-70	DNA damage inducible transcript 3	Homo sapiens	179-183
31360107-0	2019	PERK/eIF-2alpha/CHOP Pathway Dependent ROS Generation Mediates Butein-induced Non-small-cell Lung Cancer Apoptosis and G2/M Phase Arrest.	Reactive Oxygen Species	39-42	DNA damage inducible transcript 3	Homo sapiens	16-20
31281836-6	2019	The mechanistic study showed that albendazole induced endoplasmic reticulum (ER) stress, evidenced by increase of CHOP, ATF-4, caspase-4, and caspase-12.	Albendazole	34-45	DNA damage inducible transcript 3	Homo sapiens	114-118
31360107-0	2019	PERK/eIF-2alpha/CHOP Pathway Dependent ROS Generation Mediates Butein-induced Non-small-cell Lung Cancer Apoptosis and G2/M Phase Arrest.	butein	63-69	DNA damage inducible transcript 3	Homo sapiens	16-20
30848542-6	2019	In addition, Ost enhanced the levels of endoplasmic reticulum (ER) stress proteins (GRP78/Bip, CHOP, Caspase-4, IRE1alpha, PERK, JNK, P-JNK, and ATF4), decreased the cell proliferation and cycle-associated protein (Phospho-Histone H3, P-Cdc25C, Cdc25C, P-Cdc2, Cdc2, and Cyclin B1) level.	osthol	13-16	DNA damage inducible transcript 3	Homo sapiens	95-99
31092035-6	2019	In addition, pyridoxine induced reactive oxygen species (ROS) generation and alteration of mitochondrial membrane potential transition (MPT), including Bcl-2 family protein expression and consequently Ca2+ accumulation and changes of endoplasmic reticulum (ER) stress-related protein expression such as phospho-PERK, caspase-12, Grp78, and CHOP.	Pyridoxine	13-23	DNA damage inducible transcript 3	Homo sapiens	340-344
30925456-0	2019	Oxymatrine ameliorates agomelatine-induced hepatocyte injury through promoting proteasome-mediated CHOP degradation.	oxymatrine	0-10	DNA damage inducible transcript 3	Homo sapiens	99-103
30925456-0	2019	Oxymatrine ameliorates agomelatine-induced hepatocyte injury through promoting proteasome-mediated CHOP degradation.	agomelatine	23-34	DNA damage inducible transcript 3	Homo sapiens	99-103
30925456-7	2019	Agomelatine treatment resulted in accumulation of CHOP protein in L02 cells, and this phenomenon could be significantly reduced by OMT, whereas abolished by MG132 treatment.	oxymatrine	131-134	DNA damage inducible transcript 3	Homo sapiens	50-54
30925456-8	2019	CONCLUSION: We have demonstrated for the first time that OMT ameliorates the hepatocyte toxicity induced by agomelatine through decreasing CHOP on protein level.	oxymatrine	57-60	DNA damage inducible transcript 3	Homo sapiens	139-143
30925456-8	2019	CONCLUSION: We have demonstrated for the first time that OMT ameliorates the hepatocyte toxicity induced by agomelatine through decreasing CHOP on protein level.	agomelatine	108-119	DNA damage inducible transcript 3	Homo sapiens	139-143
30919222-0	2019	ABT-263 exhibits apoptosis-inducing potential in oral cancer cells by targeting C/EBP-homologous protein.	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	0-3	DNA damage inducible transcript 3	Homo sapiens	80-104
30919222-9	2019	In addition, we found that ABT-263 considerably enhanced the expression levels of the C/EBP-homologous protein (CHOP) and its mRNA, resulting in apoptosis induction in four other human oral cancer-derived cell lines (MC-3, YD-15, HN22, and Ca9.22).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	27-30	DNA damage inducible transcript 3	Homo sapiens	86-110
30919222-9	2019	In addition, we found that ABT-263 considerably enhanced the expression levels of the C/EBP-homologous protein (CHOP) and its mRNA, resulting in apoptosis induction in four other human oral cancer-derived cell lines (MC-3, YD-15, HN22, and Ca9.22).	2,2'-azino-di-(3-ethylbenzothiazoline)-6-sulfonic acid	27-30	DNA damage inducible transcript 3	Homo sapiens	112-116
30755730-0	2019	CFP suppresses breast cancer cell growth by TES-mediated upregulation of the transcription factor DDIT3.	TES	44-47	DNA damage inducible transcript 3	Homo sapiens	98-103
31126528-24	2019	Epirubicin is an alternative drug to doxorubicin in regular R-CHOP with mild long-term cardiotoxicity.	Epirubicin	0-10	DNA damage inducible transcript 3	Homo sapiens	62-66
31151970-7	2019	The patient received rituximab, cyclophosphamide, doxorubicin hydrochloride, vincristine and prednisolone (CHOP) immunochemotherapy with gradual but complete resolution of the erythroderma.	Prednisolone	93-105	DNA damage inducible transcript 3	Homo sapiens	107-111
31133013-9	2019	RESULTS: Treatment of E7-expressing TC-1 tumor cells with 3-BrPA induced significantly higher in vitro cytotoxicity and resulted in upregulation of endoplasmic reticulum stress markers (CHOP and GRP78).	bromopyruvate	58-64	DNA damage inducible transcript 3	Homo sapiens	186-190
31138775-11	2019	GA treatment increased intracellular ROS level, expression levels of GRP (glucose-regulated protein) 78, CHOP (C/EBP-homologous protein), ATF (activating transcription factor) 6 and caspase 12, as well as the phosphorylation levels of PERK (protein kinase R-like ER kinase) and IRE (inositol-requiring enzyme) 1alpha.	Gallium	0-2	DNA damage inducible transcript 3	Homo sapiens	105-109
31138775-11	2019	GA treatment increased intracellular ROS level, expression levels of GRP (glucose-regulated protein) 78, CHOP (C/EBP-homologous protein), ATF (activating transcription factor) 6 and caspase 12, as well as the phosphorylation levels of PERK (protein kinase R-like ER kinase) and IRE (inositol-requiring enzyme) 1alpha.	Gallium	0-2	DNA damage inducible transcript 3	Homo sapiens	111-135
30901302-10	2019	In patients age younger than 60 years, ibrutinib plus R-CHOP improved EFS (HR, 0.579), PFS (HR, 0.556), and OS (HR, 0.330) and slightly increased serious adverse events (35.7% v 28.6%), but the proportion of patients receiving at least six cycles of R-CHOP was similar between treatment arms (92.9% v 93.0%).	ibrutinib	39-48	DNA damage inducible transcript 3	Homo sapiens	252-256
30901302-11	2019	In patients age 60 years or older, ibrutinib plus R-CHOP worsened EFS, PFS, and OS, increased serious adverse events (63.4% v 38.2%), and decreased the proportion of patients receiving at least six cycles of R-CHOP (73.7% v 88.8%).	ibrutinib	35-44	DNA damage inducible transcript 3	Homo sapiens	210-214
30901302-14	2019	In patients age 60 years or older, ibrutinib plus R-CHOP was associated with increased toxicity, leading to compromised R-CHOP administration and worse outcomes.	ibrutinib	35-44	DNA damage inducible transcript 3	Homo sapiens	122-126
31086026-7	2019	Flaccidoxide-13-acetate also provoked endoplasmic reticulum (ER) stress and led to activation of the PERK-eIF2alpha-ATF6-CHOP pathway.	flaccidoxide-13-acetate	0-23	DNA damage inducible transcript 3	Homo sapiens	121-125
30850381-2	2019	Here, we report a phase 1b study investigating dose escalation of the BCL2 inhibitor, venetoclax, in combination with rituximab or obinutuzumab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-/G-CHOP) chemotherapy in B-cell NHL.	venetoclax	86-96	DNA damage inducible transcript 3	Homo sapiens	213-217
31190740-7	2019	Moreover, we found that the apoptotic effects of PNAP-6 proceeded through extrinsic apoptosis and ER stress pathways, by increasing the expression of Fas protein and ER stress markers, including PERK, ATF4, CHOP, p-IRE1alpha, and XBP-1s.	pnap-6	49-55	DNA damage inducible transcript 3	Homo sapiens	207-211
30801659-6	2019	Notably, tolvaptan increased the levels of unfolded protein response (UPR) marker DDIT3 and eIF2alpha phosphorylation (a UPR-induced event), which could block the translation of CYP11B2 mRNA into protein and thereby inhibit aldosterone production.	Tolvaptan	9-18	DNA damage inducible transcript 3	Homo sapiens	82-87
30730256-0	2019	Involvement of ERK1/2-mediated ELK1/CHOP/DR5 pathway in 6-(methylsulfinyl)hexyl isothiocyanate-induced apoptosis of colorectal cancer cells.	6-(Methylsulfinyl)hexyl isothiocyanate	56-94	DNA damage inducible transcript 3	Homo sapiens	36-40
30730256-6	2019	6-MSITC stimulated ERK1/2 phosphorylation, and then activated ERK1/2 signaling including ELK1 phosphorylation, and upregulation of C/EBP homologous protein (CHOP) and death receptor 5 (DR5).	6-(Methylsulfinyl)hexyl isothiocyanate	0-7	DNA damage inducible transcript 3	Homo sapiens	131-155
30730256-6	2019	6-MSITC stimulated ERK1/2 phosphorylation, and then activated ERK1/2 signaling including ELK1 phosphorylation, and upregulation of C/EBP homologous protein (CHOP) and death receptor 5 (DR5).	6-(Methylsulfinyl)hexyl isothiocyanate	0-7	DNA damage inducible transcript 3	Homo sapiens	157-161
30730256-8	2019	These results indicated that ERK1/2-mediated ELK1/CHOP/DR5 pathway is involved in 6-MSITC-induced apoptosis in colorectal cancer cells.	6-(Methylsulfinyl)hexyl isothiocyanate	82-89	DNA damage inducible transcript 3	Homo sapiens	50-54
30336657-5	2019	RESULTS: Tunicamycin increased the expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules, including spliced X-box binding protein 1 (XBP-1), transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP), and ATF6.	Tunicamycin	9-20	DNA damage inducible transcript 3	Homo sapiens	206-255
30336657-5	2019	RESULTS: Tunicamycin increased the expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules, including spliced X-box binding protein 1 (XBP-1), transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP), and ATF6.	Tunicamycin	9-20	DNA damage inducible transcript 3	Homo sapiens	257-261
30336657-7	2019	Furthermore, siRNA knockdowns of XBP-1, CHOP, and ATF6 blocked the tunicamycin-induced mRNA expressions and glycoprotein productions of MUC5AC and MUC5B.	Tunicamycin	67-78	DNA damage inducible transcript 3	Homo sapiens	40-44
30686772-12	2019	The repeated use of R-CHOP or R-CVP as first- and second-line treatment yielded high 2-year mortality rates (R-CHOP + R-CHOP, 17.3%; R-CVP + R-CVP, 21.1%).	r-cvp	30-35	DNA damage inducible transcript 3	Homo sapiens	111-115
30686772-12	2019	The repeated use of R-CHOP or R-CVP as first- and second-line treatment yielded high 2-year mortality rates (R-CHOP + R-CHOP, 17.3%; R-CVP + R-CVP, 21.1%).	r-cvp	133-138	DNA damage inducible transcript 3	Homo sapiens	22-26
30686772-12	2019	The repeated use of R-CHOP or R-CVP as first- and second-line treatment yielded high 2-year mortality rates (R-CHOP + R-CHOP, 17.3%; R-CVP + R-CVP, 21.1%).	r-cvp	30-35	DNA damage inducible transcript 3	Homo sapiens	111-115
30686772-12	2019	The repeated use of R-CHOP or R-CVP as first- and second-line treatment yielded high 2-year mortality rates (R-CHOP + R-CHOP, 17.3%; R-CVP + R-CVP, 21.1%).	r-cvp	133-138	DNA damage inducible transcript 3	Homo sapiens	22-26
30620997-7	2019	ZnO NRs and ZnO Mini-NRs significantly promoted the expression of ER stress genes HSPA5, DDIT3, XBP-1s and apoptotic gene CASP3, whereas PA also modestly promoted the expression of HSPA5, DDIT3 and CASP3.	Zinc Oxide	0-3	DNA damage inducible transcript 3	Homo sapiens	89-94
30620997-7	2019	ZnO NRs and ZnO Mini-NRs significantly promoted the expression of ER stress genes HSPA5, DDIT3, XBP-1s and apoptotic gene CASP3, whereas PA also modestly promoted the expression of HSPA5, DDIT3 and CASP3.	Zinc Oxide	0-3	DNA damage inducible transcript 3	Homo sapiens	188-193
30620997-7	2019	ZnO NRs and ZnO Mini-NRs significantly promoted the expression of ER stress genes HSPA5, DDIT3, XBP-1s and apoptotic gene CASP3, whereas PA also modestly promoted the expression of HSPA5, DDIT3 and CASP3.	Zinc Oxide	12-15	DNA damage inducible transcript 3	Homo sapiens	89-94
30620997-7	2019	ZnO NRs and ZnO Mini-NRs significantly promoted the expression of ER stress genes HSPA5, DDIT3, XBP-1s and apoptotic gene CASP3, whereas PA also modestly promoted the expression of HSPA5, DDIT3 and CASP3.	Zinc Oxide	12-15	DNA damage inducible transcript 3	Homo sapiens	188-193
30854784-8	2019	Accordingly, the proapoptotic activity of FAM175B was significantly rescued by treatment with si-ATF4 and the CHOP inhibitor 4-PBA.	4-phenylbutylamine	125-130	DNA damage inducible transcript 3	Homo sapiens	110-114
30974805-3	2019	Our data showed that EtOH induces oxidative and endoplasmic reticulum (ER) stress, as demonstrated by reactive oxygen species (ROS) and ER stress markers Grp78, ATF6, PERK and, CHOP increase.	Ethanol	21-25	DNA damage inducible transcript 3	Homo sapiens	177-181
30692634-5	2019	Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP.	Reactive Oxygen Species	70-93	DNA damage inducible transcript 3	Homo sapiens	143-147
30692634-5	2019	Overexpression of RUNX3 increased DR5 expression via induction of the reactive oxygen species (ROS)-endoplasmic reticulum (ER) stress-effector CHOP.	Reactive Oxygen Species	95-98	DNA damage inducible transcript 3	Homo sapiens	143-147
30529689-4	2019	Furthermore, Lop potentiates Btz-mediated ER stress and ER dilation due to misfolded protein accumulation and Ca2+ imbalance, leading to CHOP upregulation and subsequent paraptosis-like cell death.	Bortezomib	29-32	DNA damage inducible transcript 3	Homo sapiens	137-141
30967394-2	2019	The purpose of the present study was to investigate microRNA (miRNA) involvement in vincristine resistance in DLBCL, which was pursued by functional in vitro analysis in DLBCL cell lines and by outcome analysis of patients with DLBCL treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Vincristine	84-95	DNA damage inducible transcript 3	Homo sapiens	320-324
30618158-8	2019	Western blotting assay demonstrated that genistein increased ER stress-associated protein expression such as IRE-1alpha, Calpain 1, GRP78, GADD153, caspase-7, caspase-4, and ATF-6alpha at 20-50 muM treatment and increased apoptosis associated protein expression such as pro-apoptotic protein Bax, PARP-cleavage, caspase-9, and -3, but decreased anti-apoptotic protein such as Bcl-2 and Bid in HL-60 cells.	Genistein	41-50	DNA damage inducible transcript 3	Homo sapiens	139-146
30798142-6	2019	Furthermore, luteolin increases levels of intracellular reactive oxygen species (ROS) by activation of lethal endoplasmic reticulum stress response and mitochondrial dysfunction in glioblastoma cells, and by activation of ER stress-associated proteins expressions, including phosphorylation of eIF2alpha, PERK, CHOP, ATF4, and cleaved-caspase 12.	Reactive Oxygen Species	56-79	DNA damage inducible transcript 3	Homo sapiens	311-315
30798142-6	2019	Furthermore, luteolin increases levels of intracellular reactive oxygen species (ROS) by activation of lethal endoplasmic reticulum stress response and mitochondrial dysfunction in glioblastoma cells, and by activation of ER stress-associated proteins expressions, including phosphorylation of eIF2alpha, PERK, CHOP, ATF4, and cleaved-caspase 12.	Reactive Oxygen Species	81-84	DNA damage inducible transcript 3	Homo sapiens	311-315
30689002-0	2019	Cyclophosphamide dose adjustment based on body weight and albuminemia in elderly patients treated with R-mini-CHOP.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	110-114
30618158-9	2019	Calpain 1, GRP78, and GADD153 were increased in HL-60 cells after exposure to 40 muM of genistein.	Genistein	88-97	DNA damage inducible transcript 3	Homo sapiens	22-29
30746902-7	2019	These data indicate that gly-HDL may induce macrophage apoptosis through activating ER stress-CHOP pathway and ER stress mediates gly-HDL-induced autophagy, which in turn protects macrophages against apoptosis by alleviating CHOP pathway.	Glycine	25-28	DNA damage inducible transcript 3	Homo sapiens	94-98
30259568-10	2019	Total protein expression and ATF4 nuclear import were increased, and CEBP-homologous protein (CHOP) expression increased after treatment with 20(S)-PPD.	Sulfur	145-148	DNA damage inducible transcript 3	Homo sapiens	69-92
30259568-10	2019	Total protein expression and ATF4 nuclear import were increased, and CEBP-homologous protein (CHOP) expression increased after treatment with 20(S)-PPD.	Sulfur	145-148	DNA damage inducible transcript 3	Homo sapiens	94-98
30746902-2	2019	Our results showed that gly-HDL caused macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2alpha, and CHOP up-regulation, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and the gene silencing of PERK and CHOP.	Glycine	24-27	DNA damage inducible transcript 3	Homo sapiens	293-297
30817944-5	2019	The sensitizing effect of AC to TRAIL was well correlated with inhibition of death receptor 5 (DR5) CHOP, and p53 expression.	auriculasin	26-28	DNA damage inducible transcript 3	Homo sapiens	100-104
30746902-2	2019	Our results showed that gly-HDL caused macrophage apoptosis with concomitant activation of ER stress pathway, including nuclear translocation of activating transcription factor 6, phosphorylation of protein kinase-like ER kinase (PERK) and eukaryotic translation initiation factor 2alpha, and CHOP up-regulation, which were inhibited by 4-phenylbutyric acid (PBA, an ER stress inhibitor) and the gene silencing of PERK and CHOP.	Glycine	24-27	DNA damage inducible transcript 3	Homo sapiens	423-427
30746902-7	2019	These data indicate that gly-HDL may induce macrophage apoptosis through activating ER stress-CHOP pathway and ER stress mediates gly-HDL-induced autophagy, which in turn protects macrophages against apoptosis by alleviating CHOP pathway.	Glycine	25-28	DNA damage inducible transcript 3	Homo sapiens	225-229
30746902-5	2019	Gly-HDL-induced apoptosis, PERK phosphorylation and CHOP up-regulation were suppressed by rapamycin (an autophagy inducer), whereas aggravated by 3-methyladenine (an autophagy inhibitor) and beclin-1 siRNA.	Glycine	0-3	DNA damage inducible transcript 3	Homo sapiens	52-56
30746902-7	2019	These data indicate that gly-HDL may induce macrophage apoptosis through activating ER stress-CHOP pathway and ER stress mediates gly-HDL-induced autophagy, which in turn protects macrophages against apoptosis by alleviating CHOP pathway.	Glycine	130-133	DNA damage inducible transcript 3	Homo sapiens	225-229
30547695-5	2019	CR rates for PTCL and DLBCL patients were 46% and 49%, respectively, similar with reported CR rates with CHOP-like chemotherapy (p = .6).	Chromium	91-93	DNA damage inducible transcript 3	Homo sapiens	105-109
30746902-5	2019	Gly-HDL-induced apoptosis, PERK phosphorylation and CHOP up-regulation were suppressed by rapamycin (an autophagy inducer), whereas aggravated by 3-methyladenine (an autophagy inhibitor) and beclin-1 siRNA.	Sirolimus	90-99	DNA damage inducible transcript 3	Homo sapiens	52-56
30654087-6	2019	The findings suggested that SiO2-NPs and mSiO2-NPs exposure increased the expression levels of two ER stress markers, e.g. BiP and CHOP, which could be inhibited by the ER stress inhibitor 4-PBA, following with decreased apoptosis rates in HPAEpiC.	4-phenylbutylamine	189-194	DNA damage inducible transcript 3	Homo sapiens	131-135
30764601-8	2019	Indeed, the knockdown of C/EBP homologous protein (CHOP), a transcription factor that functions under ER stress conditions, markedly reduced DHA-mediated apoptosis, indicating that CHOP plays an essential role in the anti-cancer activity of DHA.	Docosahexaenoic Acids	141-144	DNA damage inducible transcript 3	Homo sapiens	25-49
30764601-8	2019	Indeed, the knockdown of C/EBP homologous protein (CHOP), a transcription factor that functions under ER stress conditions, markedly reduced DHA-mediated apoptosis, indicating that CHOP plays an essential role in the anti-cancer activity of DHA.	Docosahexaenoic Acids	141-144	DNA damage inducible transcript 3	Homo sapiens	51-55
30764601-8	2019	Indeed, the knockdown of C/EBP homologous protein (CHOP), a transcription factor that functions under ER stress conditions, markedly reduced DHA-mediated apoptosis, indicating that CHOP plays an essential role in the anti-cancer activity of DHA.	Docosahexaenoic Acids	141-144	DNA damage inducible transcript 3	Homo sapiens	181-185
30764601-8	2019	Indeed, the knockdown of C/EBP homologous protein (CHOP), a transcription factor that functions under ER stress conditions, markedly reduced DHA-mediated apoptosis, indicating that CHOP plays an essential role in the anti-cancer activity of DHA.	Docosahexaenoic Acids	241-244	DNA damage inducible transcript 3	Homo sapiens	25-49
30764601-8	2019	Indeed, the knockdown of C/EBP homologous protein (CHOP), a transcription factor that functions under ER stress conditions, markedly reduced DHA-mediated apoptosis, indicating that CHOP plays an essential role in the anti-cancer activity of DHA.	Docosahexaenoic Acids	241-244	DNA damage inducible transcript 3	Homo sapiens	51-55
30764601-8	2019	Indeed, the knockdown of C/EBP homologous protein (CHOP), a transcription factor that functions under ER stress conditions, markedly reduced DHA-mediated apoptosis, indicating that CHOP plays an essential role in the anti-cancer activity of DHA.	Docosahexaenoic Acids	241-244	DNA damage inducible transcript 3	Homo sapiens	181-185
30863363-10	2019	Both palmitate and brefeldin induced PERK, CHOP and BiP gene expression, which was partially, but significantly prevented by rapamycin.	Palmitates	5-14	DNA damage inducible transcript 3	Homo sapiens	43-47
30992670-1	2019	Objective: To compare cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) and CHOP plus etoposide (CHOPE) with regard to outcomes including efficacy and safety for patients with peripheral T-cell lymphoma (PTCL).	Prednisone	70-80	DNA damage inducible transcript 3	Homo sapiens	82-86
30871017-4	2019	Capsazepine can modulate Janus activated kinase (JAK)/signal transducer and activator of the transcription (STAT) pathway, intracellular Ca2+ concentration, and reactive oxygen species (ROS)-JNK-CCAAT/enhancer-binding protein homologous protein (CHOP) pathways.	capsazepine	0-11	DNA damage inducible transcript 3	Homo sapiens	246-250
30871017-4	2019	Capsazepine can modulate Janus activated kinase (JAK)/signal transducer and activator of the transcription (STAT) pathway, intracellular Ca2+ concentration, and reactive oxygen species (ROS)-JNK-CCAAT/enhancer-binding protein homologous protein (CHOP) pathways.	Reactive Oxygen Species	186-189	DNA damage inducible transcript 3	Homo sapiens	246-250
30581162-2	2019	Addition of rituximab to a reduced dose (RD) of cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy might improve patient outcomes with an improved toxicity profile when provided to elderly patients with diffuse large B-cell lymphoma.	Prednisolone	96-108	DNA damage inducible transcript 3	Homo sapiens	112-116
30820153-4	2019	The effect of tunicamycin on the expression of the unfolded protein response (UPR)-related proteins BiP and CHOP was assayed by western blotting with or without inhibition of Orai1.	Tunicamycin	14-25	DNA damage inducible transcript 3	Homo sapiens	108-112
30499118-10	2019	Both DSF/copper and CuET evoked hallmarks of UPR in PCa cells, documented by upregulation of ATF4, CHOP and phospho-eIF2alpha, with ensuing heat shock response encompassing activation of HSF1 and HSP70.	Copper	9-15	DNA damage inducible transcript 3	Homo sapiens	99-103
30893871-7	2019	Molecular modulation of endoplasmic reticulum (ER) stress induced by tunicamycin was studied by western blot analysis of the ER stress markers GRP78, CHOP and p-IRE1.	Tunicamycin	69-80	DNA damage inducible transcript 3	Homo sapiens	150-154
30708101-8	2019	Furthermore, honokiol treatment decreased cell migration and enhanced cell apoptosis, which is accompanied by the upregulation of the expressions of ER stress-induced apoptotic signaling molecules such as GRP78, phosphorylated PERK, phosphorylated eIF2alpha, CHOP, Bcl-2, Bax, and cleaved Caspase 9.	honokiol	13-21	DNA damage inducible transcript 3	Homo sapiens	259-263
30708101-9	2019	Honokiol treatment-induced increase of ER stress-related signaling molecules and apoptotic proteins in A549 and 95-D cells were reversed by CHOP siRNA.	honokiol	0-8	DNA damage inducible transcript 3	Homo sapiens	140-144
30483907-0	2019	Glycine supplementation to breast-fed piglets attenuates post-weaning jejunal epithelial apoptosis: a functional role of CHOP signaling.	Glycine	0-7	DNA damage inducible transcript 3	Homo sapiens	121-125
30483907-1	2019	This study was conducted to test the hypothesis that preweaning  glycine supplementation to breast-fed piglets alleviated the post-weaning  apoptosis of jejunal epithelium through CHOP signaling.	Glycine	65-72	DNA damage inducible transcript 3	Homo sapiens	180-184
30483907-9	2019	Among the proteins related to apoptosis, abundances of CHOP and p53 were reduced, whereas those of Bcl-2 and Bcl-xL were enhanced in the jejunum of 100-200% glycine-supplemented piglets.	Glycine	157-164	DNA damage inducible transcript 3	Homo sapiens	55-59
30483907-11	2019	The beneficial effect of glycine was associated with improved intestinal mucosal barrier and reduced apoptosis of enterocytes through CHOP signaling.	Glycine	25-32	DNA damage inducible transcript 3	Homo sapiens	134-138
30657961-6	2019	We found that ER stress marker GRP78 expression increased with CHOP and TRIB3 expression in normal endometrial stromal cells (NESCs) treated with tunicamycin, and this increase was accompanied by decreased AKT and mTOR activity and cellular invasiveness.	Tunicamycin	146-157	DNA damage inducible transcript 3	Homo sapiens	63-67
30863363-10	2019	Both palmitate and brefeldin induced PERK, CHOP and BiP gene expression, which was partially, but significantly prevented by rapamycin.	brefeldin	19-28	DNA damage inducible transcript 3	Homo sapiens	43-47
30863363-10	2019	Both palmitate and brefeldin induced PERK, CHOP and BiP gene expression, which was partially, but significantly prevented by rapamycin.	Sirolimus	125-134	DNA damage inducible transcript 3	Homo sapiens	43-47
30863363-12	2019	Compared to untreated T2D cells, rapamycin-exposed diabetic islets showed improved insulin secretion, reduced proportion of beta cells showing signs of apoptosis and better preserved insulin granules, mitochondria and ER ultrastructure; this was associated with significant reduction of PERK, CHOP and BiP gene expression.	Sirolimus	33-42	DNA damage inducible transcript 3	Homo sapiens	293-297
30674641-3	2019	In the present study, we found that palmitate treatment of human primary articular chondrocytes increased the expression of ER stress markers [activating transcription factor 4 (ATF4), C/EBP homologous protein (CHOP)] and apoptosis markers [cytochrome c and cleaved caspase-3 (CC3)].	Palmitates	36-45	DNA damage inducible transcript 3	Homo sapiens	185-209
30674641-3	2019	In the present study, we found that palmitate treatment of human primary articular chondrocytes increased the expression of ER stress markers [activating transcription factor 4 (ATF4), C/EBP homologous protein (CHOP)] and apoptosis markers [cytochrome c and cleaved caspase-3 (CC3)].	Palmitates	36-45	DNA damage inducible transcript 3	Homo sapiens	211-215
30552901-0	2019	2-Bromopalmitate sensitizes osteosarcoma cells to adriamycin-induced apoptosis via the modulation of CHOP.	Doxorubicin	50-60	DNA damage inducible transcript 3	Homo sapiens	101-105
30770792-7	2019	BV6 consistently abolishes TM-stimulated accumulation of ER stress markers such as glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) and reduces protein kinase RNA-like ER kinase (PERK) phosphorylation and X box-binding protein 1 (XBP1) splicing upon TM treatment.	Tunicamycin	27-29	DNA damage inducible transcript 3	Homo sapiens	124-148
30770792-7	2019	BV6 consistently abolishes TM-stimulated accumulation of ER stress markers such as glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) and reduces protein kinase RNA-like ER kinase (PERK) phosphorylation and X box-binding protein 1 (XBP1) splicing upon TM treatment.	Tunicamycin	27-29	DNA damage inducible transcript 3	Homo sapiens	150-154
30625303-7	2019	Exocrine acinar cells exposed to high Ins or Ins+Glu concentrations (but not Glu alone) exhibited ER-stress UPR, demonstrated by significant increase of transcript and protein levels of downstream markers in the ATF6 and IRE1 transduction arms, including: sXBP1, cleaved ATF6, XBP1, CHOP, IRE1-p and caspase-12.	Glucose	49-52	DNA damage inducible transcript 3	Homo sapiens	283-287
30552901-7	2019	Moreover, CHOP was remarkably elevated in the combination group, and silencing of CHOP almost completely blocked the apoptosis induced by the combination of 2-bromopalmitate and adriamycin.	2-bromopalmitate	157-173	DNA damage inducible transcript 3	Homo sapiens	10-14
30552901-7	2019	Moreover, CHOP was remarkably elevated in the combination group, and silencing of CHOP almost completely blocked the apoptosis induced by the combination of 2-bromopalmitate and adriamycin.	2-bromopalmitate	157-173	DNA damage inducible transcript 3	Homo sapiens	82-86
30552901-7	2019	Moreover, CHOP was remarkably elevated in the combination group, and silencing of CHOP almost completely blocked the apoptosis induced by the combination of 2-bromopalmitate and adriamycin.	Doxorubicin	178-188	DNA damage inducible transcript 3	Homo sapiens	10-14
30552901-7	2019	Moreover, CHOP was remarkably elevated in the combination group, and silencing of CHOP almost completely blocked the apoptosis induced by the combination of 2-bromopalmitate and adriamycin.	Doxorubicin	178-188	DNA damage inducible transcript 3	Homo sapiens	82-86
29948946-7	2019	Our data suggest that treatment with CFZ produces ER stress in NB without activation of CHOP-mediated apoptosis, whereas co-treatment with CFZ and LS1/71 led to apoptosis activation and CHOP expression induction.	carfilzomib	139-142	DNA damage inducible transcript 3	Homo sapiens	186-190
30159912-5	2019	The expression of endoplasmic reticulum stress marker DDIT3 was induced following an order of ZnO NRs &gt; a-ZnO MS &gt; c-ZnO MS &gt; ZnO Mini-NRs, and the apoptosis gene CASP12 was induced following an order of a-ZnO MS &gt; ZnO NRs &gt; c-ZnO MS &gt; ZnO Mini-NRs.	Zinc Oxide	94-97	DNA damage inducible transcript 3	Homo sapiens	54-59
30159912-5	2019	The expression of endoplasmic reticulum stress marker DDIT3 was induced following an order of ZnO NRs &gt; a-ZnO MS &gt; c-ZnO MS &gt; ZnO Mini-NRs, and the apoptosis gene CASP12 was induced following an order of a-ZnO MS &gt; ZnO NRs &gt; c-ZnO MS &gt; ZnO Mini-NRs.	Zinc Oxide	109-112	DNA damage inducible transcript 3	Homo sapiens	54-59
30159912-5	2019	The expression of endoplasmic reticulum stress marker DDIT3 was induced following an order of ZnO NRs &gt; a-ZnO MS &gt; c-ZnO MS &gt; ZnO Mini-NRs, and the apoptosis gene CASP12 was induced following an order of a-ZnO MS &gt; ZnO NRs &gt; c-ZnO MS &gt; ZnO Mini-NRs.	Zinc Oxide	109-112	DNA damage inducible transcript 3	Homo sapiens	54-59
30159912-5	2019	The expression of endoplasmic reticulum stress marker DDIT3 was induced following an order of ZnO NRs &gt; a-ZnO MS &gt; c-ZnO MS &gt; ZnO Mini-NRs, and the apoptosis gene CASP12 was induced following an order of a-ZnO MS &gt; ZnO NRs &gt; c-ZnO MS &gt; ZnO Mini-NRs.	Zinc Oxide	109-112	DNA damage inducible transcript 3	Homo sapiens	54-59
30511355-0	2019	Cuprizone-induced graded oligodendrocyte vulnerability is regulated by the transcription factor DNA damage-inducible transcript 3.	Cuprizone	0-9	DNA damage inducible transcript 3	Homo sapiens	96-129
30426213-5	2019	RESULTS: In colon cancer cells, treatment with bupivacaine and levobupivacaine significantly inhibited cell migration (**p &lt; 0.01, ***p &lt; 0.001; n = 4) and proliferation (**p &lt; 0.01; n = 4), while increasing the expression of CHOP (***p &lt; 0.001; n = 4) and decreased the expression of Grp78 (*p &lt; 0.05; n = 4).	Bupivacaine	47-58	DNA damage inducible transcript 3	Homo sapiens	235-239
30426213-5	2019	RESULTS: In colon cancer cells, treatment with bupivacaine and levobupivacaine significantly inhibited cell migration (**p &lt; 0.01, ***p &lt; 0.001; n = 4) and proliferation (**p &lt; 0.01; n = 4), while increasing the expression of CHOP (***p &lt; 0.001; n = 4) and decreased the expression of Grp78 (*p &lt; 0.05; n = 4).	Levobupivacaine	63-78	DNA damage inducible transcript 3	Homo sapiens	235-239
30535464-5	2019	In the present study, it was demonstrated that Ado inhibited HepG2 cell growth in a time- and concentration-dependent manner and activated endoplasmic reticulum (ER) stress, as indicated by G0/G1 cell cycle arrest, the increased mRNA and protein levels of GRP78/BiP, PERK, ATF4, CHOP, cleaved caspase-3, cytochrome c and the loss of mitochon-drial membrane potential (DeltaPsim).	Adenosine	47-50	DNA damage inducible transcript 3	Homo sapiens	279-283
30389633-10	2019	More importantly, both xanthatin and tunicamycin, an endoplasmic reticulum stress (ERS) inducing compound, increased the levels of CHOP and cleaved-caspase-3 in HepG2 cells, but their effects were significantly abolished by siRNA-mediated knockdown of CHOP.	xanthatin	23-32	DNA damage inducible transcript 3	Homo sapiens	131-135
30671964-4	2019	TUG1 was highly expressed in a cell following treatment with high glucose, and PGC-1alpha and cleaved caspase-3 levels were much lower, while CHOP level was much higher in high glucose group (HG), furthermore, CHOP inhibited PGC-1alpha expression.	Glucose	177-184	DNA damage inducible transcript 3	Homo sapiens	142-146
30674940-8	2019	Predicted vincristine resistant patients of the GCB subclass had significantly downregulated NOTCH3 -exon 16 transcript expression and tended to display adverse overall survival for R-CHOP treated patients.	Vincristine	10-21	DNA damage inducible transcript 3	Homo sapiens	184-188
30719005-5	2018	Oleic acid alone had opposite effects due to its different capacity of controlling these metabolic pathways, in particular by reduction of the ROS levels and MMP-2 activity, down-regulation of BiP, eIF2alpha, ATF6, XBP1u, CHOP, IL6, IL8 and by SOD2 and PTP-1B overexpression.	Oleic Acid	0-10	DNA damage inducible transcript 3	Homo sapiens	222-226
30340083-5	2019	Exposure to pristine ZnO NPs significantly promoted the expression of ER stress-apoptosis genes, namely DDIT3, XBP-1s, CASP9, CASP12 and BAX (p &lt; 0.05), but hydrophobic ZnO NPs only significantly promoted the expression of BAX (p &lt; 0.05).	Zinc Oxide	21-24	DNA damage inducible transcript 3	Homo sapiens	104-109
30389633-10	2019	More importantly, both xanthatin and tunicamycin, an endoplasmic reticulum stress (ERS) inducing compound, increased the levels of CHOP and cleaved-caspase-3 in HepG2 cells, but their effects were significantly abolished by siRNA-mediated knockdown of CHOP.	xanthatin	23-32	DNA damage inducible transcript 3	Homo sapiens	252-256
30389633-10	2019	More importantly, both xanthatin and tunicamycin, an endoplasmic reticulum stress (ERS) inducing compound, increased the levels of CHOP and cleaved-caspase-3 in HepG2 cells, but their effects were significantly abolished by siRNA-mediated knockdown of CHOP.	Tunicamycin	37-48	DNA damage inducible transcript 3	Homo sapiens	131-135
30389633-10	2019	More importantly, both xanthatin and tunicamycin, an endoplasmic reticulum stress (ERS) inducing compound, increased the levels of CHOP and cleaved-caspase-3 in HepG2 cells, but their effects were significantly abolished by siRNA-mediated knockdown of CHOP.	Tunicamycin	37-48	DNA damage inducible transcript 3	Homo sapiens	252-256
31276045-2	2019	Here, we report a case of PHL treated with primary hepatic resection followed by an Rituximab Cyclophosphamide Doxorubicin Vincristine Prednisone (R-CHOP) chemotherapy regimen, diagnosed after postoperative biopsy report.	rituximab cyclophosphamide	84-110	DNA damage inducible transcript 3	Homo sapiens	149-153
30315857-11	2019	Maximal CHOP expression was induced by 25 muM mitotane alone with no additional effect of B.	Mitotane	46-54	DNA damage inducible transcript 3	Homo sapiens	8-12
30621754-10	2019	Moreover, autophagy induced by XAG was mediated by activating endoplasmic reticulum stress (ERS), along with administration of XAG, the expression levels of ERS-associated proteins, including CHOP, GRP78, ATF6, p-eIF2alpha, IRE1alpha, and cleaved caspase-12 were significantly increased in HCC cells.	xanthoangelol	31-34	DNA damage inducible transcript 3	Homo sapiens	192-196
30621754-11	2019	Meanwhile, suppressing ERS with chemical chaperones (TUDCA) or CHOP shRNA could effectively abrogate the autophagy-inducing effect of XAG, and increase the apoptotic cell death.	xanthoangelol	134-137	DNA damage inducible transcript 3	Homo sapiens	63-67
30868028-3	2019	Usual chemotherapy regimen for DLBL is rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (R-CHOP).	Prednisone	101-111	DNA damage inducible transcript 3	Homo sapiens	115-119
29925224-4	2019	Shikonin induced apoptotic cell death by activating mitogen-activated protein kinase family members, and the apoptotic process was mediated by the activation of endoplasmic reticulum (ER) stress, leading to activation of the PERK/elF2alpha/CHOP apoptotic pathway, and mitochondrial Ca2+ accumulation.	shikonin	0-8	DNA damage inducible transcript 3	Homo sapiens	240-244
30209556-1	2019	Peripheral T cell lymphomas (PTCL) are less responsive to anthracycline-containing regimen such as CHOP and carry a poor prognosis.	Anthracyclines	58-71	DNA damage inducible transcript 3	Homo sapiens	99-103
30606992-6	2019	In addition, ALA significantly attenuated glutamate-induced endoplasmic reticulum (ER) stress markers; namely, glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), protein kinase regulated by RNA (PKR)-like ER-associated kinase (PERK), eukaryotic translation initiation factor 2 alpha (eIF2alpha), inositol-requiring enzyme 1 (IRE1), CCAAT/enhancer binding protein homologous protein (CHOP), and caspase-12.	Thioctic Acid	13-16	DNA damage inducible transcript 3	Homo sapiens	361-410
30606992-6	2019	In addition, ALA significantly attenuated glutamate-induced endoplasmic reticulum (ER) stress markers; namely, glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), protein kinase regulated by RNA (PKR)-like ER-associated kinase (PERK), eukaryotic translation initiation factor 2 alpha (eIF2alpha), inositol-requiring enzyme 1 (IRE1), CCAAT/enhancer binding protein homologous protein (CHOP), and caspase-12.	Thioctic Acid	13-16	DNA damage inducible transcript 3	Homo sapiens	412-416
30606992-6	2019	In addition, ALA significantly attenuated glutamate-induced endoplasmic reticulum (ER) stress markers; namely, glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), protein kinase regulated by RNA (PKR)-like ER-associated kinase (PERK), eukaryotic translation initiation factor 2 alpha (eIF2alpha), inositol-requiring enzyme 1 (IRE1), CCAAT/enhancer binding protein homologous protein (CHOP), and caspase-12.	Glutamic Acid	42-51	DNA damage inducible transcript 3	Homo sapiens	361-410
30606992-6	2019	In addition, ALA significantly attenuated glutamate-induced endoplasmic reticulum (ER) stress markers; namely, glucose-regulated protein 78 (GRP78), activating transcription factor 6 (ATF6), protein kinase regulated by RNA (PKR)-like ER-associated kinase (PERK), eukaryotic translation initiation factor 2 alpha (eIF2alpha), inositol-requiring enzyme 1 (IRE1), CCAAT/enhancer binding protein homologous protein (CHOP), and caspase-12.	Glutamic Acid	42-51	DNA damage inducible transcript 3	Homo sapiens	412-416
30606992-7	2019	We confirmed that CHOP and caspase-12 are key mediators of glutamate-induced ER stress.	Glutamic Acid	59-68	DNA damage inducible transcript 3	Homo sapiens	18-22
30606992-8	2019	Furthermore, exposure of the cells to a caspase-12-specific inhibitor and CHOP small interfering RNAs (siRNAs) led to restoration of the DeltaPsim that was damaged by glutamate treatment.	Glutamic Acid	167-176	DNA damage inducible transcript 3	Homo sapiens	74-78
30987565-14	2019	The expression of CHOP, PERK, IRE1 and ATF6 mRNA was significantly up-regulated in the presence of CCl4 or H2O2 (P < 0.05).	Hydrogen Peroxide	107-111	DNA damage inducible transcript 3	Homo sapiens	18-22
30359552-0	2019	Ixazomib promotes CHOP-dependent DR5 induction and apoptosis in colorectal cancer cells.	ixazomib	0-8	DNA damage inducible transcript 3	Homo sapiens	18-22
30307363-5	2019	She was treated with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy which was complicated by prolonged pancytopenia, without response.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	80-84
30307363-5	2019	She was treated with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy which was complicated by prolonged pancytopenia, without response.	Prednisone	68-78	DNA damage inducible transcript 3	Homo sapiens	80-84
30987565-15	2019	Whereas, GBA induced a significant decrease in these mRNA thereafter (P < 0.05), together with a decrease in CHOP and Caspase 12 proteins (P < 0.05).	8-bromoadenosine	9-12	DNA damage inducible transcript 3	Homo sapiens	109-113
31597843-2	2019	R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) remains the standard treatment for diffuse large B-cell lymphoma (DLBCL) in line with the prior 2013 guidelines.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	2-6
30423122-7	2019	Pretreatment with flutamide, as well as knockdown of androgen receptor, decreased testosterone-induced DR5 and CHOP expression, as well as apoptosis.	Flutamide	18-27	DNA damage inducible transcript 3	Homo sapiens	111-115
30423122-7	2019	Pretreatment with flutamide, as well as knockdown of androgen receptor, decreased testosterone-induced DR5 and CHOP expression, as well as apoptosis.	Testosterone	82-94	DNA damage inducible transcript 3	Homo sapiens	111-115
30423122-8	2019	Expression of DR5 and CHOP was upregulated in GLCs obtained from patients with PCOS, as well as in granulosa cells of antral follicles in ovarian sections obtained from patients with PCOS and dehydroepiandrosterone-induced PCOS mice.	Dehydroepiandrosterone	192-214	DNA damage inducible transcript 3	Homo sapiens	22-26
30332528-8	2019	Furthermore, autophagy inhibition by 3-MA significantly decreased protein expression of GRP78, p-PERK, and p-eIF2alpha and increased CHOP, ATF4, and caspase-4, whereas ERS inhibition by 4-PBA led to autophagy suppression.	3-methyladenine	37-41	DNA damage inducible transcript 3	Homo sapiens	133-137
30332528-10	2019	Additionally, both sodium hydrosulfide (NaHS) and melatonin attenuated the CSE-induced apoptosis, enhanced the CSE-induced autophagy, increased GRP78, p-PERK, and p-eIF2alpha, and decreased CHOP, ATF4, and caspase-4, via SIRT1/ORP150 pathway.	sodium bisulfide	19-38	DNA damage inducible transcript 3	Homo sapiens	190-194
30332528-10	2019	Additionally, both sodium hydrosulfide (NaHS) and melatonin attenuated the CSE-induced apoptosis, enhanced the CSE-induced autophagy, increased GRP78, p-PERK, and p-eIF2alpha, and decreased CHOP, ATF4, and caspase-4, via SIRT1/ORP150 pathway.	sodium bisulfide	40-44	DNA damage inducible transcript 3	Homo sapiens	190-194
30332528-10	2019	Additionally, both sodium hydrosulfide (NaHS) and melatonin attenuated the CSE-induced apoptosis, enhanced the CSE-induced autophagy, increased GRP78, p-PERK, and p-eIF2alpha, and decreased CHOP, ATF4, and caspase-4, via SIRT1/ORP150 pathway.	Melatonin	50-59	DNA damage inducible transcript 3	Homo sapiens	190-194
31068510-3	2019	However, several retrospective studies conducted recently have demonstrated a relatively favorable outcome with intensive chemotherapy, such as dose-adjusted EPOCH-R, than those receiving R-CHOP in patients with DHL.	Cysteamine	212-215	DNA damage inducible transcript 3	Homo sapiens	190-194
30359552-8	2019	Our findings indicated that ixazomib treatment induces CHOP-dependent DR5 induction, irrespective of p53 status.	ixazomib	28-36	DNA damage inducible transcript 3	Homo sapiens	55-59
30423122-4	2019	In this study, we found that testosterone induced expression of various UPR genes, including CHOP, as well as DR5, in cultured human granulosa-lutein cells (GLCs).	Testosterone	29-41	DNA damage inducible transcript 3	Homo sapiens	93-97
30423122-5	2019	Pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) inhibited testosterone-induced apoptosis and expression of DR5 and CHOP.	ursodoxicoltaurine	42-67	DNA damage inducible transcript 3	Homo sapiens	143-147
30423122-5	2019	Pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) inhibited testosterone-induced apoptosis and expression of DR5 and CHOP.	ursodoxicoltaurine	69-74	DNA damage inducible transcript 3	Homo sapiens	143-147
30423122-5	2019	Pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) inhibited testosterone-induced apoptosis and expression of DR5 and CHOP.	Testosterone	86-98	DNA damage inducible transcript 3	Homo sapiens	143-147
30423122-6	2019	Knockdown of CHOP inhibited testosterone-induced DR5 expression and apoptosis, and knockdown of DR5 inhibited testosterone-induced apoptosis.	Testosterone	28-40	DNA damage inducible transcript 3	Homo sapiens	13-17
30539457-5	2019	Their ribose backbone renders them sensitive to simple degradation over time and they are the target molecule for numerous and abundant ribonucleases which have evolved to chop them to pieces with extreme efficiency.	Ribose	6-12	DNA damage inducible transcript 3	Homo sapiens	172-176
30567393-3	2018	Tunicamycin (TM) treatment significantly increased mRNA levels of CHOP and GRP78, and induced lipid accumulation in the liver.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	66-70
30215789-18	2019	Of interest, C/EBP homologous protein (CHOP) signaling plays a mechanistic role in the cell death phenotype observed in iPSC progenitors, by which depletion of CHOP prevents cell death following cellular stress by thapsigargin exposure.	Thapsigargin	214-226	DNA damage inducible transcript 3	Homo sapiens	13-37
30215789-18	2019	Of interest, C/EBP homologous protein (CHOP) signaling plays a mechanistic role in the cell death phenotype observed in iPSC progenitors, by which depletion of CHOP prevents cell death following cellular stress by thapsigargin exposure.	Thapsigargin	214-226	DNA damage inducible transcript 3	Homo sapiens	39-43
30215789-18	2019	Of interest, C/EBP homologous protein (CHOP) signaling plays a mechanistic role in the cell death phenotype observed in iPSC progenitors, by which depletion of CHOP prevents cell death following cellular stress by thapsigargin exposure.	Thapsigargin	214-226	DNA damage inducible transcript 3	Homo sapiens	160-164
30606932-2	2019	While liposomal doxorubicin has been used as an effective treatment for KS patients, the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen used for PEL patients was reported to have 1-year survival rates of less than 40%.	Prednisone	137-147	DNA damage inducible transcript 3	Homo sapiens	149-153
30618588-7	2018	In addition, dual-staining for CHOP and oligodendrocyte transcription factor 2 (OLIG2) or Ionized calcium binding adaptor molecule 1 (Iba1) showed nuclear expression of CHOP in some oligodendrocyte-lineage cells in response to Tm or Tm+ferrocene, but CHOP was rarely found in microglia.	ferrocene	236-245	DNA damage inducible transcript 3	Homo sapiens	31-35
30618588-7	2018	In addition, dual-staining for CHOP and oligodendrocyte transcription factor 2 (OLIG2) or Ionized calcium binding adaptor molecule 1 (Iba1) showed nuclear expression of CHOP in some oligodendrocyte-lineage cells in response to Tm or Tm+ferrocene, but CHOP was rarely found in microglia.	ferrocene	236-245	DNA damage inducible transcript 3	Homo sapiens	169-173
30618588-7	2018	In addition, dual-staining for CHOP and oligodendrocyte transcription factor 2 (OLIG2) or Ionized calcium binding adaptor molecule 1 (Iba1) showed nuclear expression of CHOP in some oligodendrocyte-lineage cells in response to Tm or Tm+ferrocene, but CHOP was rarely found in microglia.	ferrocene	236-245	DNA damage inducible transcript 3	Homo sapiens	169-173
30567393-3	2018	Tunicamycin (TM) treatment significantly increased mRNA levels of CHOP and GRP78, and induced lipid accumulation in the liver.	Tunicamycin	13-15	DNA damage inducible transcript 3	Homo sapiens	66-70
30201260-0	2018	Dexmedetomidine alleviates cerebral ischemia-reperfusion injury by inhibiting endoplasmic reticulum stress dependent apoptosis through the PERK-CHOP-Caspase-11 pathway.	Dexmedetomidine	0-15	DNA damage inducible transcript 3	Homo sapiens	144-148
30562997-0	2018	Quantum Chemical Calculations on CHOP Derivatives-Spanning the Chemical Space of Phosphinidenes, Phosphaketenes, Oxaphosphirenes, and COP- Isomers.	phosphinidenes	81-95	DNA damage inducible transcript 3	Homo sapiens	33-37
30562997-0	2018	Quantum Chemical Calculations on CHOP Derivatives-Spanning the Chemical Space of Phosphinidenes, Phosphaketenes, Oxaphosphirenes, and COP- Isomers.	phosphaketenes	97-111	DNA damage inducible transcript 3	Homo sapiens	33-37
30562997-0	2018	Quantum Chemical Calculations on CHOP Derivatives-Spanning the Chemical Space of Phosphinidenes, Phosphaketenes, Oxaphosphirenes, and COP- Isomers.	oxaphosphirenes	113-128	DNA damage inducible transcript 3	Homo sapiens	33-37
30201260-6	2018	After Dex treatment, the expression levels of ER stress-related apoptosis pathway proteins (GRP78, p-PERK, CHOP and Cleaved-caspase-3) were significantly decreased and the apoptosis of brain cells was also significantly reduced.	Dexmedetomidine	6-9	DNA damage inducible transcript 3	Homo sapiens	107-111
30201260-7	2018	Immunohistochemistry showed that expression and nuclear localization of CHOP decreased significantly after the application of Dex.	Dexmedetomidine	126-129	DNA damage inducible transcript 3	Homo sapiens	72-76
30562997-2	2018	The present theoretical study at the CCSD(T)/def2-TZVPP level describes the chemical space of CHOP isomers in terms of structures and potential energy surfaces, using oxaphosphirene as the starting point, but also covering substituted derivatives and COP- isomers.	oxaphosphirene	167-181	DNA damage inducible transcript 3	Homo sapiens	94-98
30201260-8	2018	The downstream apoptotic protein caspase-11 mediated by PERK-CHOP was also markedly inhibited by Dex.	Dexmedetomidine	97-100	DNA damage inducible transcript 3	Homo sapiens	61-65
30101910-1	2018	Objective Although R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone) is a standard therapy for diffuse large B-cell lymphoma (DLBCL), the optimal dose for elderly patients remains unclear.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	21-25
30101910-1	2018	Objective Although R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone) is a standard therapy for diffuse large B-cell lymphoma (DLBCL), the optimal dose for elderly patients remains unclear.	Vincristine	56-67	DNA damage inducible transcript 3	Homo sapiens	21-25
30101910-1	2018	Objective Although R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone) is a standard therapy for diffuse large B-cell lymphoma (DLBCL), the optimal dose for elderly patients remains unclear.	Doxorubicin	69-80	DNA damage inducible transcript 3	Homo sapiens	21-25
30101910-1	2018	Objective Although R-CHOP (rituximab, cyclophosphamide, vincristine, doxorubicin, and prednisone) is a standard therapy for diffuse large B-cell lymphoma (DLBCL), the optimal dose for elderly patients remains unclear.	Prednisone	86-96	DNA damage inducible transcript 3	Homo sapiens	21-25
30788202-10	2018	The patient was treated with six courses of CHOP-R (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab).	Cyclophosphamide	52-68	DNA damage inducible transcript 3	Homo sapiens	44-48
30788202-10	2018	The patient was treated with six courses of CHOP-R (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab).	Doxorubicin	70-81	DNA damage inducible transcript 3	Homo sapiens	44-48
30788202-10	2018	The patient was treated with six courses of CHOP-R (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab).	Vincristine	83-94	DNA damage inducible transcript 3	Homo sapiens	44-48
30788202-10	2018	The patient was treated with six courses of CHOP-R (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab).	Prednisone	96-106	DNA damage inducible transcript 3	Homo sapiens	44-48
30709582-4	2018	They found that lico A significantly promoted the tumor-suppressor miR-144-3p expression, so as to up-regulate ER stress-response protein CHOP (CCAAT/-enhancer-binding protein homologous protein) by down-regulating nuclear factor E2-related factor 2 (Nrf2), finally inducing apoptotic cell death in lung cancer.	licochalcone A	16-22	DNA damage inducible transcript 3	Homo sapiens	138-142
30359578-0	2018	C-27-carboxylated oleanane triterpenoids up-regulate TRAIL DISC assembly via p38 MAPK and CHOP-mediated DR5 expression in human glioblastoma cells.	c-27-carboxylated oleanane	0-26	DNA damage inducible transcript 3	Homo sapiens	90-94
30359578-0	2018	C-27-carboxylated oleanane triterpenoids up-regulate TRAIL DISC assembly via p38 MAPK and CHOP-mediated DR5 expression in human glioblastoma cells.	triterpenoids	27-40	DNA damage inducible transcript 3	Homo sapiens	90-94
30262330-7	2018	Compared with the R-CHOP cohort, patients treated with DA-EPOCH-R experienced a significantly higher rate of these complications (P = .03).	da-epoch-r	55-65	DNA damage inducible transcript 3	Homo sapiens	20-24
30342372-0	2018	Sodium butyrate mitigates type 2 diabetes by inhibiting PERK-CHOP pathway of endoplasmic reticulum stress.	Butyric Acid	0-15	DNA damage inducible transcript 3	Homo sapiens	61-65
30471224-10	2018	The addition of LY294002 inhibited klotho protein downregulation of GRP78, CHOP, caspase-3, caspase-9, and caspase-12 expression.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	16-24	DNA damage inducible transcript 3	Homo sapiens	75-79
30342372-6	2018	Further research showed NaB down-regulated the expression of endoplasmic reticulum stress (ERS) related proteins, including phosphorylated type I transmembrane ER-resident protein kinase (p-PERK), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), activating transcription factor (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP).	nab	24-27	DNA damage inducible transcript 3	Homo sapiens	306-355
30342372-6	2018	Further research showed NaB down-regulated the expression of endoplasmic reticulum stress (ERS) related proteins, including phosphorylated type I transmembrane ER-resident protein kinase (p-PERK), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), activating transcription factor (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP).	nab	24-27	DNA damage inducible transcript 3	Homo sapiens	357-361
30342372-7	2018	Consequently, NaB mitigates type 2 diabetes by inhibiting PERK-CHOP pathway of ERS.	nab	14-17	DNA damage inducible transcript 3	Homo sapiens	63-67
30568444-3	2018	Results: Only ZnO NPs significantly induced cytotoxicity, accompanied by increased intracellular reactive oxygen species, Zn ions, and endoplasmic reticulum stress biomarkers (DDIT3 expression and p-Chop proteins).	Zinc Oxide	14-17	DNA damage inducible transcript 3	Homo sapiens	176-181
30568444-3	2018	Results: Only ZnO NPs significantly induced cytotoxicity, accompanied by increased intracellular reactive oxygen species, Zn ions, and endoplasmic reticulum stress biomarkers (DDIT3 expression and p-Chop proteins).	Zinc	14-16	DNA damage inducible transcript 3	Homo sapiens	176-181
30472108-3	2018	Even though the combination of rituximab, cyclophosphamide, doxorubicine, vincristine and prednisone (R-CHOP) is considered standard therapy for DLBCL, management of elderly patients remains challenging.	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	104-108
30300626-8	2018	Reactive oxygen species (ROS) overproduction by chrysophanol resulted in endoplasmic reticulum (ER) stress, leading to an increase in PERK, eIF2alpha, GADD153, and IRE1alpha levels in BT-474 and MCF-7 cells.	Reactive Oxygen Species	0-23	DNA damage inducible transcript 3	Homo sapiens	151-158
30300626-8	2018	Reactive oxygen species (ROS) overproduction by chrysophanol resulted in endoplasmic reticulum (ER) stress, leading to an increase in PERK, eIF2alpha, GADD153, and IRE1alpha levels in BT-474 and MCF-7 cells.	Reactive Oxygen Species	25-28	DNA damage inducible transcript 3	Homo sapiens	151-158
30300626-8	2018	Reactive oxygen species (ROS) overproduction by chrysophanol resulted in endoplasmic reticulum (ER) stress, leading to an increase in PERK, eIF2alpha, GADD153, and IRE1alpha levels in BT-474 and MCF-7 cells.	chrysophanic acid	48-60	DNA damage inducible transcript 3	Homo sapiens	151-158
29964331-0	2018	Inhibition of euchromatin histone-lysine N-methyltransferase 2 sensitizes breast cancer cells to tumor necrosis factor-related apoptosis-inducing ligand through reactive oxygen species-mediated activating transcription factor 4-C/EBP homologous protein-death receptor 5 pathway activation.	Reactive Oxygen Species	161-184	DNA damage inducible transcript 3	Homo sapiens	228-252
30463333-5	2018	Maritoclax-induced DR5 upregulation was regulated by induction of C/EBP homologous protein (CHOP) expression.	marinopyrrole A	0-10	DNA damage inducible transcript 3	Homo sapiens	66-90
30463333-5	2018	Maritoclax-induced DR5 upregulation was regulated by induction of C/EBP homologous protein (CHOP) expression.	marinopyrrole A	0-10	DNA damage inducible transcript 3	Homo sapiens	92-96
30431571-4	2018	INTERVENTIONS AND OUTCOMES: Fortunately, the patient"s skin lesions subsided gradually after 3 cycles of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen.	Cyclophosphamide	105-121	DNA damage inducible transcript 3	Homo sapiens	167-171
30431571-4	2018	INTERVENTIONS AND OUTCOMES: Fortunately, the patient"s skin lesions subsided gradually after 3 cycles of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen.	Doxorubicin	123-134	DNA damage inducible transcript 3	Homo sapiens	167-171
30431571-4	2018	INTERVENTIONS AND OUTCOMES: Fortunately, the patient"s skin lesions subsided gradually after 3 cycles of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) regimen.	Prednisolone	153-165	DNA damage inducible transcript 3	Homo sapiens	167-171
30194633-6	2018	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	Palmitic Acid	18-20	DNA damage inducible transcript 3	Homo sapiens	112-161
30194633-6	2018	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	Palmitic Acid	18-20	DNA damage inducible transcript 3	Homo sapiens	163-167
29964331-6	2018	Specifically, BIX-01294 induced C/EBP homologous protein (CHOP)-mediated DR5 gene transcriptional activation and DR5 promoter activation was induced by upregulation of the protein kinase R-like endoplasmic reticulum kinase-mediated activating transcription factor 4 (ATF4).	BIX 01294	14-23	DNA damage inducible transcript 3	Homo sapiens	32-56
29964331-6	2018	Specifically, BIX-01294 induced C/EBP homologous protein (CHOP)-mediated DR5 gene transcriptional activation and DR5 promoter activation was induced by upregulation of the protein kinase R-like endoplasmic reticulum kinase-mediated activating transcription factor 4 (ATF4).	BIX 01294	14-23	DNA damage inducible transcript 3	Homo sapiens	58-62
30296076-5	2018	HPO-DAEE-elicited CHOP expression and cell death were markedly suppressed by pretreatment with N-acetylcysteine (NAC), an antioxidant, by 2.40 +- 1.57-fold and 5.7 +- 1.6%, respectively.	hpo-daee	0-8	DNA damage inducible transcript 3	Homo sapiens	18-22
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Reactive Oxygen Species	24-47	DNA damage inducible transcript 3	Homo sapiens	145-149
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	Acetylcysteine	51-70	DNA damage inducible transcript 3	Homo sapiens	145-149
29964331-7	2018	Moreover, inhibition of reactive oxygen species by N-acetyl-L-cysteine efficiently blocked BIX-01294-induced DR5 upregulation by inhibiting ATF4/CHOP expression, leading to diminished sensitization to TRAIL.	BIX 01294	91-100	DNA damage inducible transcript 3	Homo sapiens	145-149
29964331-8	2018	These findings suggest that BIX-01294 sensitizes breast cancer cells to TRAIL by upregulating ATF4/CHOP-dependent DR5 expression with a reactive oxygen species-dependent manner.	BIX 01294	28-37	DNA damage inducible transcript 3	Homo sapiens	99-103
29964331-8	2018	These findings suggest that BIX-01294 sensitizes breast cancer cells to TRAIL by upregulating ATF4/CHOP-dependent DR5 expression with a reactive oxygen species-dependent manner.	Reactive Oxygen Species	136-159	DNA damage inducible transcript 3	Homo sapiens	99-103
30132536-6	2018	Furthermore, we found that the protein levels of glucose-related protein 78 (GRP78) and CCAAT-enhancer-binding protein homologous protein (CHOP) increased following treatment with 3-BP.	bromopyruvate	180-184	DNA damage inducible transcript 3	Homo sapiens	88-137
30132536-6	2018	Furthermore, we found that the protein levels of glucose-related protein 78 (GRP78) and CCAAT-enhancer-binding protein homologous protein (CHOP) increased following treatment with 3-BP.	bromopyruvate	180-184	DNA damage inducible transcript 3	Homo sapiens	139-143
30340554-1	2018	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is broadly accepted as standard for the treatment of diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	57-73	DNA damage inducible transcript 3	Homo sapiens	119-123
30340554-1	2018	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is broadly accepted as standard for the treatment of diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	75-86	DNA damage inducible transcript 3	Homo sapiens	119-123
30340554-1	2018	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is broadly accepted as standard for the treatment of diffuse large B-cell lymphoma (DLBCL).	Prednisone	105-115	DNA damage inducible transcript 3	Homo sapiens	119-123
30340554-11	2018	CONCLUSIONS: Due to its potency and low toxicity, trofosfamide/rituximab might represent an alternative therapy for DLBCL of elderly patients not suitable for R-CHOP.	trofosfamide	50-62	DNA damage inducible transcript 3	Homo sapiens	161-165
30296076-5	2018	HPO-DAEE-elicited CHOP expression and cell death were markedly suppressed by pretreatment with N-acetylcysteine (NAC), an antioxidant, by 2.40 +- 1.57-fold and 5.7 +- 1.6%, respectively.	Acetylcysteine	95-111	DNA damage inducible transcript 3	Homo sapiens	18-22
30296076-5	2018	HPO-DAEE-elicited CHOP expression and cell death were markedly suppressed by pretreatment with N-acetylcysteine (NAC), an antioxidant, by 2.40 +- 1.57-fold and 5.7 +- 1.6%, respectively.	Acetylcysteine	113-116	DNA damage inducible transcript 3	Homo sapiens	18-22
30296076-8	2018	Overall, we concluded that HPO-DAEE induces A549-cell apoptosis through the ROS-ERK-p38 pathway and, at least in part, the CHOP pathway.	hpo-daee	27-35	DNA damage inducible transcript 3	Homo sapiens	123-127
30332761-0	2018	Ciprofloxacin Enhances TRAIL-Induced Apoptosis in Lung Cancer Cells by Upregulating the Expression and Protein Stability of Death Receptors through CHOP Expression.	Ciprofloxacin	0-13	DNA damage inducible transcript 3	Homo sapiens	148-152
30314526-2	2018	Rituximab in combination with cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) therapy represents the current standard therapy, achieving a rather dissatisfying outcome in approximately 30-40% of all cases.	Prednisolone	77-89	DNA damage inducible transcript 3	Homo sapiens	93-97
30314526-6	2018	Treatment utilizing the gold standard rituximab in combination with cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) was performed, partly resulting in remission according to radiological follow-up.	Prednisolone	115-127	DNA damage inducible transcript 3	Homo sapiens	131-135
29744892-8	2018	Exposure to EGCG further increased GRP78 in the ER, and induced ATF4, spliced XBP1, CHOP, and EDEM expressions, combined with a reduction of cell surface GRP78 and a rise in caspase 3 and 8 activities.	epigallocatechin gallate	12-16	DNA damage inducible transcript 3	Homo sapiens	84-88
30243792-6	2018	Furthermore, we found that the compound 13c could inhibit cadmium-induced cell apoptosis with the downregulation of the ER stress markers GRP78, CHOP, cleaved-caspase12 and cleaved-caspase3 through western blotting.	13c	40-43	DNA damage inducible transcript 3	Homo sapiens	145-149
30243792-6	2018	Furthermore, we found that the compound 13c could inhibit cadmium-induced cell apoptosis with the downregulation of the ER stress markers GRP78, CHOP, cleaved-caspase12 and cleaved-caspase3 through western blotting.	Cadmium	58-65	DNA damage inducible transcript 3	Homo sapiens	145-149
29929133-3	2018	The results showed that direct contact with high levels of MWCNTs induced cytotoxicity and modulated expression of genes associated with ER stress (HSPA5, DDIT3 and XBP-1s) and autophagy (BECN1 and ATG12) both in A549-THP-1 macrophages cultured in the upper chambers as well as HUVECs.	mwcnts	59-65	DNA damage inducible transcript 3	Homo sapiens	155-160
30190020-4	2018	Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a highly effective but potentially neurotoxic regimen.	Cyclophosphamide	11-27	DNA damage inducible transcript 3	Homo sapiens	73-77
30190020-4	2018	Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a highly effective but potentially neurotoxic regimen.	Prednisone	59-69	DNA damage inducible transcript 3	Homo sapiens	73-77
30307162-5	2018	After 2-day exposure to palmitate, OCR and the marker of the adaptive arm of ER stress response (sorcin) were significantly raised, whereas AMPK phosphorylation, markers of pro-apoptotic arm of ER stress response (p-EIF2alpha and CHOP) and apoptosis (cleaved caspase 3) were not affected.	Palmitates	24-33	DNA damage inducible transcript 3	Homo sapiens	230-234
30307162-7	2018	After 7-day exposure to palmitate, OCR and sorcin were not significantly different from control level, p-AMPK was reduced and p-EIF2alpha, CHOP and cleaved caspase 3 were strongly upregulated.	Palmitates	24-33	DNA damage inducible transcript 3	Homo sapiens	139-143
30307162-8	2018	Presence of metformin during 7-day culture with palmitate normalized the level of p-AMPK, p-EIF2alpha, CHOP and cleaved caspase 3 but significantly increased the level of sorcin.	Metformin	12-21	DNA damage inducible transcript 3	Homo sapiens	103-107
30307162-8	2018	Presence of metformin during 7-day culture with palmitate normalized the level of p-AMPK, p-EIF2alpha, CHOP and cleaved caspase 3 but significantly increased the level of sorcin.	Palmitates	48-57	DNA damage inducible transcript 3	Homo sapiens	103-107
29959986-9	2018	Moreover, ferritin protein and CHOP mRNA expression were induced in combined iron and trigonelline incubated cells (p &lt; 0.05).	Iron	77-81	DNA damage inducible transcript 3	Homo sapiens	31-35
29783874-8	2018	Exposure to ZnO NPs promoted the expression of endoplasmic reticulum (ER) stress markers (DDIT3 and XBP-1s) and apoptosis genes (CASP9 and CASP12).	Zinc Oxide	12-15	DNA damage inducible transcript 3	Homo sapiens	90-95
30313105-6	2018	The patient was treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).Neurological symptoms improved with R-CHOP.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	146-150
30313105-6	2018	The patient was treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).Neurological symptoms improved with R-CHOP.	Doxorubicin	58-69	DNA damage inducible transcript 3	Homo sapiens	146-150
30313105-6	2018	The patient was treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).Neurological symptoms improved with R-CHOP.	Vincristine	71-82	DNA damage inducible transcript 3	Homo sapiens	146-150
30313105-6	2018	The patient was treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).Neurological symptoms improved with R-CHOP.	Prednisone	88-98	DNA damage inducible transcript 3	Homo sapiens	102-106
30313105-6	2018	The patient was treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).Neurological symptoms improved with R-CHOP.	Prednisone	88-98	DNA damage inducible transcript 3	Homo sapiens	146-150
29959986-9	2018	Moreover, ferritin protein and CHOP mRNA expression were induced in combined iron and trigonelline incubated cells (p &lt; 0.05).	trigonelline	86-98	DNA damage inducible transcript 3	Homo sapiens	31-35
29746926-6	2018	Mechanistically, we demonstrated that the fucoidan-induced, TLR4-mediated endoplasmic reticulum stress molecule CHOP promoted caspase-3 activation, which was further stimulated by the cisplatin-induced DNA damage responses, and CHOP shRNA eliminated fucoidan-induced caspase-3 cleavage but did not affect cisplatin-mediated apoptotic molecules.	Cisplatin	184-193	DNA damage inducible transcript 3	Homo sapiens	112-116
29746926-6	2018	Mechanistically, we demonstrated that the fucoidan-induced, TLR4-mediated endoplasmic reticulum stress molecule CHOP promoted caspase-3 activation, which was further stimulated by the cisplatin-induced DNA damage responses, and CHOP shRNA eliminated fucoidan-induced caspase-3 cleavage but did not affect cisplatin-mediated apoptotic molecules.	Cisplatin	305-314	DNA damage inducible transcript 3	Homo sapiens	112-116
29746926-0	2018	Fucoidan upregulates TLR4/CHOP-mediated caspase-3 and PARP activation to enhance cisplatin-induced cytotoxicity in human lung cancer cells.	Cisplatin	81-90	DNA damage inducible transcript 3	Homo sapiens	26-30
30241515-4	2018	Cyclophosphamide, hydroxydaunorubicin (doxorubicin), oncovin (vincristine), and prednisolone (CHOP) is the most common chemotherapy for non-Hodgkin lymphoma.	Prednisolone	80-92	DNA damage inducible transcript 3	Homo sapiens	94-98
29751043-8	2018	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3.	ursodoxicoltaurine	13-18	DNA damage inducible transcript 3	Homo sapiens	167-217
30107908-6	2018	Furthermore, oxicam-NSAIDs suppressed the increases in the ER stress marker CHOP (apoptosis mediator) caused by MPP+ or tunicamycin, beside suppressing eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation and the increase in ATF4 caused by MPP+.	oxicam	13-19	DNA damage inducible transcript 3	Homo sapiens	76-80
30107908-6	2018	Furthermore, oxicam-NSAIDs suppressed the increases in the ER stress marker CHOP (apoptosis mediator) caused by MPP+ or tunicamycin, beside suppressing eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation and the increase in ATF4 caused by MPP+.	mangion-purified polysaccharide (Candida albicans)	112-115	DNA damage inducible transcript 3	Homo sapiens	76-80
30107908-6	2018	Furthermore, oxicam-NSAIDs suppressed the increases in the ER stress marker CHOP (apoptosis mediator) caused by MPP+ or tunicamycin, beside suppressing eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation and the increase in ATF4 caused by MPP+.	Tunicamycin	120-131	DNA damage inducible transcript 3	Homo sapiens	76-80
30107908-7	2018	Taken together, these results suggest that oxicam-NSAIDs suppress the eIF2alpha-ATF4-CHOP pathway, one of the three signaling pathways in the ER stress response.	oxicam	43-49	DNA damage inducible transcript 3	Homo sapiens	85-89
29751043-8	2018	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3.	ursodoxicoltaurine	13-18	DNA damage inducible transcript 3	Homo sapiens	219-223
30176898-0	2018	Corosolic acid, a natural triterpenoid, induces ER stress-dependent apoptosis in human castration resistant prostate cancer cells via activation of IRE-1/JNK, PERK/CHOP and TRIB3.	corosolic acid	0-14	DNA damage inducible transcript 3	Homo sapiens	164-168
30277611-8	2018	Our results suggested that cucurbitacin-I-induced cancer cell death through the excessive ERS and CHOP-Bax and caspase-12-dependent ERS-associated apoptosis, as well as ERS-dependent autophagy, autophagy flux, and caspase-independent nonapoptotic cell death.	cucurbitacin I	27-41	DNA damage inducible transcript 3	Homo sapiens	98-102
29674443-3	2018	Treatment in the front-line setting is most often cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens, which are associated with a high failure rate and frequent relapses.	Prednisone	98-108	DNA damage inducible transcript 3	Homo sapiens	110-114
30181309-0	2018	Retraction: ROS and CHOP Are Critical for Dibenzylideneacetone to Sensitize Tumor Cells to TRAIL through Induction of Death Receptors and Downregulation of Cell Survival Proteins.	dibenzylidene acetone	42-62	DNA damage inducible transcript 3	Homo sapiens	20-24
30129387-4	2018	The results indicate that NaHS (an H2S donor) administration in uranium-intoxicated kidney cells ameliorated uranium-induced reactive oxygen species generation, caspase-3-dependent apoptosis, and endoplasmic reticulum (ER) stress identified through several key markers including GRP78, C/EBP homologous protein (CHOP), and caspase-12.	sodium bisulfide	26-30	DNA damage inducible transcript 3	Homo sapiens	286-310
30129387-4	2018	The results indicate that NaHS (an H2S donor) administration in uranium-intoxicated kidney cells ameliorated uranium-induced reactive oxygen species generation, caspase-3-dependent apoptosis, and endoplasmic reticulum (ER) stress identified through several key markers including GRP78, C/EBP homologous protein (CHOP), and caspase-12.	sodium bisulfide	26-30	DNA damage inducible transcript 3	Homo sapiens	312-316
30129387-4	2018	The results indicate that NaHS (an H2S donor) administration in uranium-intoxicated kidney cells ameliorated uranium-induced reactive oxygen species generation, caspase-3-dependent apoptosis, and endoplasmic reticulum (ER) stress identified through several key markers including GRP78, C/EBP homologous protein (CHOP), and caspase-12.	Uranium	109-116	DNA damage inducible transcript 3	Homo sapiens	286-310
30129387-4	2018	The results indicate that NaHS (an H2S donor) administration in uranium-intoxicated kidney cells ameliorated uranium-induced reactive oxygen species generation, caspase-3-dependent apoptosis, and endoplasmic reticulum (ER) stress identified through several key markers including GRP78, C/EBP homologous protein (CHOP), and caspase-12.	Uranium	109-116	DNA damage inducible transcript 3	Homo sapiens	312-316
29901077-7	2018	Treatment with MPP+ for 24 h significantly increased the expression levels of phospho-ERK1/2, phospho-p38, GRP78, CHOP, and cleaved caspase-12 in SH-SY5Y cells.	mangion-purified polysaccharide (Candida albicans)	15-19	DNA damage inducible transcript 3	Homo sapiens	114-118
29691881-7	2018	Exposure to ZnO NPs at 3 hours induced the expression of endoplasmic reticulum stress markers DDIT3 and XBP-1 s, which was suppressed by H3.	Zinc Oxide	12-15	DNA damage inducible transcript 3	Homo sapiens	94-99
30172345-1	2018	BACKGROUND: Immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a standard front-line treatment for follicular lymphoma.	Cyclophosphamide	47-63	DNA damage inducible transcript 3	Homo sapiens	109-113
30172345-1	2018	BACKGROUND: Immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a standard front-line treatment for follicular lymphoma.	Doxorubicin	65-76	DNA damage inducible transcript 3	Homo sapiens	109-113
30172345-1	2018	BACKGROUND: Immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a standard front-line treatment for follicular lymphoma.	Vincristine	78-89	DNA damage inducible transcript 3	Homo sapiens	109-113
30172345-1	2018	BACKGROUND: Immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is a standard front-line treatment for follicular lymphoma.	Prednisone	95-105	DNA damage inducible transcript 3	Homo sapiens	109-113
29957865-15	2018	In younger patients with untreated MCL, R-High-CHOP/CHASER/LEED with ASCT showed high efficacy and acceptable toxicity, and it can now be considered a standard treatment option.	asct	69-73	DNA damage inducible transcript 3	Homo sapiens	47-51
29959054-6	2018	These findings confirmed that Pimpinelol concentrations dependently increased protein aggregation and the mRNA expression of ATF-4, CHOP, GADD34 and TRIB3 in MCF-7 breast cancer cell line.	pimpinelol	30-40	DNA damage inducible transcript 3	Homo sapiens	132-136
29674443-14	2018	Anthracycline-containing regimens, mostly cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), are considered the standard of care, although the best first-line approach remains to be defined.	Anthracyclines	0-13	DNA damage inducible transcript 3	Homo sapiens	102-106
30127955-5	2018	Analysis by a polymerase chain reaction (PCR) array and confirmation via quantitative PCR technology indicated that the expression levels of growth arrest and DNA damage 153 [C/EBP homologous protein (CHOP)], a key molecule involved in ER stress-induced apoptosis, and its downstream death receptors were increased following CQ stimulation.	Chloroquine	325-327	DNA damage inducible transcript 3	Homo sapiens	175-199
29674443-14	2018	Anthracycline-containing regimens, mostly cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), are considered the standard of care, although the best first-line approach remains to be defined.	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	102-106
30127955-5	2018	Analysis by a polymerase chain reaction (PCR) array and confirmation via quantitative PCR technology indicated that the expression levels of growth arrest and DNA damage 153 [C/EBP homologous protein (CHOP)], a key molecule involved in ER stress-induced apoptosis, and its downstream death receptors were increased following CQ stimulation.	Chloroquine	325-327	DNA damage inducible transcript 3	Homo sapiens	201-205
30127955-6	2018	It was considered that the upregulation of CHOP may mediate CQ-induced extrinsic pathways and autophagy-dependent apoptosis; therefore, the role of autophagy in cholangiocarcinoma treatment was elucidated based on the data demonstrating that CQ regulates the ER-autophagy network in tumor cells.	Chloroquine	60-62	DNA damage inducible transcript 3	Homo sapiens	43-47
30214227-10	2018	Furthermore, inhibition of the endoplasmic reticulum stress by CHOP knockdown restored the effects of Mag in HepG2 cells.	magnolol	102-105	DNA damage inducible transcript 3	Homo sapiens	63-67
30127955-6	2018	It was considered that the upregulation of CHOP may mediate CQ-induced extrinsic pathways and autophagy-dependent apoptosis; therefore, the role of autophagy in cholangiocarcinoma treatment was elucidated based on the data demonstrating that CQ regulates the ER-autophagy network in tumor cells.	Chloroquine	242-244	DNA damage inducible transcript 3	Homo sapiens	43-47
29380942-1	2018	The standard of care treatment for canine lymphoma is multi-agent chemotherapy containing prednisolone, cyclophosphamide, vincristine and an anthracycline such as doxorubicin (CHOP) or epirubicin (CEOP).	Anthracyclines	141-154	DNA damage inducible transcript 3	Homo sapiens	176-180
29380942-1	2018	The standard of care treatment for canine lymphoma is multi-agent chemotherapy containing prednisolone, cyclophosphamide, vincristine and an anthracycline such as doxorubicin (CHOP) or epirubicin (CEOP).	Doxorubicin	163-174	DNA damage inducible transcript 3	Homo sapiens	176-180
29380942-2	2018	Lomustine, vincristine, procarbazine, and prednisone (LOPP) has been evaluated as a rescue, with encouraging results; however, resistance to vincristine is likely in patients relapsing on CHOP/CEOP, and this agent may enhance LOPP toxicity without improving efficacy.	Lomustine	0-9	DNA damage inducible transcript 3	Homo sapiens	188-192
29380942-2	2018	Lomustine, vincristine, procarbazine, and prednisone (LOPP) has been evaluated as a rescue, with encouraging results; however, resistance to vincristine is likely in patients relapsing on CHOP/CEOP, and this agent may enhance LOPP toxicity without improving efficacy.	Prednisone	42-52	DNA damage inducible transcript 3	Homo sapiens	188-192
29380942-2	2018	Lomustine, vincristine, procarbazine, and prednisone (LOPP) has been evaluated as a rescue, with encouraging results; however, resistance to vincristine is likely in patients relapsing on CHOP/CEOP, and this agent may enhance LOPP toxicity without improving efficacy.	lopp	54-58	DNA damage inducible transcript 3	Homo sapiens	188-192
29380942-2	2018	Lomustine, vincristine, procarbazine, and prednisone (LOPP) has been evaluated as a rescue, with encouraging results; however, resistance to vincristine is likely in patients relapsing on CHOP/CEOP, and this agent may enhance LOPP toxicity without improving efficacy.	Vincristine	141-152	DNA damage inducible transcript 3	Homo sapiens	188-192
30158521-0	2018	Kaempferol induces autophagic cell death via IRE1-JNK-CHOP pathway and inhibition of G9a in gastric cancer cells.	kaempferol	0-10	DNA damage inducible transcript 3	Homo sapiens	54-58
30158521-5	2018	Furthermore, our results showed that kaempferol induces autophagic cell death via the activation of the IRE1-JNK-CHOP signaling, indicating ER stress response.	kaempferol	37-47	DNA damage inducible transcript 3	Homo sapiens	113-117
30158521-8	2018	Taken together, our findings indicate that kaempferol activates the IRE1-JNK-CHOP signaling from cytosol to nucleus, and G9a inhibition activates autophagic cell death in GC cells.	kaempferol	43-53	DNA damage inducible transcript 3	Homo sapiens	77-81
30116009-4	2018	Human endometrial stromal cell line (HESC) after decidualization treatment with MPA + dibutyryl-cAMP (Dec) increased the expression of RS-sensors (ATF6, PERK and IRE1alpha) and UPR markers (sXBP1 and CHOP) in comparison with Non-dec cells.	Cyclic AMP	96-100	DNA damage inducible transcript 3	Homo sapiens	200-204
30120227-6	2018	ZFL-mediated ER stress enhanced anti-cancer drug-induced apoptotic cell death, and pretreatment with chemical chaperones or down-regulation of ATF4 and CHOP by small interfering RNA markedly reduced ZFL plus oxaliplatin-induced apoptosis.	zfl	0-3	DNA damage inducible transcript 3	Homo sapiens	152-156
30120227-6	2018	ZFL-mediated ER stress enhanced anti-cancer drug-induced apoptotic cell death, and pretreatment with chemical chaperones or down-regulation of ATF4 and CHOP by small interfering RNA markedly reduced ZFL plus oxaliplatin-induced apoptosis.	zfl	199-202	DNA damage inducible transcript 3	Homo sapiens	152-156
30120227-6	2018	ZFL-mediated ER stress enhanced anti-cancer drug-induced apoptotic cell death, and pretreatment with chemical chaperones or down-regulation of ATF4 and CHOP by small interfering RNA markedly reduced ZFL plus oxaliplatin-induced apoptosis.	Oxaliplatin	208-219	DNA damage inducible transcript 3	Homo sapiens	152-156
30174670-10	2018	Both inhibition of p38 MAPK by SB203580 (10 microM) and knockdown of ER stress effector CCAAT-enhancer-binding protein homologous protein (CHOP) reduced gene and protein expression of IL-6 in Tg-treated cells.	Thapsigargin	192-194	DNA damage inducible transcript 3	Homo sapiens	88-137
30174670-10	2018	Both inhibition of p38 MAPK by SB203580 (10 microM) and knockdown of ER stress effector CCAAT-enhancer-binding protein homologous protein (CHOP) reduced gene and protein expression of IL-6 in Tg-treated cells.	Thapsigargin	192-194	DNA damage inducible transcript 3	Homo sapiens	139-143
29702190-5	2018	Cisplatin-resistant lung cancer cells exhibited lower expression of CHOP compared to that in sensitive lung cancer cells, and silencing or augmenting CHOP expression enhanced or impaired cisplatin resistance, respectively.	Cisplatin	0-9	DNA damage inducible transcript 3	Homo sapiens	68-72
30071836-4	2018	CASE PRESENTATION: We present a patient with a history of Mantle cell lymphoma and treatment with R-CHOP (rituximab, doxorubicine, vincristine, cyclofosfamide, prednisone), with a meningo-encephalitis, who was treated for a suspected lymphoma relapse.	Doxorubicin	117-129	DNA damage inducible transcript 3	Homo sapiens	100-104
30071836-4	2018	CASE PRESENTATION: We present a patient with a history of Mantle cell lymphoma and treatment with R-CHOP (rituximab, doxorubicine, vincristine, cyclofosfamide, prednisone), with a meningo-encephalitis, who was treated for a suspected lymphoma relapse.	Prednisone	160-170	DNA damage inducible transcript 3	Homo sapiens	100-104
29702190-5	2018	Cisplatin-resistant lung cancer cells exhibited lower expression of CHOP compared to that in sensitive lung cancer cells, and silencing or augmenting CHOP expression enhanced or impaired cisplatin resistance, respectively.	Cisplatin	0-9	DNA damage inducible transcript 3	Homo sapiens	150-154
29702190-5	2018	Cisplatin-resistant lung cancer cells exhibited lower expression of CHOP compared to that in sensitive lung cancer cells, and silencing or augmenting CHOP expression enhanced or impaired cisplatin resistance, respectively.	Cisplatin	187-196	DNA damage inducible transcript 3	Homo sapiens	150-154
28679068-2	2018	In present study, berberine hydrochloride (BER) triggered proliferative inhibition and G2/M arrest in AGS cells, down-regulated protein expression of cyclin B1, Bcl-2, up-regulated expression of p21, p53 and cleaved caspase 3, but showed no effect on protein expression of CHOP, Bip, and caspase 4.	berberine chloride	18-41	DNA damage inducible transcript 3	Homo sapiens	273-277
30116320-9	2018	Inhibiting autophagy using 3-MA, resulted in a significant decrease in LC3-II, beclin-1 and LDH, as well as increase in the expression of BIP, CHOP, caspase 3, cleaved caspase 3 and Bax.	3-methyladenine	27-31	DNA damage inducible transcript 3	Homo sapiens	143-147
28679068-2	2018	In present study, berberine hydrochloride (BER) triggered proliferative inhibition and G2/M arrest in AGS cells, down-regulated protein expression of cyclin B1, Bcl-2, up-regulated expression of p21, p53 and cleaved caspase 3, but showed no effect on protein expression of CHOP, Bip, and caspase 4.	Berberine	43-46	DNA damage inducible transcript 3	Homo sapiens	273-277
29665051-5	2018	Mechanistic studies revealed that the sensitizing effect of hyperbaric oxygen is due to decreased ratio of Bcl-2/Bax, increased level of p53, cleaved Caspase3, GRP78, CHOP, and LC3.	Oxygen	71-77	DNA damage inducible transcript 3	Homo sapiens	167-171
30147970-5	2018	The patient was treated with two cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) which was complicated by progressive heart failure requiring substitution of liposomal doxorubicin.	Prednisone	106-116	DNA damage inducible transcript 3	Homo sapiens	120-124
30064425-7	2018	RESULTS: Combination treatment of chymostatin and aliskiren markedly suppressed PA or cholesterol-induced ER stress, as reflected by increased BiP, IRE1alpha, phosphorylated-eIF2alpha and ATF4 as well as proapoptotic transcription factor CHOP.	chymostatin	34-45	DNA damage inducible transcript 3	Homo sapiens	238-242
30064425-7	2018	RESULTS: Combination treatment of chymostatin and aliskiren markedly suppressed PA or cholesterol-induced ER stress, as reflected by increased BiP, IRE1alpha, phosphorylated-eIF2alpha and ATF4 as well as proapoptotic transcription factor CHOP.	aliskiren	50-59	DNA damage inducible transcript 3	Homo sapiens	238-242
29252084-1	2018	High-dose glucocorticoids such as prednisone are combined with cytotoxic chemotherapy in the R-CHOP or dose adjusted R-EPOCH regimens used for non-Hodgkin lymphoma (NHL).	Prednisone	34-44	DNA damage inducible transcript 3	Homo sapiens	95-99
30108506-9	2018	Docking studies indicated that CHOP-mediated pathway was potentially blocked by high dose of lico A.	licochalcone A	93-99	DNA damage inducible transcript 3	Homo sapiens	31-35
30108506-10	2018	Our results suggested that lico A could cause UPR, autophagy and apoptosis, and the underlying mechanism involved up-regulation of miR-144-3p, and increased lico A level would also increase the potential for lico A inhibiting CHOP-dependent apoptosis in H292 cells.	licochalcone A	27-33	DNA damage inducible transcript 3	Homo sapiens	226-230
30108506-10	2018	Our results suggested that lico A could cause UPR, autophagy and apoptosis, and the underlying mechanism involved up-regulation of miR-144-3p, and increased lico A level would also increase the potential for lico A inhibiting CHOP-dependent apoptosis in H292 cells.	licochalcone A	157-163	DNA damage inducible transcript 3	Homo sapiens	226-230
30108506-10	2018	Our results suggested that lico A could cause UPR, autophagy and apoptosis, and the underlying mechanism involved up-regulation of miR-144-3p, and increased lico A level would also increase the potential for lico A inhibiting CHOP-dependent apoptosis in H292 cells.	licochalcone A	157-163	DNA damage inducible transcript 3	Homo sapiens	226-230
29750632-2	2018	We assessed whether PET can guide therapy in patients who are treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Prednisone	123-133	DNA damage inducible transcript 3	Homo sapiens	135-139
30123071-6	2018	Importantly, we have first observed marked induction of ER stress and CHOP-dependent SCLC cell apoptosis in MLN0128 and AZD1775-primed cells.	adavosertib	120-127	DNA damage inducible transcript 3	Homo sapiens	70-74
29753740-8	2018	Furthermore, we found endoplasmic reticulum (ER) stress accompanied by increased expression of ER stress markers, such as glucose response protein 78 (GRP78) and C/EBP-homologous protein (CHOP), in 2DG-treated cells.	Deoxyglucose	198-201	DNA damage inducible transcript 3	Homo sapiens	162-186
29327364-6	2018	Downregulation of Bax/Bcl-2, CHOP, GRP78, inflammatory factors, and reactive oxygen species generation, and the increase of MMP level detected after 4-PBA treatment indicated an inhibitory effect of 4-PBA on cell apoptosis, inflammatory response, and ER stress in OA.	4-phenylbutyric acid	199-204	DNA damage inducible transcript 3	Homo sapiens	29-33
29749522-6	2018	The results demonstrated that LPS stimulation increased the expression levels of GRP78, CHOP, NF-kappaB and GrB, and decreased the expression of IkappaBalpha, and these changes were inhibited by SA3N, which indicated that inhibition of GrB activity may suppress endoplasmic reticulum (ER) stress signaling.	sa3n	195-199	DNA damage inducible transcript 3	Homo sapiens	88-92
29753740-8	2018	Furthermore, we found endoplasmic reticulum (ER) stress accompanied by increased expression of ER stress markers, such as glucose response protein 78 (GRP78) and C/EBP-homologous protein (CHOP), in 2DG-treated cells.	Deoxyglucose	198-201	DNA damage inducible transcript 3	Homo sapiens	188-192
29933620-12	2018	Moreover, SH-EAE strikingly suppressed the protein expression of two ER stress sensors, including inositol requiring enzyme-1alpha (IRE-1alpha) and protein kinase R-like ER kinase (PERK), and antagonized the induction of C/EBP homologous protein (CHOP) expression by thapsigargin, an ER stress inducer.	Thapsigargin	267-279	DNA damage inducible transcript 3	Homo sapiens	221-245
29946110-2	2018	We hypothesized that adding lenalidomide to R-CHOP (R2CHOP) may decrease the risk of CNS relapse.	Lenalidomide	28-40	DNA damage inducible transcript 3	Homo sapiens	46-50
29974072-8	2018	In particular, salinomycin-induced ER Ca2+ depletion up-regulates C/EBP homologous protein (CHOP), which inhibits Wnt signaling by down-regulating beta-catenin.	salinomycin	15-26	DNA damage inducible transcript 3	Homo sapiens	66-90
29974072-8	2018	In particular, salinomycin-induced ER Ca2+ depletion up-regulates C/EBP homologous protein (CHOP), which inhibits Wnt signaling by down-regulating beta-catenin.	salinomycin	15-26	DNA damage inducible transcript 3	Homo sapiens	92-96
29676829-4	2018	Furthermore, we found that DMAS stimulated endoplasmic reticulum stress and mediated autophagy through the PERK-eIF2alpha-ATF4-CHOP and IRE1-TRAF2-JNK axes of the unfolded protein response in human lung adenocarcinoma cells.	beta, beta-dimethylacrylshikonin	27-31	DNA damage inducible transcript 3	Homo sapiens	127-131
29921924-6	2018	We compared the roles of the ATF4/CHOP and IRE1alpha/XBP1s UPR pathways, which were both induced by GA.	18alpha-glycyrrhetinic acid	100-102	DNA damage inducible transcript 3	Homo sapiens	34-38
29921924-7	2018	The ATF4/CHOP cascade induced autophagy and was indispensable for the induction of apoptosis in GA-treated HCC cells.	18alpha-glycyrrhetinic acid	96-98	DNA damage inducible transcript 3	Homo sapiens	9-13
29963517-2	2018	The R-CHOP therapy [rituximab (R), cyclophosphamide, hydroxy-doxorubicin, vincristine, and prednisone] is a popular and recommended regimen for primary therapy, prescribed by several treatment guidelines for WM.	Cyclophosphamide	35-51	DNA damage inducible transcript 3	Homo sapiens	6-10
29963517-2	2018	The R-CHOP therapy [rituximab (R), cyclophosphamide, hydroxy-doxorubicin, vincristine, and prednisone] is a popular and recommended regimen for primary therapy, prescribed by several treatment guidelines for WM.	Vincristine	74-85	DNA damage inducible transcript 3	Homo sapiens	6-10
29963517-2	2018	The R-CHOP therapy [rituximab (R), cyclophosphamide, hydroxy-doxorubicin, vincristine, and prednisone] is a popular and recommended regimen for primary therapy, prescribed by several treatment guidelines for WM.	Prednisone	91-101	DNA damage inducible transcript 3	Homo sapiens	6-10
29930756-9	2018	Limiting the availability of glutamine significantly ameliorates the lipotoxic effects of palmitate, reduces CHOP and XBP1(s) induction and restores the expression levels of HER2 and HER3.	Glutamine	29-38	DNA damage inducible transcript 3	Homo sapiens	109-113
29357413-6	2018	Activating transcription factor 4 arising from the UPR mediates cell death via expression of CCAAT/enhancer-binding protein (c/EBP) homologous protein (CHOP), impairs the generation of pyrophosphate, a potent inhibitor of mineralization, and potentiates VSMC transdifferentiation to the osteochondrocytic phenotype.	diphosphoric acid	185-198	DNA damage inducible transcript 3	Homo sapiens	152-156
29764928-11	2018	Furthermore, our in vivo results also showed that GRP78, CHOP expression and apoptosis were significantly increased in endometrial cells during the secretory phase as well as by in vitro treatment with progesterone.	Progesterone	202-214	DNA damage inducible transcript 3	Homo sapiens	57-61
29483217-8	2018	Mechanistically, we found that the apoptosis following combined Carfilzomib/ACY-1215 treatment is mediated through increased CHOP expression.	carfilzomib	64-75	DNA damage inducible transcript 3	Homo sapiens	125-129
29483217-8	2018	Mechanistically, we found that the apoptosis following combined Carfilzomib/ACY-1215 treatment is mediated through increased CHOP expression.	ricolinostat	76-84	DNA damage inducible transcript 3	Homo sapiens	125-129
29748013-8	2018	Overexpression of LIP restored cisplatin"s pro-apoptotic effect by activating CHOP/TRB3/caspase 3 axis and up-regulating calreticulin, that triggered MPM cell phagocytosis by dendritic cells and expanded autologous anti-tumor CD8+CD107+T-cytotoxic lymphocytes.	Cisplatin	31-40	DNA damage inducible transcript 3	Homo sapiens	78-82
29891461-8	2018	LiCl, an inhibitor of GSK-3beta, attenuated HG-induced ERS and significantly lowered the expression levels of GRP78 and CHOP (P&lt;0.01).	Lithium Chloride	0-4	DNA damage inducible transcript 3	Homo sapiens	120-124
29761908-7	2018	Regarding first-line induction, a shift from R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) to R-bendamustine was observed over time, as well as a decline in radiotherapy.	Prednisone	108-118	DNA damage inducible transcript 3	Homo sapiens	47-51
29891454-7	2018	In HTR-8/SVneo cells treated with different doses of DCA (0, 10, 50, and 100 micromol/L), the mRNA expressions of GRP78, CHOP, caspase-3 and caspase-7 were significantly increased in a dose-dependent manner (P&lt;0.05) and the protein levels of GRP78 and CHOP were also increased dose-dependently.	Deoxycholic Acid	53-56	DNA damage inducible transcript 3	Homo sapiens	121-125
29891454-7	2018	In HTR-8/SVneo cells treated with different doses of DCA (0, 10, 50, and 100 micromol/L), the mRNA expressions of GRP78, CHOP, caspase-3 and caspase-7 were significantly increased in a dose-dependent manner (P&lt;0.05) and the protein levels of GRP78 and CHOP were also increased dose-dependently.	Deoxycholic Acid	53-56	DNA damage inducible transcript 3	Homo sapiens	255-259
30082570-9	2018	Interpretation &amp; conclusions: Except for ALCL, ALK positive, all other PTCLs showed poor long-term outcome with CHOP-based chemotherapy.	Adenosine Monophosphate	16-19	DNA damage inducible transcript 3	Homo sapiens	116-120
28826228-3	2018	RESULTS: Culturing islets in CO-saturated medium protected them from hypoxia-induced apoptosis and preserved beta cell function by suppressing expression of proapoptotic (Bim, PARP, Cas-3), proinflammatory (TNF-alpha), and endoplasmic reticulum (ER) stress (glucose-regulated protein 94, grp94, CHOP) proteins.	co-saturated medium	29-48	DNA damage inducible transcript 3	Homo sapiens	295-299
29577663-11	2018	MPPa-PDT caused increasing of ER stress markers (GRP78, CHOP) as MPPa accumulated in ER.	15-phenyl-beta-methylpentadecanoic acid	0-4	DNA damage inducible transcript 3	Homo sapiens	56-60
29734677-7	2018	Bornyl cis-4-hydroxycinnamate-related cell death also implied that the protein kinase R-like endoplasmic reticulum kinase (PERK)-eIF2&amp;alpha;-ATF4-CHOP signal pathways was activated upon bornyl cis-4-hydroxycinnamate treatment.	Adenosine Monophosphate	134-137	DNA damage inducible transcript 3	Homo sapiens	150-154
29716630-2	2018	Chemo-immunotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP) is the current first-line treatment.	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	94-98
29546614-10	2018	Moreover, the growth inhibitory effect of gambogic acid on pancreatic cancer cells was modulated through up-regulation of DDIT3, DUSP1, and DUSP5 and down-regulation of ALDOA, TOP2A, and ATG4B.	gambogic acid	42-55	DNA damage inducible transcript 3	Homo sapiens	122-127
29664056-14	2018	Exposure of HUVECs to ox-LDL also markedly induced caspase-3 activity together with increased CHOP mRNA level; these effects were inhibited by simvastatin treatment.	Simvastatin	143-154	DNA damage inducible transcript 3	Homo sapiens	94-98
29505783-11	2018	In sesamin group, the expression of Bax, caspase-12, GRP78, GADD153, p-IRE1alpha, p-JNK, LC3I/II and beclin-1 was up-regulated while Bcl-2 was down-regulated compared to control group.	sesamin	3-10	DNA damage inducible transcript 3	Homo sapiens	60-67
29724297-5	2018	Further study showed that ibrutinib treatment increased ERS-related protein expression, including Bip, ATF4 and CHOP, suggesting the induction of ER-stress in Reh cells.	ibrutinib	26-35	DNA damage inducible transcript 3	Homo sapiens	112-116
29724297-6	2018	More importantly, once ER-stress was suppressed by tauroursodeoxycholic acid (TUDCA), an ER-stress inhibitor, the upregulation of Bip, ATF4, CHOP, cleaved-caspase3 and cleaved-PARP after ibrutinib treatment was partially reversed, suggesting that induction of ALL cell apoptosis by ibrutinib was partially attributed to activation of ER stress.	ursodoxicoltaurine	51-76	DNA damage inducible transcript 3	Homo sapiens	141-145
29724297-6	2018	More importantly, once ER-stress was suppressed by tauroursodeoxycholic acid (TUDCA), an ER-stress inhibitor, the upregulation of Bip, ATF4, CHOP, cleaved-caspase3 and cleaved-PARP after ibrutinib treatment was partially reversed, suggesting that induction of ALL cell apoptosis by ibrutinib was partially attributed to activation of ER stress.	ursodoxicoltaurine	78-83	DNA damage inducible transcript 3	Homo sapiens	141-145
29477024-4	2018	NLR &gt;=6 was associated with lower CR rate to R-CHOP (46% vs. 74%; p = 0.02) and there was a trend towards significance in multivariate regression analyses (OR 0.36, 95% CI 0.11-1.00; p = 0.05).	Chromium	37-39	DNA damage inducible transcript 3	Homo sapiens	50-54
30046327-8	2018	The use of depot injectable steroids with a CHOP-based protocol seems to result in a longer survival time in patients with mediastinal lymphoma when comparing the survival distribution for those receiving oral steroids with a CHOP-based protocol.	Steroids	28-36	DNA damage inducible transcript 3	Homo sapiens	44-48
30046327-8	2018	The use of depot injectable steroids with a CHOP-based protocol seems to result in a longer survival time in patients with mediastinal lymphoma when comparing the survival distribution for those receiving oral steroids with a CHOP-based protocol.	Steroids	28-36	DNA damage inducible transcript 3	Homo sapiens	226-230
30046327-8	2018	The use of depot injectable steroids with a CHOP-based protocol seems to result in a longer survival time in patients with mediastinal lymphoma when comparing the survival distribution for those receiving oral steroids with a CHOP-based protocol.	Steroids	210-218	DNA damage inducible transcript 3	Homo sapiens	44-48
29719411-2	2018	Patients with peripheral T-cell lymphoma (PTCL) generally have a poor prognosis when treated with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy; once relapse occurs, it is mostly regarded as an incurable disease.	Prednisolone	146-158	DNA damage inducible transcript 3	Homo sapiens	160-164
29317554-1	2018	BACKGROUND: Rituximab plus bendamustine (R-B) has been demonstrated to improve outcomes and reduce toxicity compared with rituximab, cyclophosphamide, doxorubicin, and prednisone (R-CHOP) in follicular lymphoma (FL).	Bendamustine Hydrochloride	27-39	DNA damage inducible transcript 3	Homo sapiens	182-186
29317554-3	2018	Therefore, we retrospectively assessed patients with FL3A treated with either R-CHOP or R-B in five European cancer centers and compared their outcomes.	fl3a	53-57	DNA damage inducible transcript 3	Homo sapiens	80-84
29317554-12	2018	IMPLICATIONS FOR PRACTICE: Rituximab plus bendamustine (R-B) has shown to be less toxic and more effective than rituximab, cyclophosphamide, doxorubicin, and prednisone (R-CHOP) in follicular lymphoma grade 3A.	Bendamustine Hydrochloride	42-54	DNA damage inducible transcript 3	Homo sapiens	172-176
29587440-0	2018	7-Acetylsinumaximol B Induces Apoptosis and Autophagy in Human Gastric Carcinoma Cells through Mitochondria Dysfunction and Activation of the PERK/eIF2alpha/ATF4/CHOP Signaling Pathway.	7-acetylsinumaximol B	0-21	DNA damage inducible transcript 3	Homo sapiens	162-166
30146638-7	2018	Treatment with tunicamycin resulted in up-regulation of ER stress genes, such as splicing x-box binding protein-1(sXBP1), activating transcription factor 4(ATF4), glucose-regulated protein 78(GRP78) and C/EBP homologous protein (CHOP).	Tunicamycin	15-26	DNA damage inducible transcript 3	Homo sapiens	203-227
30146638-7	2018	Treatment with tunicamycin resulted in up-regulation of ER stress genes, such as splicing x-box binding protein-1(sXBP1), activating transcription factor 4(ATF4), glucose-regulated protein 78(GRP78) and C/EBP homologous protein (CHOP).	Tunicamycin	15-26	DNA damage inducible transcript 3	Homo sapiens	229-233
29587440-6	2018	The 7-AB treatment also triggered endoplasmic reticulum (ER) stress, leading to activation of the PERK/elF2alpha/ATF4/CHOP apoptotic pathway.	7-acetylsinumaximol B	4-8	DNA damage inducible transcript 3	Homo sapiens	118-122
30026676-7	2018	Results: BME significantly decreased expression levels of ER-stress markers (including phospho-eIF2alpha, CHOP, and phospho-JNK [Jun N-terminal kinases]) in PA-treated HepG2 cells.	Palmitates	157-159	DNA damage inducible transcript 3	Homo sapiens	106-110
29744288-0	2018	Dasatinib promotes TRAIL-mediated apoptosis by upregulating CHOP-dependent death receptor 5 in gastric cancer.	Dasatinib	0-9	DNA damage inducible transcript 3	Homo sapiens	60-64
29744288-7	2018	Moreover, increased DR5 expression facilitated dasatinib-induced apoptosis; the dasatinib-induced increase in DR5 expression was mediated by CCAAT/enhancer-binding protein homologous protein (CHOP).	Dasatinib	80-89	DNA damage inducible transcript 3	Homo sapiens	141-190
29744288-7	2018	Moreover, increased DR5 expression facilitated dasatinib-induced apoptosis; the dasatinib-induced increase in DR5 expression was mediated by CCAAT/enhancer-binding protein homologous protein (CHOP).	Dasatinib	80-89	DNA damage inducible transcript 3	Homo sapiens	192-196
29744288-9	2018	Our results show that dasatinib promoted TRAIL-mediated apoptosis via upregulation of CHOP-dependent DR5 expression in GC, suggesting that DR5 induction can be used as an indicator of dasatinib sensitivity.	Dasatinib	22-31	DNA damage inducible transcript 3	Homo sapiens	86-90
29744288-9	2018	Our results show that dasatinib promoted TRAIL-mediated apoptosis via upregulation of CHOP-dependent DR5 expression in GC, suggesting that DR5 induction can be used as an indicator of dasatinib sensitivity.	Dasatinib	184-193	DNA damage inducible transcript 3	Homo sapiens	86-90
29239061-0	2018	Progesterone inhibited endoplasmic reticulum stress associated apoptosis induced by interleukin-1beta via the GRP78/PERK/CHOP pathway in BeWo cells.	Progesterone	0-12	DNA damage inducible transcript 3	Homo sapiens	121-125
29167125-8	2018	Expression of Bnip3 and CHOP, two proapoptotic targets of HIF-1alpha and ROS pathways, respectively, was suppressed by hMSC-CM, while Bcl-2 expression was restored.	Reactive Oxygen Species	73-76	DNA damage inducible transcript 3	Homo sapiens	24-28
29301832-12	2018	Coupling docetaxel with NOS inhibition increased EnR-stress response via coactivation of ATF4 and CHOP, which triggered the pASK1/JNK proapoptotic pathway, promoting cleavage of caspases 3 and 9.Conclusions: iNOS is a critical target for docetaxel resistance in TNBC.	Docetaxel	9-18	DNA damage inducible transcript 3	Homo sapiens	98-102
29301832-12	2018	Coupling docetaxel with NOS inhibition increased EnR-stress response via coactivation of ATF4 and CHOP, which triggered the pASK1/JNK proapoptotic pathway, promoting cleavage of caspases 3 and 9.Conclusions: iNOS is a critical target for docetaxel resistance in TNBC.	Docetaxel	238-247	DNA damage inducible transcript 3	Homo sapiens	98-102
29314656-8	2018	Moreover, rapamycin significantly mitigated MI/R-induced endoplasmic reticulum stress and mitochondrial impairment demonstrated by reduced Caspase-12 activity, inhibited CHOP activation, decreased cytoplasmic Cyto-C release and preserved intact mitochondria.	Sirolimus	10-19	DNA damage inducible transcript 3	Homo sapiens	170-174
29314656-8	2018	Moreover, rapamycin significantly mitigated MI/R-induced endoplasmic reticulum stress and mitochondrial impairment demonstrated by reduced Caspase-12 activity, inhibited CHOP activation, decreased cytoplasmic Cyto-C release and preserved intact mitochondria.	r	47-48	DNA damage inducible transcript 3	Homo sapiens	170-174
29253068-15	2018	Future approaches should incorporate targeted agents such as everolimus with R-CHOP rather than as adjuvant therapy after CR has been obtained.	Everolimus	61-71	DNA damage inducible transcript 3	Homo sapiens	79-83
29239061-10	2018	IL-1beta could induce ERS and associated cell apoptosis by activating the GRP78/PERK/CHOP signal pathway, which could be inhibited by progesterone.	Progesterone	134-146	DNA damage inducible transcript 3	Homo sapiens	85-89
29328482-16	2018	These findings suggest that cytisine induced the ER stress-mediated apoptotic pathway via activation of CHOP, JNK and caspase-4 in HepG2 cells, and cytisine is a potential new target compound for nAchRs (nicotinic acetylcholine receptors) to treat liver cancer.	cytisine	28-36	DNA damage inducible transcript 3	Homo sapiens	104-108
29328423-6	2018	Knockdown of TXNDC5 markedly augmented cisplatin-induced levels of CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-3 activity and apoptosis; while overexpression of TXNDC5 largely eliminated cetuximab-induced levels of CHOP, caspase-3 activity and apoptosis.	Cisplatin	39-48	DNA damage inducible transcript 3	Homo sapiens	67-116
29328423-6	2018	Knockdown of TXNDC5 markedly augmented cisplatin-induced levels of CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-3 activity and apoptosis; while overexpression of TXNDC5 largely eliminated cetuximab-induced levels of CHOP, caspase-3 activity and apoptosis.	Cisplatin	39-48	DNA damage inducible transcript 3	Homo sapiens	118-122
29328423-6	2018	Knockdown of TXNDC5 markedly augmented cisplatin-induced levels of CCAAT/enhancer-binding protein homologous protein (CHOP), caspase-3 activity and apoptosis; while overexpression of TXNDC5 largely eliminated cetuximab-induced levels of CHOP, caspase-3 activity and apoptosis.	Cisplatin	39-48	DNA damage inducible transcript 3	Homo sapiens	237-241
29328423-7	2018	Cisplatin and cetuximab demonstrated a combinatorial effect on increasing the levels of CHOP, caspase-3 activity and apoptosis, which was largely eliminated by overexpression of TXNDC5 or a reactive oxygen species (ROS) scavenger/antagonist.	Cisplatin	0-9	DNA damage inducible transcript 3	Homo sapiens	88-92
29328423-7	2018	Cisplatin and cetuximab demonstrated a combinatorial effect on increasing the levels of CHOP, caspase-3 activity and apoptosis, which was largely eliminated by overexpression of TXNDC5 or a reactive oxygen species (ROS) scavenger/antagonist.	Reactive Oxygen Species	190-213	DNA damage inducible transcript 3	Homo sapiens	88-92
29328482-14	2018	In the present study, we observed that cytisine induced ER stress-inducing factors and CHOP and p-JNK1/2 protein expression, and it increased the JNK protein expression in the HepG2 cells.	cytisine	39-47	DNA damage inducible transcript 3	Homo sapiens	87-91
29198881-5	2018	With the existing literature, this review exhibits the effect of arsenic on adipose tissue and its signalling events such as SIRT3- FOXO3a signalling pathway, Ras -MAP -AP-1 cascade, PI(3)-K-Akt pathway, endoplasmic reticulum stress protein, C/EBP homologous protein (CHOP10) and GPCR pathway with role of adipokines.	Arsenic	65-72	DNA damage inducible transcript 3	Homo sapiens	268-274
29280296-0	2018	Lock and chop: A novel method for the generation of a PICK1 PDZ domain and piperidine-based inhibitor co-crystal structure.	piperidine	75-85	DNA damage inducible transcript 3	Homo sapiens	9-13
29467881-1	2018	Treatment with rituximab plus a regimen of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) for patients with diffuse large B-cell lymphoma (DLBCL) has proven efficacy in clinical trials.	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	104-108
29467881-1	2018	Treatment with rituximab plus a regimen of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) for patients with diffuse large B-cell lymphoma (DLBCL) has proven efficacy in clinical trials.	Prednisolone	90-102	DNA damage inducible transcript 3	Homo sapiens	104-108
29458389-9	2018	Gene expression analysis identified endoplasmic reticulum (ER) stress and the unfolded protein response as the most affected pathways and artesunate-induced expression of the ER stress markers ATF-4 and DDIT3 was specifically upregulated in malignant B-cells, but not in normal B-cells.	Artesunate	138-148	DNA damage inducible transcript 3	Homo sapiens	203-208
28508557-1	2018	BACKGROUND: The aim of this study was to describe the use of a lomustine (CCNU), vincristine, procarbazine and prednisolone (LOPP) protocol used for treatment of chemotherapy naive T-cell lymphoma patients and to describe the response rate, toxicity and disease-free interval compared historically to CHOP chemotherapy.	Lomustine	63-72	DNA damage inducible transcript 3	Homo sapiens	301-305
28508557-1	2018	BACKGROUND: The aim of this study was to describe the use of a lomustine (CCNU), vincristine, procarbazine and prednisolone (LOPP) protocol used for treatment of chemotherapy naive T-cell lymphoma patients and to describe the response rate, toxicity and disease-free interval compared historically to CHOP chemotherapy.	lopp	125-129	DNA damage inducible transcript 3	Homo sapiens	301-305
29686956-4	2018	Since she was in her second trimester, we decided to treat her with rituximab-cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP).	Prednisone	122-132	DNA damage inducible transcript 3	Homo sapiens	136-140
28681934-3	2018	When human SH-SY5Y neuroblastoma cells were treated with DBL or CAPE, the expression of endoplasmic reticulum (ER) stress-related genes such as HSPA5, HYOU1, DDIT3, and SEC61b increased to a larger extent in response to CAPE treatment, while that of antioxidant genes such as HMOX1, GCLM, and NQO1 increased to a larger extent in response to DBL treatment.	3,4-dihydroxybenzalacetone	57-60	DNA damage inducible transcript 3	Homo sapiens	158-163
29434187-6	2018	Activation of the amino-acid-sensing kinase general control nonderepressible 2 (GCN2) upon glutamine deprivation is responsible for TRAIL-R2 upregulation through a signaling pathway involving ATF4 and CHOP transcription factors.	Glutamine	91-100	DNA damage inducible transcript 3	Homo sapiens	201-205
29207036-7	2018	The results of the present study are the first, to the best of our knowledge, to demonstrate that melatonin induced apoptosis in hFOB 1.19 human osteoblastic cells by activating the ERS-associated eIF2alpha-ATF4 pathway and subsequently triggered the cascade effects of CHOP, caspase-3 and JNK.	Melatonin	98-107	DNA damage inducible transcript 3	Homo sapiens	270-274
29926678-13	2018	CONCLUSIONS: Dex has notable effects against H/R injury, which may be related to effective inhibition of apoptosis mediated by the CHOP"s signal path.	Dexmedetomidine	13-16	DNA damage inducible transcript 3	Homo sapiens	131-135
29135079-3	2018	Western blot assay revealed that the protein expressions of p53, Bax, and CCAAT-enhancer-binding protein homologous protein (CHOP) increased, while the levels of Bcl-2 were reduced following CS extract treatment.	Cesium	191-193	DNA damage inducible transcript 3	Homo sapiens	74-123
29135079-3	2018	Western blot assay revealed that the protein expressions of p53, Bax, and CCAAT-enhancer-binding protein homologous protein (CHOP) increased, while the levels of Bcl-2 were reduced following CS extract treatment.	Cesium	191-193	DNA damage inducible transcript 3	Homo sapiens	125-129
28524259-10	2018	Nonpegylated liposomal doxorubicin instead of doxorubicin in the R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) regimen is a feasible option for patients with diffuse large B-cell lymphoma presenting with concomitant cardiac disorders.	Doxorubicin	23-34	DNA damage inducible transcript 3	Homo sapiens	67-71
28681934-3	2018	When human SH-SY5Y neuroblastoma cells were treated with DBL or CAPE, the expression of endoplasmic reticulum (ER) stress-related genes such as HSPA5, HYOU1, DDIT3, and SEC61b increased to a larger extent in response to CAPE treatment, while that of antioxidant genes such as HMOX1, GCLM, and NQO1 increased to a larger extent in response to DBL treatment.	caffeic acid phenethyl ester	64-68	DNA damage inducible transcript 3	Homo sapiens	158-163
29721381-1	2018	Diminished overall survival rate of non-Hodgkin lymphoma (NHL) patients treated with a combination regimen of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) has been recently linked to recurrent somatic mutations activating FOXO1.	Prednisone	168-178	DNA damage inducible transcript 3	Homo sapiens	182-186
29442009-8	2018	Showing no significant effect on the expression of protein kinase RNA-like ER kinase (PERK), cisplatin and 14G2a exhibited a marked synergistic effect on inducing phosphorylation/activation of PERK, phosphorylation/inactivation of eukaryotic translation initiation factor 2alpha (eIF2alpha), expression of CHOP, in parallel to inducing the caspase-3 activity and apoptosis in MG-63 and Saos-2 cells.	Cisplatin	93-102	DNA damage inducible transcript 3	Homo sapiens	306-310
29391535-5	2018	We have shown that kaempferol pre-incubation significantly inhibits the expression of GRP78 (a chaperone) and CHOP (ER stress associated pro-apoptotic transcription factor) under stressed condition.	kaempferol	19-29	DNA damage inducible transcript 3	Homo sapiens	110-114
28986289-7	2018	The data showed that PQ significantly reduced A549 cell viability, changed cell morphology, induced cell apoptosis and significantly upregulated the levels of GRP78, CHOP, p-PERK, c-ATF6 and p-IRE1alpha.	Paraquat	21-23	DNA damage inducible transcript 3	Homo sapiens	166-170
29342125-5	2018	The cytotoxic mechanism of NEO214 involved severe ER stress and prolonged induction of CCAAT/enhancer-binding protein homologous protein (CHOP), a key pro-apoptotic component of the ER stress response.	neo214	27-33	DNA damage inducible transcript 3	Homo sapiens	87-136
29410666-2	2018	However, this model involves animals with high tumor burden, whereas in the clinics B-NHL patients are usually treated with chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, and prednisone) as first-line therapy prior to immunotherapy.	Cyclophosphamide	144-160	DNA damage inducible transcript 3	Homo sapiens	138-142
29342125-5	2018	The cytotoxic mechanism of NEO214 involved severe ER stress and prolonged induction of CCAAT/enhancer-binding protein homologous protein (CHOP), a key pro-apoptotic component of the ER stress response.	neo214	27-33	DNA damage inducible transcript 3	Homo sapiens	138-142
29433671-8	2018	The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP).	Reactive Oxygen Species	39-42	DNA damage inducible transcript 3	Homo sapiens	245-269
29339762-6	2018	Previous studies revealed that the release of calcium from the ER induces ER stress, leading to the conversion of X-box binding protein 1 (Xbp1) pre-mRNA to spliced Xbp1 (sXbp1) as well as the up-regulation of Chop expression.	Calcium	46-53	DNA damage inducible transcript 3	Homo sapiens	210-214
29339762-7	2018	Capsaicin treatment increased the expression of sXbp1 and Chop in brown preadipocytes and did not enhance lipid accumulation or Ucp1 expression in Xbp1 knockdown cells.	Capsaicin	0-9	DNA damage inducible transcript 3	Homo sapiens	58-62
29433671-8	2018	The three phytochemicals activated the ROS-p38-p53 apoptotic pathway by increasing the level of phosphorylated p38 MAPK and p53, and they activated the ER stress-mediated apoptotic pathway by increasing the level of phosphorylated eIF2alpha and C/EBP homologous protein (CHOP).	Reactive Oxygen Species	39-42	DNA damage inducible transcript 3	Homo sapiens	271-275
30280609-6	2018	Finally, the pro-apoptotic factor CHOP was a common target of both ATF6 and IRE1alpha pathways and was associated with elongated CIT and increased cell death.	cit	129-132	DNA damage inducible transcript 3	Homo sapiens	34-38
29324796-4	2018	It is concluded based on our result that QA induces apoptosis and ER stress just as QA-induced ER stress pathway may mediate apoptosis by upregulating mRNA expression levels of eIF2alpha, ATF4, IRE1, XBP1, ATF6, PERK and CHOP in the HeLa cells.	quinovic acid	84-86	DNA damage inducible transcript 3	Homo sapiens	221-225
29086009-4	2018	According to the chemotherapy regimens, patients were classified in four groups: combination of vincristine, cyclophosphamide, doxorubicin, and prednisone (CHOP group) with rituximab (RCHOP group) and combination of vincristine, cyclophosphamide, pegylated liposomal doxorubicin and prednisone (CDOP group) with rituximab (RCDOP group).	Prednisone	144-154	DNA damage inducible transcript 3	Homo sapiens	156-160
29940794-8	2018	Finally, the 2 autophagic genes LC3B and ATG12 were found to be transcriptionally upregulated by downstream ATF4 and DDIT3 in ER stress, which contributed to the SiNP-enhanced autophagosome synthesis.	sinp	162-166	DNA damage inducible transcript 3	Homo sapiens	117-122
30238070-11	2018	The ontology can be used to reason individual components from regimens mentioned in electronic health records (eg, R-CHOP maps to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) and also to probabilistically reconstruct regimens from individual drug components.	Prednisone	189-199	DNA damage inducible transcript 3	Homo sapiens	117-121
29157092-8	2018	ONC201 combined with bortezomib in a Burkitt"s lymphoma xenograft model reduced tumor cell density and improved CHOP induction compared to either agent alone.	Bortezomib	21-31	DNA damage inducible transcript 3	Homo sapiens	112-116
29554648-12	2018	Increased phospho-AMPKalpha, CHOP and Grp78 as well as cellular apoptosis were prevented by mTOR inhibitor rapamycin in HG-treated podocytes.	Sirolimus	107-116	DNA damage inducible transcript 3	Homo sapiens	29-33
30025493-12	2018	Our results demonstrated that FKB induced protective autophagy through the ATF4-DDIT3-TRIB3-AKT-MTOR-RPS6KB1 signaling pathway in GBM cells, indicating that the combination treatment of FKB with autophagy inhibitors may potentially be an effective therapeutic strategy for GBM.	flavokawain B	30-33	DNA damage inducible transcript 3	Homo sapiens	80-85
30025493-12	2018	Our results demonstrated that FKB induced protective autophagy through the ATF4-DDIT3-TRIB3-AKT-MTOR-RPS6KB1 signaling pathway in GBM cells, indicating that the combination treatment of FKB with autophagy inhibitors may potentially be an effective therapeutic strategy for GBM.	flavokawain B	186-189	DNA damage inducible transcript 3	Homo sapiens	80-85
29618689-2	2018	Treatment with five cycles of doxorubicin, vincristine, cyclophosphamide, and prednisolone (CHOP) therapy was initiated, which resulted in insufficient improvement in anemia.	Prednisolone	78-90	DNA damage inducible transcript 3	Homo sapiens	92-96
29387400-6	2018	The patient received chemotherapy with six cycles of cyclophosphamide, hydroxydaunomycin, oncovin and prednisone (CHOP regimen) and a complete radiological response was achieved after six cycles of treatment.	Prednisone	102-112	DNA damage inducible transcript 3	Homo sapiens	114-118
29415941-7	2018	Although the patient received two courses of cyclophosphamide, hydroxydaunorubicin, oncovin, and prednisone (CHOP) and dexamethasone, etoposide, ifosfamide, and carboplatin (DeVIC) therapy, facial nerve and lower limb paralysis manifested.	Prednisone	97-107	DNA damage inducible transcript 3	Homo sapiens	109-113
29190494-6	2018	The involvement of SRC/FAK activation in FUS-CHOP-mediated invasion was further confirmed using the SRC inhibitor dasatinib, the specific FAK inhibitor PF-573228, and FAK siRNA.	Dasatinib	114-123	DNA damage inducible transcript 3	Homo sapiens	45-49
29190494-6	2018	The involvement of SRC/FAK activation in FUS-CHOP-mediated invasion was further confirmed using the SRC inhibitor dasatinib, the specific FAK inhibitor PF-573228, and FAK siRNA.	6-(4-(3-(methylsulfonyl)benzylamino)-5-(trifluoromethyl)pyrimidin-2-ylamino)-3,4-dihydroquinolin-2(1H)-one	152-161	DNA damage inducible transcript 3	Homo sapiens	45-49
29190494-8	2018	Downstream of SRC/FAK signaling, we found that FUS-CHOP expression increases the levels of the RHO/ROCK downstream effector phospho-MLC2 (T18/S19) and that this activation was prevented by dasatinib or PF573228.	Dasatinib	189-198	DNA damage inducible transcript 3	Homo sapiens	51-55
29877250-1	2018	Prior to the 2000, patients with extranodal NK/T-cell lymphoma, nasal type (ENKL) were typically treated with anthracycline-containing chemotherapy, such as CHOP therapy, and the therapeutic outcomes were unsatisfactory.	Anthracyclines	110-123	DNA damage inducible transcript 3	Homo sapiens	157-161
29737107-7	2018	R-CHOP (rituximab,cyclophosphamide,epirubicin,vindesine,prednisone) or CHOP regimen chemotherapy significantly improved the survival of the patients (P=0.000 2).	Epirubicin	35-45	DNA damage inducible transcript 3	Homo sapiens	2-6
29737107-7	2018	R-CHOP (rituximab,cyclophosphamide,epirubicin,vindesine,prednisone) or CHOP regimen chemotherapy significantly improved the survival of the patients (P=0.000 2).	Vindesine	46-55	DNA damage inducible transcript 3	Homo sapiens	2-6
29737107-7	2018	R-CHOP (rituximab,cyclophosphamide,epirubicin,vindesine,prednisone) or CHOP regimen chemotherapy significantly improved the survival of the patients (P=0.000 2).	Prednisone	56-66	DNA damage inducible transcript 3	Homo sapiens	2-6
29737107-7	2018	R-CHOP (rituximab,cyclophosphamide,epirubicin,vindesine,prednisone) or CHOP regimen chemotherapy significantly improved the survival of the patients (P=0.000 2).	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	2-6
29383150-5	2017	Moreover, erastin and ART induced endoplasmic reticulum (ER) stress and promoted p53 upregulated modulator of apoptosis (PUMA) expression via C/EBP-homologous protein (CHOP).	erastin	10-17	DNA damage inducible transcript 3	Homo sapiens	168-172
28766099-2	2018	We conducted a prospective clinical trial to assess the efficacy of palonosetron in patients receiving the CHOP regimen.	Palonosetron	68-80	DNA damage inducible transcript 3	Homo sapiens	107-111
28766099-5	2018	Palonosetron (0.75 mg) was administered before chemotherapy on day 1 of both the first and second CHOP cycles.	Palonosetron	0-12	DNA damage inducible transcript 3	Homo sapiens	98-102
29164887-10	2017	Overall, our results showed that PTER potentiated TRAIL-induced apoptosis via ROS-mediated CHOP activation leading to the expression of DR4 and DR5.	Reactive Oxygen Species	78-81	DNA damage inducible transcript 3	Homo sapiens	91-95
29206200-6	2017	Finally, in the milieu of TUNI-induced ERS, l-glutamine was found to maintain a high level of GRP78, alleviate CHOP-mediated apoptosis and activate the inositol requiring enzyme 1alpha (IRE1alpha)-X-box binding protein 1 (XBP1) axis.	Glutamine	44-55	DNA damage inducible transcript 3	Homo sapiens	111-115
29206200-8	2017	We propose that the functional effect of l-glutamine on intestinal health may be partly due to its modulation of ERS and CHOP-mediated apoptosis.	Glutamine	41-52	DNA damage inducible transcript 3	Homo sapiens	121-125
28966297-7	2017	In addition, NAC (N-acetylcysteine, a reactive oxygen species (ROS) scavenger) treatment dramatically decreased ROS generation in H1299 cells; both of NAC and 4-PBA (4-phenylbutyrate, a specific endoplasmic reticulum (ER) stress inhibitor) administration impaired apoptosis and expression levels of ATF4, CHOP and caspase-4 in G-Rh2 incubated H1299 cells.	Acetylcysteine	18-34	DNA damage inducible transcript 3	Homo sapiens	305-309
29535810-8	2018	Silibinin further induced endoplasmic reticulum (ER) stress as was indicated by the increase in ER marker proteins such as PERK, eIF2alpha, and ATF-4, which stimulate the expression of CCAAT/enhancer binding protein homologous protein (CHOP).	Silybin	0-9	DNA damage inducible transcript 3	Homo sapiens	185-234
29535810-8	2018	Silibinin further induced endoplasmic reticulum (ER) stress as was indicated by the increase in ER marker proteins such as PERK, eIF2alpha, and ATF-4, which stimulate the expression of CCAAT/enhancer binding protein homologous protein (CHOP).	Silybin	0-9	DNA damage inducible transcript 3	Homo sapiens	236-240
29354290-6	2017	Interleukin (IL)-1beta and the nucleoside reverse transcriptase inhibitor abacavir upregulated expression of ER stress markers in human astrocytes, including binding immunoglobulin protein (BiP), C/EBP homologous protein (CHOP), and calnexin.	abacavir	74-82	DNA damage inducible transcript 3	Homo sapiens	196-220
29354290-6	2017	Interleukin (IL)-1beta and the nucleoside reverse transcriptase inhibitor abacavir upregulated expression of ER stress markers in human astrocytes, including binding immunoglobulin protein (BiP), C/EBP homologous protein (CHOP), and calnexin.	abacavir	74-82	DNA damage inducible transcript 3	Homo sapiens	222-226
29340089-7	2017	MiR-185-5p affected the expansion of MDSCs and reversed the effect of RNCR3 on MDSC differentiation and function through directly targeting Chop.	mir-185-5p	0-10	DNA damage inducible transcript 3	Homo sapiens	140-144
29535810-9	2018	CHOP-targeted siRNA eliminated the induction of DR5 and resulted in a significant decrease in silibinin/TRAIL-mediated apoptosis.	Silybin	94-103	DNA damage inducible transcript 3	Homo sapiens	0-4
29333403-1	2017	Background: While cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is the most commonly used chemotherapeutic regimen for patients with peripheral T-cell lymphomas (PTCLs), elderly patients are more vulnerable to associated toxicities.	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	80-84
29333403-1	2017	Background: While cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is the most commonly used chemotherapeutic regimen for patients with peripheral T-cell lymphomas (PTCLs), elderly patients are more vulnerable to associated toxicities.	Doxorubicin	36-47	DNA damage inducible transcript 3	Homo sapiens	80-84
29333403-1	2017	Background: While cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is the most commonly used chemotherapeutic regimen for patients with peripheral T-cell lymphomas (PTCLs), elderly patients are more vulnerable to associated toxicities.	Prednisolone	66-78	DNA damage inducible transcript 3	Homo sapiens	80-84
29390581-8	2017	The patient attained partial remission after undergoing 2 rounds of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP regimen) before autologous stem cell transplantation, however, he quickly relapsed and developed new cutaneous lesions.	Prednisone	116-126	DNA damage inducible transcript 3	Homo sapiens	128-132
28964970-5	2017	Mechanistically, metformin altered UPR activated by bortezomib, leading to a reduced expression of BiP, up-regulation of CHOP and down-regulation of Bcl-2.	Metformin	17-26	DNA damage inducible transcript 3	Homo sapiens	121-125
28964970-5	2017	Mechanistically, metformin altered UPR activated by bortezomib, leading to a reduced expression of BiP, up-regulation of CHOP and down-regulation of Bcl-2.	Bortezomib	52-62	DNA damage inducible transcript 3	Homo sapiens	121-125
29121349-10	2017	In addition, naringenin increased ROS, ER stress, through activation of eIF2alpha and IRE1alpha, GADD153 and GRP78 proteins in a dose-dependent manner.	naringenin	13-23	DNA damage inducible transcript 3	Homo sapiens	97-104
29163689-6	2017	Pretreatment with N-acetylcystein, a ROS scavenger, significantly abrogated TCS7010-induced accumulation of CHOP, BIM, cleaved caspase-7 and cleaved PARP.	N-Acetyl-L-cysteine	18-33	DNA damage inducible transcript 3	Homo sapiens	108-112
29163689-6	2017	Pretreatment with N-acetylcystein, a ROS scavenger, significantly abrogated TCS7010-induced accumulation of CHOP, BIM, cleaved caspase-7 and cleaved PARP.	Aurora A Inhibitor I	76-83	DNA damage inducible transcript 3	Homo sapiens	108-112
28789937-7	2017	rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone (R-CHOP) was initial treatment in 15 (79%) of patients with aggFL and 21 (72%) of those with FL3A; rituximab was included in initial therapy in 18 (95%) and 24 (83%), respectively.	Prednisone	55-65	DNA damage inducible transcript 3	Homo sapiens	69-73
29152653-13	2017	It induced glucose-regulated protein 78 (GRP78) expression, whereas the expression levels of activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP) were upregulated and then downregulated following treatment with various doses of elaidic acid.	elaidic acid	277-289	DNA damage inducible transcript 3	Homo sapiens	138-187
29152653-13	2017	It induced glucose-regulated protein 78 (GRP78) expression, whereas the expression levels of activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP) were upregulated and then downregulated following treatment with various doses of elaidic acid.	elaidic acid	277-289	DNA damage inducible transcript 3	Homo sapiens	189-193
29152653-14	2017	These results indicated that elaidic acid inhibited SH-SY5Y cell growth and induced apoptosis by enhancing oxidative stress and activating the ER stress/UPR signaling pathway and the GRP78/ATF4/CHOP pathway.	elaidic acid	29-41	DNA damage inducible transcript 3	Homo sapiens	194-198
29163689-5	2017	In addition, TCS7010 resulted in the production of reactive oxygen species (ROS) and stimulation of the unfolded protein response (UPR), leading to the upregulation of CCAAT/enhancer-binding protein-homologous protein (CHOP), and its downstream target BCL2 like 11 (BIM).	Aurora A Inhibitor I	13-20	DNA damage inducible transcript 3	Homo sapiens	168-217
29163689-5	2017	In addition, TCS7010 resulted in the production of reactive oxygen species (ROS) and stimulation of the unfolded protein response (UPR), leading to the upregulation of CCAAT/enhancer-binding protein-homologous protein (CHOP), and its downstream target BCL2 like 11 (BIM).	Aurora A Inhibitor I	13-20	DNA damage inducible transcript 3	Homo sapiens	219-223
28951205-4	2017	In cultured VSMC, tunicamycin caused cell death accompanied by an increase in caspase-3 processing and C/EBP homologous protein (CHOP) expression.	Tunicamycin	18-29	DNA damage inducible transcript 3	Homo sapiens	103-127
28988120-3	2017	We found that leflunomide caused endoplasmic reticulum (ER) stress and activated an unfolded protein response, as evidenced by increased expression of related genes including CHOP and GADD34; and elevated protein levels of typical ER stress markers including CHOP, ATF-4, p-eIF2alpha, and spliced XBP1.	Leflunomide	14-25	DNA damage inducible transcript 3	Homo sapiens	175-179
28988120-3	2017	We found that leflunomide caused endoplasmic reticulum (ER) stress and activated an unfolded protein response, as evidenced by increased expression of related genes including CHOP and GADD34; and elevated protein levels of typical ER stress markers including CHOP, ATF-4, p-eIF2alpha, and spliced XBP1.	Leflunomide	14-25	DNA damage inducible transcript 3	Homo sapiens	259-263
28988120-5	2017	Inhibition of ER stress with an ER stress inhibitor 4-phenylbutyrate, and knockdown of ATF-4 and CHOP genes partially protected cells upon leflunomide exposure.	Leflunomide	139-150	DNA damage inducible transcript 3	Homo sapiens	97-101
29344266-0	2017	Erratum: HBV suppresses thapsigargin-induced apoptosis via inhibiting CHOP expression in hepatocellular carcinoma cells.	Thapsigargin	24-36	DNA damage inducible transcript 3	Homo sapiens	70-74
29046367-10	2017	Further, PA treatment significantly increased the expression of ERS markers, Ig heavy chain binding protein (Bip), and homologous proteins of CCAAT-enhancer binding proteins (CHOP).	Palmitic Acid	9-11	DNA damage inducible transcript 3	Homo sapiens	175-179
28951205-4	2017	In cultured VSMC, tunicamycin caused cell death accompanied by an increase in caspase-3 processing and C/EBP homologous protein (CHOP) expression.	Tunicamycin	18-29	DNA damage inducible transcript 3	Homo sapiens	129-133
29142472-7	2017	PGE1 enhanced the TG-induced expression of C/EBP homologous protein (CHOP), glucose-regulated protein (GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and mRNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phospho-eukaryotic initiation factor 2alpha and CHOP.	Alprostadil	0-4	DNA damage inducible transcript 3	Homo sapiens	444-448
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Arginine	70-73	DNA damage inducible transcript 3	Homo sapiens	29-33
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Arginine	70-73	DNA damage inducible transcript 3	Homo sapiens	37-41
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Arginine	74-77	DNA damage inducible transcript 3	Homo sapiens	29-33
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Arginine	74-77	DNA damage inducible transcript 3	Homo sapiens	37-41
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Arginine	74-77	DNA damage inducible transcript 3	Homo sapiens	29-33
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Arginine	74-77	DNA damage inducible transcript 3	Homo sapiens	37-41
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Proline	86-89	DNA damage inducible transcript 3	Homo sapiens	29-33
29061791-14	2017	Furthermore, confocal microscopy examination revealed that Tetrandrine induced expression of ER stress-related proteins GADD153 and GRP78.	tetrandrine	59-70	DNA damage inducible transcript 3	Homo sapiens	120-127
28668332-6	2017	Ethanol stimulated reactive oxygen species (ROS) production, which induced CHOP expression and eIF2alpha phosphorylation.	Ethanol	0-7	DNA damage inducible transcript 3	Homo sapiens	75-79
28668332-6	2017	Ethanol stimulated reactive oxygen species (ROS) production, which induced CHOP expression and eIF2alpha phosphorylation.	Reactive Oxygen Species	19-42	DNA damage inducible transcript 3	Homo sapiens	75-79
28668332-6	2017	Ethanol stimulated reactive oxygen species (ROS) production, which induced CHOP expression and eIF2alpha phosphorylation.	Reactive Oxygen Species	44-47	DNA damage inducible transcript 3	Homo sapiens	75-79
29263552-4	2017	Early and accurate diagnosis is required as these patients respond well to systemic anthracycline-based chemotherapy (R-CHOP).	Anthracyclines	84-97	DNA damage inducible transcript 3	Homo sapiens	120-124
28862883-1	2017	Purpose To evaluate the impact of the addition of bortezomib to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) on outcomes in previously untreated patients with non-germinal center B-cell-like (non-GCB) diffuse large B-cell lymphoma (DLBCL).	Bortezomib	50-60	DNA damage inducible transcript 3	Homo sapiens	137-141
28875258-7	2017	Oxalate stress significantly up-regulated expression of ER stress markers GRP78 and CHOP both in vitro and in vivo.	Oxalates	0-7	DNA damage inducible transcript 3	Homo sapiens	84-88
29382010-10	2017	OUTCOMES: After 4 rounds of chemotherapy using the rituximab-cyclophosphamide hydroxydaunorubicin oncovin prednisolone (R-CHOP) regimen, the patient"s pain was significantly relieved.	rituximab-cyclophosphamide hydroxydaunorubicin oncovin prednisolone	51-118	DNA damage inducible transcript 3	Homo sapiens	122-126
29296861-2	2017	Despite producing somewhat less-than-satisfactory results, the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remains the de facto standard in PTCL treatment.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	138-142
29296861-2	2017	Despite producing somewhat less-than-satisfactory results, the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remains the de facto standard in PTCL treatment.	Prednisone	126-136	DNA damage inducible transcript 3	Homo sapiens	138-142
29126407-8	2017	In the subgroup treated with CHOP or CHOP-like therapy, patients with Arg/Arg and Arg/Pro showed a higher 5-year overall survival (OS) rate than those with Pro/Pro (68.8% vs. 23.2%, P = 0.001).	Proline	86-89	DNA damage inducible transcript 3	Homo sapiens	37-41
29291017-6	2017	Moreover, DDIT3 deregulation promoted letrozole-resistance by acting as a potent corepressor of ESR1 transcription.	Letrozole	38-47	DNA damage inducible transcript 3	Homo sapiens	10-15
29291017-7	2017	Taken together, we have identified that disruption of the miR-1271/DDIT3/ERalpha cascade plays a causative role in the pathogenesis of letrozole resistance in BCa.	Letrozole	135-144	DNA damage inducible transcript 3	Homo sapiens	67-72
28831584-6	2017	The Deauville scores from 18-fluorodeoxyglucose positron emission tomography after R-CHOP showed low (2-3) in 58.0% and high (4) in 42.0% of the patients.	18-fluorodeoxyglucose	26-47	DNA damage inducible transcript 3	Homo sapiens	85-89
28831584-11	2017	In conclusion, DLBCL patients who partially responded to R-CHOP are still a heterogeneous group, for which IPI2 and Deauville scores should be evaluated for prediction of prognosis.	ipi2	107-111	DNA damage inducible transcript 3	Homo sapiens	59-63
28688954-8	2017	Treatment with tauroursodeoxycholic acid (TUDCA) increased the expression levels of the bile acid transporters and Nrf2, decreased the expression levels of glucose-regulated protein 78 (GRP78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), and C/EBP-homologous protein (CHOP), and inhibited RFP-induced oxidative stress.	ursodoxicoltaurine	15-40	DNA damage inducible transcript 3	Homo sapiens	267-291
28688954-8	2017	Treatment with tauroursodeoxycholic acid (TUDCA) increased the expression levels of the bile acid transporters and Nrf2, decreased the expression levels of glucose-regulated protein 78 (GRP78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), and C/EBP-homologous protein (CHOP), and inhibited RFP-induced oxidative stress.	ursodoxicoltaurine	15-40	DNA damage inducible transcript 3	Homo sapiens	293-297
28688954-8	2017	Treatment with tauroursodeoxycholic acid (TUDCA) increased the expression levels of the bile acid transporters and Nrf2, decreased the expression levels of glucose-regulated protein 78 (GRP78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), and C/EBP-homologous protein (CHOP), and inhibited RFP-induced oxidative stress.	ursodoxicoltaurine	42-47	DNA damage inducible transcript 3	Homo sapiens	267-291
28688954-8	2017	Treatment with tauroursodeoxycholic acid (TUDCA) increased the expression levels of the bile acid transporters and Nrf2, decreased the expression levels of glucose-regulated protein 78 (GRP78), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4), and C/EBP-homologous protein (CHOP), and inhibited RFP-induced oxidative stress.	ursodoxicoltaurine	42-47	DNA damage inducible transcript 3	Homo sapiens	293-297
28949381-8	2017	ER stress was stimulated by caffeine as demonstrated by increased levels of GRP78/Bip, CHOP and inositol-requiring enzyme 1 (IRE1)-alpha as well as many enlarged ERs detected by electron microscopy.	Caffeine	28-36	DNA damage inducible transcript 3	Homo sapiens	87-91
29142472-7	2017	PGE1 enhanced the TG-induced expression of C/EBP homologous protein (CHOP), glucose-regulated protein (GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and mRNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phospho-eukaryotic initiation factor 2alpha and CHOP.	Alprostadil	0-4	DNA damage inducible transcript 3	Homo sapiens	43-67
29142472-7	2017	PGE1 enhanced the TG-induced expression of C/EBP homologous protein (CHOP), glucose-regulated protein (GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and mRNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phospho-eukaryotic initiation factor 2alpha and CHOP.	Alprostadil	0-4	DNA damage inducible transcript 3	Homo sapiens	69-73
29142472-7	2017	PGE1 enhanced the TG-induced expression of C/EBP homologous protein (CHOP), glucose-regulated protein (GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and mRNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phospho-eukaryotic initiation factor 2alpha and CHOP.	Thapsigargin	18-20	DNA damage inducible transcript 3	Homo sapiens	43-67
29142472-7	2017	PGE1 enhanced the TG-induced expression of C/EBP homologous protein (CHOP), glucose-regulated protein (GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and mRNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phospho-eukaryotic initiation factor 2alpha and CHOP.	Thapsigargin	18-20	DNA damage inducible transcript 3	Homo sapiens	69-73
29079731-7	2017	We demonstrated that bleomycin can activate ER stress associated proteins, including GRP78, CHOP, and ATF-4, both in vitro and in vivo.	Bleomycin	21-30	DNA damage inducible transcript 3	Homo sapiens	92-96
29142472-7	2017	PGE1 enhanced the TG-induced expression of C/EBP homologous protein (CHOP), glucose-regulated protein (GRP) 78 and spliced X box-binding protein 1 at 6 h. However, it attenuated their expressions after 24 h. PGE1 alone induced protein and mRNA expressions of GRP78; PGE1 also induced protein expression of DNA damage-inducible gene 34 and inhibited the expressions of phospho-PKR-like ER kinase, phospho-eukaryotic initiation factor 2alpha and CHOP.	Thapsigargin	18-20	DNA damage inducible transcript 3	Homo sapiens	444-448
28467689-7	2017	Inhibition of CHOP with a siRNA diminished DR5 expression and vernodalol-induced sensitization to the TRAIL treatment.	vernodalol	62-72	DNA damage inducible transcript 3	Homo sapiens	14-18
29070784-0	2017	Kaempferol Sensitizes Human Ovarian Cancer Cells-OVCAR-3 and SKOV-3 to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-Induced Apoptosis via JNK/ERK-CHOP Pathway and Up-Regulation of Death Receptors 4 and 5.	kaempferol	0-10	DNA damage inducible transcript 3	Homo sapiens	165-169
29070784-10	2017	RESULTS Kaempferol enhanced apoptosis and drastically up-regulated DR4, DR5, CHOP, JNK, ERK1/2, p38 and apoptotic protein expression with decline in the expression of anti-apoptotic proteins.	kaempferol	8-18	DNA damage inducible transcript 3	Homo sapiens	77-81
29070784-11	2017	Further transfection with siRNA specific to CHOP and DR5 indicated the involvement of CHOP in DR5 up-regulation and also the contribution of DR5 in kaempferol-enhanced TRAIL-induced apoptosis.	kaempferol	148-158	DNA damage inducible transcript 3	Homo sapiens	44-48
29070784-12	2017	CONCLUSIONS Kaempferol sensitized ovarian cancer cells to TRAIL-induced apoptosis via up-regulation of DR4 and DR5 through ERK/JNK/CHOP pathways.	kaempferol	12-22	DNA damage inducible transcript 3	Homo sapiens	131-135
28630460-11	2017	Interestingly, CHOP was positively correlated with TNFalpha and total ROS production and GRP78 was negatively correlated with glutathione levels.	Reactive Oxygen Species	70-73	DNA damage inducible transcript 3	Homo sapiens	15-19
28467689-11	2017	Based on our results, vernodalol enhanced TRAIL-induced apoptosis by down-regulating Mcl-1 and up-regulating DR5, and the effects of DR5 depended on JNK activation and CHOP induction.	vernodalol	22-32	DNA damage inducible transcript 3	Homo sapiens	168-172
28843399-7	2017	CB-5083 induced ER stress, as documented through: 1) prominent expression of chaperones (GRP78, GRP94, PDI, DNAJC3, and DNAJB9); 2) increased activation of IRE1-alpha, as demonstrated by the splicing of XBP1; and 3) activation of PERK, which resulted in a significant overexpression of CHOP, and its downstream genes.	CB-5083	0-7	DNA damage inducible transcript 3	Homo sapiens	286-290
29152143-9	2017	PGPIPN alleviated alcohol-induced cell steatosis and injuries by regulating the gene expressions and/or activities of ACC, PPAR-gamma, CHOP and Caspase-3.	pgpipn	0-6	DNA damage inducible transcript 3	Homo sapiens	135-139
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	91-95
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Doxorubicin	126-137	DNA damage inducible transcript 3	Homo sapiens	91-95
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Vincristine	139-150	DNA damage inducible transcript 3	Homo sapiens	91-95
28791403-10	2017	Among DLBCL cases, the TP53 mutations shortened both OS and PFS of patients treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and decreased both OS and PFS of patients with secondary DLBCL disease.	Prednisone	155-165	DNA damage inducible transcript 3	Homo sapiens	91-95
28943956-0	2017	HBV suppresses thapsigargin-induced apoptosis via inhibiting CHOP expression in hepatocellular carcinoma cells.	Thapsigargin	15-27	DNA damage inducible transcript 3	Homo sapiens	61-65
29152143-9	2017	PGPIPN alleviated alcohol-induced cell steatosis and injuries by regulating the gene expressions and/or activities of ACC, PPAR-gamma, CHOP and Caspase-3.	Alcohols	18-25	DNA damage inducible transcript 3	Homo sapiens	135-139
28931802-9	2017	Although basal expression of CHOP mRNA was enhanced in OR6 cells compared to cured cells, it was similarly upregulated in both cell lines following palmitate treatment.	Palmitates	148-157	DNA damage inducible transcript 3	Homo sapiens	29-33
29033794-7	2017	Enhanced expression of GRP78, CHOP and eIF2alpha and activation of caspase 12 were additionally confirmed that endoplasmic reticulum (ER) stress pathway of apoptosis was involved in the cytotoxicity of DHA.	artenimol	202-205	DNA damage inducible transcript 3	Homo sapiens	30-34
29081194-7	2017	NCCN-IPI was outstanding to identify the subgroup of low risk patients with PTCL, who may benefit from conventional chemotherapy such as CHOP or CHOP-like regimen.	diprotin A	5-8	DNA damage inducible transcript 3	Homo sapiens	137-141
28712870-6	2017	Both CHOP and TFPI mRNA levels were upregulated after CC treatment, especially in the M2 phenotype, and the ER stress inhibitor 4-phenylbutyric acid (PBA) reversed this effect.	4-phenylbutyric acid	128-148	DNA damage inducible transcript 3	Homo sapiens	5-9
29081194-7	2017	NCCN-IPI was outstanding to identify the subgroup of low risk patients with PTCL, who may benefit from conventional chemotherapy such as CHOP or CHOP-like regimen.	diprotin A	5-8	DNA damage inducible transcript 3	Homo sapiens	145-149
28603046-8	2017	HCPT-induced apoptosis was correlated with elevation of GRP78 and CHOP, which were hallmarks of ER stress.	hydroxycamptothecinum	0-4	DNA damage inducible transcript 3	Homo sapiens	66-70
28886181-6	2017	In vitro studies demonstrated that the induction of SSAT and elevated polyamine catabolism in cells increases the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha) and enhances the expression of binding immunoglobulin protein BiP/GRP78) and CCAAT-enhancer-binding protein homologous protein (CHOP/GADD153).	Polyamines	70-79	DNA damage inducible transcript 3	Homo sapiens	270-319
28886181-6	2017	In vitro studies demonstrated that the induction of SSAT and elevated polyamine catabolism in cells increases the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha) and enhances the expression of binding immunoglobulin protein BiP/GRP78) and CCAAT-enhancer-binding protein homologous protein (CHOP/GADD153).	Polyamines	70-79	DNA damage inducible transcript 3	Homo sapiens	321-325
28886181-6	2017	In vitro studies demonstrated that the induction of SSAT and elevated polyamine catabolism in cells increases the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha) and enhances the expression of binding immunoglobulin protein BiP/GRP78) and CCAAT-enhancer-binding protein homologous protein (CHOP/GADD153).	Polyamines	70-79	DNA damage inducible transcript 3	Homo sapiens	326-333
28603046-10	2017	Knockdown of PERK decreased the ratio of Bax/Bcl-2, GRP78 and CHOP expression, suggesting that PERK signal pathway was involved in HCPT-induced fibroblast apoptosis.	hydroxycamptothecinum	131-135	DNA damage inducible transcript 3	Homo sapiens	62-66
28753442-7	2017	The combination of IMGN529 and rituximab was highly efficacious in multiple xenograft models, with superior antitumor efficacy seen compared to either agent alone or treatment with R-CHOP therapy.	naratuximab emtansine	19-26	DNA damage inducible transcript 3	Homo sapiens	183-187
28647884-5	2017	Inhibition of ER stress by treatment with the ER stress inhibitors, salubrinal and 4-phenylbutyric acid or CHOP siRNA transfection reduced FLX-induced cell death.	Fluoxetine	139-142	DNA damage inducible transcript 3	Homo sapiens	107-111
28631090-12	2017	In addition, we conclude that pseudoceramide-dominant emollient suppresses excessive ER stress induction and CHOP activation following UVB in barrier damaged skin, providing evidence that pseudoceramide-dominant emollients can be promising strategies for photoprotection of the barrier damaged skin.	pseudoceramide	30-44	DNA damage inducible transcript 3	Homo sapiens	109-113
28631090-12	2017	In addition, we conclude that pseudoceramide-dominant emollient suppresses excessive ER stress induction and CHOP activation following UVB in barrier damaged skin, providing evidence that pseudoceramide-dominant emollients can be promising strategies for photoprotection of the barrier damaged skin.	pseudoceramide	188-202	DNA damage inducible transcript 3	Homo sapiens	109-113
28643892-5	2017	Knockdown of Atf4 or Ddit3 restored cell viability after calcitriol treatment, indicating that the ER stress response was indeed responsible for the anti-proliferative effect in AXT cells.	Calcitriol	57-67	DNA damage inducible transcript 3	Homo sapiens	21-26
28711572-3	2017	Several observational studies and retrospective series have demonstrated that patients with DHL carry a poor prognosis and respond less and for a shorter duration to standard R-CHOP (rituximab, cyclophosphamide, vincristine, adriamycin, and prednisone).	Cysteamine	92-95	DNA damage inducible transcript 3	Homo sapiens	177-181
26999778-0	2017	A salvage chemotherapy of R-P-IMVP16/CBDCA consisting of rituximab, methylprednisolone, ifosfamide, methotrexate, etoposide, and carboplatin for patients with diffuse large B cell lymphoma who had previously received R-CHOP therapy as first-line chemotherapy.	r-p-imvp16	26-36	DNA damage inducible transcript 3	Homo sapiens	219-223
26999778-1	2017	We have reported the efficacy of the salvage chemotherapy P-IMVP16/CBDCA for patients with diffuse large B cell lymphoma (DLBCL) who had previously received CHOP before the availability of rituximab (R).	p-imvp16	58-66	DNA damage inducible transcript 3	Homo sapiens	157-161
26999778-1	2017	We have reported the efficacy of the salvage chemotherapy P-IMVP16/CBDCA for patients with diffuse large B cell lymphoma (DLBCL) who had previously received CHOP before the availability of rituximab (R).	Carboplatin	67-72	DNA damage inducible transcript 3	Homo sapiens	157-161
26999778-2	2017	Here, we confirmed the efficacy of R combined with P-IMVP16/CBDCA as a salvage chemotherapy for patients with DLBCL, who had previously received R-CHOP.	p-imvp16	51-59	DNA damage inducible transcript 3	Homo sapiens	147-151
31966830-11	2017	We deduce that the traditional chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is inadequate for the treatment of IVNKTL.	Prednisone	96-106	DNA damage inducible transcript 3	Homo sapiens	108-112
28647884-4	2017	FLX induced apoptotic cell death, activation of caspase-4, -9, and -3, and expression of endoplasmic reticulum (ER) stress-associated proteins, including C/EBP homologous protein (CHOP).	Fluoxetine	0-3	DNA damage inducible transcript 3	Homo sapiens	154-178
28647884-4	2017	FLX induced apoptotic cell death, activation of caspase-4, -9, and -3, and expression of endoplasmic reticulum (ER) stress-associated proteins, including C/EBP homologous protein (CHOP).	Fluoxetine	0-3	DNA damage inducible transcript 3	Homo sapiens	180-184
28860664-0	2017	Cadmium-induced ER stress and inflammation are mediated through C/EBP-DDIT3 signaling in human bronchial epithelial cells.	Cadmium	0-7	DNA damage inducible transcript 3	Homo sapiens	70-75
28860664-3	2017	Here, we identified a cluster of genes that are altered in response to Cd exposure in human bronchial epithelial cells (BEAS-2B) and demonstrated that Cd-induced ER stress and inflammation are mediated via CCAAT-enhancer-binding proteins (C/EBP)-DNA-damaged-inducible transcript 3 (DDIT3) signaling in BEAS-2B cells.	Cadmium	71-73	DNA damage inducible transcript 3	Homo sapiens	282-287
28860664-3	2017	Here, we identified a cluster of genes that are altered in response to Cd exposure in human bronchial epithelial cells (BEAS-2B) and demonstrated that Cd-induced ER stress and inflammation are mediated via CCAAT-enhancer-binding proteins (C/EBP)-DNA-damaged-inducible transcript 3 (DDIT3) signaling in BEAS-2B cells.	Cadmium	151-153	DNA damage inducible transcript 3	Homo sapiens	282-287
28860664-5	2017	Gene set enrichment analysis revealed that Cd treatment stimulated the C/EBP signaling pathway and induced transcriptional activation of its downstream target genes, including DDIT3.	Cadmium	43-45	DNA damage inducible transcript 3	Homo sapiens	176-181
28860664-6	2017	Suppression of DDIT3 expression using specific small interfering RNA effectively alleviated Cd-induced ER stress and inflammatory responses in both BEAS-2B and normal primary normal human bronchial epithelial cells.	Cadmium	92-94	DNA damage inducible transcript 3	Homo sapiens	15-20
32300390-1	2017	Rituximab (R) with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is the current standard of care as first-line treatment for diffuse large B-cell lymphoma (DLBCL), the most common lymphoma subtype.	Prednisone	66-76	DNA damage inducible transcript 3	Homo sapiens	78-82
28841673-5	2017	Furthermore, CHOP was shown to be significantly upregulated upon treatment with tunicamycin in HCC cells.	Tunicamycin	80-91	DNA damage inducible transcript 3	Homo sapiens	13-17
28870016-8	2017	The response was relatively long-lived compared with previously reported CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens, but the above regimens do not result in long-term remission.	Doxorubicin	79-90	DNA damage inducible transcript 3	Homo sapiens	73-77
28545881-9	2017	Treatment of human chondrocytes with palmitate induced expression of CHOP, activated JNK and inhibited IGF-1 function.	Palmitates	37-46	DNA damage inducible transcript 3	Homo sapiens	69-73
28863158-8	2017	Moreover, pemetrexed or cisplatin alone increased the protein expression of the endoplasmic reticulum stress markers IRE1alpha, Bip and CHOP.	Pemetrexed	10-20	DNA damage inducible transcript 3	Homo sapiens	136-140
28863158-8	2017	Moreover, pemetrexed or cisplatin alone increased the protein expression of the endoplasmic reticulum stress markers IRE1alpha, Bip and CHOP.	Cisplatin	24-33	DNA damage inducible transcript 3	Homo sapiens	136-140
28841673-6	2017	Specific knockdown of CHOP not only enhanced tunicamycin-induced autophagy, but also significantly attenuated ER stress-induced apoptosis in HCC cells.	Tunicamycin	45-56	DNA damage inducible transcript 3	Homo sapiens	22-26
28811603-11	2017	Finally, the cells transfected with CHOP siRNA significantly reversed the TNT-induced apoptosis, which indicated that ER stress led to apoptosis.	Trinitrotoluene	74-77	DNA damage inducible transcript 3	Homo sapiens	36-40
28808300-4	2017	These effects were reversed by CHOP siRNA which inhibited the ERS signaling pathway, but were promoted by thapsigargin (a classical ERS inducer) in vitro.	Thapsigargin	106-118	DNA damage inducible transcript 3	Homo sapiens	31-35
28798402-6	2017	Mechanistically, proteasomal-impairment-induced ER stress, CHOP upregulation and disruption of Ca2+ homeostasis were found to be critically involved in the bortezomib/nutlin-3-induced dilation of the ER.	Bortezomib	156-166	DNA damage inducible transcript 3	Homo sapiens	59-63
28798402-6	2017	Mechanistically, proteasomal-impairment-induced ER stress, CHOP upregulation and disruption of Ca2+ homeostasis were found to be critically involved in the bortezomib/nutlin-3-induced dilation of the ER.	nutlin 3	167-175	DNA damage inducible transcript 3	Homo sapiens	59-63
28767099-7	2017	In contrast, fisetin induced up-regulation of CHOP expression and reactive oxygen species production, which had no effect on fisetin-induced apoptosis.	fisetin	13-20	DNA damage inducible transcript 3	Homo sapiens	46-50
28471808-0	2017	3-Bromopyruvate enhances TRAIL-induced apoptosis in human nasopharyngeal carcinoma cells through CHOP-dependent upregulation of TRAIL-R2.	bromopyruvate	0-15	DNA damage inducible transcript 3	Homo sapiens	97-101
31966674-5	2017	RESULTS: PQ significantly increased the cell apoptosis as well as the expression of p58ipk and CHOP, but decreased the expression of pAKT.	Paraquat	9-11	DNA damage inducible transcript 3	Homo sapiens	95-99
28652211-4	2017	Plk2 expression was dramatically decreased under ER stress induced by brefeldin A (BFA), thapsigargin (TG), or tunicamycin (TM), and this down regulation of Plk2 expression was dependent on activating transcription factor 4 (ATF4) and C/EBP homology protein (CHOP).	Tunicamycin	124-126	DNA damage inducible transcript 3	Homo sapiens	235-257
28652211-4	2017	Plk2 expression was dramatically decreased under ER stress induced by brefeldin A (BFA), thapsigargin (TG), or tunicamycin (TM), and this down regulation of Plk2 expression was dependent on activating transcription factor 4 (ATF4) and C/EBP homology protein (CHOP).	Tunicamycin	124-126	DNA damage inducible transcript 3	Homo sapiens	259-263
28624529-5	2017	Mechanistically, cyclopamine induces endoplasmic reticulum (ER) stress via reactive oxygen species (ROS) and CHOP, the last protein of the ER stress pathway and it regulates the proteasome degradation of survivin.	cyclopamine	17-28	DNA damage inducible transcript 3	Homo sapiens	109-113
29137257-7	2017	Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy.	kaempferol	155-165	DNA damage inducible transcript 3	Homo sapiens	76-125
28725323-3	2017	Patients with an advanced stage B-cell malignant lymphoma are typically treated with a combination therapy of rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP).	Prednisolone	172-184	DNA damage inducible transcript 3	Homo sapiens	188-192
28482072-8	2017	In contrast, CHOP overexpression mimicked inhibition of PGC-1alpha by high glucose.	Glucose	75-82	DNA damage inducible transcript 3	Homo sapiens	13-17
28482072-10	2017	Moreover, maternal diabetes in vivo and high glucose in vitro promoted the interaction between CHOP and the PGC-1alpha transcriptional regulator CCAAT/enhancer binding protein-beta (C/EBPbeta), and reduced C/EBPbeta binding to the PGC-1alpha promoter leading to markedly decrease in PGC-1alpha expression.	Glucose	45-52	DNA damage inducible transcript 3	Homo sapiens	95-99
28522441-2	2017	We hypothesized that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) could decrease rates of relapse and transformation.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	98-102
28522441-2	2017	We hypothesized that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) could decrease rates of relapse and transformation.	Doxorubicin	54-65	DNA damage inducible transcript 3	Homo sapiens	98-102
28522441-2	2017	We hypothesized that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) could decrease rates of relapse and transformation.	Prednisone	84-94	DNA damage inducible transcript 3	Homo sapiens	98-102
28743963-6	2017	miR-183-5p post-transcriptionally downregulates CHOP and inhibits endoplasmic reticulum stress-induced apoptosis.	mir-183-5p	0-10	DNA damage inducible transcript 3	Homo sapiens	48-52
28725161-1	2017	BACKGROUND: Rituximab combined with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is used as standard frontline regimen for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	95-99
29137257-7	2017	Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy.	4-phenylbutyric acid	280-285	DNA damage inducible transcript 3	Homo sapiens	127-131
29137257-7	2017	Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy.	kaempferol	289-299	DNA damage inducible transcript 3	Homo sapiens	76-125
29137257-7	2017	Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy.	kaempferol	289-299	DNA damage inducible transcript 3	Homo sapiens	127-131
28652211-7	2017	Notably, we identified two C/EBPalpha responsive elements at positions -2002 and -948, to which C/EBPalpha or CHOP binding was enhanced by BFA under in vitro and in vivo conditions.	Brefeldin A	139-142	DNA damage inducible transcript 3	Homo sapiens	110-114
28652211-10	2017	CHOP may up-regulate DNA-binding affinities after BFA treatment, via recruiting C/EBPalpha to the upstream-promoter of Plk2.	Brefeldin A	50-53	DNA damage inducible transcript 3	Homo sapiens	0-4
28426350-11	2017	Conclusion Lenalidomide maintenance for 24 months after obtaining a CR or PR to R-CHOP significantly prolonged PFS in elderly patients with DLBCL.	Lenalidomide	11-23	DNA damage inducible transcript 3	Homo sapiens	82-86
28725161-1	2017	BACKGROUND: Rituximab combined with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is used as standard frontline regimen for diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	54-65	DNA damage inducible transcript 3	Homo sapiens	95-99
28725161-1	2017	BACKGROUND: Rituximab combined with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is used as standard frontline regimen for diffuse large B-cell lymphoma (DLBCL).	Prednisone	83-93	DNA damage inducible transcript 3	Homo sapiens	95-99
29137257-7	2017	Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy.	kaempferol	155-165	DNA damage inducible transcript 3	Homo sapiens	127-131
29137257-7	2017	Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy.	kaempferol	155-165	DNA damage inducible transcript 3	Homo sapiens	252-256
29137257-7	2017	Indeed, blocking ER stress by 4-phenyl butyric acid (4-PBA) or knockdown of CCAAT/enhancer-binding protein homologous protein (CHOP) with siRNA alleviated kaempferol-induced HepG2 or Huh7 cells autophagy; while transfection with plasmid overexpressing CHOP reversed the effect of 4-PBA on kaempferol-induced autophagy.	4-phenylbutyric acid	280-285	DNA damage inducible transcript 3	Homo sapiens	76-125
28400209-9	2017	Here we found that AST attenuated glutamate-induced elevation of CHOP and ER chaperone glucose-regulated protein (GRP78).	Glutamic Acid	34-43	DNA damage inducible transcript 3	Homo sapiens	65-69
28475457-12	2017	When considered in conjunction with reports of patients with newly diagnosed DHL, which demonstrate lower rates of disease response to R-CHOP compared with intensive front-line therapy, our findings further support the use of intensive front-line therapy for this patient population.	Cysteamine	77-80	DNA damage inducible transcript 3	Homo sapiens	137-141
28453460-6	2017	RESULTS: The cell survival rate in the Tun group was enhanced than that in the CHOP-si group, both of which were declined with the passage of time.	Silicon	84-86	DNA damage inducible transcript 3	Homo sapiens	79-83
28344322-5	2017	AS-IV treatment also concentration-dependently attenuated FFA-induced hepatic ER stress evidenced by the reduction of the key markers, GRP78, CHOP and p-PERK.	Fatty Acids, Nonesterified	58-61	DNA damage inducible transcript 3	Homo sapiens	142-146
28181380-9	2017	We also used ATF-6alpha, ATF-6beta, GADD153, and GRP78 which indicated that fisetin induced cell death through ER stress.	fisetin	76-83	DNA damage inducible transcript 3	Homo sapiens	36-43
28808400-0	2017	Induction of Apoptosis and Cell Cycle Arrest by Flavokawain C on HT-29 Human Colon Adenocarcinoma via Enhancement of Reactive Oxygen Species Generation, Upregulation of p21, p27, and GADD153, and Inactivation of Inhibitor of Apoptosis Proteins.	flavokawain C	48-61	DNA damage inducible transcript 3	Homo sapiens	183-190
28630443-6	2017	Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP.	Tunicamycin	25-36	DNA damage inducible transcript 3	Homo sapiens	65-69
27253186-20	2017	Treatment with R-CHOP (rituximab, cyclophosphamide, doxorubicine, vincristine, and prednisolone) was initiated with very good clinical and biochemical response, yet only mild recovery of kidney function.	Prednisolone	83-95	DNA damage inducible transcript 3	Homo sapiens	17-21
28573788-9	2017	Increased production of ROS was accompanied by upregulation of CHOP and Noxa.	Reactive Oxygen Species	24-27	DNA damage inducible transcript 3	Homo sapiens	63-67
26860883-10	2017	The patient received CHOP-R with intrathecal methotrexate followed by consolidation high dose methotrexate obtaining a complete response which is ongoing.	Methotrexate	45-57	DNA damage inducible transcript 3	Homo sapiens	21-25
28326487-8	2017	In addition, cisplatin resulted in a more pronounced increase of endoplasmic reticulum (ER) stress in MG63 cells than in their resistant variants, which was evidenced by the activation of molecular markers of ER stress, GRP78, CHOP and ATF4.	Cisplatin	13-22	DNA damage inducible transcript 3	Homo sapiens	227-231
28251435-7	2017	Moreover, HMGB1-mediated EPC apoptosis and CHOP expression were dramatically suppressed by PERK shRNA or a specific eIF2alpha inhibitor (salubrinal).	salubrinal	137-147	DNA damage inducible transcript 3	Homo sapiens	43-47
28808400-11	2017	The protein levels of XIAP, c-IAP1, and c-IAP2 were downregulated, whereas the GADD153 was upregulated after FKC treatment.	flavokawain C	109-112	DNA damage inducible transcript 3	Homo sapiens	79-86
28706487-4	2017	In addition, PE-mediated endoplasmic reticulum (ER) stress caused increasing expressions of C/EBP homologous protein (CHOP), leading to apoptosis in HCC cells both in vitro and in vivo.	pe	13-15	DNA damage inducible transcript 3	Homo sapiens	92-116
28706487-4	2017	In addition, PE-mediated endoplasmic reticulum (ER) stress caused increasing expressions of C/EBP homologous protein (CHOP), leading to apoptosis in HCC cells both in vitro and in vivo.	pe	13-15	DNA damage inducible transcript 3	Homo sapiens	118-122
28706487-5	2017	Inhibition of ER stress with CHOP small interfering RNA or 4-phenyl-butyric acid partially reversed PE-induced cell death.	pe	100-102	DNA damage inducible transcript 3	Homo sapiens	29-33
28402965-6	2017	Blocking ROS production attenuated the expression of two markers of ER stress: binding of immunoglobulin protein (BIP) and CCAAT/enhancer-binding protein homologous protein (CHOP).	Reactive Oxygen Species	9-12	DNA damage inducible transcript 3	Homo sapiens	123-172
28402965-6	2017	Blocking ROS production attenuated the expression of two markers of ER stress: binding of immunoglobulin protein (BIP) and CCAAT/enhancer-binding protein homologous protein (CHOP).	Reactive Oxygen Species	9-12	DNA damage inducible transcript 3	Homo sapiens	174-178
28402965-7	2017	Blocking CHOP expression using RNA interference also inhibited ROS generation.	Reactive Oxygen Species	63-66	DNA damage inducible transcript 3	Homo sapiens	9-13
28642847-5	2017	Bax is essential for endoplasmic reticulum (ER) stress-triggered apoptosis, and our RNAi experiments showed that the PERK-eIF2-CHOP pathway and reactive oxygen species (ROS) are also main participants in this process.	Reactive Oxygen Species	169-172	DNA damage inducible transcript 3	Homo sapiens	127-131
28642847-6	2017	LT-induced ROS generation was decreased in CHOP-knockdown HCT-8 cells compared to that in control cells.	Reactive Oxygen Species	11-14	DNA damage inducible transcript 3	Homo sapiens	43-47
28642847-7	2017	Moreover, pretreatment with the ROS inhibitor NAC down-regulated GRP78, CHOP, Bim, and cleaved caspase-3 expression, resulting in a reduction in the apoptosis rate from 36.2 to 20.3% in LT-treated HCT-8 cells.	Reactive Oxygen Species	32-35	DNA damage inducible transcript 3	Homo sapiens	72-76
27530507-12	2017	Teneligliptin ameliorates high glucose-induced endoplasmic reticulum stress reducing the expression of several markers (BIP, PERK, ATF4, CHOP, IRE1a and ATF6).	3-(4-(4-(3-methyl-1-phenyl-1H-pyrazol-5-yl)piperazin-1-yl)pyrrolidin-2-ylcarbonyl)thiazolidine	0-13	DNA damage inducible transcript 3	Homo sapiens	137-141
27530507-12	2017	Teneligliptin ameliorates high glucose-induced endoplasmic reticulum stress reducing the expression of several markers (BIP, PERK, ATF4, CHOP, IRE1a and ATF6).	Glucose	31-38	DNA damage inducible transcript 3	Homo sapiens	137-141
28323103-7	2017	Moreover, inhibition of C/EBA homologous protein (CHOP) expression by siRNA partially prevented Cr(VI)-induced cell apoptosis, mitochondrial dysfunction and ROS generation.	chromium hexavalent ion	96-102	DNA damage inducible transcript 3	Homo sapiens	24-48
26449182-1	2017	The CHOP regimen consisting of cyclophosphamide, doxorubicin (DOX), vincristine and prednisolone has been the most used regimen for peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS).	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	4-8
26449182-1	2017	The CHOP regimen consisting of cyclophosphamide, doxorubicin (DOX), vincristine and prednisolone has been the most used regimen for peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS).	Doxorubicin	49-60	DNA damage inducible transcript 3	Homo sapiens	4-8
26449182-1	2017	The CHOP regimen consisting of cyclophosphamide, doxorubicin (DOX), vincristine and prednisolone has been the most used regimen for peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS).	Doxorubicin	62-65	DNA damage inducible transcript 3	Homo sapiens	4-8
26449182-1	2017	The CHOP regimen consisting of cyclophosphamide, doxorubicin (DOX), vincristine and prednisolone has been the most used regimen for peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS).	Vincristine	68-79	DNA damage inducible transcript 3	Homo sapiens	4-8
26449182-1	2017	The CHOP regimen consisting of cyclophosphamide, doxorubicin (DOX), vincristine and prednisolone has been the most used regimen for peripheral T-cell lymphoma, not otherwise specified (PTCL-NOS).	Prednisolone	84-96	DNA damage inducible transcript 3	Homo sapiens	4-8
28323103-7	2017	Moreover, inhibition of C/EBA homologous protein (CHOP) expression by siRNA partially prevented Cr(VI)-induced cell apoptosis, mitochondrial dysfunction and ROS generation.	chromium hexavalent ion	96-102	DNA damage inducible transcript 3	Homo sapiens	50-54
28323103-7	2017	Moreover, inhibition of C/EBA homologous protein (CHOP) expression by siRNA partially prevented Cr(VI)-induced cell apoptosis, mitochondrial dysfunction and ROS generation.	Reactive Oxygen Species	157-160	DNA damage inducible transcript 3	Homo sapiens	24-48
28323103-7	2017	Moreover, inhibition of C/EBA homologous protein (CHOP) expression by siRNA partially prevented Cr(VI)-induced cell apoptosis, mitochondrial dysfunction and ROS generation.	Reactive Oxygen Species	157-160	DNA damage inducible transcript 3	Homo sapiens	50-54
28415782-8	2017	Mechanistically, CB-839 enhanced Crflz-induced ER stress and apoptosis, characterized by a robust induction of ATF4 and CHOP and the activation of caspases.	CB-839	17-23	DNA damage inducible transcript 3	Homo sapiens	120-124
28631572-8	2017	With tunicamycin treatment, phosphorylation of PERK and eIF2alpha and CHOP expression increased.	Tunicamycin	5-16	DNA damage inducible transcript 3	Homo sapiens	70-74
28618969-5	2017	In this study, we demonstrated that penfluridol induced endoplasmic reticulum stress in BxPC-3, AsPC-1, and Panc-1 pancreatic cancer cell lines as indicated by upregulation of endoplasmic reticulum stress markers such as binding protein (BIP), C/EBP homologous protein (CHOP) and inositol requiring 1alpha (IRE1alpha) after treatment with penfluridol in a concentration-dependent manner.	Penfluridol	36-47	DNA damage inducible transcript 3	Homo sapiens	244-268
28618969-5	2017	In this study, we demonstrated that penfluridol induced endoplasmic reticulum stress in BxPC-3, AsPC-1, and Panc-1 pancreatic cancer cell lines as indicated by upregulation of endoplasmic reticulum stress markers such as binding protein (BIP), C/EBP homologous protein (CHOP) and inositol requiring 1alpha (IRE1alpha) after treatment with penfluridol in a concentration-dependent manner.	Penfluridol	36-47	DNA damage inducible transcript 3	Homo sapiens	270-274
28618969-6	2017	Inhibiting endoplasmic reticulum stress by pretreatment with pharmacological inhibitors such as sodium phenylbutyrate and mithramycin or by silencing CHOP using CHOP small interfering RNA, blocked penfluridol-induced autophagy.	Penfluridol	197-208	DNA damage inducible transcript 3	Homo sapiens	150-154
28618969-6	2017	Inhibiting endoplasmic reticulum stress by pretreatment with pharmacological inhibitors such as sodium phenylbutyrate and mithramycin or by silencing CHOP using CHOP small interfering RNA, blocked penfluridol-induced autophagy.	Penfluridol	197-208	DNA damage inducible transcript 3	Homo sapiens	161-165
28641632-5	2017	RESULTS: The complete rate in EPOCH+-R followed by DICE+-R regimen group was higher than that in the CHOP+-R group (84.2% vs 70.8%), and the relapsed rate was lower in EPOCH+-R followed by DICE+-R regimen group than that in the CHOP+-R group (6.25% vs 35.3%).	epoch+-r	30-38	DNA damage inducible transcript 3	Homo sapiens	228-232
28415782-8	2017	Mechanistically, CB-839 enhanced Crflz-induced ER stress and apoptosis, characterized by a robust induction of ATF4 and CHOP and the activation of caspases.	carfilzomib	33-38	DNA damage inducible transcript 3	Homo sapiens	120-124
28282786-4	2017	Promoted expression of CHOP, a down-streaming transcription factor for endoplasmic reticulum stress (ER stress), enhanced death factor 4 (DR4) activity and accelerated reactive oxygen species (ROS) as well as cell death.	Reactive Oxygen Species	168-191	DNA damage inducible transcript 3	Homo sapiens	23-27
28420235-0	2017	Garcinol from Garcinia indica Downregulates Cancer Stem-like Cell Biomarker ALDH1A1 in Nonsmall Cell Lung Cancer A549 Cells through DDIT3 Activation.	garcinol	0-8	DNA damage inducible transcript 3	Homo sapiens	132-137
28420235-7	2017	We also found that garcinol enriched DNA damage-inducible transcript 3 (DDIT3) and then altered DDIT3-CCAAT-enhancer-binding proteins beta (C/EBPbeta) interaction resulting in a decreased binding of C/EBPbeta to the endogenous ALDH1A1 promoter.	garcinol	19-27	DNA damage inducible transcript 3	Homo sapiens	37-70
28420235-7	2017	We also found that garcinol enriched DNA damage-inducible transcript 3 (DDIT3) and then altered DDIT3-CCAAT-enhancer-binding proteins beta (C/EBPbeta) interaction resulting in a decreased binding of C/EBPbeta to the endogenous ALDH1A1 promoter.	garcinol	19-27	DNA damage inducible transcript 3	Homo sapiens	72-77
28420235-7	2017	We also found that garcinol enriched DNA damage-inducible transcript 3 (DDIT3) and then altered DDIT3-CCAAT-enhancer-binding proteins beta (C/EBPbeta) interaction resulting in a decreased binding of C/EBPbeta to the endogenous ALDH1A1 promoter.	garcinol	19-27	DNA damage inducible transcript 3	Homo sapiens	96-101
28420235-9	2017	Garcinol repressed ALDH1A1 transcription in A549 cells through alterations in the interaction between DDIT3 and C/EBPbeta.	garcinol	0-8	DNA damage inducible transcript 3	Homo sapiens	102-107
28211011-5	2017	Further analysis illustrated that TEOA promoted the phosphorylation of PERK and elF2alpha, followed by up-regulation of the downstream protein CHOP, suggesting the involvement of PERK/eIF2alpha/CHOP pathway and ER stress in TEOA-induced autophagy in SW620 cells.	triethanolamine	34-38	DNA damage inducible transcript 3	Homo sapiens	143-147
28211011-5	2017	Further analysis illustrated that TEOA promoted the phosphorylation of PERK and elF2alpha, followed by up-regulation of the downstream protein CHOP, suggesting the involvement of PERK/eIF2alpha/CHOP pathway and ER stress in TEOA-induced autophagy in SW620 cells.	triethanolamine	34-38	DNA damage inducible transcript 3	Homo sapiens	194-198
28461685-6	2017	She received treatment with steroids, rituximab, cyclophosphamide, vincristine, and doxorubicin (R-CHOP).	Doxorubicin	84-95	DNA damage inducible transcript 3	Homo sapiens	99-103
28275987-0	2017	Smenospongidine suppresses the proliferation of multiple myeloma cells by promoting CCAAT/enhancer-binding protein homologous protein-mediated beta-catenin degradation.	Smenospongidine	0-15	DNA damage inducible transcript 3	Homo sapiens	84-133
28275987-6	2017	In addition, smenospongidine-induced beta-catenin degradation was mediated by up-regulating CCAAT/enhancer-binding protein homologous protein (CHOP).	Smenospongidine	13-28	DNA damage inducible transcript 3	Homo sapiens	92-141
28275987-6	2017	In addition, smenospongidine-induced beta-catenin degradation was mediated by up-regulating CCAAT/enhancer-binding protein homologous protein (CHOP).	Smenospongidine	13-28	DNA damage inducible transcript 3	Homo sapiens	143-147
28282786-4	2017	Promoted expression of CHOP, a down-streaming transcription factor for endoplasmic reticulum stress (ER stress), enhanced death factor 4 (DR4) activity and accelerated reactive oxygen species (ROS) as well as cell death.	Reactive Oxygen Species	193-196	DNA damage inducible transcript 3	Homo sapiens	23-27
28460451-5	2017	In addition, tunicamycin caused pronounced endoplasmatic reticulum stress and apoptosis through activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and activation of the gene encoding CCAAT-enhancer-binding protein homologous protein (CHOP).	Tunicamycin	13-24	DNA damage inducible transcript 3	Homo sapiens	206-255
27736260-1	2017	Treatment of diffuse large B-cell lymphoma (DLBCL) with R-CHOP(-like) regimens include large cumulative doses of prednisolone.	Prednisolone	113-125	DNA damage inducible transcript 3	Homo sapiens	58-62
28358434-10	2017	In addition, GSK2606414 treatment inhibited eIF2alpha phosphorylation and reduced CHOP and VEGF mRNA expression levels in RPE cells under TG-induced ER stress.	7-methyl-5-(1-((3-(trifluoromethyl)phenyl)acetyl)-2,3-dihydro-1H-indol-5-yl)-7H-pyrrolo(2,3-d)pyrimidin-4-amine	13-23	DNA damage inducible transcript 3	Homo sapiens	82-86
28358434-10	2017	In addition, GSK2606414 treatment inhibited eIF2alpha phosphorylation and reduced CHOP and VEGF mRNA expression levels in RPE cells under TG-induced ER stress.	Thapsigargin	138-140	DNA damage inducible transcript 3	Homo sapiens	82-86
28459209-10	2017	In MCF-7 cells treated with tunicamycin, cell viability decreased significantly, but PEAK, eIF2, and CHOP were upregulated markedly and p-PI3K, p-AKT, and p-MTOR were downregulated in dose- and time-dependent manners.	Tunicamycin	28-39	DNA damage inducible transcript 3	Homo sapiens	101-105
28412728-7	2017	Andrographolide-induced cell death, UPR signaling, and CHOP, Bax, and caspase 3 apoptosis elements were all inhibited in the presence of the ROS scavenger NAC.	andrographolide	0-15	DNA damage inducible transcript 3	Homo sapiens	55-59
28412728-7	2017	Andrographolide-induced cell death, UPR signaling, and CHOP, Bax, and caspase 3 apoptosis elements were all inhibited in the presence of the ROS scavenger NAC.	Reactive Oxygen Species	141-144	DNA damage inducible transcript 3	Homo sapiens	55-59
28460451-5	2017	In addition, tunicamycin caused pronounced endoplasmatic reticulum stress and apoptosis through activation of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and activation of the gene encoding CCAAT-enhancer-binding protein homologous protein (CHOP).	Tunicamycin	13-24	DNA damage inducible transcript 3	Homo sapiens	257-261
28212571-6	2017	Notably, Tan I upregulated CCAAT-enhancer-binding protein homologous protein (CHOP), inositol-requiring protein-1 (IRE1) and p-c-Jun N-terminal kinase (p-JNK), but silencing of IRE1 or p62 and JNK inhibitor SP600125 blocked the LC3II accumulation in Tan I-treated H28 cells.	tanshinone	9-14	DNA damage inducible transcript 3	Homo sapiens	27-76
28212571-6	2017	Notably, Tan I upregulated CCAAT-enhancer-binding protein homologous protein (CHOP), inositol-requiring protein-1 (IRE1) and p-c-Jun N-terminal kinase (p-JNK), but silencing of IRE1 or p62 and JNK inhibitor SP600125 blocked the LC3II accumulation in Tan I-treated H28 cells.	tanshinone	9-14	DNA damage inducible transcript 3	Homo sapiens	78-82
28096087-6	2017	Longitudinal analysis of plasma samples collected under rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) chemotherapy showed a rapid clearance of DLBCL mutations from cfDNA among responding patients.	rituximab-cyclophosphamide	56-82	DNA damage inducible transcript 3	Homo sapiens	121-125
28445949-6	2017	These cells survived longer following treatment with a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	70-86	DNA damage inducible transcript 3	Homo sapiens	129-133
28445949-6	2017	These cells survived longer following treatment with a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Doxorubicin	88-99	DNA damage inducible transcript 3	Homo sapiens	129-133
28445949-6	2017	These cells survived longer following treatment with a combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Prednisone	117-127	DNA damage inducible transcript 3	Homo sapiens	129-133
28096087-6	2017	Longitudinal analysis of plasma samples collected under rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) chemotherapy showed a rapid clearance of DLBCL mutations from cfDNA among responding patients.	Doxorubicin	83-94	DNA damage inducible transcript 3	Homo sapiens	121-125
28096087-6	2017	Longitudinal analysis of plasma samples collected under rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) chemotherapy showed a rapid clearance of DLBCL mutations from cfDNA among responding patients.	vincristine-prednisone	95-117	DNA damage inducible transcript 3	Homo sapiens	121-125
28103509-6	2017	The results showed that DTMF-induced enhanced ROS production at higher concentration (100muM) as evidenced by upregulated expression of ER stress and apoptotic proteins with concomitant increase in PERK, CHOP, and JNK levels, when compared to N-acetyl cysteine (NAC, ROS inhibitor) treated HCT-116 cells, which depicts that DTMF might act as a crucial mediator of apoptosis signaling.	3',5-dihydroxy-3,4',7-trimethoxyflavone	24-28	DNA damage inducible transcript 3	Homo sapiens	204-208
28100868-8	2017	In contrast, retinol treatment significantly increased the mRNA expression of endoplasmic reticulum (ER) stress factors (heme oxygenase 1 (HMOX1), CCAAT/enhancer-binding protein homologous protein (CHOP), 78 kDa glucose-regulated protein (GRP78), and DnaJ (Hsp40) homolog, subfamily B, member 9 (DNAJB9)).	Vitamin A	13-20	DNA damage inducible transcript 3	Homo sapiens	147-196
27995330-5	2017	Hcy increased annexin V-positive cells, DHE oxidation, GRP78 and CHOP expression and Xbp-1 mRNA splicing, indicating that Hcy induces apoptosis, oxidative stress and ER stress.	Homocysteine	0-3	DNA damage inducible transcript 3	Homo sapiens	65-69
27578021-6	2017	UCB toxicity was enhanced in undifferentiated SH-SY5Y cells and correlated with a higher mRNA expression of pro-apoptotic CHOP.	ucb	0-3	DNA damage inducible transcript 3	Homo sapiens	122-126
28202415-8	2017	Additionally, TRAIL/Gln deprivation upregulated the expression of endoplasmic reticulum (ER) stress markers such as ATF4 and phosphorylated eIF2alpha, thereby enhancing the C/EBP homologous protein (CHOP) protein level.	Glutamine	20-23	DNA damage inducible transcript 3	Homo sapiens	173-197
28202415-8	2017	Additionally, TRAIL/Gln deprivation upregulated the expression of endoplasmic reticulum (ER) stress markers such as ATF4 and phosphorylated eIF2alpha, thereby enhancing the C/EBP homologous protein (CHOP) protein level.	Glutamine	20-23	DNA damage inducible transcript 3	Homo sapiens	199-203
28202415-9	2017	Transient knockdown of CHOP partically reversed TRAIL/Gln deprivation-mediated apoptosis.	Glutamine	54-57	DNA damage inducible transcript 3	Homo sapiens	23-27
28100868-8	2017	In contrast, retinol treatment significantly increased the mRNA expression of endoplasmic reticulum (ER) stress factors (heme oxygenase 1 (HMOX1), CCAAT/enhancer-binding protein homologous protein (CHOP), 78 kDa glucose-regulated protein (GRP78), and DnaJ (Hsp40) homolog, subfamily B, member 9 (DNAJB9)).	Vitamin A	13-20	DNA damage inducible transcript 3	Homo sapiens	198-202
28103509-7	2017	Collectively, our results suggest that DTMF stimulates ROS-mediated oxidative stress, which in turn induces PERK-CHOP and JNK pathway of apoptosis to promote HCT-116 cell death.	3',5-dihydroxy-3,4',7-trimethoxyflavone	39-43	DNA damage inducible transcript 3	Homo sapiens	113-117
28103509-7	2017	Collectively, our results suggest that DTMF stimulates ROS-mediated oxidative stress, which in turn induces PERK-CHOP and JNK pathway of apoptosis to promote HCT-116 cell death.	ros	55-58	DNA damage inducible transcript 3	Homo sapiens	113-117
27341688-4	2017	The results showed that oxLDL induced in THP-1 macrophages: (i) increase of MMP-9 gene expression and its pro-form secretion, (ii) intracellular accumulation of 7-ketocholesterol, (iii) ERS activation (increased eIF2alpha phosphorylation, XBP1 and CHOP mRNA levels, and Grp78 protein expression), and (iv) oxidative stress (increased levels of reactive oxygen species and NADPH oxidase activity).	oxldl	24-29	DNA damage inducible transcript 3	Homo sapiens	248-252
28162804-7	2017	Furthermore, MC-LR-induced ER stress significantly promoted the expression of PERK/eIF2alpha and their downstream targets (ATF4, CHOP, and Gadd34), which indicates that PERK-eIF2alpha-ATF4 pathway is involved in MC-LR-induced insulin deficiency.	cyanoginosin LR	13-18	DNA damage inducible transcript 3	Homo sapiens	129-133
28397039-8	2017	Moreover, silencing CHOP by shRNA enhanced the release of EDA+ FN from hepatocytes following palmitate treatment, which was involved in ER stress-related cell damage.	Palmitates	93-102	DNA damage inducible transcript 3	Homo sapiens	20-24
28259956-9	2017	Treatment with NaHS attenuated ROS production, inhibited CHOP and GRP78 expression, and decreased cell apoptosis.	sodium bisulfide	15-19	DNA damage inducible transcript 3	Homo sapiens	57-61
28103535-3	2017	Our experiments showed that the combination of EGCG and Am80 synergistically induced both apoptosis in human lung cancer cell line PC-9 and up-regulated expressions of growth arrest and DNA damage-inducible gene 153 (GADD153), death receptor 5, and p21waf1 genes in the cells.	epigallocatechin gallate	47-51	DNA damage inducible transcript 3	Homo sapiens	168-215
28103535-3	2017	Our experiments showed that the combination of EGCG and Am80 synergistically induced both apoptosis in human lung cancer cell line PC-9 and up-regulated expressions of growth arrest and DNA damage-inducible gene 153 (GADD153), death receptor 5, and p21waf1 genes in the cells.	epigallocatechin gallate	47-51	DNA damage inducible transcript 3	Homo sapiens	217-224
28103535-3	2017	Our experiments showed that the combination of EGCG and Am80 synergistically induced both apoptosis in human lung cancer cell line PC-9 and up-regulated expressions of growth arrest and DNA damage-inducible gene 153 (GADD153), death receptor 5, and p21waf1 genes in the cells.	tamibarotene	56-60	DNA damage inducible transcript 3	Homo sapiens	168-215
28103535-3	2017	Our experiments showed that the combination of EGCG and Am80 synergistically induced both apoptosis in human lung cancer cell line PC-9 and up-regulated expressions of growth arrest and DNA damage-inducible gene 153 (GADD153), death receptor 5, and p21waf1 genes in the cells.	tamibarotene	56-60	DNA damage inducible transcript 3	Homo sapiens	217-224
28553347-8	2017	Furthermore, mitomycin C induced endoplasmic reticulum stress by increasing the expression of glucose-regulated protein 78, CAAT/enhancer-binding protein homologous protein (CHOP) and caspase-4 in a dose-dependent manner.	Mitomycin	13-24	DNA damage inducible transcript 3	Homo sapiens	174-178
28413663-6	2017	The patient completed three cycles of combination chemotherapy consisting of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP regimen) followed by radiation consolidation therapy, and has maintained a complete remission ever since.	Prednisone	124-134	DNA damage inducible transcript 3	Homo sapiens	136-140
28553347-9	2017	Salubrinal significantly inhibited the mitomycin C-induced cell viability loss and apoptosis, and these effects were accompanied by a reduction in CHOP expression.	salubrinal	0-10	DNA damage inducible transcript 3	Homo sapiens	147-151
28294183-4	2017	ER stress-associated proteins glucose-regulated protein (GRP) 78, activating transcription factor (ATF) 4 and C/EBP homologous protein (CHOP), as was phosphorylation of eukaryotic initiation factor (EIF) 2alpha, were all up-regulated by cholesterol.	Cholesterol	237-248	DNA damage inducible transcript 3	Homo sapiens	110-134
28559645-7	2017	TREATMENT AND OUTCOME: The patient had a good initial response to a CHOP scheme (cyclophosphamide, doxorubicin, vincristine and prednisone) with filgrastim.	Cyclophosphamide	81-97	DNA damage inducible transcript 3	Homo sapiens	68-72
28559645-7	2017	TREATMENT AND OUTCOME: The patient had a good initial response to a CHOP scheme (cyclophosphamide, doxorubicin, vincristine and prednisone) with filgrastim.	Doxorubicin	99-110	DNA damage inducible transcript 3	Homo sapiens	68-72
28559645-7	2017	TREATMENT AND OUTCOME: The patient had a good initial response to a CHOP scheme (cyclophosphamide, doxorubicin, vincristine and prednisone) with filgrastim.	Vincristine	112-123	DNA damage inducible transcript 3	Homo sapiens	68-72
28559645-7	2017	TREATMENT AND OUTCOME: The patient had a good initial response to a CHOP scheme (cyclophosphamide, doxorubicin, vincristine and prednisone) with filgrastim.	Prednisone	128-138	DNA damage inducible transcript 3	Homo sapiens	68-72
29142990-10	2017	Sodium 4-phenylbutyrate treatment increased COL4A5 transcript levels (P &lt; 0.01), and reduced ER size (P &lt; 0.01 by EM and P &lt; 0.001 by immunostaining), ER stress (p HSPA5 and DDIT3, all P values &lt; 0.01) and autophagy (ATG7, P &lt; 0.01).	4-phenylbutyric acid	0-23	DNA damage inducible transcript 3	Homo sapiens	183-188
28185329-8	2017	Mechanistic investigations revealed that matrine treatment causes ER dilation and up-regulated the expression of ER stress markers GRP78, eIF2alpha, and CHOP, increases the levels of apoptotic in Michigan Cancer Foundation cells, subsequently, blocking the ER stress-mediated apoptosis pathway, significantly decreased matrine-induced apoptotic but still has significant difference between control group.	matrine	41-48	DNA damage inducible transcript 3	Homo sapiens	153-157
28159805-5	2017	We further found that palmitate, but not oleate or oleate with palmitate, increases endoplasmic reticulum (ER) stress, signaling through the unfolded protein response, and yielding CHOP-mediated induction of apoptosis.	Palmitates	22-31	DNA damage inducible transcript 3	Homo sapiens	181-185
28159805-7	2017	The data show palmitate is toxic to human syncytiotrophoblasts, through the induction of ER stress and apoptosis mediated by CHOP, whereas oleate is not toxic, abrogates palmitate toxicity and induces fat accumulation.	Palmitates	14-23	DNA damage inducible transcript 3	Homo sapiens	125-129
28300830-3	2017	Here we show that Smad7 inhibition with a specific Smad7 antisense oligonucleotide upregulates eukaryotic translation initiation factor 2alpha (eIF2alpha) phosphorylation, a transcription factor involved in the regulation of cell cycle arrest and induction of cell death, and induces activating transcription factor 4 (ATF4) and CCAAT/enhancer binding protein homology protein (CHOP), two downstream targets of eIF2alpha.	Oligonucleotides	67-82	DNA damage inducible transcript 3	Homo sapiens	378-382
28270124-10	2017	Cyproterone acetate treatment also increased DR5 gene promoter activity, which could be abolished by mutation of a consensus binding domain of transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP) in the DR5 gene promoter.	Cyproterone Acetate	0-19	DNA damage inducible transcript 3	Homo sapiens	164-213
28270124-10	2017	Cyproterone acetate treatment also increased DR5 gene promoter activity, which could be abolished by mutation of a consensus binding domain of transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP) in the DR5 gene promoter.	Cyproterone Acetate	0-19	DNA damage inducible transcript 3	Homo sapiens	215-219
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	Cyproterone Acetate	0-19	DNA damage inducible transcript 3	Homo sapiens	30-34
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	Cyproterone Acetate	0-19	DNA damage inducible transcript 3	Homo sapiens	189-193
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	4-phenylbutyric acid	132-148	DNA damage inducible transcript 3	Homo sapiens	189-193
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	Cyproterone Acetate	161-180	DNA damage inducible transcript 3	Homo sapiens	30-34
28270124-11	2017	Cyproterone acetate increases CHOP expression in a concentration and time-dependent manner and endoplasmic reticulum stress reducer 4-phenylbutyrate could block cyproterone acetate-induced CHOP and DR5 up-regulation.	Cyproterone Acetate	161-180	DNA damage inducible transcript 3	Homo sapiens	189-193
28270124-12	2017	More importantly, siRNA silencing of CHOP significantly reduced cyproterone acetate-induced DR5 up-regulation and TRAIL sensitivity in prostate cancer cells.	Cyproterone Acetate	64-83	DNA damage inducible transcript 3	Homo sapiens	37-41
27928587-1	2017	Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy has been mostly applied to patients with untreated peripheral T cell lymphoma (PTCL).	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	62-66
28115372-2	2017	Anthracycline-containing regimens, namely cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), nowadays represent the standard first-line treatment; for patients who achieve a satisfactory response, a consolidation by means of autologous stem cell transplantation may offer a greater chance of long-term survival.	Anthracyclines	0-13	DNA damage inducible transcript 3	Homo sapiens	102-106
28115372-2	2017	Anthracycline-containing regimens, namely cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), nowadays represent the standard first-line treatment; for patients who achieve a satisfactory response, a consolidation by means of autologous stem cell transplantation may offer a greater chance of long-term survival.	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	102-106
27928587-1	2017	Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy has been mostly applied to patients with untreated peripheral T cell lymphoma (PTCL).	Doxorubicin	18-29	DNA damage inducible transcript 3	Homo sapiens	62-66
27928587-1	2017	Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)/CHOP-like chemotherapy has been mostly applied to patients with untreated peripheral T cell lymphoma (PTCL).	Prednisolone	48-60	DNA damage inducible transcript 3	Homo sapiens	62-66
28265411-17	2017	CONCLUSIONS: Implementation of the CHOP inpatient nutritional rehabilitation protocol aimed at rapid, efficient, and safe weight gain and integration of caregivers in treatment of patients with diverse ED diagnoses led to excellent QI outcomes in percentage MBMI at discharge and 4-weeks follow-up, while maintaining a short LOS and low rates of RH phosphorus supplementation.	Phosphorus	349-359	DNA damage inducible transcript 3	Homo sapiens	35-39
27677346-8	2017	In addition, curcumin and IFN-beta/RA combination inhibited the expression of COX-2 and up-regulated GADD153.	Curcumin	13-21	DNA damage inducible transcript 3	Homo sapiens	101-108
27677346-8	2017	In addition, curcumin and IFN-beta/RA combination inhibited the expression of COX-2 and up-regulated GADD153.	Tretinoin	35-37	DNA damage inducible transcript 3	Homo sapiens	101-108
28205354-3	2017	We take this opportunity to report a case of a 65 year-old man who developed a rapidly progressive glomerulonephritis within days after completing his first cycle of R-CHOP (Rituximab, Cyclophosphamide, Doxorubicin, Vincristine, Prednisolone) chemotherapy for newly diagnosed mantle cell lymphoma.	Doxorubicin	203-214	DNA damage inducible transcript 3	Homo sapiens	168-172
27627987-0	2017	Carriers of a VEGFA enhancer polymorphism selectively binding CHOP/DDIT3 are predisposed to increased circulating levels of thyroid-stimulating hormone.	Thyrotropin	124-151	DNA damage inducible transcript 3	Homo sapiens	67-72
27627987-13	2017	Because CHOP is induced by several types of intracellular stress, this indicates that cellular stress could be involved in the normal or pathophysiological response of the thyroid to TSH.	Thyrotropin	183-186	DNA damage inducible transcript 3	Homo sapiens	8-12
27627987-0	2017	Carriers of a VEGFA enhancer polymorphism selectively binding CHOP/DDIT3 are predisposed to increased circulating levels of thyroid-stimulating hormone.	Thyrotropin	124-151	DNA damage inducible transcript 3	Homo sapiens	62-66
27996348-6	2017	Meanwhile, curcumin pretreatment prevented FZD induced ER stress, evidenced by the inhibition of glucose-regulated protein 78 and DNA damage inducible gene 153/C/EBP-homologous protein (GADD153/CHOP) protein expression.	Curcumin	11-19	DNA damage inducible transcript 3	Homo sapiens	186-193
27996348-6	2017	Meanwhile, curcumin pretreatment prevented FZD induced ER stress, evidenced by the inhibition of glucose-regulated protein 78 and DNA damage inducible gene 153/C/EBP-homologous protein (GADD153/CHOP) protein expression.	Curcumin	11-19	DNA damage inducible transcript 3	Homo sapiens	194-198
27996348-6	2017	Meanwhile, curcumin pretreatment prevented FZD induced ER stress, evidenced by the inhibition of glucose-regulated protein 78 and DNA damage inducible gene 153/C/EBP-homologous protein (GADD153/CHOP) protein expression.	Furazolidone	43-46	DNA damage inducible transcript 3	Homo sapiens	186-193
27996348-6	2017	Meanwhile, curcumin pretreatment prevented FZD induced ER stress, evidenced by the inhibition of glucose-regulated protein 78 and DNA damage inducible gene 153/C/EBP-homologous protein (GADD153/CHOP) protein expression.	Furazolidone	43-46	DNA damage inducible transcript 3	Homo sapiens	194-198
28208696-10	2017	Furthermore, the levels of the ER stress-induced apoptosis response proteins CHOP, cleaved caspase-12 and cleaved caspase-3 were inhibited by VPA treatment.	Valproic Acid	142-145	DNA damage inducible transcript 3	Homo sapiens	77-81
28228218-10	2017	The induction of DR5 and pro-apoptotic effect were mediated through activation of ER stress accompanying by increased synthesis of GRP78 and CHOP, which can be blocked by adding of ER stress inhibitor 4-PBA.	4-phenylbutylamine	201-206	DNA damage inducible transcript 3	Homo sapiens	141-145
27908660-6	2017	Mechanistic studies showed that triptonide induced senescence followed by apoptosis mainly by suppressing transcription of TERT and oncogenic c-Myc, while concomitantly promoting transcription of senescence-promoting genes p16 and p21 and the pro-apoptotic gene encoding DNA damage-inducible transcript 3.	triptonide	32-42	DNA damage inducible transcript 3	Homo sapiens	271-304
28063906-0	2017	Pyrazinamide-induced hepatotoxicity is alleviated by 4-PBA via inhibition of the PERK-eIF2alpha-ATF4-CHOP pathway.	Pyrazinamide	0-12	DNA damage inducible transcript 3	Homo sapiens	101-105
28063906-0	2017	Pyrazinamide-induced hepatotoxicity is alleviated by 4-PBA via inhibition of the PERK-eIF2alpha-ATF4-CHOP pathway.	4-phenylbutyric acid	53-58	DNA damage inducible transcript 3	Homo sapiens	101-105
28024901-4	2017	The results showed that along with induction of Cdk5 and apoptosis, GRP78 and its two sensors as well as CHOP and cleaved caspase-12 were induced in high glucose treated podocytes.	Glucose	154-161	DNA damage inducible transcript 3	Homo sapiens	105-109
27809414-8	2017	The underlying mechanisms involve the inhibition of Hcy-induced activation of binding protein (Bip) and C/EBP homologous protein (CHOP), as well as the phosphorylation of protein kinase RNA-like ER kinase (PERK) or inositol-requiring enzyme 1 alpha (IRE1alpha).	Homocysteine	52-55	DNA damage inducible transcript 3	Homo sapiens	104-128
27809414-8	2017	The underlying mechanisms involve the inhibition of Hcy-induced activation of binding protein (Bip) and C/EBP homologous protein (CHOP), as well as the phosphorylation of protein kinase RNA-like ER kinase (PERK) or inositol-requiring enzyme 1 alpha (IRE1alpha).	Homocysteine	52-55	DNA damage inducible transcript 3	Homo sapiens	130-134
27852055-0	2017	Isochaihulactone-induced DDIT3 causes ER stress-PERK independent apoptosis in glioblastoma multiforme cells.	isochaihulactone	0-16	DNA damage inducible transcript 3	Homo sapiens	25-30
27810161-10	2017	After treatment, sperm production was significantly lowered 3 and 6 months after ABVD +- radiotherapy or CHOP/MOPP-ABV.	MOPP-ABV protocol	110-118	DNA damage inducible transcript 3	Homo sapiens	105-109
28159976-7	2017	Oxotremorine altered DNA damage inducible 3 (CHOP) gene expression, glucose-regulated protein 78 kDa (GRP78) and activating transcription factor 4 (ATF4) protein expression, and protein carbonyl and 8-OHdG levels.	Oxotremorine	0-12	DNA damage inducible transcript 3	Homo sapiens	45-49
28075474-13	2017	The expression levels of PERK, CHOP and phosphorylated MAPK (p38, ERK1/2 and JNK1/2) were upregulated following isomahanine treatment.	mahanine	112-123	DNA damage inducible transcript 3	Homo sapiens	31-35
28225499-3	2017	To improve the clinical diagnosis and treatment for PCDLBCL-O, we report a case of PCDLBCL-O successfully treated by the combination of R-CHOP (A chemotherapy protocol consists of cyclophosphamide, doxorubicin, vincristine, prednisone plus Rituximab) chemotherapy and surgery.	pcdlbcl-o	52-61	DNA damage inducible transcript 3	Homo sapiens	138-142
28225499-3	2017	To improve the clinical diagnosis and treatment for PCDLBCL-O, we report a case of PCDLBCL-O successfully treated by the combination of R-CHOP (A chemotherapy protocol consists of cyclophosphamide, doxorubicin, vincristine, prednisone plus Rituximab) chemotherapy and surgery.	pcdlbcl-o	83-92	DNA damage inducible transcript 3	Homo sapiens	138-142
28088783-3	2017	Nontoxic alpha-asarone at 1-20 muM attenuated 7beta-hydroxycholesterol-induced activation of eukaryotic initiation factor 2alpha in macrophages leading to C/EBP homologous protein (CHOP) expression and apoptosis due to sustained ER stress.	asarone	9-22	DNA damage inducible transcript 3	Homo sapiens	155-179
28088783-3	2017	Nontoxic alpha-asarone at 1-20 muM attenuated 7beta-hydroxycholesterol-induced activation of eukaryotic initiation factor 2alpha in macrophages leading to C/EBP homologous protein (CHOP) expression and apoptosis due to sustained ER stress.	asarone	9-22	DNA damage inducible transcript 3	Homo sapiens	181-185
28088783-3	2017	Nontoxic alpha-asarone at 1-20 muM attenuated 7beta-hydroxycholesterol-induced activation of eukaryotic initiation factor 2alpha in macrophages leading to C/EBP homologous protein (CHOP) expression and apoptosis due to sustained ER stress.	cholest-5-en-3 beta,7 alpha-diol	46-70	DNA damage inducible transcript 3	Homo sapiens	155-179
28088783-3	2017	Nontoxic alpha-asarone at 1-20 muM attenuated 7beta-hydroxycholesterol-induced activation of eukaryotic initiation factor 2alpha in macrophages leading to C/EBP homologous protein (CHOP) expression and apoptosis due to sustained ER stress.	cholest-5-en-3 beta,7 alpha-diol	46-70	DNA damage inducible transcript 3	Homo sapiens	181-185
27852055-6	2017	Isochaihulactone induced DDIT3 led to the expression of NAG-1.	isochaihulactone	0-16	DNA damage inducible transcript 3	Homo sapiens	25-30
27852055-8	2017	Overall, the data revealed that isochaihulactone disrupted ER homeostasis in cancer cells by increasing DDIT3 and NAG-1 expression.	isochaihulactone	32-48	DNA damage inducible transcript 3	Homo sapiens	104-109
27894091-4	2017	At the signaling level, CBG treatment in CRC cells provoked endoplasmic reticulum stress (ER stress), the latter was evidenced by caspase-12 activation, CHOP expression, as well as PERK and IRE1 phosphorylations.	cinobufagin	24-27	DNA damage inducible transcript 3	Homo sapiens	153-157
27894091-5	2017	Contrarily, the ER stress inhibitor salubrinal, the caspase-12 inhibitor and CHOP shRNA remarkably attenuated CBG-induced CRC cell death and apoptosis.	cinobufagin	110-113	DNA damage inducible transcript 3	Homo sapiens	77-81
27888615-3	2017	Deoxycholic acid (DCA), Chemodeoxycholic acid (CDCA) and Lithocholic acid (LCA) activated the PERK arm of the UPR, via phosphorylation of eIF2alpha and up-regulation of ATF3, CHOP and BiP/GRP78.	Lithocholic Acid	75-78	DNA damage inducible transcript 3	Homo sapiens	175-179
27888615-3	2017	Deoxycholic acid (DCA), Chemodeoxycholic acid (CDCA) and Lithocholic acid (LCA) activated the PERK arm of the UPR, via phosphorylation of eIF2alpha and up-regulation of ATF3, CHOP and BiP/GRP78.	Deoxycholic Acid	0-16	DNA damage inducible transcript 3	Homo sapiens	175-179
27894091-9	2017	CHOP upregulation and mTORC1 in-activation were also noticed in CBG-treated HCT-116 tumors.	cinobufagin	64-67	DNA damage inducible transcript 3	Homo sapiens	0-4
27888615-3	2017	Deoxycholic acid (DCA), Chemodeoxycholic acid (CDCA) and Lithocholic acid (LCA) activated the PERK arm of the UPR, via phosphorylation of eIF2alpha and up-regulation of ATF3, CHOP and BiP/GRP78.	Deoxycholic Acid	18-21	DNA damage inducible transcript 3	Homo sapiens	175-179
27903966-3	2017	[Pemetrexed + sildenafil] activated an eIF2alpha - ATF4 - CHOP - Beclin1 pathway causing formation of toxic autophagosomes; activated a protective IRE1 - XBP-1 - chaperone induction pathway; and activated a toxic eIF2alpha - CHOP - DR4 / DR5 / CD95 induction pathway.	Sildenafil Citrate	14-24	DNA damage inducible transcript 3	Homo sapiens	58-62
27888615-3	2017	Deoxycholic acid (DCA), Chemodeoxycholic acid (CDCA) and Lithocholic acid (LCA) activated the PERK arm of the UPR, via phosphorylation of eIF2alpha and up-regulation of ATF3, CHOP and BiP/GRP78.	chemodeoxycholic acid	24-45	DNA damage inducible transcript 3	Homo sapiens	175-179
27888615-3	2017	Deoxycholic acid (DCA), Chemodeoxycholic acid (CDCA) and Lithocholic acid (LCA) activated the PERK arm of the UPR, via phosphorylation of eIF2alpha and up-regulation of ATF3, CHOP and BiP/GRP78.	Chenodeoxycholic Acid	47-51	DNA damage inducible transcript 3	Homo sapiens	175-179
27888615-3	2017	Deoxycholic acid (DCA), Chemodeoxycholic acid (CDCA) and Lithocholic acid (LCA) activated the PERK arm of the UPR, via phosphorylation of eIF2alpha and up-regulation of ATF3, CHOP and BiP/GRP78.	Lithocholic Acid	57-73	DNA damage inducible transcript 3	Homo sapiens	175-179
27903966-3	2017	[Pemetrexed + sildenafil] activated an eIF2alpha - ATF4 - CHOP - Beclin1 pathway causing formation of toxic autophagosomes; activated a protective IRE1 - XBP-1 - chaperone induction pathway; and activated a toxic eIF2alpha - CHOP - DR4 / DR5 / CD95 induction pathway.	Pemetrexed	1-11	DNA damage inducible transcript 3	Homo sapiens	58-62
27903966-3	2017	[Pemetrexed + sildenafil] activated an eIF2alpha - ATF4 - CHOP - Beclin1 pathway causing formation of toxic autophagosomes; activated a protective IRE1 - XBP-1 - chaperone induction pathway; and activated a toxic eIF2alpha - CHOP - DR4 / DR5 / CD95 induction pathway.	Pemetrexed	1-11	DNA damage inducible transcript 3	Homo sapiens	225-229
27903966-3	2017	[Pemetrexed + sildenafil] activated an eIF2alpha - ATF4 - CHOP - Beclin1 pathway causing formation of toxic autophagosomes; activated a protective IRE1 - XBP-1 - chaperone induction pathway; and activated a toxic eIF2alpha - CHOP - DR4 / DR5 / CD95 induction pathway.	Sildenafil Citrate	14-24	DNA damage inducible transcript 3	Homo sapiens	225-229
27903966-4	2017	[Pemetrexed + sildenafil] reduced the expression of c-FLIP-s, MCL-1 and BCL-XL that was blocked in a cell-type -dependent fashion by either over-expression of HSP90 / GRP78 / HSP70 / HSP27 or by blockade of eIF2alpha-CHOP signaling.	Pemetrexed	1-11	DNA damage inducible transcript 3	Homo sapiens	217-221
27903966-4	2017	[Pemetrexed + sildenafil] reduced the expression of c-FLIP-s, MCL-1 and BCL-XL that was blocked in a cell-type -dependent fashion by either over-expression of HSP90 / GRP78 / HSP70 / HSP27 or by blockade of eIF2alpha-CHOP signaling.	Sildenafil Citrate	14-24	DNA damage inducible transcript 3	Homo sapiens	217-221
29212067-2	2017	Standard treatment is usually a combined immune chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Doxorubicin	95-106	DNA damage inducible transcript 3	Homo sapiens	139-143
29212067-0	2017	Lenalidomide Maintenance after R-CHOP Therapy in Diffuse Large B-Cell Lymphoma: Can It Be a Standard of Care.	Lenalidomide	0-12	DNA damage inducible transcript 3	Homo sapiens	33-37
29212067-2	2017	Standard treatment is usually a combined immune chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	125-135	DNA damage inducible transcript 3	Homo sapiens	139-143
27960150-2	2017	The use of the anthracycline doxorubicin has been associated with arrhythmias and cardiomyopathy, making patients with cardiac dysfunction poor candidates for R-CHOP.	Anthracyclines	15-28	DNA damage inducible transcript 3	Homo sapiens	161-165
28458356-1	2017	Management of constipation in patients receiving cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) or CHOP-like chemotherapy regimens is important for prevention of paralytic ileus.	Prednisolone	96-108	DNA damage inducible transcript 3	Homo sapiens	110-114
28458356-8	2017	Therefore, it is important to avoid negative drug interaction between magnesium oxide and antacids in patients receiving CHOP chemotherapy.	Magnesium Oxide	70-85	DNA damage inducible transcript 3	Homo sapiens	121-125
27603596-0	2017	Tunicamycin enhances human colon cancer cells to TRAIL-induced apoptosis by JNK-CHOP-mediated DR5 upregulation and the inhibition of the EGFR pathway.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	80-84
27603596-5	2017	DR5 induction was regulated by C/EBP homologous protein (CHOP) and JNK as CHOP siRNA or JNK inhibitor SP600125 considerably abolished the DR5 induction.	pyrazolanthrone	102-110	DNA damage inducible transcript 3	Homo sapiens	31-55
27603596-5	2017	DR5 induction was regulated by C/EBP homologous protein (CHOP) and JNK as CHOP siRNA or JNK inhibitor SP600125 considerably abolished the DR5 induction.	pyrazolanthrone	102-110	DNA damage inducible transcript 3	Homo sapiens	57-61
27603596-7	2017	In summary, tunicamycin effectively enhanced TRAIL-induced apoptosis might through JNK-CHOP-mediated DR5 upregulation and the inhibition of the epidermal growth factor receptor pathway.	Tunicamycin	12-23	DNA damage inducible transcript 3	Homo sapiens	87-91
27283030-4	2017	The patient was diagnosed with PEL-LL and treated with six cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP), which resulted in a complete remission.	Cyclophosphamide	84-100	DNA damage inducible transcript 3	Homo sapiens	148-152
27283030-4	2017	The patient was diagnosed with PEL-LL and treated with six cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP), which resulted in a complete remission.	Prednisolone	132-144	DNA damage inducible transcript 3	Homo sapiens	148-152
27960150-2	2017	The use of the anthracycline doxorubicin has been associated with arrhythmias and cardiomyopathy, making patients with cardiac dysfunction poor candidates for R-CHOP.	Doxorubicin	29-40	DNA damage inducible transcript 3	Homo sapiens	161-165
28304295-0	2017	Palmitate Increases beta-site AbetaPP-Cleavage Enzyme 1 Activity and Amyloid-beta Genesis by Evoking Endoplasmic Reticulum Stress and Subsequent C/EBP Homologous Protein Activation.	Palmitates	0-9	DNA damage inducible transcript 3	Homo sapiens	145-169
29234397-6	2017	ACE also protected HepG2 cells from PA- (300 muM-) induced endoplasmic reticulum (ER) stress and apoptosis and attenuated the related key molecules including GRP78, eIF2, and CHOP, respectively.	Palmitic Acid	36-38	DNA damage inducible transcript 3	Homo sapiens	175-179
28304295-8	2017	We further show that CHOP is an indispensable molecular mediator of palmitate-induced upregulation in BACE1 activity and Abeta genesis.	Palmitates	68-77	DNA damage inducible transcript 3	Homo sapiens	21-25
29279550-7	2017	Patients with ALK-positive ALCL are usually treated with anthracycline-based regimens, such as combination cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) or CHOEP (CHOP plus etoposide), which provide a favorable prognosis, except in patients with multiple International Prognostic Index factors.	Anthracyclines	57-70	DNA damage inducible transcript 3	Homo sapiens	169-173
29279550-7	2017	Patients with ALK-positive ALCL are usually treated with anthracycline-based regimens, such as combination cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) or CHOEP (CHOP plus etoposide), which provide a favorable prognosis, except in patients with multiple International Prognostic Index factors.	Anthracyclines	57-70	DNA damage inducible transcript 3	Homo sapiens	185-189
29279550-7	2017	Patients with ALK-positive ALCL are usually treated with anthracycline-based regimens, such as combination cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) or CHOEP (CHOP plus etoposide), which provide a favorable prognosis, except in patients with multiple International Prognostic Index factors.	Doxorubicin	125-136	DNA damage inducible transcript 3	Homo sapiens	169-173
29279550-7	2017	Patients with ALK-positive ALCL are usually treated with anthracycline-based regimens, such as combination cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) or CHOEP (CHOP plus etoposide), which provide a favorable prognosis, except in patients with multiple International Prognostic Index factors.	Prednisolone	155-167	DNA damage inducible transcript 3	Homo sapiens	169-173
27895089-7	2017	Moreover, HDL isolated from patients with metabolic syndrome induced macrophage apoptosis, oxidative stress, and CHOP upregulation, which were blocked by PBA and DPI.	4-phenylbutyric acid	154-157	DNA damage inducible transcript 3	Homo sapiens	113-117
27895089-7	2017	Moreover, HDL isolated from patients with metabolic syndrome induced macrophage apoptosis, oxidative stress, and CHOP upregulation, which were blocked by PBA and DPI.	diphenyleneiodonium	162-165	DNA damage inducible transcript 3	Homo sapiens	113-117
28123744-1	2017	The standard of care for first-line therapy in diffuse large B-cell lymphoma (DLBCL) is the rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) regimen.	Prednisone	150-160	DNA damage inducible transcript 3	Homo sapiens	164-168
27061377-7	2017	However, knocking down CHOP reversed E Platinum-induced apoptosis by blocking mitochondrial apoptotic pathway.	Platinum	39-47	DNA damage inducible transcript 3	Homo sapiens	23-27
27697610-3	2016	Induction of ATF4 and CHOP was observed in myeloma cells under Thapsigargin independently of cell death.	Thapsigargin	63-75	DNA damage inducible transcript 3	Homo sapiens	22-26
27816613-6	2017	Exposure to TDCIPP led to the activation of protein markers of endoplasmic reticulum (ER) stress, including eukaryotic translation initiation factor 2a subunit (p-EIF2a), activation transcription factor (ATF4), glucose-regulated protein (GRP78), and the proapoptotic factor C/EBP homologous protein (CHOP).	tris(1,3-dichloro-2-propyl)phosphate	12-18	DNA damage inducible transcript 3	Homo sapiens	274-298
27816613-6	2017	Exposure to TDCIPP led to the activation of protein markers of endoplasmic reticulum (ER) stress, including eukaryotic translation initiation factor 2a subunit (p-EIF2a), activation transcription factor (ATF4), glucose-regulated protein (GRP78), and the proapoptotic factor C/EBP homologous protein (CHOP).	tris(1,3-dichloro-2-propyl)phosphate	12-18	DNA damage inducible transcript 3	Homo sapiens	300-304
28978846-6	2017	From recent prospective trials, conventional R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) regimen, which is the current standard regimen for DLBCL, has been acknowledged as a well-established regimen for DLBCL.	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	47-51
28978846-6	2017	From recent prospective trials, conventional R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) regimen, which is the current standard regimen for DLBCL, has been acknowledged as a well-established regimen for DLBCL.	Doxorubicin	82-93	DNA damage inducible transcript 3	Homo sapiens	47-51
28978846-6	2017	From recent prospective trials, conventional R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) regimen, which is the current standard regimen for DLBCL, has been acknowledged as a well-established regimen for DLBCL.	Vincristine	95-106	DNA damage inducible transcript 3	Homo sapiens	47-51
28978846-6	2017	From recent prospective trials, conventional R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone) regimen, which is the current standard regimen for DLBCL, has been acknowledged as a well-established regimen for DLBCL.	Prednisolone	112-124	DNA damage inducible transcript 3	Homo sapiens	47-51
27760757-9	2016	The combined molecular and clinical prognostic indices, M-IPI-R and IPI+IHC, have remarkable predictive values in R-CHOP-treated DLBCL.	ipi-r	58-63	DNA damage inducible transcript 3	Homo sapiens	116-120
27760757-9	2016	The combined molecular and clinical prognostic indices, M-IPI-R and IPI+IHC, have remarkable predictive values in R-CHOP-treated DLBCL.	diprotin A	58-61	DNA damage inducible transcript 3	Homo sapiens	116-120
27959410-9	2017	Treatment with SFN for 48 h also significantly upregulated the protein expression levels of Bip/GRP78, XBP-1, caspase-12, CHOP/GADD153 and Bid in HepG2 cells.	sulforaphane	15-18	DNA damage inducible transcript 3	Homo sapiens	122-126
27959410-9	2017	Treatment with SFN for 48 h also significantly upregulated the protein expression levels of Bip/GRP78, XBP-1, caspase-12, CHOP/GADD153 and Bid in HepG2 cells.	sulforaphane	15-18	DNA damage inducible transcript 3	Homo sapiens	127-134
28123531-12	2017	In addition, the levels of phosphorylated JNK and the transcription factor, C/EBP homologous protein (CHOP), an ER stress-associated apoptotic molecule, were increased in the goniothalamin-treated cells.	goniothalamin	175-188	DNA damage inducible transcript 3	Homo sapiens	76-100
28123531-12	2017	In addition, the levels of phosphorylated JNK and the transcription factor, C/EBP homologous protein (CHOP), an ER stress-associated apoptotic molecule, were increased in the goniothalamin-treated cells.	goniothalamin	175-188	DNA damage inducible transcript 3	Homo sapiens	102-106
27895312-3	2016	Mechanistically, LZ-205 triggers reactive oxygen species (ROS)-induced endoplasmic reticulum (ER) stress and unfolded protein response, which could be reversed by silencing CHOP, a mediator of the ER stress-associated apoptosis.	lz	17-19	DNA damage inducible transcript 3	Homo sapiens	173-177
28039491-7	2016	Additionally, our in vitro study found that apoptotic rate was decreased with remarkable down-regulation of the cleaved caspase-12, CHOP, p-JNK after ER stress was inhibited by 4-Phenylbutyric acid (4-PBA) treatment.	4-phenylbutyric acid	177-197	DNA damage inducible transcript 3	Homo sapiens	132-136
27895312-3	2016	Mechanistically, LZ-205 triggers reactive oxygen species (ROS)-induced endoplasmic reticulum (ER) stress and unfolded protein response, which could be reversed by silencing CHOP, a mediator of the ER stress-associated apoptosis.	Reactive Oxygen Species	33-56	DNA damage inducible transcript 3	Homo sapiens	173-177
27895312-3	2016	Mechanistically, LZ-205 triggers reactive oxygen species (ROS)-induced endoplasmic reticulum (ER) stress and unfolded protein response, which could be reversed by silencing CHOP, a mediator of the ER stress-associated apoptosis.	Reactive Oxygen Species	58-61	DNA damage inducible transcript 3	Homo sapiens	173-177
27977675-7	2016	CHOP knockdown by siRNA in the CAL 27 cells significantly suppressed macrolide-induced cell death under the AAD culture condition.	Macrolides	69-78	DNA damage inducible transcript 3	Homo sapiens	0-4
27930712-11	2016	Cantharidin could also increase the endoplasmic reticulum (ER) stress signals, including the expressions of phosphorylated eIF-2alpha and CHOP, but not Grp78 and Grp94.	Cantharidin	0-11	DNA damage inducible transcript 3	Homo sapiens	138-142
27835875-9	2016	Patients with high TLG level were more likely to relapse than those with low TLG level even though they had got complete or partial remission in R-CHOP therapy (40% versus 9%, p=0.012).	(5r)-3-Acetyl-4-Hydroxy-5-Methyl-5-[(1z)-2-Methylbuta-1,3-Dien-1-Yl]thiophen-2(5h)-One	19-22	DNA damage inducible transcript 3	Homo sapiens	147-151
27931220-17	2016	Native musk and synthetic musk ketone can up-regulate IL-24 (interleukin family) and DDIT3 (MAPK signalling pathway) in lung cancer cells.	Ketones	31-37	DNA damage inducible transcript 3	Homo sapiens	85-90
27845899-6	2016	We then reveal that BDMC upregulates GRP78 and facilitates apoptosis through eIF2alpha/CHOP pathway.	bisdemethoxycurcumin	20-24	DNA damage inducible transcript 3	Homo sapiens	87-91
27913503-1	2016	Although rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard treatment for patients with diffuse large B-cell lymphoma (DLBCL), ~30% to 50% of patients are not cured by this treatment, depending on disease stage or prognostic index.	Doxorubicin	42-53	DNA damage inducible transcript 3	Homo sapiens	86-90
27913503-1	2016	Although rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard treatment for patients with diffuse large B-cell lymphoma (DLBCL), ~30% to 50% of patients are not cured by this treatment, depending on disease stage or prognostic index.	Prednisone	72-82	DNA damage inducible transcript 3	Homo sapiens	86-90
28154512-11	2016	In the additive genetic model results for each IL10 polymorphism, the rs1800871 and rs1800872 polymorphisms represented a marginal association with OS (p = 0.09 and p = 0.06) and PFS (p = 0.05 and p = 0.08) in B-cell lymphoma patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Osmium	148-150	DNA damage inducible transcript 3	Homo sapiens	325-329
27676154-5	2016	Genistein (a specific Tyr phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein) with C/EBP-beta, thus negatively regulating it.	Genistein	0-9	DNA damage inducible transcript 3	Homo sapiens	81-85
27676154-5	2016	Genistein (a specific Tyr phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein) with C/EBP-beta, thus negatively regulating it.	Genistein	0-9	DNA damage inducible transcript 3	Homo sapiens	87-111
27676154-5	2016	Genistein (a specific Tyr phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein) with C/EBP-beta, thus negatively regulating it.	Tyrosine	22-25	DNA damage inducible transcript 3	Homo sapiens	81-85
27676154-5	2016	Genistein (a specific Tyr phosphorylation inhibitor) leads to the interaction of CHOP (C/EBP Homologous Protein) with C/EBP-beta, thus negatively regulating it.	Tyrosine	22-25	DNA damage inducible transcript 3	Homo sapiens	87-111
27315156-0	2016	Rituximab plus reduced-dose cyclophosphamide, doxorubicin, vincristine and prednisone (RD R-CHOP) chemotherapy is feasible for very elderly patients (&gt;=80 years) with B-cell lymphoma: analysis of treatment outcome.	Prednisone	75-85	DNA damage inducible transcript 3	Homo sapiens	92-96
27980366-4	2016	Protein and mRNA levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and ARPE-19 cell viability were measured in the presence of tunicamycin-induced ER stress in control or PTX3 small hairpin RNA (shRNA)-transfected ARPE-19 cells.	Tunicamycin	144-155	DNA damage inducible transcript 3	Homo sapiens	78-82
27980366-8	2016	Decreased cell viability and prolonged protein and mRNA expression of CHOP were observed under tunicamycin-induced ER stress in PTX3 shRNA transfected ARPE-19 cells.	Tunicamycin	95-106	DNA damage inducible transcript 3	Homo sapiens	70-74
27729194-8	2016	Here, we show that VCP inhibitors act synergistically with Salubrinal, an inhibitor of eIF2alpha dephosphorylation, by enhancing CHOP expression in ovarian cancer cell lines.	salubrinal	59-69	DNA damage inducible transcript 3	Homo sapiens	129-133
27697863-7	2016	In summary, cytoplasmic CHOP plays a central role in coordinating the interaction of MAM proteins with the outer mitochondrial membrane translocase, Tom22, to activate metabolic activity in the IMS by enhanced phosphate circulation.	Phosphates	210-219	DNA damage inducible transcript 3	Homo sapiens	24-28
27994685-0	2016	Intra-patient Variability of FDG Standardized Uptake Values in Mediastinal Blood Pool, Liver, and Myocardium during R-CHOP Chemotherapy in Patients with Diffuse Large B-cell Lymphoma.	Fluorodeoxyglucose F18	29-32	DNA damage inducible transcript 3	Homo sapiens	118-122
28030899-8	2016	In univariate analysis, the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen resulted in a better PFS than the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen (88.9% vs. 50.0%; p = 0.053).	Cyclophosphamide	39-55	DNA damage inducible transcript 3	Homo sapiens	209-213
28030899-8	2016	In univariate analysis, the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen resulted in a better PFS than the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen (88.9% vs. 50.0%; p = 0.053).	Doxorubicin	57-68	DNA damage inducible transcript 3	Homo sapiens	209-213
28030899-8	2016	In univariate analysis, the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen resulted in a better PFS than the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen (88.9% vs. 50.0%; p = 0.053).	Vincristine	70-81	DNA damage inducible transcript 3	Homo sapiens	209-213
28030899-8	2016	In univariate analysis, the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen resulted in a better PFS than the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen (88.9% vs. 50.0%; p = 0.053).	Prednisone	87-97	DNA damage inducible transcript 3	Homo sapiens	101-105
28030899-8	2016	In univariate analysis, the rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen resulted in a better PFS than the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen (88.9% vs. 50.0%; p = 0.053).	Prednisone	87-97	DNA damage inducible transcript 3	Homo sapiens	209-213
27613715-4	2016	We found that nefazodone induced endoplasmic reticulum (ER) stress in HepG2 cells, as the expression of typical ER stress markers, including CHOP, ATF-4, and p-eIF2alpha, was significantly increased, and splicing of XBP1 was observed.	nefazodone	14-24	DNA damage inducible transcript 3	Homo sapiens	141-145
28101356-6	2016	After treatment with chemotherapy regimens comprising cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP), followed by high-dose treatment with methotrexate, dexamethasone, ifosfamide, etoposide and L-asparaginasum (SMILE), the patient succumbed to the disease.	Prednisone	101-111	DNA damage inducible transcript 3	Homo sapiens	113-117
27748868-9	2016	Western blot analyses demonstrated that the levels of Fas, FasL, cytochrome c, Apaf-1, GADD153 and GRP78 were upregulated in GdCl3-treated U-2 OS cells.	gadolinium chloride	125-130	DNA damage inducible transcript 3	Homo sapiens	87-94
27902770-7	2016	Glycolytic inhibitor 2-deoxyglucose (2-DG) induced ER stress as detected by qPCR (BiP, ATF4) and immunoblotting (BiP, CHOP) and increased dihydroethidium probe oxidation both CD138low and CD138high cells.	Deoxyglucose	21-35	DNA damage inducible transcript 3	Homo sapiens	118-122
27902770-7	2016	Glycolytic inhibitor 2-deoxyglucose (2-DG) induced ER stress as detected by qPCR (BiP, ATF4) and immunoblotting (BiP, CHOP) and increased dihydroethidium probe oxidation both CD138low and CD138high cells.	Deoxyglucose	37-41	DNA damage inducible transcript 3	Homo sapiens	118-122
27769859-6	2016	MGO-induced endothelial apoptosis was significantly diminished by the depletion of CHOP with si-RNA against human CHOP, but not by SP600125, a specific inhibitor of JNK.	Pyruvaldehyde	0-3	DNA damage inducible transcript 3	Homo sapiens	83-87
27769859-6	2016	MGO-induced endothelial apoptosis was significantly diminished by the depletion of CHOP with si-RNA against human CHOP, but not by SP600125, a specific inhibitor of JNK.	Pyruvaldehyde	0-3	DNA damage inducible transcript 3	Homo sapiens	114-118
27769859-9	2016	Taken together, these findings indicate that MGO specifically induces endothelial dysfunction in a CHOP-dependent manner, suggesting the therapeutic potential of CHOP inhibition in diabetic cardiovascular complications.	Pyruvaldehyde	45-48	DNA damage inducible transcript 3	Homo sapiens	99-103
27769859-9	2016	Taken together, these findings indicate that MGO specifically induces endothelial dysfunction in a CHOP-dependent manner, suggesting the therapeutic potential of CHOP inhibition in diabetic cardiovascular complications.	Pyruvaldehyde	45-48	DNA damage inducible transcript 3	Homo sapiens	162-166
27896021-4	2016	LCA induced ER stress-related proteins, such as CCAAT-enhancer-binding protein homologous protein (CHOP), and the phosphorylation of eukaryotic initiation factor 2-alpha (p-eIF2alpha) and c-Jun N-terminal kinases (p-JNK) in both cancer cell-types.	Lithocholic Acid	0-3	DNA damage inducible transcript 3	Homo sapiens	48-97
27896021-4	2016	LCA induced ER stress-related proteins, such as CCAAT-enhancer-binding protein homologous protein (CHOP), and the phosphorylation of eukaryotic initiation factor 2-alpha (p-eIF2alpha) and c-Jun N-terminal kinases (p-JNK) in both cancer cell-types.	Lithocholic Acid	0-3	DNA damage inducible transcript 3	Homo sapiens	99-103
27896021-8	2016	Salubrinal, an inhibitor of eIF2alpha dephosphorylation and ER stress, reduced LCA-induced CHOP levels slightly in PC-3, but not DU-145 cells.	salubrinal	0-10	DNA damage inducible transcript 3	Homo sapiens	91-95
27896021-8	2016	Salubrinal, an inhibitor of eIF2alpha dephosphorylation and ER stress, reduced LCA-induced CHOP levels slightly in PC-3, but not DU-145 cells.	Lithocholic Acid	79-82	DNA damage inducible transcript 3	Homo sapiens	91-95
27601063-8	2016	Combined treatment using BZ and VNR, but not PTX, enhanced the cytotoxic effect and apoptosis induction along with pronounced ER stress loading such as upregulation of GRP78 and CHOP/GADD153.	Bortezomib	25-27	DNA damage inducible transcript 3	Homo sapiens	178-182
27477167-0	2016	Rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) in the management of primary mediastinal B-cell lymphoma: a subgroup analysis of the UK NCRI R-CHOP 14 versus 21 trial.	Prednisolone	58-70	DNA damage inducible transcript 3	Homo sapiens	74-78
27555288-13	2016	Our study implicates for the first time ER stress-induced CHOP activation in the brain as a mechanistic link in the palmitate-induced negative regulation of leptin and IGF1, two neurotrophic cytokines that play an indispensable role in the mammalian brain.	Palmitates	116-125	DNA damage inducible transcript 3	Homo sapiens	58-62
27339788-4	2016	Homocysteine significantly increased mRNA levels of CHOP and p53, resulting in the upregulation of their downstream target gene, p53 up-regulated modulator of apoptosis (PUMA).	Homocysteine	0-12	DNA damage inducible transcript 3	Homo sapiens	52-56
27629794-7	2016	Interestingly, SP600125 also inhibits the expression CHOP, yet CHOP has no impact on death receptor expressions.	pyrazolanthrone	15-23	DNA damage inducible transcript 3	Homo sapiens	53-57
27601063-8	2016	Combined treatment using BZ and VNR, but not PTX, enhanced the cytotoxic effect and apoptosis induction along with pronounced ER stress loading such as upregulation of GRP78 and CHOP/GADD153.	Bortezomib	25-27	DNA damage inducible transcript 3	Homo sapiens	183-190
27872741-5	2016	demonstrated that approximately 20% of patients with FL relapse within two years after achieving remission with R-CHOP and have a poor prognosis.	fl	53-55	DNA damage inducible transcript 3	Homo sapiens	114-118
27650555-6	2016	Mechanistically, AMPKalpha1 was found to coimmunoprecipitate with CHOP and phosphorylate CHOP at serine 30.	Serine	97-103	DNA damage inducible transcript 3	Homo sapiens	89-93
26513129-12	2016	Furthermore, Trolox inhibited AEA-induced CHOP10 expression and caspase 3 activity, indicating that oxidative stress was required for AEA-induced ER stress-apoptosis.	6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid	13-19	DNA damage inducible transcript 3	Homo sapiens	42-48
26513129-12	2016	Furthermore, Trolox inhibited AEA-induced CHOP10 expression and caspase 3 activity, indicating that oxidative stress was required for AEA-induced ER stress-apoptosis.	anandamide	30-33	DNA damage inducible transcript 3	Homo sapiens	42-48
26513129-12	2016	Furthermore, Trolox inhibited AEA-induced CHOP10 expression and caspase 3 activity, indicating that oxidative stress was required for AEA-induced ER stress-apoptosis.	anandamide	134-137	DNA damage inducible transcript 3	Homo sapiens	42-48
27748814-5	2016	Inhibition of ER stress using ER stress antagonist, salubrinal, attenuated the expression of CHOP and alleviated neuronal death.	salubrinal	52-62	DNA damage inducible transcript 3	Homo sapiens	93-97
27489231-6	2016	Interestingly, obovatol upregulated the expression of endoplasmic reticulum stress proteins such as C/EBP homologous protein (CHOP), IRE1alpha, ATF4 and p-elF2 in A549 and H460 NSCLCs.	obovatol	15-23	DNA damage inducible transcript 3	Homo sapiens	100-124
27489231-6	2016	Interestingly, obovatol upregulated the expression of endoplasmic reticulum stress proteins such as C/EBP homologous protein (CHOP), IRE1alpha, ATF4 and p-elF2 in A549 and H460 NSCLCs.	obovatol	15-23	DNA damage inducible transcript 3	Homo sapiens	126-130
27489231-7	2016	Conversely, depletion of CHOP blocked the apoptotic activity of obovatol to increase sub-G1 accumulation in A549 and H460 NSCLCs.	obovatol	64-72	DNA damage inducible transcript 3	Homo sapiens	25-29
27489231-8	2016	Overall, our findings support scientific evidences that obovatol induces apoptosis via CHOP activation in A549 and H460 NSCLCs.	obovatol	56-64	DNA damage inducible transcript 3	Homo sapiens	87-91
27634458-6	2016	Treatments of SH-SY5Y cells with the chemical chaperone, 4-phenylbutyric acid and the ROS scavenger, N-acetyl-cysteine reduced the AA-induced expression of ATF4 protein and CHOP mRNA, and resulted in the suppression of apoptosis.	4-phenylbutyric acid	57-77	DNA damage inducible transcript 3	Homo sapiens	173-177
27634458-6	2016	Treatments of SH-SY5Y cells with the chemical chaperone, 4-phenylbutyric acid and the ROS scavenger, N-acetyl-cysteine reduced the AA-induced expression of ATF4 protein and CHOP mRNA, and resulted in the suppression of apoptosis.	Reactive Oxygen Species	86-89	DNA damage inducible transcript 3	Homo sapiens	173-177
27634458-6	2016	Treatments of SH-SY5Y cells with the chemical chaperone, 4-phenylbutyric acid and the ROS scavenger, N-acetyl-cysteine reduced the AA-induced expression of ATF4 protein and CHOP mRNA, and resulted in the suppression of apoptosis.	Acetylcysteine	101-118	DNA damage inducible transcript 3	Homo sapiens	173-177
27650555-7	2016	Furthermore, serine 30 phosphorylation of CHOP triggered its ubiquitination and proteasomal degradation.	Serine	13-19	DNA damage inducible transcript 3	Homo sapiens	42-46
27650555-11	2016	CONCLUSIONS: Our results indicate that AMPKalpha1 mediates CHOP ubiquitination and proteasomal degradation in macrophages by promoting the phosphorylation of CHOP at serine 30.	Serine	166-172	DNA damage inducible transcript 3	Homo sapiens	59-63
27754332-9	2016	Western blotting indicated that TET increased endoplasmic reticulum (ER) stress associated protein expression such as GADD153, GRP78, ATF-6alpha and ATF-6 betawhich indicated that TET induced cell death through ER stress.	tetrandrine	32-35	DNA damage inducible transcript 3	Homo sapiens	118-125
27801783-6	2016	The unfolded protein response signaling pathway-related proteins were also activated on 11-epi-SA treatment, and these changes were accompanied by the upregulated expression of growth arrest and DNA damage-inducible protein (GADD153) and CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP), the genes encoding transcription factors associated with growth arrest and apoptosis under prolonged ER stress.	11-epi-sa	88-97	DNA damage inducible transcript 3	Homo sapiens	177-232
27801783-6	2016	The unfolded protein response signaling pathway-related proteins were also activated on 11-epi-SA treatment, and these changes were accompanied by the upregulated expression of growth arrest and DNA damage-inducible protein (GADD153) and CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP), the genes encoding transcription factors associated with growth arrest and apoptosis under prolonged ER stress.	11-epi-sa	88-97	DNA damage inducible transcript 3	Homo sapiens	297-301
27801783-7	2016	Two inhibitors, namely salubrinal (Sal) and SP600125, partially abrogated 11-epi-SA-related cell death, implying that the protein kinase R (PKR)-like endoplasmic reticulum kinase (PERK)-activating transcription factor (ATF) 6-CHOP or the inositol-requiring enzyme 1 alpha (IRE1alpha)-c-Jun N-terminal kinase (JNK)-cJun signal pathway was activated after 11-epi-SA treatment.	11-epi-sa	74-83	DNA damage inducible transcript 3	Homo sapiens	226-230
27732567-4	2016	We report that overexpression of wild-type CYPB attenuated aldosterone-induced oxidative stress (evidenced by reduced production of reactive oxygen species and improved mitochondrial dysfunction), ERS (indicated by reduced expression of the ERS markers glucose-regulated protein 78 [GRP78] and C/-EBP homologous protein [CHOP]), and tubular cell apoptosis in comparison with aldosterone-induced human kidney-2 (HK-2) cells.	Aldosterone	59-70	DNA damage inducible transcript 3	Homo sapiens	294-319
27732567-4	2016	We report that overexpression of wild-type CYPB attenuated aldosterone-induced oxidative stress (evidenced by reduced production of reactive oxygen species and improved mitochondrial dysfunction), ERS (indicated by reduced expression of the ERS markers glucose-regulated protein 78 [GRP78] and C/-EBP homologous protein [CHOP]), and tubular cell apoptosis in comparison with aldosterone-induced human kidney-2 (HK-2) cells.	Aldosterone	59-70	DNA damage inducible transcript 3	Homo sapiens	321-325
27351173-14	2016	CONCLUSIONS: With anthracycline-based regimens such as R-CHOP and R-EPOCH, very elderly patients with DLBCL had superior outcomes similar to those achieved for younger patients with DLBCL.	Anthracyclines	18-31	DNA damage inducible transcript 3	Homo sapiens	57-61
27754332-9	2016	Western blotting indicated that TET increased endoplasmic reticulum (ER) stress associated protein expression such as GADD153, GRP78, ATF-6alpha and ATF-6 betawhich indicated that TET induced cell death through ER stress.	tetrandrine	180-183	DNA damage inducible transcript 3	Homo sapiens	118-125
27620489-7	2016	In both cell lines, Cd exposure resulted in caspase-3-mediated PARP-1 cleavage and the induction of CHOP, LC3-II, and HO-1, which were limited in YD10B and H1299 cells exposed to high concentrations of Cd.	Cadmium	20-22	DNA damage inducible transcript 3	Homo sapiens	100-104
27620489-9	2016	The inhibition of autophagy using small interfering RNA (siRNA) for the autophagy-related gene atg5 enhanced HO-1, CHOP, and PARP-1 cleavage induced by Cd.	Cadmium	152-154	DNA damage inducible transcript 3	Homo sapiens	115-119
27392939-0	2016	Mephebrindole, a synthetic indole analog coordinates the crosstalk between p38MAPK and eIF2alpha/ATF4/CHOP signalling pathways for induction of apoptosis in human breast carcinoma cells.	mephebrindole	0-13	DNA damage inducible transcript 3	Homo sapiens	102-106
27392939-0	2016	Mephebrindole, a synthetic indole analog coordinates the crosstalk between p38MAPK and eIF2alpha/ATF4/CHOP signalling pathways for induction of apoptosis in human breast carcinoma cells.	indole	7-13	DNA damage inducible transcript 3	Homo sapiens	102-106
28011957-11	2016	Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	76-80
27731378-3	2016	In this study, we show that ER stress mediated by thapsigargin promoted CHOP and DR5 synthesis thus sensitizing TRAIL treatment, which induced ESCC cells apoptosis.	Thapsigargin	50-62	DNA damage inducible transcript 3	Homo sapiens	72-76
27813604-8	2016	Furthermore, GRP78, IRE1alpha, XBP1s, and CHOP expression was downregulated as a result of rosuvastatin administration.	Rosuvastatin Calcium	91-103	DNA damage inducible transcript 3	Homo sapiens	42-46
27077778-10	2016	CONCLUSION: CHOPE has a trend to improve CR rate, 1-year PFS and OS compared with CHOP alone.	Chromium	41-43	DNA damage inducible transcript 3	Homo sapiens	12-16
27470132-0	2016	Rifampicin-induced injury in L02 cells is alleviated by 4-PBA via inhibition of the PERK-ATF4-CHOP pathway.	Rifampin	0-10	DNA damage inducible transcript 3	Homo sapiens	94-98
27599983-6	2016	The expressions of HSP90B1 and DDIT3 proteins were detected in all paraffin-embedded biopsy samples by immunochemistry.	Paraffin	67-75	DNA damage inducible transcript 3	Homo sapiens	31-36
27573888-9	2016	Elevated expression of spliced X-box binding protein 1 (XBP1) and CCAAT/enhancer-binding protein homologous protein (CHOP) further confirmed that ROS generated by NTGP induces apoptosis through the ER stress signaling pathway.	Reactive Oxygen Species	146-149	DNA damage inducible transcript 3	Homo sapiens	66-115
27573888-9	2016	Elevated expression of spliced X-box binding protein 1 (XBP1) and CCAAT/enhancer-binding protein homologous protein (CHOP) further confirmed that ROS generated by NTGP induces apoptosis through the ER stress signaling pathway.	Reactive Oxygen Species	146-149	DNA damage inducible transcript 3	Homo sapiens	117-121
27470132-0	2016	Rifampicin-induced injury in L02 cells is alleviated by 4-PBA via inhibition of the PERK-ATF4-CHOP pathway.	4-phenylbutylamine	56-61	DNA damage inducible transcript 3	Homo sapiens	94-98
27470132-8	2016	Treatment with 4-PBA decreased the protein and gene expression of GRP78, PERK, ATF4 and CHOP.	4-phenylbutylamine	15-20	DNA damage inducible transcript 3	Homo sapiens	88-92
27470132-10	2016	These results indicate that 4-PBA alleviates RFP-induced injury in L02 cells via inhibition of the PERK-ATF4-CHOP pathway.	4-phenylbutylamine	28-33	DNA damage inducible transcript 3	Homo sapiens	109-113
27665710-7	2016	Inhibition of ER stress with 4-phenylbutyric acid effectively inhibited the activation of eIF2alpha and CHOP signals and reversed AGEs-induced cell apoptosis.	4-phenylbutyric acid	29-49	DNA damage inducible transcript 3	Homo sapiens	104-108
27498033-6	2016	We found that DHAA upregulated ER stress-related genes such as GRP78, CHOP, and spliced XBP1.	Dehydroascorbic Acid	14-18	DNA damage inducible transcript 3	Homo sapiens	70-74
27636901-6	2016	Induction of Chop/CHOP and p58IPK/P58IPK by oxidized LDL was mimicked by hydrogen peroxide and was blocked by co-treatment with the N-acetylcystein antioxidant.	Hydrogen Peroxide	73-90	DNA damage inducible transcript 3	Homo sapiens	13-17
27636901-6	2016	Induction of Chop/CHOP and p58IPK/P58IPK by oxidized LDL was mimicked by hydrogen peroxide and was blocked by co-treatment with the N-acetylcystein antioxidant.	Hydrogen Peroxide	73-90	DNA damage inducible transcript 3	Homo sapiens	18-22
27264312-0	2016	Novel CHOP activator LGH00168 induces necroptosis in A549 human lung cancer cells via ROS-mediated ER stress and NF-kappaB inhibition.	LGH00168	21-29	DNA damage inducible transcript 3	Homo sapiens	6-10
27026200-7	2016	Consequently, the transcription factor CCAAT/enhancer-binding protein homology protein (CHOP) accumulated in response to carfilzomib, and CHOP depletion conferred protection against cytotoxicity.	carfilzomib	121-132	DNA damage inducible transcript 3	Homo sapiens	39-86
27026200-7	2016	Consequently, the transcription factor CCAAT/enhancer-binding protein homology protein (CHOP) accumulated in response to carfilzomib, and CHOP depletion conferred protection against cytotoxicity.	carfilzomib	121-132	DNA damage inducible transcript 3	Homo sapiens	88-92
27026200-10	2016	CONCLUSIONS: Collectively, carfilzomib induced ER stress culminating in activation of intrinsic and extrinsic caspase pathways, and we identified the CHOP protein level as a biomarker that could predict sensitivity to carfilzomib in CLL.	carfilzomib	218-229	DNA damage inducible transcript 3	Homo sapiens	150-154
27264312-0	2016	Novel CHOP activator LGH00168 induces necroptosis in A549 human lung cancer cells via ROS-mediated ER stress and NF-kappaB inhibition.	ros	86-89	DNA damage inducible transcript 3	Homo sapiens	6-10
27264312-12	2016	Moreover, NAC significantly diminished LGH00168-induced CHOP activation, NF-kappaB inhibition and necroptosis in A549 cells.	LGH00168	39-47	DNA damage inducible transcript 3	Homo sapiens	56-60
27481183-3	2016	At the protein expression level, compared to the lean, the phosphorylation of AMPK, and p-Akt at serine 473 were significantly reduced from the overweight (OW) and/or obese (OB); while the protein expression of p-JNK, cleaved caspase 3, CHOP and p-eIF2alpha were elevated from the OW and/or OB.	Serine	97-103	DNA damage inducible transcript 3	Homo sapiens	237-241
27628560-5	2016	She was initially started on R-CHOP(rituximab and doxorubicin, vincristine, cyclophosphamide, and prednisolone), but after one course the regimen was changed to dose-adjusted EPOCH-R(rituximab and doxorubicin, etoposide, vincristine, cyclophosphamide, and prednisolone).	r	29-30	DNA damage inducible transcript 3	Homo sapiens	31-35
27156492-6	2016	For the latter, the patient was receiving rituximab cyclophosphamide hydroxydaunorubicin oncovin vincristine prednisone (R-CHOP) regimen.	rituximab cyclophosphamide hydroxydaunorubicin	42-88	DNA damage inducible transcript 3	Homo sapiens	123-127
27581364-4	2016	Physapubescin decreases the expression of HIF-2alpha and increases the expression of CCAAT/enhancer-binding protein homologus protein (CHOP), which leads to up-regulation of death receptor 5 (DR5), activation of caspase-8 and -3, cleavage of poly (ADP-Ribose) polymerase (PARP) and apoptosis.	physapubescin	0-13	DNA damage inducible transcript 3	Homo sapiens	135-139
27496964-0	2016	Gossypol induces death receptor-5 through activation of ROS-ERK-CHOP pathway and sensitizes colon cancer cells to TRAIL.	Gossypol	0-8	DNA damage inducible transcript 3	Homo sapiens	64-68
27496964-0	2016	Gossypol induces death receptor-5 through activation of ROS-ERK-CHOP pathway and sensitizes colon cancer cells to TRAIL.	ros	56-59	DNA damage inducible transcript 3	Homo sapiens	64-68
27312042-2	2016	The CHOP regimen is the standard treatment for non-Hodgkin"s lymphoma (NHL) and is categorized as highly or moderately emetogenic in the CINV guidelines.	cinv	137-141	DNA damage inducible transcript 3	Homo sapiens	4-8
26923251-12	2016	ASM siRNA, DES, recombinant AC, and ER stress inhibitor 4-phenylbutyric acid were blocked by elevated levels of C/EBP homologous protein (CHOP); ox-LDL induced elevated levels of CHOP.	4-phenylbutyric acid	56-76	DNA damage inducible transcript 3	Homo sapiens	112-136
26923251-12	2016	ASM siRNA, DES, recombinant AC, and ER stress inhibitor 4-phenylbutyric acid were blocked by elevated levels of C/EBP homologous protein (CHOP); ox-LDL induced elevated levels of CHOP.	4-phenylbutyric acid	56-76	DNA damage inducible transcript 3	Homo sapiens	138-142
27382104-1	2016	PURPOSE: Utility of combined-modality therapy for patients with limited-stage diffuse large B-cell lymphoma (DLBCL) was shown in the Southwest Oncology Group (SWOG) S8736 study, where three cycles of CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus radiotherapy (CHOP3RT) improved 5-year progression-free (PFS) and overall survival (OS) compared with eight cycles of CHOP (CHOP8).	Cyclophosphamide	206-222	DNA damage inducible transcript 3	Homo sapiens	200-204
27382104-1	2016	PURPOSE: Utility of combined-modality therapy for patients with limited-stage diffuse large B-cell lymphoma (DLBCL) was shown in the Southwest Oncology Group (SWOG) S8736 study, where three cycles of CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus radiotherapy (CHOP3RT) improved 5-year progression-free (PFS) and overall survival (OS) compared with eight cycles of CHOP (CHOP8).	Doxorubicin	224-235	DNA damage inducible transcript 3	Homo sapiens	200-204
27382104-1	2016	PURPOSE: Utility of combined-modality therapy for patients with limited-stage diffuse large B-cell lymphoma (DLBCL) was shown in the Southwest Oncology Group (SWOG) S8736 study, where three cycles of CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) plus radiotherapy (CHOP3RT) improved 5-year progression-free (PFS) and overall survival (OS) compared with eight cycles of CHOP (CHOP8).	Vincristine	237-248	DNA damage inducible transcript 3	Homo sapiens	200-204
27621650-2	2016	Although the majority of patients with diffuse large B-cell lymphoma (DLBCL) can be cured with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), chemoresistance is a common cause of treatment failure.	Prednisone	143-153	DNA damage inducible transcript 3	Homo sapiens	155-159
27481183-5	2016	In cultured PBMCs, high glucose and FFAs induced GRP78, CHOP and XBP-1 mRNA, and high glucose also induced APP, PS1 and PS2 mRNA.	Glucose	24-31	DNA damage inducible transcript 3	Homo sapiens	56-60
27267997-5	2016	Carnosic acid also promoted the expression of ER proteins including BiP and CHOP in a dose-dependent manner.	salvin	0-13	DNA damage inducible transcript 3	Homo sapiens	76-80
27350212-9	2016	Increased level of spliced XBP-1, ATF6 nuclear translocation and CHOP protein expression were detected in CD44+/CD24- and original MCF7 cells treated with tunicamycin.	Tunicamycin	155-166	DNA damage inducible transcript 3	Homo sapiens	65-69
27391761-6	2016	Treatment with 1.0 ng/mL of melatonin also significantly elevated MT2, SOD1, and GPX4 while lowering FASL, CHOP, and GRP78 mRNA abundance compared to the untreated control.	Melatonin	28-37	DNA damage inducible transcript 3	Homo sapiens	107-111
27233943-2	2016	Unbiased genomic and proteomic screenings using ovarian cancer cell lines of different genetic backgrounds and sensitivities to platinum led to the identification of two key genes upregulated by mifepristone and involved in the unfolded protein response (UPR): the master chaperone of the endoplasmic reticulum (ER), glucose regulated protein (GRP) of 78 kDa, and the CCAAT/enhancer binding protein homologous transcription factor (CHOP).	Platinum	128-136	DNA damage inducible transcript 3	Homo sapiens	368-430
27233943-2	2016	Unbiased genomic and proteomic screenings using ovarian cancer cell lines of different genetic backgrounds and sensitivities to platinum led to the identification of two key genes upregulated by mifepristone and involved in the unfolded protein response (UPR): the master chaperone of the endoplasmic reticulum (ER), glucose regulated protein (GRP) of 78 kDa, and the CCAAT/enhancer binding protein homologous transcription factor (CHOP).	Platinum	128-136	DNA damage inducible transcript 3	Homo sapiens	432-436
27233943-2	2016	Unbiased genomic and proteomic screenings using ovarian cancer cell lines of different genetic backgrounds and sensitivities to platinum led to the identification of two key genes upregulated by mifepristone and involved in the unfolded protein response (UPR): the master chaperone of the endoplasmic reticulum (ER), glucose regulated protein (GRP) of 78 kDa, and the CCAAT/enhancer binding protein homologous transcription factor (CHOP).	Mifepristone	195-207	DNA damage inducible transcript 3	Homo sapiens	368-430
27233943-2	2016	Unbiased genomic and proteomic screenings using ovarian cancer cell lines of different genetic backgrounds and sensitivities to platinum led to the identification of two key genes upregulated by mifepristone and involved in the unfolded protein response (UPR): the master chaperone of the endoplasmic reticulum (ER), glucose regulated protein (GRP) of 78 kDa, and the CCAAT/enhancer binding protein homologous transcription factor (CHOP).	Mifepristone	195-207	DNA damage inducible transcript 3	Homo sapiens	432-436
27233943-3	2016	GRP78 and CHOP were upregulated by mifepristone in ovarian cancer cells regardless of p53 status and platinum sensitivity.	Mifepristone	35-47	DNA damage inducible transcript 3	Homo sapiens	10-14
27392906-5	2016	Serum and glucose deprivation significantly induced a variety of ER stress-inducible genes, but a 12-h treatment of 2-Cl-Phen down-regulated expression of several ER stress-related genes, with the exception of GADD153.	2-cl-phen	116-125	DNA damage inducible transcript 3	Homo sapiens	210-217
27392906-7	2016	This study also observed that a 24-h treatment of 2-Cl-Phen attenuated the expression levels of GRP78, GADD153, and c-Myc protein.	2-cl-phen	50-59	DNA damage inducible transcript 3	Homo sapiens	103-110
27432061-0	2016	Echinacoside Protects Against MPP(+)-Induced Neuronal Apoptosis via ROS/ATF3/CHOP Pathway Regulation.	echinacoside	0-12	DNA damage inducible transcript 3	Homo sapiens	77-81
27432061-0	2016	Echinacoside Protects Against MPP(+)-Induced Neuronal Apoptosis via ROS/ATF3/CHOP Pathway Regulation.	mangion-purified polysaccharide (Candida albicans)	30-36	DNA damage inducible transcript 3	Homo sapiens	77-81
27432061-4	2016	In addition, ECH suppressed the ROS and MPP(+)-induced expression of apoptotic genes (ATF3, CHOP, and SCNA).	Reactive Oxygen Species	32-35	DNA damage inducible transcript 3	Homo sapiens	92-96
27432061-9	2016	Taken together, these data suggest that the ROS/ATF3/CHOP pathway plays a critical role in mechanisms by which ECH protects against MPP(+)-induced apoptosis in PD.	Reactive Oxygen Species	44-47	DNA damage inducible transcript 3	Homo sapiens	53-57
27278525-0	2016	Fluoxetine synergizes with temozolomide to induce the CHOP-dependent endoplasmic reticulum stress-related apoptosis pathway in glioma cells.	Fluoxetine	0-10	DNA damage inducible transcript 3	Homo sapiens	54-58
27064126-5	2016	l-Serine inhibited homocysteine-induced ER stress as verified by decreased glucose-regulated protein 78kDa (GRP78) and C/EBP homologous protein (CHOP) expression as well as X-box binding protein 1 (xbp1) mRNA splicing.	Serine	0-8	DNA damage inducible transcript 3	Homo sapiens	119-143
27278525-0	2016	Fluoxetine synergizes with temozolomide to induce the CHOP-dependent endoplasmic reticulum stress-related apoptosis pathway in glioma cells.	Temozolomide	27-39	DNA damage inducible transcript 3	Homo sapiens	54-58
27278525-14	2016	Knockdown of CHOP expression abolished the synergistic effect of FLT and TMZ in the C6 cells, which suggests that FLT may sensitize glioma cells to TMZ through activation of the CHOP-dependent apoptosis pathway.	Temozolomide	73-76	DNA damage inducible transcript 3	Homo sapiens	13-17
27278525-14	2016	Knockdown of CHOP expression abolished the synergistic effect of FLT and TMZ in the C6 cells, which suggests that FLT may sensitize glioma cells to TMZ through activation of the CHOP-dependent apoptosis pathway.	Temozolomide	73-76	DNA damage inducible transcript 3	Homo sapiens	178-182
27064126-5	2016	l-Serine inhibited homocysteine-induced ER stress as verified by decreased glucose-regulated protein 78kDa (GRP78) and C/EBP homologous protein (CHOP) expression as well as X-box binding protein 1 (xbp1) mRNA splicing.	Serine	0-8	DNA damage inducible transcript 3	Homo sapiens	145-149
27064126-5	2016	l-Serine inhibited homocysteine-induced ER stress as verified by decreased glucose-regulated protein 78kDa (GRP78) and C/EBP homologous protein (CHOP) expression as well as X-box binding protein 1 (xbp1) mRNA splicing.	Homocysteine	19-31	DNA damage inducible transcript 3	Homo sapiens	119-143
27064126-5	2016	l-Serine inhibited homocysteine-induced ER stress as verified by decreased glucose-regulated protein 78kDa (GRP78) and C/EBP homologous protein (CHOP) expression as well as X-box binding protein 1 (xbp1) mRNA splicing.	Homocysteine	19-31	DNA damage inducible transcript 3	Homo sapiens	145-149
27461002-8	2016	In melanoma cells, delta-TT exerted its antitumor effect through activation of the PERK/p-eIF2alpha/ATF4/CHOP, IRE1alpha and caspase-4 ER stress-related branches.	tocotrienol, delta	19-27	DNA damage inducible transcript 3	Homo sapiens	105-109
27464732-13	2016	In the lipogenic HER2/neu-positive SKBR3 cell line, palmitate induces a G2 phase cell cycle delay and CHOP-dependent apoptosis as well as a partial activation of the ER stress response network via XBP1 and ATF6.	Palmitates	52-61	DNA damage inducible transcript 3	Homo sapiens	102-106
27467006-9	2016	Genistein triggered ER stress in HeLa cells, as indicated by the upregulation of glucose-regulated protein 78 (GRP78) and CHOP expression.	Genistein	0-9	DNA damage inducible transcript 3	Homo sapiens	122-126
27166181-7	2016	Moreover, chemical inhibition of ER stress or IRE-1 depletion with siRNA in andrographolide treated cells significantly limited expression of IRE-1 and CHOP as determined by immunofluorescence staining, real time PCR, or immunobloting.	andrographolide	76-91	DNA damage inducible transcript 3	Homo sapiens	152-156
27166181-10	2016	These data demonstrate that andrographolide associated ER stress contributes to apoptosis through the activation of a pro-apoptotic GRP-78/IRE-1/XBP-1/CHOP signaling pathway.	andrographolide	28-43	DNA damage inducible transcript 3	Homo sapiens	151-155
27131989-6	2016	We examined the neuroprotective effects of SAL administration on significantly reducing ER stress: janus-N-terminal kinase (JNK) phosphorylation and C/EBP homology protein (CHOP), oxidative stress: superoxide and carbonyls, and neuroinflammation: nuclear factor kappa beta (NFkappaB) activity, inducible nitric oxide synthase (iNOS) protein expression, and pro-inflammatory cytokines at 24h post-TBI.	salubrinal	43-46	DNA damage inducible transcript 3	Homo sapiens	149-171
27262990-5	2016	In addition, FA, Bz, and IP increased the protein expression of pro-apoptotic genes, C/EBP homologous protein (CHOP) and Bax, and reduced the protein expression of anti-apoptotic gene, Bcl-2.	Benzene	17-19	DNA damage inducible transcript 3	Homo sapiens	85-109
27262990-5	2016	In addition, FA, Bz, and IP increased the protein expression of pro-apoptotic genes, C/EBP homologous protein (CHOP) and Bax, and reduced the protein expression of anti-apoptotic gene, Bcl-2.	Benzene	17-19	DNA damage inducible transcript 3	Homo sapiens	111-115
27262990-5	2016	In addition, FA, Bz, and IP increased the protein expression of pro-apoptotic genes, C/EBP homologous protein (CHOP) and Bax, and reduced the protein expression of anti-apoptotic gene, Bcl-2.	isoprene	25-27	DNA damage inducible transcript 3	Homo sapiens	85-109
27262990-5	2016	In addition, FA, Bz, and IP increased the protein expression of pro-apoptotic genes, C/EBP homologous protein (CHOP) and Bax, and reduced the protein expression of anti-apoptotic gene, Bcl-2.	isoprene	25-27	DNA damage inducible transcript 3	Homo sapiens	111-115
27262990-8	2016	As CHOP is an endoplasmic reticulum (ER)-stress related apoptosis marker of which production is induced by ROS, it was considered that these CS components induce apoptosis of SW620 cells by increasing ROS synthesis and ER-stress.	Reactive Oxygen Species	107-110	DNA damage inducible transcript 3	Homo sapiens	3-7
27262990-8	2016	As CHOP is an endoplasmic reticulum (ER)-stress related apoptosis marker of which production is induced by ROS, it was considered that these CS components induce apoptosis of SW620 cells by increasing ROS synthesis and ER-stress.	Cesium	141-143	DNA damage inducible transcript 3	Homo sapiens	3-7
27262990-8	2016	As CHOP is an endoplasmic reticulum (ER)-stress related apoptosis marker of which production is induced by ROS, it was considered that these CS components induce apoptosis of SW620 cells by increasing ROS synthesis and ER-stress.	Reactive Oxygen Species	201-204	DNA damage inducible transcript 3	Homo sapiens	3-7
27133915-5	2016	The combination of vitamin D &amp; resveratrol completely reversed tunicamycin and Abeta25-35 induced cytotoxicity in SH-SY5Y cells, as well as elevation in ER stress markers (i.e.GRP78, p-eIF2alpha and CHOP), insulin signaling disruption (i.e. elevation in p-IRS-1serine307 and reduction in p-Akt serine473) and tau phosphorylation (i.e. reduction in p-GSK3beta serine9, and elevation in p-Tau serine396 &amp;404).	Vitamin D	19-28	DNA damage inducible transcript 3	Homo sapiens	203-207
27089170-2	2016	In Phase II studies, lenalidomide combined with R-CHOP (R(2)-CHOP) improved outcomes relative to historical R-CHOP in newly diagnosed DLBCL, particularly in non-GCB cases.	Lenalidomide	21-33	DNA damage inducible transcript 3	Homo sapiens	61-65
27089170-2	2016	In Phase II studies, lenalidomide combined with R-CHOP (R(2)-CHOP) improved outcomes relative to historical R-CHOP in newly diagnosed DLBCL, particularly in non-GCB cases.	Lenalidomide	21-33	DNA damage inducible transcript 3	Homo sapiens	61-65
27089170-0	2016	ROBUST: Lenalidomide-R-CHOP versus placebo-R-CHOP in previously untreated ABC-type diffuse large B-cell lymphoma.	Lenalidomide	8-20	DNA damage inducible transcript 3	Homo sapiens	23-27
27133915-5	2016	The combination of vitamin D &amp; resveratrol completely reversed tunicamycin and Abeta25-35 induced cytotoxicity in SH-SY5Y cells, as well as elevation in ER stress markers (i.e.GRP78, p-eIF2alpha and CHOP), insulin signaling disruption (i.e. elevation in p-IRS-1serine307 and reduction in p-Akt serine473) and tau phosphorylation (i.e. reduction in p-GSK3beta serine9, and elevation in p-Tau serine396 &amp;404).	Adenosine Monophosphate	30-33	DNA damage inducible transcript 3	Homo sapiens	203-207
27133915-5	2016	The combination of vitamin D &amp; resveratrol completely reversed tunicamycin and Abeta25-35 induced cytotoxicity in SH-SY5Y cells, as well as elevation in ER stress markers (i.e.GRP78, p-eIF2alpha and CHOP), insulin signaling disruption (i.e. elevation in p-IRS-1serine307 and reduction in p-Akt serine473) and tau phosphorylation (i.e. reduction in p-GSK3beta serine9, and elevation in p-Tau serine396 &amp;404).	Resveratrol	35-46	DNA damage inducible transcript 3	Homo sapiens	203-207
27311010-9	2016	We further demonstrated that propofol pretreatment attenuated or inhibited the effects caused by TG, such as upregulation of Bax, BiP, C/EBP homologous protein (CHOP), active caspase 12, and cleaved caspase 3, and downregulation of Bcl2.	Propofol	29-37	DNA damage inducible transcript 3	Homo sapiens	135-159
27260301-0	2016	Caffeic acid phenethyl ester enhances TRAIL-mediated apoptosis via CHOP-induced death receptor 5 upregulation in hepatocarcinoma Hep3B cells.	caffeic acid phenethyl ester	0-28	DNA damage inducible transcript 3	Homo sapiens	67-71
27176604-9	2016	Manu A caused depolarization of the mitochondrial membrane with induction of CHOP, DR4 and DR5.	manumycin	0-6	DNA damage inducible transcript 3	Homo sapiens	77-81
27374464-3	2016	These data provide the rationale to combine everolimus with standard treatment for DLBCL of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone delivered in a 21-day cycle (R-CHOP-21) for six cycles.	Everolimus	44-54	DNA damage inducible transcript 3	Homo sapiens	197-201
27374464-25	2016	INTERPRETATION: The mTORC1 inhibitor everolimus given for 14 days in combination with R-CHOP-21 for patients with DLBCL is safe.	Everolimus	37-47	DNA damage inducible transcript 3	Homo sapiens	88-92
27311010-9	2016	We further demonstrated that propofol pretreatment attenuated or inhibited the effects caused by TG, such as upregulation of Bax, BiP, C/EBP homologous protein (CHOP), active caspase 12, and cleaved caspase 3, and downregulation of Bcl2.	Thapsigargin	97-99	DNA damage inducible transcript 3	Homo sapiens	161-165
27311010-9	2016	We further demonstrated that propofol pretreatment attenuated or inhibited the effects caused by TG, such as upregulation of Bax, BiP, C/EBP homologous protein (CHOP), active caspase 12, and cleaved caspase 3, and downregulation of Bcl2.	Propofol	29-37	DNA damage inducible transcript 3	Homo sapiens	161-165
27311010-9	2016	We further demonstrated that propofol pretreatment attenuated or inhibited the effects caused by TG, such as upregulation of Bax, BiP, C/EBP homologous protein (CHOP), active caspase 12, and cleaved caspase 3, and downregulation of Bcl2.	Thapsigargin	97-99	DNA damage inducible transcript 3	Homo sapiens	135-159
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	gldl	14-18	DNA damage inducible transcript 3	Homo sapiens	144-148
27270209-4	2016	In SKOV-3 cells, citral induces the ER stress markers CHOP, GADD45, EDEM, ATF4, Hsp90, ATG5, and phospho-eIF2alpha.	citral	17-23	DNA damage inducible transcript 3	Homo sapiens	54-58
27307990-5	2016	In Burkitt lymphoma, the CXCR4 antagonist plerixafor has already been shown to enhance the therapeutic effect of rituximab, the immunotherapeutic agent of R-CHOP; but this is yet to be confirmed for DLBCL.	plerixafor	42-52	DNA damage inducible transcript 3	Homo sapiens	157-161
27307990-14	2016	CONCLUSIONS: Based on our results, implying that the anti-proliferative/pro-apoptotic effect of rituximab on DLBCL cells can be synergistically enhanced by the CXCR4 antagonist plerixafor, addition of plerixafor to the R-CHOP regimen can be suggested to improve treatment outcome for DLBCL patients.	plerixafor	177-187	DNA damage inducible transcript 3	Homo sapiens	221-225
27462230-10	2016	Two years after, the patient suffered a relapse and underwent 6 cycles of CHOP-R (cyclophosphamide, hydroxydaunomycin, oncovin, prednisone, and rituximab), achieving partial remission.	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	74-78
27103007-2	2016	Recently, the StiL and the BRIGHT trials showed that the combination of rituximab and bendamustine (R-B) is non-inferior to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) with a better toxicity profile.	Bendamustine Hydrochloride	86-98	DNA damage inducible transcript 3	Homo sapiens	197-201
27035631-8	2016	Downregulation of CHOP with siRNA blocked the autophagy inhibition and erlotinib co-treatment induced apoptosis and prevented cancer cells from this co-treatment-induced cell death.	Erlotinib Hydrochloride	71-80	DNA damage inducible transcript 3	Homo sapiens	18-22
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	55-72	DNA damage inducible transcript 3	Homo sapiens	144-148
27206739-6	2016	Incubation of gLDL-exposed cells with the anti-oxidant N-acetyl-cysteine (NAC) reduced ERS, revealed by decreased eIF2alpha phosphorylation and CHOP gene expression and increased GRP78 expression, thus validating the interconnection between ERS and oxidative stress.	Acetylcysteine	74-77	DNA damage inducible transcript 3	Homo sapiens	144-148
27115471-10	2016	Reduced expression of heat shock proteins (HSPs) was observed in AA cells, whereas DCA induced expression of CHOP, C/EBP, HSP60, and HSP90 in CA cells.	Dichloroacetic Acid	83-86	DNA damage inducible transcript 3	Homo sapiens	109-113
27129176-0	2016	Thalidomide enhanced the efficacy of CHOP chemotherapy in the treatment of diffuse large B cell lymphoma: A phase II study.	Thalidomide	0-11	DNA damage inducible transcript 3	Homo sapiens	37-41
27129176-1	2016	Cyclophosphamide, doxorubicin, vincristine, and prednisolone plus rituximab (R-CHOP) is the standard treatment for patients with diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	79-83
27129176-11	2016	We concluded that the addition of thalidomide to the CHOP regimen significantly improved the CRR and showed a trend of improving clinical outcome in patients with DLBCL, especially for patients with Bcl-2 positive and Bcl-6 negative B-cell phenotype, without increased toxicity.	Thalidomide	34-45	DNA damage inducible transcript 3	Homo sapiens	53-57
27222248-6	2016	PLX4032 induces DR5 expression at transcriptional levels, largely due to enhancing CHOP/Elk1-mediated DR5 transcription.	Vemurafenib	0-7	DNA damage inducible transcript 3	Homo sapiens	83-87
27342502-1	2016	OBJECTIVE: To explore the clinical efficiency and safety of CHOP regimen containing pegylated liposomal doxorubicin (PLD) for the aged patients with advanced diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	104-115	DNA damage inducible transcript 3	Homo sapiens	60-64
27133040-11	2016	Simultaneously, ALA could inhibit activation of ER stress-associated sensors GRP78, IRE1alpha, ATF6, P-PERK, P-eIF2alpha, CHOP and ATF4 induced by HCY.	Thioctic Acid	16-19	DNA damage inducible transcript 3	Homo sapiens	122-126
27041458-9	2016	Furthermore, sevoflurane treatment markedly increased the expression of CHOP and GRP78, two hallmark proteins of ER stress.	Sevoflurane	13-24	DNA damage inducible transcript 3	Homo sapiens	72-76
27041458-11	2016	Moreover, sevoflurane-stimulated expression of CHOP and GRP78 was inhibited by rapamycin, but further enhanced by 3-MA.	Sevoflurane	10-21	DNA damage inducible transcript 3	Homo sapiens	47-51
27041458-11	2016	Moreover, sevoflurane-stimulated expression of CHOP and GRP78 was inhibited by rapamycin, but further enhanced by 3-MA.	3-methyladenine	114-118	DNA damage inducible transcript 3	Homo sapiens	47-51
26990931-1	2016	BACKGROUND: Chemoimmunotherapy containing rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) is the standard treatment for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	53-69	DNA damage inducible transcript 3	Homo sapiens	117-121
26990931-1	2016	BACKGROUND: Chemoimmunotherapy containing rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) is the standard treatment for diffuse large B-cell lymphoma (DLBCL).	Prednisolone	101-113	DNA damage inducible transcript 3	Homo sapiens	117-121
25980682-6	2016	CHOP, a key factor involved in ER stress-mediated apoptosis, was also activated by curcumin.	Curcumin	83-91	DNA damage inducible transcript 3	Homo sapiens	0-4
27330716-13	2016	The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA.	Tunicamycin	87-98	DNA damage inducible transcript 3	Homo sapiens	74-78
27330716-15	2016	CONCLUSIONS: Endoplasmic reticulum stress induced by tunicamycin increased resistin mRNA through the PERK-ATF4-CHOP pathway in THP-1 human monocytes.	Tunicamycin	53-64	DNA damage inducible transcript 3	Homo sapiens	111-115
26983803-7	2016	Tanshinone IIA also increased CHOP and activated the PERK-ATF4 pathway suggesting that tanshinone IIA increased DR5 and CHOP by activating the PERK-ATF4 pathway.	tanshinone	87-97	DNA damage inducible transcript 3	Homo sapiens	30-34
26983803-7	2016	Tanshinone IIA also increased CHOP and activated the PERK-ATF4 pathway suggesting that tanshinone IIA increased DR5 and CHOP by activating the PERK-ATF4 pathway.	tanshinone	87-97	DNA damage inducible transcript 3	Homo sapiens	120-124
27320607-9	2016	CHOP/GADD153 expression was increased 48 hours after FK506 treatment.	Tacrolimus	53-58	DNA damage inducible transcript 3	Homo sapiens	0-4
27320607-9	2016	CHOP/GADD153 expression was increased 48 hours after FK506 treatment.	Tacrolimus	53-58	DNA damage inducible transcript 3	Homo sapiens	5-12
27182548-1	2016	The data presented in this article are related to the research article entitled "14-deoxy-11,12-didehydroandrographolide induces DDIT3-dependent endoplasmic reticulum stress-mediated autophagy in T-47D breast carcinoma cells", which the mechanistic toxicology properties of 14-deoxy-11,12-didehydroandrographolide (14-DDA) were investigated (Tan et al., 2016 [1]).	14-deoxy-11,12-didehydroandrographolide	81-120	DNA damage inducible transcript 3	Homo sapiens	129-134
27009865-9	2016	Importantly, interruption of CHOP rendered HCC cells sensitive to IMB-6G-induced apoptosis via inactivation of Bim, PUMA and Bax.	IMB-6G	66-72	DNA damage inducible transcript 3	Homo sapiens	29-33
27009865-10	2016	Thus, the IRE1alpha-ASK1 and PERK-CHOP pathways may be a novel molecular mechanism of IMB-6G-induced apoptosis.	IMB-6G	86-92	DNA damage inducible transcript 3	Homo sapiens	34-38
27182548-1	2016	The data presented in this article are related to the research article entitled "14-deoxy-11,12-didehydroandrographolide induces DDIT3-dependent endoplasmic reticulum stress-mediated autophagy in T-47D breast carcinoma cells", which the mechanistic toxicology properties of 14-deoxy-11,12-didehydroandrographolide (14-DDA) were investigated (Tan et al., 2016 [1]).	14-deoxy-11,12-didehydroandrographolide	274-313	DNA damage inducible transcript 3	Homo sapiens	129-134
27182548-1	2016	The data presented in this article are related to the research article entitled "14-deoxy-11,12-didehydroandrographolide induces DDIT3-dependent endoplasmic reticulum stress-mediated autophagy in T-47D breast carcinoma cells", which the mechanistic toxicology properties of 14-deoxy-11,12-didehydroandrographolide (14-DDA) were investigated (Tan et al., 2016 [1]).	14-deoxy-11,12-didehydroandrographolide	315-321	DNA damage inducible transcript 3	Homo sapiens	129-134
26139302-5	2016	RESULTS: During February 2014, 6 patients (50% women; mean age: 61.5 years; age range: 44-76 years) admitted to the ICU of the Hospital of Pontevedra (CHOP) presented resistant E.cloacae complex isolates to extended-spectrum cephalosporins.	Cephalosporins	225-239	DNA damage inducible transcript 3	Homo sapiens	151-155
27045839-2	2016	The most common regimen, R-CHOP, consists of a combination of anthracycline- and immuno-based drugs including Rituximab.	Anthracyclines	62-75	DNA damage inducible transcript 3	Homo sapiens	27-31
26960952-4	2016	The patient was then treated with 8 cycles of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, which resulted in histological and functional improvement of her salivary glands.	Cyclophosphamide	65-81	DNA damage inducible transcript 3	Homo sapiens	48-52
26521941-6	2016	Cariporide (20 muM), a pharmacological inhibitor of NHE-1, also attenuated ERS-induced apoptosis in cardiomyocytes and CHOP protein expression, suggesting that NHE-1 plays an important role in ERS-associated apoptosis in cardiomyocytes.	cariporide	0-10	DNA damage inducible transcript 3	Homo sapiens	119-123
26931344-5	2016	RESULTS: Celecoxib (&gt;=60 microM) up-regulated the expression of ER stress markers (GRP78 and CHOP) and induced cell apoptosis accompanying with a correlated increased expression of VEGF in HT29 cells.	Celecoxib	9-18	DNA damage inducible transcript 3	Homo sapiens	96-100
26847145-7	2016	Moreover, Lico B promoted the generation of reactive oxygen species (ROS), which, in turn, can induce CHOP, death receptor (DR) 4 and DR5.	licochalcone B	10-16	DNA damage inducible transcript 3	Homo sapiens	102-106
26847145-7	2016	Moreover, Lico B promoted the generation of reactive oxygen species (ROS), which, in turn, can induce CHOP, death receptor (DR) 4 and DR5.	Reactive Oxygen Species	44-67	DNA damage inducible transcript 3	Homo sapiens	102-106
26847145-7	2016	Moreover, Lico B promoted the generation of reactive oxygen species (ROS), which, in turn, can induce CHOP, death receptor (DR) 4 and DR5.	Reactive Oxygen Species	69-72	DNA damage inducible transcript 3	Homo sapiens	102-106
26506947-5	2016	She was treated with two courses of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) for B-cell lymphoma, rituximab once every 3 weeks for five cycles, steroid pulse therapy, oral prednisolone, cyclosporin and high-dose i.v.	Prednisolone	95-107	DNA damage inducible transcript 3	Homo sapiens	111-115
27530021-2	2016	After completion of one course of rituximab plus cyclophosphamide, pirarubicin, vincristine, and prednisolone (R-CHOP) chemotherapy, the patient developed lung abscess and sepsis caused by Streptococcus intermedius.	Prednisolone	97-109	DNA damage inducible transcript 3	Homo sapiens	113-117
26787261-5	2016	Furthermore, arjunic acid upregulated the expression of endoplasmic reticulum (ER) stress proteins such as IRE1 alpha, ATF4, p-eIF2alpha, and C/EBP homologous protein (CHOP) in A549 and H460 cells.	arjunic acid	13-25	DNA damage inducible transcript 3	Homo sapiens	142-166
27015684-5	2016	In addition, Amblyomin-X promoted accumulation of ER stress markers (GRP78 and GADD153) in sensitive (SK-MEL-28) and bortezomib-resistant (Mia-PaCa-2) tumor cells.	amblyomin-x	13-24	DNA damage inducible transcript 3	Homo sapiens	79-86
27073670-1	2016	The cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) regimen is considered to be a standard treatment for non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	4-20	DNA damage inducible transcript 3	Homo sapiens	65-69
27073670-1	2016	The cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) regimen is considered to be a standard treatment for non-Hodgkin"s lymphoma (NHL).	Doxorubicin	22-33	DNA damage inducible transcript 3	Homo sapiens	65-69
27073670-1	2016	The cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) regimen is considered to be a standard treatment for non-Hodgkin"s lymphoma (NHL).	Prednisolone	51-63	DNA damage inducible transcript 3	Homo sapiens	65-69
26787261-5	2016	Furthermore, arjunic acid upregulated the expression of endoplasmic reticulum (ER) stress proteins such as IRE1 alpha, ATF4, p-eIF2alpha, and C/EBP homologous protein (CHOP) in A549 and H460 cells.	arjunic acid	13-25	DNA damage inducible transcript 3	Homo sapiens	168-172
26787261-6	2016	Conversely, CHOP depletion attenuated the increase of sub-G1 population by arjunic acid, and also JNK inhibitor SP600125 blocked the cytotoxicity and upregulation of IRE1 alpha and CHOP induced by arjunic acid in A549 and H460 cells.	arjunic acid	75-87	DNA damage inducible transcript 3	Homo sapiens	12-16
26787261-6	2016	Conversely, CHOP depletion attenuated the increase of sub-G1 population by arjunic acid, and also JNK inhibitor SP600125 blocked the cytotoxicity and upregulation of IRE1 alpha and CHOP induced by arjunic acid in A549 and H460 cells.	arjunic acid	75-87	DNA damage inducible transcript 3	Homo sapiens	181-185
26787261-6	2016	Conversely, CHOP depletion attenuated the increase of sub-G1 population by arjunic acid, and also JNK inhibitor SP600125 blocked the cytotoxicity and upregulation of IRE1 alpha and CHOP induced by arjunic acid in A549 and H460 cells.	pyrazolanthrone	112-120	DNA damage inducible transcript 3	Homo sapiens	181-185
26787261-6	2016	Conversely, CHOP depletion attenuated the increase of sub-G1 population by arjunic acid, and also JNK inhibitor SP600125 blocked the cytotoxicity and upregulation of IRE1 alpha and CHOP induced by arjunic acid in A549 and H460 cells.	arjunic acid	197-209	DNA damage inducible transcript 3	Homo sapiens	12-16
26787261-6	2016	Conversely, CHOP depletion attenuated the increase of sub-G1 population by arjunic acid, and also JNK inhibitor SP600125 blocked the cytotoxicity and upregulation of IRE1 alpha and CHOP induced by arjunic acid in A549 and H460 cells.	arjunic acid	197-209	DNA damage inducible transcript 3	Homo sapiens	181-185
26917416-7	2016	niclosamide also significantly increase activating transcription factor 3 (ATF3), activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-homologous protein (CHOP) expression in HCC cells.	Niclosamide	0-11	DNA damage inducible transcript 3	Homo sapiens	127-176
26845695-7	2016	The apoptosis ratio, the expression of GRP78, CHOP and Caspase-12 mRNA and protein and p-JNK protein increase in the H/R and TG groups, weaken in the lycopene+H/R, 4-PBA+H/R and lycopene+TG groups.	Thapsigargin	125-127	DNA damage inducible transcript 3	Homo sapiens	46-50
26847723-4	2016	Additionally, kaempferol-induced apoptosis possibly acts via the endoplasmic reticulum (ER) stress pathway, due to the significant increase in the protein expression levels of glucose-regulated protein 78, glucose-regulated protein 94, protein kinase R-like ER kinase, inositol-requiring enzyme 1alpha, partial activating transcription factor 6 cleavage, caspase-4, C/EBP homologous protein (CHOP) and cleaved caspase-3.	kaempferol	14-24	DNA damage inducible transcript 3	Homo sapiens	366-390
26847723-4	2016	Additionally, kaempferol-induced apoptosis possibly acts via the endoplasmic reticulum (ER) stress pathway, due to the significant increase in the protein expression levels of glucose-regulated protein 78, glucose-regulated protein 94, protein kinase R-like ER kinase, inositol-requiring enzyme 1alpha, partial activating transcription factor 6 cleavage, caspase-4, C/EBP homologous protein (CHOP) and cleaved caspase-3.	kaempferol	14-24	DNA damage inducible transcript 3	Homo sapiens	392-396
26847723-6	2016	Thus, kaempferol promoted HepG2 cell apoptosis via induction of the ER stress-CHOP signaling pathway.	kaempferol	6-16	DNA damage inducible transcript 3	Homo sapiens	78-82
26704305-7	2016	Resveratrol-mediated disruption of protein glycosylation induced cellular apoptosis as indicated by the up-regulation of GADD153, followed by the activation of ER-stress sensors (PERK and ATF6alpha).	Resveratrol	0-11	DNA damage inducible transcript 3	Homo sapiens	121-128
26893368-4	2016	In vitro, acute exposure to cinacalcet induced endoplasmic reticulum stress coupled to apoptosis via ATF4-CHOP-TRB3 in CaSR-positive, MYCN-amplified cells.	Cinacalcet	28-38	DNA damage inducible transcript 3	Homo sapiens	106-110
26887051-7	2016	AR-12 combined with sildenafil in a GRP78 plus HSP27 -dependent fashion to profoundly activate an eIF2alpha/ATF4/CHOP/Beclin1 pathway in parallel with inactivating mTOR and increasing ATG13 phosphorylation, collectively resulting in formation of punctate toxic autophagosomes.	OSU 03012	0-5	DNA damage inducible transcript 3	Homo sapiens	113-117
26887051-7	2016	AR-12 combined with sildenafil in a GRP78 plus HSP27 -dependent fashion to profoundly activate an eIF2alpha/ATF4/CHOP/Beclin1 pathway in parallel with inactivating mTOR and increasing ATG13 phosphorylation, collectively resulting in formation of punctate toxic autophagosomes.	Sildenafil Citrate	20-30	DNA damage inducible transcript 3	Homo sapiens	113-117
26793997-10	2016	Collectively, PTX triggers ER stress response followed by induction of autophagy via involvement of Ca(2+) CHOP Atg5 signalling cascade.	Pentoxifylline	14-17	DNA damage inducible transcript 3	Homo sapiens	107-111
26424560-0	2016	MYC and BCL-2 adjusted-International Prognostic Index (A-IPI) is a better predictor of outcome than the standard IPI for patients with diffuse large B-cell lymphoma treated with R-CHOP.	diprotin A	57-60	DNA damage inducible transcript 3	Homo sapiens	180-184
26424560-8	2016	In the era of R-CHOP treatment, MYC and BCL-2 adjusted-IPI is more powerful than the IPI for helping guide treatment planning and interpretation of clinical trials.	diprotin A	55-58	DNA damage inducible transcript 3	Homo sapiens	16-20
26584763-5	2016	We showed that cell treatment with alpha-ZOL/beta-ZOL generated endoplasmic reticulum (ER) stress and activated the Unfolded Protein Response (UPR) as evidenced by XBP1 mRNA splicing and up-regulation of GADD34, GRP78, ATF4 and CHOP.	zearalenol	35-44	DNA damage inducible transcript 3	Homo sapiens	228-232
26584763-5	2016	We showed that cell treatment with alpha-ZOL/beta-ZOL generated endoplasmic reticulum (ER) stress and activated the Unfolded Protein Response (UPR) as evidenced by XBP1 mRNA splicing and up-regulation of GADD34, GRP78, ATF4 and CHOP.	zearalenol	45-53	DNA damage inducible transcript 3	Homo sapiens	228-232
29227599-1	2016	We have studied hypoxic regulation of the expression of genes encoded GADD (growth arrest and DNAdamage) family proteins in U87 glioma cells in relation to inhibition of IRE1 (inositol requiring enzyme-1),which controls cell proliferation and tumor growth as a central mediator of endoplasmic reticulum stress.We have shown that hypoxia up-regulates the expression of GADD34, GADD45A, GADD45B, and GADD153genes, which are related to cell proliferation and apoptosis, in control (transfected by empty vector) gliomacells in gene specific manner.	gadd	70-74	DNA damage inducible transcript 3	Homo sapiens	398-405
28352766-9	2016	After the case was treated by cyclophosphamide pirarubicin vindesine dexamethasone (CHOP) chemotherapy for six courses, her clinical symptoms were partially alleviated, while CT showed progression disease.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	84-88
28352766-9	2016	After the case was treated by cyclophosphamide pirarubicin vindesine dexamethasone (CHOP) chemotherapy for six courses, her clinical symptoms were partially alleviated, while CT showed progression disease.	pirarubicin	47-58	DNA damage inducible transcript 3	Homo sapiens	84-88
28352766-9	2016	After the case was treated by cyclophosphamide pirarubicin vindesine dexamethasone (CHOP) chemotherapy for six courses, her clinical symptoms were partially alleviated, while CT showed progression disease.	vindesine dexamethasone	59-82	DNA damage inducible transcript 3	Homo sapiens	84-88
26917416-7	2016	niclosamide also significantly increase activating transcription factor 3 (ATF3), activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-homologous protein (CHOP) expression in HCC cells.	Niclosamide	0-11	DNA damage inducible transcript 3	Homo sapiens	178-182
26849807-9	2016	Rottlerin treatment also induced rapid, sustained PERK/CHOP UPR signaling.	rottlerin	0-9	DNA damage inducible transcript 3	Homo sapiens	55-59
26891914-5	2016	Administration of 2-DG increased the expression of the ER molecular chaperones GRP78 and GRP94, the prodeath protein C/EBP homology protein (CHOP) and the phosphorylation of Akt at S473, T450 and T308.	Deoxyglucose	18-22	DNA damage inducible transcript 3	Homo sapiens	117-139
26891914-5	2016	Administration of 2-DG increased the expression of the ER molecular chaperones GRP78 and GRP94, the prodeath protein C/EBP homology protein (CHOP) and the phosphorylation of Akt at S473, T450 and T308.	Deoxyglucose	18-22	DNA damage inducible transcript 3	Homo sapiens	141-145
26891914-6	2016	Combined treatment with both RSV and 2-DG reduced GRP78, GRP94 and Akt phosphorylation but increased CHOP and NB cell death when compared with the administration of 2-DG alone.	Resveratrol	29-32	DNA damage inducible transcript 3	Homo sapiens	101-105
26891914-6	2016	Combined treatment with both RSV and 2-DG reduced GRP78, GRP94 and Akt phosphorylation but increased CHOP and NB cell death when compared with the administration of 2-DG alone.	Deoxyglucose	37-41	DNA damage inducible transcript 3	Homo sapiens	101-105
26891914-7	2016	The selective inhibition of Akt activity also decreased 2-DG-induced GRP78 and GRP94 expression and increased CHOP expression, suggesting that Akt can modulate ER stress.	Deoxyglucose	56-60	DNA damage inducible transcript 3	Homo sapiens	110-114
26859847-7	2016	FKC was also found to cause endoplasmic reticulum (ER) stress, as suggested by the elevation of GADD153 protein after FKC treatment.	flavokawain C	0-3	DNA damage inducible transcript 3	Homo sapiens	96-103
26849807-12	2016	Moreover, CHOP genetic deletion, but not AMPK knock-down, prevented rottlerin-induced apoptosis and supported cell survival, suggesting that UPR signaling is a major modulator of cell fate in PaSC during metabolic stress.	rottlerin	68-77	DNA damage inducible transcript 3	Homo sapiens	10-14
26174226-0	2016	RU486 Induces Pro-Apoptotic Endoplasmic Reticulum Stress Through the Induction of CHOP Expression by Enhancing C/EBPdelta Expression in Human Renal Carcinoma Caki Cells.	Mifepristone	0-5	DNA damage inducible transcript 3	Homo sapiens	82-86
26174226-3	2016	Treatment of Caki cells with RU486 was found to induce several signature ER stress markers; including ER stress-specific XBP1 splicing, and the up-regulation of glucose-regulated protein (GRP)-78 and CCAAT/enhancer-binding protein homologous protein (CHOP) expression.	Mifepristone	29-34	DNA damage inducible transcript 3	Homo sapiens	200-249
26174226-3	2016	Treatment of Caki cells with RU486 was found to induce several signature ER stress markers; including ER stress-specific XBP1 splicing, and the up-regulation of glucose-regulated protein (GRP)-78 and CCAAT/enhancer-binding protein homologous protein (CHOP) expression.	Mifepristone	29-34	DNA damage inducible transcript 3	Homo sapiens	251-255
26174226-4	2016	RU486-induced expression of CHOP involves the putative C/EBPdelta site within the CHOP promoter region.	Mifepristone	0-5	DNA damage inducible transcript 3	Homo sapiens	28-32
26174226-4	2016	RU486-induced expression of CHOP involves the putative C/EBPdelta site within the CHOP promoter region.	Mifepristone	0-5	DNA damage inducible transcript 3	Homo sapiens	82-86
26174226-6	2016	In addition, RU486-induced CHOP expression is down-regulated by inhibition of the p38 MAPK and JNK signaling pathways at the post-translational levels.	Mifepristone	13-18	DNA damage inducible transcript 3	Homo sapiens	27-31
26174226-8	2016	Suppression of CHOP expression by CHOP siRNA attenuated RU486-induced apoptosis.	Mifepristone	56-61	DNA damage inducible transcript 3	Homo sapiens	15-19
26174226-8	2016	Suppression of CHOP expression by CHOP siRNA attenuated RU486-induced apoptosis.	Mifepristone	56-61	DNA damage inducible transcript 3	Homo sapiens	34-38
26174226-9	2016	Taken together, RU486 induces pro-apoptotic ER stress through the induction of CHOP expression.	Mifepristone	16-21	DNA damage inducible transcript 3	Homo sapiens	79-83
26784903-12	2016	Furthermore, sodium butyrate treatment markedly enhanced the expression of endoplasmic reticulum stress-associated proteins, including BIP, CHOP, PDI, and IRE-1a.	Butyric Acid	13-28	DNA damage inducible transcript 3	Homo sapiens	140-144
25557612-6	2016	In tumorigenic keratinocytes that overexpress COX-2, AEA activated the PKR-like ER kinase (PERK), inositol requiring kinase-1 (IRE1), and activating transcription factor-6 (ATF6) ER stress pathways and the ER stress apoptosis-associated proteins, C/EBP homologous protein-10 (CHOP10), caspase-12, and caspase-3.	anandamide	53-56	DNA damage inducible transcript 3	Homo sapiens	247-274
25557612-6	2016	In tumorigenic keratinocytes that overexpress COX-2, AEA activated the PKR-like ER kinase (PERK), inositol requiring kinase-1 (IRE1), and activating transcription factor-6 (ATF6) ER stress pathways and the ER stress apoptosis-associated proteins, C/EBP homologous protein-10 (CHOP10), caspase-12, and caspase-3.	anandamide	53-56	DNA damage inducible transcript 3	Homo sapiens	276-282
26816615-8	2016	The results showed that knockdown of CLIC4 with or without 100 muM adenosine triphosphate (ATP) treatment significantly increased the expression of Bax, active caspase 3, active caspase 4 and CHOP but suppressed Bcl-2 expression in HN4 cells.	Adenosine Triphosphate	67-89	DNA damage inducible transcript 3	Homo sapiens	192-196
26816615-8	2016	The results showed that knockdown of CLIC4 with or without 100 muM adenosine triphosphate (ATP) treatment significantly increased the expression of Bax, active caspase 3, active caspase 4 and CHOP but suppressed Bcl-2 expression in HN4 cells.	Adenosine Triphosphate	91-94	DNA damage inducible transcript 3	Homo sapiens	192-196
26834485-7	2016	CONCLUSION: It is generally believed that the regimen consisting of cyclophosphamide, hydroxydaunorubicin (doxorubicin), vincristine, and prednisolone (CHOP) is also applicable to ALCL.	Cyclophosphamide	68-84	DNA damage inducible transcript 3	Homo sapiens	152-156
27186398-6	2016	Our results also revealed that guggulsterone-induced apoptosis was coupled with endoplasmic reticulum stress (ERS) in CHOP-dependent pathway.	pregna-4,17-diene-3,16-dione	31-44	DNA damage inducible transcript 3	Homo sapiens	118-122
26834485-7	2016	CONCLUSION: It is generally believed that the regimen consisting of cyclophosphamide, hydroxydaunorubicin (doxorubicin), vincristine, and prednisolone (CHOP) is also applicable to ALCL.	Doxorubicin	86-105	DNA damage inducible transcript 3	Homo sapiens	152-156
26834485-7	2016	CONCLUSION: It is generally believed that the regimen consisting of cyclophosphamide, hydroxydaunorubicin (doxorubicin), vincristine, and prednisolone (CHOP) is also applicable to ALCL.	Prednisolone	138-150	DNA damage inducible transcript 3	Homo sapiens	152-156
27188649-1	2016	BACKGROUND/AIMS: Rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) every 14 days seems to achieve better outcomes than R-CHOP every 21 days in diffuse large B-cell lymphoma (DLBCL) patients.	rituximab-cyclophosphamide	17-43	DNA damage inducible transcript 3	Homo sapiens	89-93
27188649-1	2016	BACKGROUND/AIMS: Rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) every 14 days seems to achieve better outcomes than R-CHOP every 21 days in diffuse large B-cell lymphoma (DLBCL) patients.	Doxorubicin	45-56	DNA damage inducible transcript 3	Homo sapiens	89-93
27188649-1	2016	BACKGROUND/AIMS: Rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) every 14 days seems to achieve better outcomes than R-CHOP every 21 days in diffuse large B-cell lymphoma (DLBCL) patients.	Doxorubicin	45-56	DNA damage inducible transcript 3	Homo sapiens	149-153
27188649-1	2016	BACKGROUND/AIMS: Rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) every 14 days seems to achieve better outcomes than R-CHOP every 21 days in diffuse large B-cell lymphoma (DLBCL) patients.	Vincristine	58-69	DNA damage inducible transcript 3	Homo sapiens	89-93
27188649-1	2016	BACKGROUND/AIMS: Rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) every 14 days seems to achieve better outcomes than R-CHOP every 21 days in diffuse large B-cell lymphoma (DLBCL) patients.	Vincristine	58-69	DNA damage inducible transcript 3	Homo sapiens	149-153
27188649-1	2016	BACKGROUND/AIMS: Rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) every 14 days seems to achieve better outcomes than R-CHOP every 21 days in diffuse large B-cell lymphoma (DLBCL) patients.	Prednisone	75-85	DNA damage inducible transcript 3	Homo sapiens	89-93
27188649-1	2016	BACKGROUND/AIMS: Rituximab-cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) every 14 days seems to achieve better outcomes than R-CHOP every 21 days in diffuse large B-cell lymphoma (DLBCL) patients.	Prednisone	75-85	DNA damage inducible transcript 3	Homo sapiens	149-153
24675549-1	2016	This article describes the first reported case of dramatic lymphocytosis flare after initiation of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy for an indolent lymphoma.	Cyclophosphamide	118-134	DNA damage inducible transcript 3	Homo sapiens	101-105
24675549-1	2016	This article describes the first reported case of dramatic lymphocytosis flare after initiation of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy for an indolent lymphoma.	Doxorubicin	136-147	DNA damage inducible transcript 3	Homo sapiens	101-105
24675549-1	2016	This article describes the first reported case of dramatic lymphocytosis flare after initiation of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy for an indolent lymphoma.	Vincristine	149-160	DNA damage inducible transcript 3	Homo sapiens	101-105
24675549-1	2016	This article describes the first reported case of dramatic lymphocytosis flare after initiation of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy for an indolent lymphoma.	Prednisone	166-176	DNA damage inducible transcript 3	Homo sapiens	101-105
28116298-7	2016	In addition, treatment of 7,8-DHF decreased CCAAT/enhancer-binding protein homologous protein (CHOP) expression, which is a marker protein during endoplasmic reticulum (ER) stress activation.	6,7-dihydroxyflavone	26-33	DNA damage inducible transcript 3	Homo sapiens	44-93
26435364-0	2016	Influence of dose reduction of vincristine in R-CHOP on outcomes of diffuse large B cell lymphoma.	Vincristine	31-42	DNA damage inducible transcript 3	Homo sapiens	48-52
27039799-1	2016	BACKGROUND: A combination of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat B-cell non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	42-58	DNA damage inducible transcript 3	Homo sapiens	104-108
27039799-1	2016	BACKGROUND: A combination of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat B-cell non-Hodgkin"s lymphoma (NHL).	Doxorubicin	60-71	DNA damage inducible transcript 3	Homo sapiens	104-108
27039799-1	2016	BACKGROUND: A combination of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat B-cell non-Hodgkin"s lymphoma (NHL).	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	104-108
28116298-7	2016	In addition, treatment of 7,8-DHF decreased CCAAT/enhancer-binding protein homologous protein (CHOP) expression, which is a marker protein during endoplasmic reticulum (ER) stress activation.	6,7-dihydroxyflavone	26-33	DNA damage inducible transcript 3	Homo sapiens	95-99
26492567-11	2016	Combination R-CHOP with bortezomib followed by maintenance bortezomib appears to improve outcomes compared historically with R-CHOP alone, with prolonged remissions in a subset of patients.	Bortezomib	24-34	DNA damage inducible transcript 3	Homo sapiens	127-131
26809026-4	2016	Traditionally, both forms of primary systemic ALCL have been treated upfront with an anthracycline based combination chemotherapy such as CHOP.	Anthracyclines	85-98	DNA damage inducible transcript 3	Homo sapiens	138-142
26764304-5	2016	His symptoms were improved after rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) therapy.	Prednisolone	92-104	DNA damage inducible transcript 3	Homo sapiens	108-112
27383764-5	2016	Both of monocytes (%) and M-MDSCs were decreased in different R-IPI groups after 4-course of R-CHOP chemotherapy (P &lt; 0.05).	r-ipi	62-67	DNA damage inducible transcript 3	Homo sapiens	95-99
26917260-9	2016	Conversely, pretreated with salubrinal (a selective inhibition of protein phosphatase 1-mediated eIF2alpha dephosphorylation), JEG-3 cells were rescued from JMR-132-mediated cell growth inhibition, and abolished JMR-132-induced cleaved caspase-3, CHOP, phospho-p53, and ubiquitinated proteins accumulation.	salubrinal	28-38	DNA damage inducible transcript 3	Homo sapiens	247-251
27034868-10	2016	The patient was initiated on cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, demonstrating a striking response.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
27034868-10	2016	The patient was initiated on cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, demonstrating a striking response.	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	89-93
27563337-3	2016	IRE1-JNK and eIF2alpha-CHOP signaling pathways are the two important players of ER stress, which is also modulated by ROS production, calcium disturbance, and inflammatory factors.	ros	118-121	DNA damage inducible transcript 3	Homo sapiens	23-27
27563337-3	2016	IRE1-JNK and eIF2alpha-CHOP signaling pathways are the two important players of ER stress, which is also modulated by ROS production, calcium disturbance, and inflammatory factors.	Calcium	134-141	DNA damage inducible transcript 3	Homo sapiens	23-27
26986862-5	2016	We present a patient with T/myeloid mixed-phenotype acute leukemia secondary to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma.	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	152-156
26986862-11	2016	We describe a case of therapy-related T/myeloid mixed phenotype acute leukemia following rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma DLBCL.	Cyclophosphamide	100-116	DNA damage inducible transcript 3	Homo sapiens	161-165
26986862-11	2016	We describe a case of therapy-related T/myeloid mixed phenotype acute leukemia following rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma DLBCL.	Doxorubicin	118-129	DNA damage inducible transcript 3	Homo sapiens	161-165
26986862-5	2016	We present a patient with T/myeloid mixed-phenotype acute leukemia secondary to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma.	Doxorubicin	109-120	DNA damage inducible transcript 3	Homo sapiens	152-156
26986862-11	2016	We describe a case of therapy-related T/myeloid mixed phenotype acute leukemia following rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma DLBCL.	Prednisone	148-158	DNA damage inducible transcript 3	Homo sapiens	161-165
26986862-5	2016	We present a patient with T/myeloid mixed-phenotype acute leukemia secondary to rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone R-CHOP chemotherapy for primary cutaneous diffuse large B-cell lymphoma.	Prednisone	139-149	DNA damage inducible transcript 3	Homo sapiens	152-156
27665771-7	2016	Treatment with BIMP increased the mRNA levels of the ER stress marker genes binding immunoglobulin protein (BiP) and the transcription factor C/EBP homologous protein (CHOP).	bis(isopropyl methyl)phosphonate	15-19	DNA damage inducible transcript 3	Homo sapiens	142-166
27665771-7	2016	Treatment with BIMP increased the mRNA levels of the ER stress marker genes binding immunoglobulin protein (BiP) and the transcription factor C/EBP homologous protein (CHOP).	bis(isopropyl methyl)phosphonate	15-19	DNA damage inducible transcript 3	Homo sapiens	168-172
27665771-8	2016	Furthermore, BIMP increased the protein expressions and phosphorylation of BiP, CHOP, and protein kinase RNA-like ER kinase and the phosphorylation of eukaryotic translation initiation factor 2.	bis(isopropyl methyl)phosphonate	13-17	DNA damage inducible transcript 3	Homo sapiens	80-84
27665771-9	2016	Compared to BIMP treatment alone, pretreatment with the CHOP siRNA, siCHOP, decreased BIMP-dependent CHOP expression and improved CCF-STTG1 cell viability.	bis(isopropyl methyl)phosphonate	12-16	DNA damage inducible transcript 3	Homo sapiens	56-60
27665771-9	2016	Compared to BIMP treatment alone, pretreatment with the CHOP siRNA, siCHOP, decreased BIMP-dependent CHOP expression and improved CCF-STTG1 cell viability.	bis(isopropyl methyl)phosphonate	12-16	DNA damage inducible transcript 3	Homo sapiens	70-74
27665771-9	2016	Compared to BIMP treatment alone, pretreatment with the CHOP siRNA, siCHOP, decreased BIMP-dependent CHOP expression and improved CCF-STTG1 cell viability.	bis(isopropyl methyl)phosphonate	86-90	DNA damage inducible transcript 3	Homo sapiens	56-60
27665771-9	2016	Compared to BIMP treatment alone, pretreatment with the CHOP siRNA, siCHOP, decreased BIMP-dependent CHOP expression and improved CCF-STTG1 cell viability.	bis(isopropyl methyl)phosphonate	86-90	DNA damage inducible transcript 3	Homo sapiens	70-74
26867637-0	2016	Rapid Assessment of DNA Methylation Changes in Response to Salicylic Acid by Chop-qPCR.	Salicylic Acid	59-73	DNA damage inducible transcript 3	Homo sapiens	77-81
27178822-8	2016	2DG altered the N-glycosylation status of EGFR and induced the endoplasmic reticulum (ER) stress markers CHOP and BiP in vitro.	Deoxyglucose	0-3	DNA damage inducible transcript 3	Homo sapiens	105-109
26996008-7	2016	Compared with the control group, tanshinone IIA could apparently induce apoptosis of Ec-109 cells, and the level of Caspase-4 and CHOP (p &lt; 0.01) obviously increased.	tanshinone	33-47	DNA damage inducible transcript 3	Homo sapiens	130-134
27096481-5	2016	The patient was treated with multiagent cytotoxic chemotherapy, consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Prednisone	126-136	DNA damage inducible transcript 3	Homo sapiens	138-142
26885255-2	2015	The combined chemotherapy of rituximab, cyclophosphamide, Adriamycin, vincristine, and prednisone (R-CHOP) is considered as the standard therapy for DLBCL; however, nearly half of the patients become refractory to the R-CHOP regimen.	Doxorubicin	58-68	DNA damage inducible transcript 3	Homo sapiens	101-105
27057275-7	2016	Furthermore, in an animal model of ER stress involving tunicamycin, combinatorial treatment with cilostazol and probucol significantly increased the expression of HO-1 and mitochondrial biogenesis-related genes and proteins, whereas it downregulated serum ALT, eIF2 phosphorylation, and CHOP expression, as well as the lipogenesis-related genes SREBP-1c and FAS.	Cilostazol	97-107	DNA damage inducible transcript 3	Homo sapiens	287-291
27057275-7	2016	Furthermore, in an animal model of ER stress involving tunicamycin, combinatorial treatment with cilostazol and probucol significantly increased the expression of HO-1 and mitochondrial biogenesis-related genes and proteins, whereas it downregulated serum ALT, eIF2 phosphorylation, and CHOP expression, as well as the lipogenesis-related genes SREBP-1c and FAS.	Probucol	112-120	DNA damage inducible transcript 3	Homo sapiens	287-291
26559613-3	2016	In the present study we show that BMAA at low levels does not cause an acute toxicity in neuroblastoma cells but increases the expression of the ER stress marker, C/EBP homologous protein (CHOP) and increases the activity of the pro-apoptotic enzyme caspase-3.	beta-N-methylamino-L-alanine	34-38	DNA damage inducible transcript 3	Homo sapiens	163-187
26559613-3	2016	In the present study we show that BMAA at low levels does not cause an acute toxicity in neuroblastoma cells but increases the expression of the ER stress marker, C/EBP homologous protein (CHOP) and increases the activity of the pro-apoptotic enzyme caspase-3.	beta-N-methylamino-L-alanine	34-38	DNA damage inducible transcript 3	Homo sapiens	189-193
26577412-6	2015	Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation.	Carbenoxolone	0-13	DNA damage inducible transcript 3	Homo sapiens	108-112
26577412-6	2015	Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation.	Tunicamycin	25-36	DNA damage inducible transcript 3	Homo sapiens	108-112
26885255-2	2015	The combined chemotherapy of rituximab, cyclophosphamide, Adriamycin, vincristine, and prednisone (R-CHOP) is considered as the standard therapy for DLBCL; however, nearly half of the patients become refractory to the R-CHOP regimen.	Prednisone	87-97	DNA damage inducible transcript 3	Homo sapiens	101-105
26885255-2	2015	The combined chemotherapy of rituximab, cyclophosphamide, Adriamycin, vincristine, and prednisone (R-CHOP) is considered as the standard therapy for DLBCL; however, nearly half of the patients become refractory to the R-CHOP regimen.	Prednisone	87-97	DNA damage inducible transcript 3	Homo sapiens	220-224
26419929-6	2015	Furthermore, CTRP9 decreased palmitate- or tunicamycin-induced ER stress markers, such as eIF2alpha, CHOP and IRE-1, in HepG2 cells.	Tunicamycin	43-54	DNA damage inducible transcript 3	Homo sapiens	101-105
25953530-7	2015	The patient was in partial response after four cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP).	Prednisone	119-129	DNA damage inducible transcript 3	Homo sapiens	133-137
26419929-6	2015	Furthermore, CTRP9 decreased palmitate- or tunicamycin-induced ER stress markers, such as eIF2alpha, CHOP and IRE-1, in HepG2 cells.	Palmitates	29-38	DNA damage inducible transcript 3	Homo sapiens	101-105
26884853-8	2015	We concluded that CD30 may be useful as a prognostic marker in rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) treated DLBCLs, indicating favorable outcomes in a Chinese population.	Prednisone	122-132	DNA damage inducible transcript 3	Homo sapiens	136-140
26241884-5	2015	Cisplatin also upregulated ER stress-associated apoptotic protein 153/C/EBP homology protein (CHOP) in SKOV3 cells.	Cisplatin	0-9	DNA damage inducible transcript 3	Homo sapiens	66-92
26241884-5	2015	Cisplatin also upregulated ER stress-associated apoptotic protein 153/C/EBP homology protein (CHOP) in SKOV3 cells.	Cisplatin	0-9	DNA damage inducible transcript 3	Homo sapiens	94-98
26241884-6	2015	While treatment with 2-DG alone could not upregulate the CHOP expression, a combination of both 2-DG and cisplatin increased the protein levels of CHOP above those induced by Cisplatin alone.	Deoxyglucose	96-100	DNA damage inducible transcript 3	Homo sapiens	147-151
26241884-6	2015	While treatment with 2-DG alone could not upregulate the CHOP expression, a combination of both 2-DG and cisplatin increased the protein levels of CHOP above those induced by Cisplatin alone.	Cisplatin	105-114	DNA damage inducible transcript 3	Homo sapiens	147-151
26241884-6	2015	While treatment with 2-DG alone could not upregulate the CHOP expression, a combination of both 2-DG and cisplatin increased the protein levels of CHOP above those induced by Cisplatin alone.	Cisplatin	175-184	DNA damage inducible transcript 3	Homo sapiens	147-151
26248489-5	2015	The results showed that meglumine diatrizoate caused significant cell apoptosis by up-regulating the expression of ER stress markers, including glucose-regulated protein 78 (GRP78), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein-homologous protein (CHOP) and caspase 12, in a time- and dose-dependent manner, which could be alleviated by preincubation with valsartan.	Diatrizoate Meglumine	24-45	DNA damage inducible transcript 3	Homo sapiens	224-273
26248489-5	2015	The results showed that meglumine diatrizoate caused significant cell apoptosis by up-regulating the expression of ER stress markers, including glucose-regulated protein 78 (GRP78), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein-homologous protein (CHOP) and caspase 12, in a time- and dose-dependent manner, which could be alleviated by preincubation with valsartan.	Diatrizoate Meglumine	24-45	DNA damage inducible transcript 3	Homo sapiens	275-279
25172906-10	2015	The expression of GRP78 and CHOP increased in the simple scald and scald and 50 mug/kg dexmedetomidine groups (p &lt; 0.05).	Dexmedetomidine	87-102	DNA damage inducible transcript 3	Homo sapiens	28-32
26486079-5	2015	Inhibition of both AMPK and PERK/CHOP pathways by siRNA or chemical inhibitor could block CGK733-induced p21Waf1/Cip1 expression as well as caspase-3 cleavage.	CGK 733	90-96	DNA damage inducible transcript 3	Homo sapiens	33-37
26546056-8	2015	The reduction of CHOP expression by siRNA partially abrogated WZ35-induced cell apoptosis.	wz35	62-66	DNA damage inducible transcript 3	Homo sapiens	17-21
26885117-3	2015	This study aimed to investigate the effect of atorvastatin on the ATF4-CHOP-TRIB3 pathway.	Atorvastatin	46-58	DNA damage inducible transcript 3	Homo sapiens	71-75
26885117-11	2015	CONCLUSIONS: Atorvastatin has an effect on ER stress through ATF4-CHOP pathway.	Atorvastatin	13-25	DNA damage inducible transcript 3	Homo sapiens	66-70
26396188-8	2015	Additionally, polyamine depletion resulted in elevation of mRNA and protein levels of the stress-induced C/EBP homologous protein (CHOP), whose dominant negative function is known to inhibit C/EBPbeta DNA binding activity.	Polyamines	14-23	DNA damage inducible transcript 3	Homo sapiens	105-129
26396188-9	2015	Conditional knockdown of CHOP in polyamine-depleted preadipocytes restored PPARgamma and C/EBPalpha expression, but failed to recover MCE and differentiation.	Polyamines	33-42	DNA damage inducible transcript 3	Homo sapiens	25-29
26396188-11	2015	We conclude that de novo synthesis of polyamines during adipogenesis is required for down-regulation of CHOP to allow C/EBPbeta activation, and for promoting MCE.	Polyamines	38-48	DNA damage inducible transcript 3	Homo sapiens	104-108
26396188-8	2015	Additionally, polyamine depletion resulted in elevation of mRNA and protein levels of the stress-induced C/EBP homologous protein (CHOP), whose dominant negative function is known to inhibit C/EBPbeta DNA binding activity.	Polyamines	14-23	DNA damage inducible transcript 3	Homo sapiens	131-135
26349783-6	2015	Chaetocin treatment activated endoplasmic reticulum (ER) stress which gave rise to the up-regulation of ATF3 and CHOP.	chaetocin	0-9	DNA damage inducible transcript 3	Homo sapiens	113-117
26349783-10	2015	In summary, chaetocin pharmacologically inhibits the activity of SUV39H1 which provokes ER stress and results in up-regulation of ATF3 and CHOP, leading to DR5-dependent apoptosis eventually.	chaetocin	12-21	DNA damage inducible transcript 3	Homo sapiens	139-143
26887774-11	2015	RESULTS: (1) The mRNA expressions of GRP78, beclin1, Bcl-2 and CHOP in the group of BAPTA-AM were 0.583+-0.025, 0.860+-0.055, 0.714+-0.032 and 0.811+-0.004, respectively.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	84-92	DNA damage inducible transcript 3	Homo sapiens	63-67
26540043-5	2015	MEAO significantly inhibited tunicamycin-induced ER stress marker expression including GRP78, CHOP, and XBP-1 in tunicamycin-treated Human hepatocellular carcinoma (HepG2) cells and the livers of tunicamycin-injected mice.	meao	0-4	DNA damage inducible transcript 3	Homo sapiens	94-98
26540043-5	2015	MEAO significantly inhibited tunicamycin-induced ER stress marker expression including GRP78, CHOP, and XBP-1 in tunicamycin-treated Human hepatocellular carcinoma (HepG2) cells and the livers of tunicamycin-injected mice.	Tunicamycin	29-40	DNA damage inducible transcript 3	Homo sapiens	94-98
26134454-5	2015	We show that ZEN treatment induces ER stress and activates the unfolded protein response (UPR) as evidenced by XBP1 mRNA splicing and upregulation of GRP78, ATF4, GADD34, PDIA6, and CHOP.	Zearalenone	13-16	DNA damage inducible transcript 3	Homo sapiens	182-186
26305886-7	2015	ER stress marker CHOP was strongly induced and the two upstream ER stress signalling events XBP1-mRNA splicing and eukaryotic initiation factor 2 A (eIF2alpha) phosphorylation were activated by mitotane in NCI-H295 cells but to a much lesser extent in four nonsteroidogenic cell lines.	Mitotane	194-202	DNA damage inducible transcript 3	Homo sapiens	17-21
26246051-10	2015	Zerumbone induced mitochondrial damage and endoplasmic reticulum (ER) stress as evidenced by the loss of mitochondrial membrane potential and upregulation of GRP-78 and CHOP/GADD153 expression.	zerumbone	0-9	DNA damage inducible transcript 3	Homo sapiens	169-173
26246051-10	2015	Zerumbone induced mitochondrial damage and endoplasmic reticulum (ER) stress as evidenced by the loss of mitochondrial membrane potential and upregulation of GRP-78 and CHOP/GADD153 expression.	zerumbone	0-9	DNA damage inducible transcript 3	Homo sapiens	174-181
26887774-14	2015	While the protein expressions of GRP78, beclin1, Bcl-2 and CHOP in the group of BAPTA-AM were 0.423+-0.035, 0.952+-0.022, 0.385+-0.032, 0.681+-0.095, respectively.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	80-88	DNA damage inducible transcript 3	Homo sapiens	59-63
26370079-9	2015	Consistently, TLR4 activation by LPS abolished cAMP-induced up-regulation of uncoupling protein 1 (UCP1) in primary human adipocytes, which was reversed by silencing of C/EBP homologous protein (CHOP).	Cyclic AMP	47-51	DNA damage inducible transcript 3	Homo sapiens	169-193
26370079-9	2015	Consistently, TLR4 activation by LPS abolished cAMP-induced up-regulation of uncoupling protein 1 (UCP1) in primary human adipocytes, which was reversed by silencing of C/EBP homologous protein (CHOP).	Cyclic AMP	47-51	DNA damage inducible transcript 3	Homo sapiens	195-199
26887774-15	2015	The protein expressions of GRP78, beclin1, Bcl-2 and CHOP in the group of A23187 were 0.743+-0.032, 0.638+-0.025, 0.596+-0.029, 0.431+-0.095, respectively.	Calcimycin	74-80	DNA damage inducible transcript 3	Homo sapiens	53-57
26887774-17	2015	The mRNA and protein expressions of beclin and CHOP in the group of BAPTA-AM were both higher than those in the control group (P&lt;0.05).	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	68-76	DNA damage inducible transcript 3	Homo sapiens	47-51
26887774-26	2015	CONCLUSION: GRP78 could regulate autophagy and apoptosis of ovarian cancer cells by regulating the expressions of beclin1, Bcl-2 and CHOP, thereby affecting the sensitivity to cisplatin in ovarian carcinoma, which may be a new method for the treatment and improvement of the sensitivity to cisplatin in ovarian carcinoma.	Cisplatin	176-185	DNA damage inducible transcript 3	Homo sapiens	133-137
26770342-5	2015	The addition of R to standard CHOP were showed to increase the proportion of CR (RR=1.23, 95% CI=1.13-1.35, P&lt;0.00001) and OR (RR=1.39, 95% CI=1.24-1.55, P&lt;0.00001) in a fixed-effect model, indicating that rituximab combined with CHOP regimen is efficacy than CHOP alone.	Chromium	77-79	DNA damage inducible transcript 3	Homo sapiens	30-34
26459308-6	2015	Furthermore, increased levels of GADD153/CHOP and GRP78 indicated hesperidin-induced apoptosis in HeLa cells involved a caspase-dependent pathway, presumably downstream of the endoplasmic reticulum stress pathway.	Hesperidin	66-76	DNA damage inducible transcript 3	Homo sapiens	33-40
26459308-6	2015	Furthermore, increased levels of GADD153/CHOP and GRP78 indicated hesperidin-induced apoptosis in HeLa cells involved a caspase-dependent pathway, presumably downstream of the endoplasmic reticulum stress pathway.	Hesperidin	66-76	DNA damage inducible transcript 3	Homo sapiens	41-45
26225471-8	2015	In conclusion, these findings provide evidence that under the celecoxib treatment, GRP78 plays a protective role by modulating Akt activation and abrogating CHOP expression.	Celecoxib	62-71	DNA damage inducible transcript 3	Homo sapiens	157-161
26275811-0	2015	Farnesol activates the intrinsic pathway of apoptosis and the ATF4-ATF3-CHOP cascade of ER stress in human T lymphoblastic leukemia Molt4 cells.	Farnesol	0-8	DNA damage inducible transcript 3	Homo sapiens	72-76
26275811-4	2015	Analysis of the gene expression profiles by microarray analysis revealed that farnesol increased the expression of several genes related to the unfolded protein response (UPR), including CHOP and CHAC1.	Farnesol	78-86	DNA damage inducible transcript 3	Homo sapiens	187-191
26439795-5	2015	Esculetin also induced the expression of the CCAAT/enhancer-binding protein-homologous protein (CHOP) and pro-apoptotic factors caspase-12.	esculetin	0-9	DNA damage inducible transcript 3	Homo sapiens	45-94
26439795-5	2015	Esculetin also induced the expression of the CCAAT/enhancer-binding protein-homologous protein (CHOP) and pro-apoptotic factors caspase-12.	esculetin	0-9	DNA damage inducible transcript 3	Homo sapiens	96-100
26439795-6	2015	Moreover, transfection of colon cancer cells with a small interfering ribonucleic acid targeting CHOP attenuated esculetin-induced apoptosis.	esculetin	113-122	DNA damage inducible transcript 3	Homo sapiens	97-101
26314270-7	2015	Second, PA time-dependently activated the pro-apoptotic ER stress pathway, as evidenced by increased expression levels of BiP, CHOP, IRE1-alpha, phospho-PERK, and phospho-JNK.	podophyllotoxin acetate	8-10	DNA damage inducible transcript 3	Homo sapiens	127-131
26238415-4	2015	As compared with the effects of the parent molecule, 3-O-HT glucuronide and 4-O-HT glucuronide at 10 muM and 25 muM alone induced a milder change in mRNA expression levels of both CCAAT-enhancer-binding protein homologous protein (CHOP) and glucose regulated protein GRP78 immunoglobulin heavy chain binding protein (BiP).	3-O-hydroxytyrosol glucuronide	53-71	DNA damage inducible transcript 3	Homo sapiens	180-229
26238415-4	2015	As compared with the effects of the parent molecule, 3-O-HT glucuronide and 4-O-HT glucuronide at 10 muM and 25 muM alone induced a milder change in mRNA expression levels of both CCAAT-enhancer-binding protein homologous protein (CHOP) and glucose regulated protein GRP78 immunoglobulin heavy chain binding protein (BiP).	3-O-hydroxytyrosol glucuronide	53-71	DNA damage inducible transcript 3	Homo sapiens	231-235
26238415-4	2015	As compared with the effects of the parent molecule, 3-O-HT glucuronide and 4-O-HT glucuronide at 10 muM and 25 muM alone induced a milder change in mRNA expression levels of both CCAAT-enhancer-binding protein homologous protein (CHOP) and glucose regulated protein GRP78 immunoglobulin heavy chain binding protein (BiP).	Glucuronides	60-71	DNA damage inducible transcript 3	Homo sapiens	180-229
26238415-4	2015	As compared with the effects of the parent molecule, 3-O-HT glucuronide and 4-O-HT glucuronide at 10 muM and 25 muM alone induced a milder change in mRNA expression levels of both CCAAT-enhancer-binding protein homologous protein (CHOP) and glucose regulated protein GRP78 immunoglobulin heavy chain binding protein (BiP).	Glucuronides	60-71	DNA damage inducible transcript 3	Homo sapiens	231-235
26259235-0	2015	PERK/CHOP contributes to the CGK733-induced vesicular calcium sequestration which is accompanied by non-apoptotic cell death.	Calcium	54-61	DNA damage inducible transcript 3	Homo sapiens	5-9
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	92-96
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Cyclophosphamide	30-46	DNA damage inducible transcript 3	Homo sapiens	206-210
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Doxorubicin	48-59	DNA damage inducible transcript 3	Homo sapiens	92-96
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Doxorubicin	48-59	DNA damage inducible transcript 3	Homo sapiens	206-210
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Prednisone	78-88	DNA damage inducible transcript 3	Homo sapiens	92-96
26315113-1	2015	Treatment with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has greatly improved clinical outcomes in patients with diffuse large B-cell lymphoma (DLBCL) compared with CHOP.	Prednisone	78-88	DNA damage inducible transcript 3	Homo sapiens	206-210
26458444-2	2015	The current standard therapy for DLBCL is R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, which allows many patients to achieve disease cure.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	44-48
26458444-2	2015	The current standard therapy for DLBCL is R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, which allows many patients to achieve disease cure.	Doxorubicin	79-90	DNA damage inducible transcript 3	Homo sapiens	44-48
26458444-2	2015	The current standard therapy for DLBCL is R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, which allows many patients to achieve disease cure.	Vincristine	92-103	DNA damage inducible transcript 3	Homo sapiens	44-48
26458444-2	2015	The current standard therapy for DLBCL is R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone) therapy, which allows many patients to achieve disease cure.	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	44-48
26259235-4	2015	Ionomycin, an ER stress drug and calcium ionophore, can activate PERK/CHOP signaling and accelerate CGK733-induced calcium sequestration.	Ionomycin	0-9	DNA damage inducible transcript 3	Homo sapiens	70-74
26259235-4	2015	Ionomycin, an ER stress drug and calcium ionophore, can activate PERK/CHOP signaling and accelerate CGK733-induced calcium sequestration.	Calcium	33-40	DNA damage inducible transcript 3	Homo sapiens	70-74
26259235-5	2015	Knockdown of CHOP diminished CGK733-induced vesicular calcium sequestration, but had no effects on the cell death.	Calcium	54-61	DNA damage inducible transcript 3	Homo sapiens	13-17
26259235-7	2015	Our study reveals that CGK733-induced intracellular calcium sequestration is correlated with the PERK/CHOP signaling pathway and may also be involved in the dysregulations of calcium-binding proteins.	Calcium	52-59	DNA damage inducible transcript 3	Homo sapiens	102-106
26355342-10	2015	In contrast, the LPS challenge is blocked by the ER stress inhibitor TUDCA, resulting in: CHOP downregulation, reduced caspase-1, caspase-11, caspase-3 activities, lowered interleukin-1beta secretion and rescue from cell death.	ursodoxicoltaurine	69-74	DNA damage inducible transcript 3	Homo sapiens	90-94
26370464-1	2015	BACKGROUND: The regimen of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is an efficient treatment of non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	27-43	DNA damage inducible transcript 3	Homo sapiens	89-93
26370464-1	2015	BACKGROUND: The regimen of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is an efficient treatment of non-Hodgkin"s lymphoma (NHL).	Doxorubicin	45-56	DNA damage inducible transcript 3	Homo sapiens	89-93
26370464-1	2015	BACKGROUND: The regimen of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is an efficient treatment of non-Hodgkin"s lymphoma (NHL).	Prednisolone	75-87	DNA damage inducible transcript 3	Homo sapiens	89-93
26353013-10	2015	We demonstrated that EBR treatment downregulated calnexin and upregulated BiP and IRE1alpha expression levels and induced CHOP translocation from the cytoplasm to nucleus.	EBR	21-24	DNA damage inducible transcript 3	Homo sapiens	122-126
26353013-11	2015	The translocation of CHOP was associated with caspase-9 and caspase-3 activation after a 12 h EBR treatment.	EBR	94-97	DNA damage inducible transcript 3	Homo sapiens	21-25
26617965-0	2015	Borrelidin Induces the Unfolded Protein Response in Oral Cancer Cells and Chop-Dependent Apoptosis.	borrelidin	0-10	DNA damage inducible transcript 3	Homo sapiens	74-78
26049256-4	2015	Furthermore, ICA treatment increased the expression of ERS-related molecules (p-PERK, ATF6, GRP78, p-eIF2alpha, and CHOP), up-regulated the apoptosis-related protein PUMA and down-regulated the anti-apoptosis-related protein Bcl2.	icariin	13-16	DNA damage inducible transcript 3	Homo sapiens	116-120
26049256-6	2015	Additionally, ICA inhibited the growth of human lung adenocarcinoma A549 cell xenografts by increasing the expression of ERS-related molecules (p-PERK and CHOP), up-regulating PUMA, and down-regulating Bcl2.	icariin	14-17	DNA damage inducible transcript 3	Homo sapiens	155-159
25666327-4	2015	We present a 52-year-old male with lymphoma who was treated with R-CHOP (R: Rituximab; C: Cyclophosphamide; H: Doxorubicin; O: Vincristine; P: Prednisone).	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	67-71
25701954-7	2015	We further detected the upregulated expression of CAAT/enhancer binding protein homologous protein (CHOP) in DHA-treated HCT-116 cells.	artenimol	109-112	DNA damage inducible transcript 3	Homo sapiens	100-104
25701954-8	2015	Conversely, silencing CHOP resulted in a decrease of DHA-induced apoptosis.	artenimol	53-56	DNA damage inducible transcript 3	Homo sapiens	22-26
25701954-11	2015	Overall, our data indicated that DHA triggered endoplasmic reticulum (ER) stress through inhibiting SERCA activity to release intracellular Ca(2+) from ER, the upregulated expression of CHOP activated mitochondrial apoptosis pathway to induce apoptosis of HCT-116 cells.	artenimol	33-36	DNA damage inducible transcript 3	Homo sapiens	186-190
26617729-7	2015	Administration of cisplatin substantially increased the levels of GRP78 and CHOP.	Cisplatin	18-27	DNA damage inducible transcript 3	Homo sapiens	76-80
25544670-4	2015	RESULTS AND DISCUSSION: The combination of GTE and NSAIDs synergistically inhibited tumor development in rodents through the activation of the GADD153-DR5-TRAIL apoptotic pathway.	epigallocatechin gallate	43-46	DNA damage inducible transcript 3	Homo sapiens	143-150
25998512-3	2015	METHODS: Patients who were newly diagnosed with DLBCL and treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) were analysed.	Prednisone	133-143	DNA damage inducible transcript 3	Homo sapiens	147-151
26035406-7	2015	CONCLUSIONS: The NCCN-IPI retains its prognostic value in diffuse large B-cell lymphoma patients with F-fluoro-2-deoxy-d-glucose positron emission tomography-based complete response after first-line R-CHOP therapy.	diprotin A	22-25	DNA damage inducible transcript 3	Homo sapiens	201-205
25666327-4	2015	We present a 52-year-old male with lymphoma who was treated with R-CHOP (R: Rituximab; C: Cyclophosphamide; H: Doxorubicin; O: Vincristine; P: Prednisone).	Doxorubicin	111-122	DNA damage inducible transcript 3	Homo sapiens	67-71
25666327-4	2015	We present a 52-year-old male with lymphoma who was treated with R-CHOP (R: Rituximab; C: Cyclophosphamide; H: Doxorubicin; O: Vincristine; P: Prednisone).	Vincristine	127-138	DNA damage inducible transcript 3	Homo sapiens	67-71
25801913-7	2015	As with HDAC4 knockdown, TMP269 significantly enhanced cytotoxicity induced by CFZ in MM cell lines, upregulating ATF4 and CHOP and inducing apoptosis.	A 269A	25-31	DNA damage inducible transcript 3	Homo sapiens	123-127
26376594-2	2015	We present a 64-year-old man who was treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone) chemoimmunotherapy for mantle cell lymphoma and developed purulent meningitis, probably caused by Leuconostoc sp.	Cyclophosphamide	73-89	DNA damage inducible transcript 3	Homo sapiens	52-56
26264395-7	2015	O-demethyldemethoxycurcumin also downregulated the expression of ER stress signaling proteins, including the phosphorylation of PKR-like endoplasmic reticulum kinase (p-PERK), the phosphorylation of inositol-requiring enzyme 1 (p-IRE1), activating transcription factor 6 (ATF6), binding immunoglobulin protein (BiP) and C/EBP homologous protein (CHOP).	O-demethyldemethoxycurcumin	0-27	DNA damage inducible transcript 3	Homo sapiens	320-344
26264395-7	2015	O-demethyldemethoxycurcumin also downregulated the expression of ER stress signaling proteins, including the phosphorylation of PKR-like endoplasmic reticulum kinase (p-PERK), the phosphorylation of inositol-requiring enzyme 1 (p-IRE1), activating transcription factor 6 (ATF6), binding immunoglobulin protein (BiP) and C/EBP homologous protein (CHOP).	O-demethyldemethoxycurcumin	0-27	DNA damage inducible transcript 3	Homo sapiens	346-350
25916210-8	2015	Western blot analysis revealed that the levels of intrinsic-related apoptotic proteins Bax and extrinsic-related proteins (DR5, CHOP) were significantly increased in nimbolide-treated 786-O and A-498 cells.	nimbolide	166-175	DNA damage inducible transcript 3	Homo sapiens	128-132
26376594-2	2015	We present a 64-year-old man who was treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone) chemoimmunotherapy for mantle cell lymphoma and developed purulent meningitis, probably caused by Leuconostoc sp.	Prednisolone	121-133	DNA damage inducible transcript 3	Homo sapiens	52-56
25844964-5	2015	gamma-Tocotrienol treatment was also found to cause a decrease in mitogenic Erk1/2 signaling, an increase in stress-dependent p38 and JNK1/2 signaling, as well as an increase in ER stress apoptotic markers, including phospho-PERK, phospho-eIF2alpha, Bip, IRE1alpha, ATF-4, CHOP, and TRB3.	plastochromanol 8	0-17	DNA damage inducible transcript 3	Homo sapiens	273-277
26307968-7	2015	Furthermore, treating the cells with the ER stress inhibitors 4-phenylbutyrate (4-PBA) or knocking down CHOP, using lentivirus encoded short hairpin interfering RNAs (shRNAs), significantly diminished the ZEA-induced increases in GRP78 and CHOP, and cell death.	Zearalenone	205-208	DNA damage inducible transcript 3	Homo sapiens	104-108
26307968-7	2015	Furthermore, treating the cells with the ER stress inhibitors 4-phenylbutyrate (4-PBA) or knocking down CHOP, using lentivirus encoded short hairpin interfering RNAs (shRNAs), significantly diminished the ZEA-induced increases in GRP78 and CHOP, and cell death.	Zearalenone	205-208	DNA damage inducible transcript 3	Homo sapiens	240-244
26307968-8	2015	In summary, our results suggest that ZEA induces the apoptosis and necrosis of RAW 264.7 macrophages in a dose- and time-dependent manner via the ER stress pathway in which the activation of CHOP plays a critical role.	Zearalenone	37-40	DNA damage inducible transcript 3	Homo sapiens	191-195
26203587-14	2015	In addition, the quenching of ROS using NAC prevented the induction of JNK phosphorylation and CHOP induction.	ros	30-33	DNA damage inducible transcript 3	Homo sapiens	95-99
26247732-2	2015	Herein we demonstrated evidence that CHOP-related ER stress is associated with the development of renal fibrosis in both CKD patients and unilateral ureteral obstruction (UUO)-induced animals, and specifically, mice deficient in Chop were protected from UUO-induced renal fibrosis.	uuo	171-174	DNA damage inducible transcript 3	Homo sapiens	37-41
25958041-9	2015	Along with the induction of FABP4 and apoptosis, GRP78 and its three sensors as well as C/EBP homologous protein (CHOP) and Caspase-12 were induced in HMCs treated with NEFA or high glucose and these responses were attenuated or even abrogated by treating with FABP4 inhibitor or FABP4 siRNA.	Fatty Acids, Nonesterified	169-173	DNA damage inducible transcript 3	Homo sapiens	88-112
25958041-9	2015	Along with the induction of FABP4 and apoptosis, GRP78 and its three sensors as well as C/EBP homologous protein (CHOP) and Caspase-12 were induced in HMCs treated with NEFA or high glucose and these responses were attenuated or even abrogated by treating with FABP4 inhibitor or FABP4 siRNA.	Fatty Acids, Nonesterified	169-173	DNA damage inducible transcript 3	Homo sapiens	114-118
25958041-9	2015	Along with the induction of FABP4 and apoptosis, GRP78 and its three sensors as well as C/EBP homologous protein (CHOP) and Caspase-12 were induced in HMCs treated with NEFA or high glucose and these responses were attenuated or even abrogated by treating with FABP4 inhibitor or FABP4 siRNA.	Glucose	182-189	DNA damage inducible transcript 3	Homo sapiens	88-112
25958041-9	2015	Along with the induction of FABP4 and apoptosis, GRP78 and its three sensors as well as C/EBP homologous protein (CHOP) and Caspase-12 were induced in HMCs treated with NEFA or high glucose and these responses were attenuated or even abrogated by treating with FABP4 inhibitor or FABP4 siRNA.	Glucose	182-189	DNA damage inducible transcript 3	Homo sapiens	114-118
25857226-0	2015	CHOP mediates XBP1S-induced renal mesangial cell necrosis following high glucose treatment.	Glucose	73-80	DNA damage inducible transcript 3	Homo sapiens	0-4
26081590-7	2015	Furthermore, TUDCA decreased SAN-induced ROS production, and NAC attenuated SAN-induced GRP78 and CHOP expression.	Acetylcysteine	61-64	DNA damage inducible transcript 3	Homo sapiens	98-102
26314441-4	2015	RESULTS: In CHOP group 16 patients achieved CR+PR, the total remission rate (TRR) was 47.06%; in ASP+CHOP group 24 patients achieved CR+PR, the TRR was 70.58%, and the TRR in ASP+CHOP group was higher than that in CHOP group, there was statistical significance between these 2 groups (X(2) = 3.886, P &lt; 0.05).	Praseodymium	47-49	DNA damage inducible transcript 3	Homo sapiens	12-16
26314441-5	2015	The time of PFS in CHOP group was 24.7 months, and the time of PFS in ASP+CHOP group was 47.5 months which was significantly longer than that in CHOP group, and there was statistical siguificance between these 2 groups (P &lt; 0.05).	Aspartic Acid	70-73	DNA damage inducible transcript 3	Homo sapiens	74-78
26314441-5	2015	The time of PFS in CHOP group was 24.7 months, and the time of PFS in ASP+CHOP group was 47.5 months which was significantly longer than that in CHOP group, and there was statistical siguificance between these 2 groups (P &lt; 0.05).	Aspartic Acid	70-73	DNA damage inducible transcript 3	Homo sapiens	74-78
26314441-12	2015	The grade II serum creatinine was elevated in 2 cases of ASP+CHOP group and in 1 case of CHOP group who was inproved after symptomatic therapy.	Creatinine	19-29	DNA damage inducible transcript 3	Homo sapiens	61-65
26314441-12	2015	The grade II serum creatinine was elevated in 2 cases of ASP+CHOP group and in 1 case of CHOP group who was inproved after symptomatic therapy.	Creatinine	19-29	DNA damage inducible transcript 3	Homo sapiens	89-93
26284193-7	2015	The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM).	Reactive Oxygen Species	260-263	DNA damage inducible transcript 3	Homo sapiens	45-49
26284193-7	2015	The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM).	Reactive Oxygen Species	260-263	DNA damage inducible transcript 3	Homo sapiens	50-57
26284193-7	2015	The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM).	phenethyl isothiocyanate	288-293	DNA damage inducible transcript 3	Homo sapiens	45-49
26284193-7	2015	The key regulator of UPR-mediated apoptosis, CHOP/GADD153 and endoplasmic reticulum resident chaperone BiP/GRP78 were parallely up-regulated with activation of two major sensors of the UPR [PERK and ATF-6 in PA-1; PERK, and IRE1alpha in SKOV-3) in response to ROS accumulation induced by PEITC (5 muM).	phenethyl isothiocyanate	288-293	DNA damage inducible transcript 3	Homo sapiens	50-57
26284193-8	2015	ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the effect of PEITC on UPR signatures (P-PERK, IRE1alpha, CHOP/GADD153, and BiP/GRP78), suggesting the involvement of ROS in UPR-mediated apoptosis.	Reactive Oxygen Species	0-3	DNA damage inducible transcript 3	Homo sapiens	111-115
26284193-8	2015	ROS scavenger, N-acetyl-L-cysteine (NAC), attenuated the effect of PEITC on UPR signatures (P-PERK, IRE1alpha, CHOP/GADD153, and BiP/GRP78), suggesting the involvement of ROS in UPR-mediated apoptosis.	Reactive Oxygen Species	0-3	DNA damage inducible transcript 3	Homo sapiens	116-123
26116180-0	2015	Identification of 5-nitrofuran-2-amide derivatives that induce apoptosis in triple negative breast cancer cells by activating C/EBP-homologous protein expression.	5-nitrofuran-2-amide	18-38	DNA damage inducible transcript 3	Homo sapiens	126-150
26116180-4	2015	Here, we identified 5-nitrofuran-2-amide derivatives as small molecule activators of CHOP expression that induced apoptosis in triple negative breast cancer (TNBC) cells.	5-nitrofuran-2-amide	20-40	DNA damage inducible transcript 3	Homo sapiens	85-89
25899891-0	2015	Nonpegylated Liposomal Doxorubicin as a Component of R-CHOP Is an Effective and Safe Alternative to Conventional Doxorubicin in the Treatment of Patients With Diffuse Large B-Cell Lymphoma and Preexisting Cardiac Diseases.	Doxorubicin	23-34	DNA damage inducible transcript 3	Homo sapiens	55-59
26710957-6	2015	Then the protein expression level of CCAAT/enhancer binding protein homologous protein (CHOP) was measured by Western blot to define the effect of various concentrations of nicotine and different dosing periods of nicotine on the protein expression level of CHOP.	Nicotine	173-181	DNA damage inducible transcript 3	Homo sapiens	37-86
26710957-6	2015	Then the protein expression level of CCAAT/enhancer binding protein homologous protein (CHOP) was measured by Western blot to define the effect of various concentrations of nicotine and different dosing periods of nicotine on the protein expression level of CHOP.	Nicotine	173-181	DNA damage inducible transcript 3	Homo sapiens	88-92
26710957-6	2015	Then the protein expression level of CCAAT/enhancer binding protein homologous protein (CHOP) was measured by Western blot to define the effect of various concentrations of nicotine and different dosing periods of nicotine on the protein expression level of CHOP.	Nicotine	173-181	DNA damage inducible transcript 3	Homo sapiens	258-262
26710957-6	2015	Then the protein expression level of CCAAT/enhancer binding protein homologous protein (CHOP) was measured by Western blot to define the effect of various concentrations of nicotine and different dosing periods of nicotine on the protein expression level of CHOP.	Nicotine	214-222	DNA damage inducible transcript 3	Homo sapiens	37-86
26710957-6	2015	Then the protein expression level of CCAAT/enhancer binding protein homologous protein (CHOP) was measured by Western blot to define the effect of various concentrations of nicotine and different dosing periods of nicotine on the protein expression level of CHOP.	Nicotine	214-222	DNA damage inducible transcript 3	Homo sapiens	88-92
26710957-6	2015	Then the protein expression level of CCAAT/enhancer binding protein homologous protein (CHOP) was measured by Western blot to define the effect of various concentrations of nicotine and different dosing periods of nicotine on the protein expression level of CHOP.	Nicotine	214-222	DNA damage inducible transcript 3	Homo sapiens	258-262
26710957-10	2015	RESULTS: Nicotine could concentration and time-dependently improve the expression of CHOP in 16HBE cells.	Nicotine	9-17	DNA damage inducible transcript 3	Homo sapiens	85-89
26710957-11	2015	The ratio of CHOP to average absorbance of glyceraldehyde phosphate dehydrogenase (GAPDH) was significantly higher in 40 micromol/L nicotine group than that in control group (1.04 +- 0.32 vs 0.30 +- 0.17, P &lt; 0.05).	Nicotine	132-140	DNA damage inducible transcript 3	Homo sapiens	13-17
26394465-3	2015	In the Archean hydrothermal conditions under the action of the phosphorus chemical potential the C-H-O system was transformed into a four-component system C-H-O-P setting up a gluconeogenic system, which became the basis of power supply for a protometabolism, and formation of a new cycle of CO2 fixation (reductive pentose phosphate pathway).	N2,N6-bis(4-(2-aminoethoxy)quinolin-2-yl)-4-((4-fluorobenzyl)oxy)pyridine-2,6-dicarboxamide	292-295	DNA damage inducible transcript 3	Homo sapiens	155-162
25869285-7	2015	Anthracycline-based regimens such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remain the standard first-line treatment choice for systemic ALCL, but in many patients with ALK- ALCL, it is ineffective, and thus it is often followed by consolidative autologous stem cell transplantation.	Anthracyclines	0-13	DNA damage inducible transcript 3	Homo sapiens	97-101
25869285-7	2015	Anthracycline-based regimens such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remain the standard first-line treatment choice for systemic ALCL, but in many patients with ALK- ALCL, it is ineffective, and thus it is often followed by consolidative autologous stem cell transplantation.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	97-101
25869285-7	2015	Anthracycline-based regimens such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remain the standard first-line treatment choice for systemic ALCL, but in many patients with ALK- ALCL, it is ineffective, and thus it is often followed by consolidative autologous stem cell transplantation.	Prednisone	85-95	DNA damage inducible transcript 3	Homo sapiens	97-101
26394465-3	2015	In the Archean hydrothermal conditions under the action of the phosphorus chemical potential the C-H-O system was transformed into a four-component system C-H-O-P setting up a gluconeogenic system, which became the basis of power supply for a protometabolism, and formation of a new cycle of CO2 fixation (reductive pentose phosphate pathway).	Phosphorus	63-73	DNA damage inducible transcript 3	Homo sapiens	155-162
26394465-3	2015	In the Archean hydrothermal conditions under the action of the phosphorus chemical potential the C-H-O system was transformed into a four-component system C-H-O-P setting up a gluconeogenic system, which became the basis of power supply for a protometabolism, and formation of a new cycle of CO2 fixation (reductive pentose phosphate pathway).	Pentosephosphates	316-333	DNA damage inducible transcript 3	Homo sapiens	155-162
25648098-1	2015	PURPOSE: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard chemotherapy in diffuse large B-cell lymphoma (DLBCL) patients.	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	86-90
25648098-1	2015	PURPOSE: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard chemotherapy in diffuse large B-cell lymphoma (DLBCL) patients.	Doxorubicin	42-53	DNA damage inducible transcript 3	Homo sapiens	86-90
25648098-1	2015	PURPOSE: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the standard chemotherapy in diffuse large B-cell lymphoma (DLBCL) patients.	Prednisone	72-82	DNA damage inducible transcript 3	Homo sapiens	86-90
25841776-4	2015	In primary human hepatocytes, a lipotoxic concentration of PA triggered endoplasmic reticulum stress, induced the apoptotic transcription factor CHOP, and increased the percentage of apoptotic cells.	Palmitic Acid	59-61	DNA damage inducible transcript 3	Homo sapiens	145-149
26076798-2	2015	Historically, PTCL was treated like aggressive B-cell lymphomas, and to date cyclophosphamide, prednisone, vincristine, and doxorubicin (CHOP) remains the most commonly used regimen, despite disappointing results.	Prednisone	95-105	DNA damage inducible transcript 3	Homo sapiens	137-141
26076798-2	2015	Historically, PTCL was treated like aggressive B-cell lymphomas, and to date cyclophosphamide, prednisone, vincristine, and doxorubicin (CHOP) remains the most commonly used regimen, despite disappointing results.	Doxorubicin	124-135	DNA damage inducible transcript 3	Homo sapiens	137-141
25737469-4	2015	Although NaF and tunicamycin both induced PERK activation followed by eIF2alpha phosphorylation and ATF4 expression, CHOP expression was only induced by tunicamycin.	Tunicamycin	153-164	DNA damage inducible transcript 3	Homo sapiens	117-121
25737469-8	2015	The GADD34 siRNA increased CHOP expression, which corresponded to increased ATF4 in tunicamycin-treated cells; however, the increased ATF4 did not induce CHOP expression in NaF-treated cells.	Tunicamycin	84-95	DNA damage inducible transcript 3	Homo sapiens	27-31
24988111-7	2015	Induction of ER stress by DON was confirmed by immunocytology demonstrating increased protein expression of two major ER stress markers ATF3 and DDIT3.	deoxynivalenol	26-29	DNA damage inducible transcript 3	Homo sapiens	145-150
25904325-3	2015	Using HepG2 and primary human hepatocytes, we found that CHOP induces cell death and inflammatory responses after saturated free fatty acid exposure by activating NF-kappaB through a pathway involving IRAK2 expression, resulting in secretion of cytokines IL-8 and TNFalpha directly from hepatocytes.	saturated free fatty acid	114-139	DNA damage inducible transcript 3	Homo sapiens	57-61
26009870-1	2015	BACKGROUND: Previously we have reported that generation of reactive oxygen species is the prime event responsible for calcium mediated activation of PERK-eIF2alpha-CHOP pathway and apoptosis in UV-B irradiated human skin fibroblasts (Hs68).	Reactive Oxygen Species	59-82	DNA damage inducible transcript 3	Homo sapiens	164-168
25817893-13	2015	In contrast to ascorbic acid, trolox, and deferoxamine, N-acetylcysteine suppressed the EA-induced upregulation of GADD153, although not of HO-1.	Acetylcysteine	56-72	DNA damage inducible transcript 3	Homo sapiens	115-122
25817893-13	2015	In contrast to ascorbic acid, trolox, and deferoxamine, N-acetylcysteine suppressed the EA-induced upregulation of GADD153, although not of HO-1.	Ethacrynic Acid	88-90	DNA damage inducible transcript 3	Homo sapiens	115-122
25870318-5	2015	We found that usnic acid causes endoplasmic reticulum (ER) stress demonstrated by the increased expression of typical ER stress markers, including CHOP, ATF-4, p-eIF2alpha, and spliced XBP1.	usnic acid	14-24	DNA damage inducible transcript 3	Homo sapiens	147-151
25950987-8	2015	PCB29-pQ markedly increased the hallmark genes of ER stress, namely, glucose-regulated protein 78 (GRP78), GRP94, and C/EBP homologous protein (CHOP) on both protein and mRNA levels in HepG2 cells.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	DNA damage inducible transcript 3	Homo sapiens	118-142
25950987-8	2015	PCB29-pQ markedly increased the hallmark genes of ER stress, namely, glucose-regulated protein 78 (GRP78), GRP94, and C/EBP homologous protein (CHOP) on both protein and mRNA levels in HepG2 cells.	2,3,5-trichloro-6-phenyl-(1,4)benzoquinone	0-8	DNA damage inducible transcript 3	Homo sapiens	144-148
26075749-5	2015	Meanwhile, the unfolded protein response regulator CHOP, p-eIF2alpha, calreticulin, GRP78 and ATP2A1, all of which are also considered as ER stress markers, are upregulated by metformin and miR-708-5p.	Metformin	176-185	DNA damage inducible transcript 3	Homo sapiens	51-55
26009870-1	2015	BACKGROUND: Previously we have reported that generation of reactive oxygen species is the prime event responsible for calcium mediated activation of PERK-eIF2alpha-CHOP pathway and apoptosis in UV-B irradiated human skin fibroblasts (Hs68).	Calcium	118-125	DNA damage inducible transcript 3	Homo sapiens	164-168
26013662-7	2015	Mechanistic investigations revealed that curcumin treatment upregulated the ER stress markers CHOP and Bip/GRP78 and the autophagic marker LC3-II.	Curcumin	41-49	DNA damage inducible transcript 3	Homo sapiens	94-98
26063499-11	2015	Furthermore, LA induced ROS generation which could be involved in the CHOP induction which is known to activate the Bim translation.	ros	24-27	DNA damage inducible transcript 3	Homo sapiens	70-74
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged &gt;80 years are less clear.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	113-117
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged &gt;80 years are less clear.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	229-233
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged &gt;80 years are less clear.	Doxorubicin	69-80	DNA damage inducible transcript 3	Homo sapiens	113-117
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged &gt;80 years are less clear.	Doxorubicin	69-80	DNA damage inducible transcript 3	Homo sapiens	229-233
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged &gt;80 years are less clear.	Vincristine	82-93	DNA damage inducible transcript 3	Homo sapiens	229-233
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged &gt;80 years are less clear.	Prednisone	99-109	DNA damage inducible transcript 3	Homo sapiens	113-117
25675909-1	2015	BACKGROUND: Although the combination of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is considered standard therapy for diffuse large B-cell lymphoma (DLBCL), patterns of use and the impact of R-CHOP on survival in patients aged &gt;80 years are less clear.	Prednisone	99-109	DNA damage inducible transcript 3	Homo sapiens	229-233
25975443-8	2015	Randomized clinical trials have (a) established that bendamustine-rituximab (BR) is more efficacious and less toxic than rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP); (b) established that bortezomib should replace vincristine if using an R-CHOP backbone; and (c) established that maintenance rituximab (MR) is beneficial after an R-CHOP induction.	Bendamustine Hydrochloride	53-65	DNA damage inducible transcript 3	Homo sapiens	194-198
25975443-8	2015	Randomized clinical trials have (a) established that bendamustine-rituximab (BR) is more efficacious and less toxic than rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP); (b) established that bortezomib should replace vincristine if using an R-CHOP backbone; and (c) established that maintenance rituximab (MR) is beneficial after an R-CHOP induction.	Bendamustine Hydrochloride	53-65	DNA damage inducible transcript 3	Homo sapiens	274-278
25975443-8	2015	Randomized clinical trials have (a) established that bendamustine-rituximab (BR) is more efficacious and less toxic than rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP); (b) established that bortezomib should replace vincristine if using an R-CHOP backbone; and (c) established that maintenance rituximab (MR) is beneficial after an R-CHOP induction.	Bendamustine Hydrochloride	53-65	DNA damage inducible transcript 3	Homo sapiens	274-278
26166660-0	2015	Apigenin inhibits indoxyl sulfate-induced endoplasmic reticulum stress and anti-proliferative pathways, CHOP and IL-6/p21, in human renal proximal tubular cells.	Indican	18-33	DNA damage inducible transcript 3	Homo sapiens	104-108
26166660-6	2015	RESULTS: In HK-2 cells, apigenin completely inhibited IS-induced ER stress, as indicated by decreased expression of CHOP, ATF4 and GRP78, although the phosphorylated level of eIF2alpha did not decrease.	Apigenin	24-32	DNA damage inducible transcript 3	Homo sapiens	116-120
25522790-6	2015	Moreover, the ER stress-associated binding immunoglobulin protein (BiP), PKR-like ER kinase (PERK), activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP) were also upregulated at both mRNA and protein levels by lidocaine treatment.	Lidocaine	259-268	DNA damage inducible transcript 3	Homo sapiens	145-194
25964548-7	2015	SB203580, SP600125, and salubrinal effectively inhibited apoptosis and attenuated expression of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK) and CCAAT-enhancer-binding protein homologous protein (CHOP).	SB 203580	0-8	DNA damage inducible transcript 3	Homo sapiens	175-224
25964548-7	2015	SB203580, SP600125, and salubrinal effectively inhibited apoptosis and attenuated expression of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK) and CCAAT-enhancer-binding protein homologous protein (CHOP).	SB 203580	0-8	DNA damage inducible transcript 3	Homo sapiens	226-230
25964548-7	2015	SB203580, SP600125, and salubrinal effectively inhibited apoptosis and attenuated expression of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK) and CCAAT-enhancer-binding protein homologous protein (CHOP).	pyrazolanthrone	10-18	DNA damage inducible transcript 3	Homo sapiens	175-224
25964548-7	2015	SB203580, SP600125, and salubrinal effectively inhibited apoptosis and attenuated expression of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK) and CCAAT-enhancer-binding protein homologous protein (CHOP).	pyrazolanthrone	10-18	DNA damage inducible transcript 3	Homo sapiens	226-230
25964548-7	2015	SB203580, SP600125, and salubrinal effectively inhibited apoptosis and attenuated expression of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK) and CCAAT-enhancer-binding protein homologous protein (CHOP).	salubrinal	24-34	DNA damage inducible transcript 3	Homo sapiens	175-224
25964548-7	2015	SB203580, SP600125, and salubrinal effectively inhibited apoptosis and attenuated expression of phosphorylated protein kinase RNA-like endoplasmic reticulum kinase (PERK) and CCAAT-enhancer-binding protein homologous protein (CHOP).	salubrinal	24-34	DNA damage inducible transcript 3	Homo sapiens	226-230
26214636-9	2015	The 5-year OS was 61% in the R-CHOP compared to 38% in the CHOP group (p=0.007).	Osmium	11-13	DNA damage inducible transcript 3	Homo sapiens	31-35
26056479-7	2015	The patient underwent cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regime of chemotherapy and achieved a complete remission after four cycles.	Cyclophosphamide	22-38	DNA damage inducible transcript 3	Homo sapiens	82-86
26056479-7	2015	The patient underwent cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regime of chemotherapy and achieved a complete remission after four cycles.	Prednisone	70-80	DNA damage inducible transcript 3	Homo sapiens	82-86
26175857-9	2015	Furthermore, PCF treatment inhibited the expression of GRP78 at 4 h after UVB irradiation, and suppressed CHOP expression at 18 h post-irradiation, indicating that PCF could inhibit UVB-evoked ER stress in the early stage post-irradiation, and suppress the ER stress-induced apoptosis in the late stage.	PHENYL CHLOROFORMATE	13-16	DNA damage inducible transcript 3	Homo sapiens	106-110
25263322-5	2015	R-CVP was associated with lower 5-year overall survival (R-CVP 76%, R-CHOP 86%, R-Flu 86%; p = 0.021) and progression-free survival (R-CVP 49%, R-CHOP 58%, R-Flu 64%; p = 0.029).	r-cvp	0-5	DNA damage inducible transcript 3	Homo sapiens	70-74
25263322-5	2015	R-CVP was associated with lower 5-year overall survival (R-CVP 76%, R-CHOP 86%, R-Flu 86%; p = 0.021) and progression-free survival (R-CVP 49%, R-CHOP 58%, R-Flu 64%; p = 0.029).	r-cvp	0-5	DNA damage inducible transcript 3	Homo sapiens	146-150
25594392-6	2015	We further confirmed that the PA-induced apoptosis was mediated by prolonged ER stress at least in part via the PERK/eIF2alpha/ATF4/CHOP pathway.	panduratin A	30-32	DNA damage inducible transcript 3	Homo sapiens	132-136
25813094-12	2015	Furthermore, DMC promoted expression of ER stress-associated proteins such as GRP78, GADD153, IRE1beta, ATF-6alpha, ATF-6beta and caspase-4.	demethoxycurcumin	13-16	DNA damage inducible transcript 3	Homo sapiens	85-92
25608104-9	2015	Mechanistic studies demonstrated that Fatsioside A induces growth inhibition of U87MG cells via the induction of endoplasmic reticulum (ER) stress, which was supported by the upregulation of ER stress markers, including elevated levels of phosphorylation of PERK and eIF2alpha, the increased expression levels of CHOP and the accelerated cleavage of caspase-4.	3,15,18-trihydroxy-18,19-secolupane-12,19-dione 3-O-glucopyranosyl(1-2)glucopyranoside	38-50	DNA damage inducible transcript 3	Homo sapiens	313-317
25608104-10	2015	The downregulation of CHOP via CHOP-specific siRNA reduced the growth-inhibitive effect of Fatsioside A on U87MG cells, further confirming the role of the ER stress response in mediating Fatsioside A-induced growth inhibition.	3,15,18-trihydroxy-18,19-secolupane-12,19-dione 3-O-glucopyranosyl(1-2)glucopyranoside	91-103	DNA damage inducible transcript 3	Homo sapiens	22-26
25608104-10	2015	The downregulation of CHOP via CHOP-specific siRNA reduced the growth-inhibitive effect of Fatsioside A on U87MG cells, further confirming the role of the ER stress response in mediating Fatsioside A-induced growth inhibition.	3,15,18-trihydroxy-18,19-secolupane-12,19-dione 3-O-glucopyranosyl(1-2)glucopyranoside	91-103	DNA damage inducible transcript 3	Homo sapiens	31-35
25608104-10	2015	The downregulation of CHOP via CHOP-specific siRNA reduced the growth-inhibitive effect of Fatsioside A on U87MG cells, further confirming the role of the ER stress response in mediating Fatsioside A-induced growth inhibition.	3,15,18-trihydroxy-18,19-secolupane-12,19-dione 3-O-glucopyranosyl(1-2)glucopyranoside	187-199	DNA damage inducible transcript 3	Homo sapiens	22-26
25608104-10	2015	The downregulation of CHOP via CHOP-specific siRNA reduced the growth-inhibitive effect of Fatsioside A on U87MG cells, further confirming the role of the ER stress response in mediating Fatsioside A-induced growth inhibition.	3,15,18-trihydroxy-18,19-secolupane-12,19-dione 3-O-glucopyranosyl(1-2)glucopyranoside	187-199	DNA damage inducible transcript 3	Homo sapiens	31-35
26039024-5	2015	The present case reports ten years progression-free survival in a female patient with mantle cell lymphoma with baseline clinical stage IVB (MIPI 5), treated with nine courses of CHOP chemotherapy.	mipi	141-145	DNA damage inducible transcript 3	Homo sapiens	179-183
25594392-7	2015	Pretreatment with cycloheximide, an ER stress inhibitor rescued PA-induced cell death, which was accompanied by the suppression of ER-stress-related HSPA5 and CHOP proteins.	Cycloheximide	18-31	DNA damage inducible transcript 3	Homo sapiens	159-163
25594392-7	2015	Pretreatment with cycloheximide, an ER stress inhibitor rescued PA-induced cell death, which was accompanied by the suppression of ER-stress-related HSPA5 and CHOP proteins.	panduratin A	64-66	DNA damage inducible transcript 3	Homo sapiens	159-163
25894488-0	2015	Avarol induces apoptosis in pancreatic ductal adenocarcinoma cells by activating PERK-eIF2alpha-CHOP signaling.	avarol	0-6	DNA damage inducible transcript 3	Homo sapiens	96-100
25897662-5	2015	In addition, NASTRp induced expression of endoplasmic reticulum stress markers such as DDIT3/CHOP, and led to apoptosis along with Bim induction.	naphthol AS-TR phosphate	13-19	DNA damage inducible transcript 3	Homo sapiens	87-92
25897662-5	2015	In addition, NASTRp induced expression of endoplasmic reticulum stress markers such as DDIT3/CHOP, and led to apoptosis along with Bim induction.	naphthol AS-TR phosphate	13-19	DNA damage inducible transcript 3	Homo sapiens	93-97
25894488-4	2015	Analyses of the molecular mechanisms of avarol-induced apoptosis indicated upregulation of ER stress marker BiP and ER stress-dependent apoptosis inducer CHOP in PDAC cells but not in normal cells, suggesting that avarol selectively induces ER stress responses.	avarol	40-46	DNA damage inducible transcript 3	Homo sapiens	154-158
25894488-6	2015	Moreover, CHOP downregulation was significantly suppressed by avarol-induced apoptosis.	avarol	62-68	DNA damage inducible transcript 3	Homo sapiens	10-14
25894488-7	2015	Thus, the PERK-eIF2alpha-CHOP signaling pathway may be a novel molecular mechanism of avarol-induced apoptosis.	avarol	86-92	DNA damage inducible transcript 3	Homo sapiens	25-29
25492236-9	2015	CONCLUSIONS: There was a trend of higher OS and FFS rates for patients who had received consolidation RT after R-CHOP (especially for patients with stage III/IV disease), but the difference did not reach statistical significance.	Osmium	41-43	DNA damage inducible transcript 3	Homo sapiens	113-117
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	125-141	DNA damage inducible transcript 3	Homo sapiens	108-112
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Vincristine	156-167	DNA damage inducible transcript 3	Homo sapiens	108-112
25430047-1	2015	This study aimed to clarify the association between the TP53 rs1625895 polymorphism and the efficiency of R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisolone) therapy in 106 patients with diffuse large B cell lymphoma (DLBCL).	Prednisolone	169-181	DNA damage inducible transcript 3	Homo sapiens	108-112
25881228-4	2015	METHODS: First, B-cell cancer cell lines were tested successively for resistance towards the chemotherapeutic components of R-CHOP: cyclophosphamide (C), doxorubicin (H), and vincristine (O).	Cyclophosphamide	132-148	DNA damage inducible transcript 3	Homo sapiens	126-130
25492236-9	2015	CONCLUSIONS: There was a trend of higher OS and FFS rates for patients who had received consolidation RT after R-CHOP (especially for patients with stage III/IV disease), but the difference did not reach statistical significance.	CHEMBL1198227	48-51	DNA damage inducible transcript 3	Homo sapiens	113-117
25322957-5	2015	Thapsigargin/tunicamycin treatment induced a significant increase in endoplasmic reticulum stress and of cell death, represented by higher GADD153 and GRP78 expression and propidium iodide flow cytometry, respectively.	Thapsigargin	0-12	DNA damage inducible transcript 3	Homo sapiens	139-146
25322957-5	2015	Thapsigargin/tunicamycin treatment induced a significant increase in endoplasmic reticulum stress and of cell death, represented by higher GADD153 and GRP78 expression and propidium iodide flow cytometry, respectively.	Tunicamycin	13-24	DNA damage inducible transcript 3	Homo sapiens	139-146
25445468-0	2015	Pegylated liposomal doxorubicin replacing conventional doxorubicin in standard R-CHOP chemotherapy for elderly patients with diffuse large B-cell lymphoma: an open label, single arm, phase II trial.	Doxorubicin	20-31	DNA damage inducible transcript 3	Homo sapiens	81-85
25872712-4	2015	Moreover, the antioxidant N-acetylcysteine (NAC) and pro-apoptotic transcription factor CHOP knockdown were used to clarify the precise interplay between reactive oxygen species (ROS), ER stress and their roles in NaF-induced apoptosis in Sertoli cells.	Reactive Oxygen Species	154-177	DNA damage inducible transcript 3	Homo sapiens	88-92
24956143-3	2015	In this prospective cohort study of 44 patients aged 70 years or older with NHL receiving rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP), a GA was administered before the start of chemotherapy.	Prednisone	148-158	DNA damage inducible transcript 3	Homo sapiens	162-166
25039351-5	2015	These results suggest that patients with primary SN-DLBCL treated with R-CHOP have a relatively low CNS relapse rate and better OS compared to previous studies before the introduction of R.	Osmium	128-130	DNA damage inducible transcript 3	Homo sapiens	73-77
25788268-0	2015	Piperlongumine selectively kills hepatocellular carcinoma cells and preferentially inhibits their invasion via ROS-ER-MAPKs-CHOP.	piperlonguminine	0-14	DNA damage inducible transcript 3	Homo sapiens	124-128
25788268-0	2015	Piperlongumine selectively kills hepatocellular carcinoma cells and preferentially inhibits their invasion via ROS-ER-MAPKs-CHOP.	Reactive Oxygen Species	111-114	DNA damage inducible transcript 3	Homo sapiens	124-128
25788268-3	2015	Here, we reported that PL specifically suppressed HCC cell migration/invasion via endoplasmic reticulum (ER)-MAPKs-CHOP signaling pathway.	piperlonguminine	23-25	DNA damage inducible transcript 3	Homo sapiens	115-119
25647410-5	2015	Using TEM and western blot analysis, we observed increased ER stress in response to PA, as indicated by the increased levels of the ER stress markers, BiP, activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP), and the phosphoralytion of eukaryotic translation initiation factor 2alpha and c-Jun N-terminal kinase (JNK).	Palmitates	84-86	DNA damage inducible transcript 3	Homo sapiens	201-225
25647410-5	2015	Using TEM and western blot analysis, we observed increased ER stress in response to PA, as indicated by the increased levels of the ER stress markers, BiP, activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP), and the phosphoralytion of eukaryotic translation initiation factor 2alpha and c-Jun N-terminal kinase (JNK).	Palmitates	84-86	DNA damage inducible transcript 3	Homo sapiens	227-231
26687958-2	2015	Although it has limited efficacy, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy is widely used for treatment of de-novo peripheral T-cell lymphoma.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	94-98
26687958-2	2015	Although it has limited efficacy, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy is widely used for treatment of de-novo peripheral T-cell lymphoma.	Prednisone	82-92	DNA damage inducible transcript 3	Homo sapiens	94-98
25960846-9	2015	Also our study showed that controlled CINV episodes in patients who received CMF regimen were better than the regimen including adriamycin (CAF, CHOP) into both granisetron (p=0.06) and metoclopramid (p=0.04).	Doxorubicin	128-138	DNA damage inducible transcript 3	Homo sapiens	145-149
26045770-10	2015	HCPT treatment induced the upregulation of CHOP and downregulation of XIAP in HTCFs.	hydroxycamptothecinum	0-4	DNA damage inducible transcript 3	Homo sapiens	43-47
25960846-9	2015	Also our study showed that controlled CINV episodes in patients who received CMF regimen were better than the regimen including adriamycin (CAF, CHOP) into both granisetron (p=0.06) and metoclopramid (p=0.04).	Granisetron	161-172	DNA damage inducible transcript 3	Homo sapiens	145-149
25938832-6	2015	In addition, the palmitate sodium treatment also activated the PI3K/Akt pathway,induced expression of CHOP and Bax of the UPR and non-UPR signaling pathways respectively.	Palmitic Acid	17-33	DNA damage inducible transcript 3	Homo sapiens	102-106
25498902-5	2015	Contrastingly, cells with hyper-active mTORC1 displayed basally elevated levels of ER stress which was greatly exaggerated following nelfinavir treatment, seen through increased CHOP mRNA and XBP1 splicing.	Nelfinavir	133-143	DNA damage inducible transcript 3	Homo sapiens	178-182
25938832-7	2015	Moreover, Pretreatment with LY294002 inhibited the palmitate sodium induced-phosphorylation of PI3K and Akt, and promoted upregulation of CHOP and Bax induced by palmitate sodium.	2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one	28-36	DNA damage inducible transcript 3	Homo sapiens	138-142
25938832-7	2015	Moreover, Pretreatment with LY294002 inhibited the palmitate sodium induced-phosphorylation of PI3K and Akt, and promoted upregulation of CHOP and Bax induced by palmitate sodium.	Palmitic Acid	162-178	DNA damage inducible transcript 3	Homo sapiens	138-142
25938832-8	2015	CONCLUSION: The PI3K/Akt pathway may be involved in regulation of the UPR and non-UPR signaling pathways of endoplasmic reticulum stress and may promote apoptosis of hepatocytes by enhancing the expression of CHOP and Bax protein in saturated fatty acid-induced steatotic hepatocytes.	Fatty Acids	233-253	DNA damage inducible transcript 3	Homo sapiens	209-213
25635435-1	2015	BACKGROUND: Rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival in first-line chemotherapy for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	42-58	DNA damage inducible transcript 3	Homo sapiens	102-106
25635435-1	2015	BACKGROUND: Rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival in first-line chemotherapy for patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	60-71	DNA damage inducible transcript 3	Homo sapiens	102-106
25635435-1	2015	BACKGROUND: Rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival in first-line chemotherapy for patients with diffuse large B-cell lymphoma (DLBCL).	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	102-106
25685062-4	2015	Moreover, our data show BIX-01294 stimulates endoplasmic reticulum stress (ER stress) and up-regulated expression of PMAIP1 through DDIT3 up-regulation.	BIX 01294	24-33	DNA damage inducible transcript 3	Homo sapiens	132-137
25418196-3	2015	A total of 197 patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) were enrolled between October 2005 and July 2011; PET/CT was performed at the time of diagnosis (PET/CT0), after 2 and 4 cycles of chemotherapy (PET/CT2 and PET/CT4, respectively), and at the end of treatment (F-PET/CT).	Prednisone	96-106	DNA damage inducible transcript 3	Homo sapiens	110-114
25428129-4	2015	Tunicamycin induced the phosphorylation and activation of PERK and eIF2alpha within 2 h in RPTC, which was followed by the induction of GRP78 and CHOP.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	146-150
25428129-7	2015	Inhibition of mTOR with rapamycin partially suppressed the phosphorylation of PERK and eIF2a and the induction of CHOP and GRP78 induction during tunicamycin treatment.	Sirolimus	24-33	DNA damage inducible transcript 3	Homo sapiens	114-118
25428129-7	2015	Inhibition of mTOR with rapamycin partially suppressed the phosphorylation of PERK and eIF2a and the induction of CHOP and GRP78 induction during tunicamycin treatment.	Tunicamycin	146-157	DNA damage inducible transcript 3	Homo sapiens	114-118
25395425-0	2015	Ibritumomab consolidation after 3 cycles of CHOP plus radiotherapy in high-risk limited-stage aggressive B-cell lymphoma: SWOG S0313.	ibritumomab tiuxetan	0-11	DNA damage inducible transcript 3	Homo sapiens	44-48
25174772-7	2015	Intensifying therapy with R-HyperCVAD induction or ASCT consolidation after R-CHOP is associated with prolonged PFS and similar rates of toxicity.	r-hypercvad	26-37	DNA damage inducible transcript 3	Homo sapiens	78-82
24531715-4	2015	We first demonstrated that cisplatin-induced apoptosis in ovarian cancer cell lines was associated with endoplasmic reticulum (ER) stress, evidenced by induction of Glucose-Regulated Protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153) and increased intracellular Ca(2+) release.	Cisplatin	27-36	DNA damage inducible transcript 3	Homo sapiens	203-251
24531715-4	2015	We first demonstrated that cisplatin-induced apoptosis in ovarian cancer cell lines was associated with endoplasmic reticulum (ER) stress, evidenced by induction of Glucose-Regulated Protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153) and increased intracellular Ca(2+) release.	Cisplatin	27-36	DNA damage inducible transcript 3	Homo sapiens	253-260
26167311-6	2015	The patient received cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) followed by salvage ifosfamide, carboplatin, and etoposide (ICE) but had continuous progression of cutaneous involvement.	Prednisone	69-79	DNA damage inducible transcript 3	Homo sapiens	81-85
25261037-8	2015	Zonisamide not only suppressed MPP+-induced cell death, but also inhibited ER stress-induced cell death and suppressed the expression of ER stress-related factors such as C/EBO homologous protein (CHOP) in vivo.	Zonisamide	0-10	DNA damage inducible transcript 3	Homo sapiens	171-195
25261037-8	2015	Zonisamide not only suppressed MPP+-induced cell death, but also inhibited ER stress-induced cell death and suppressed the expression of ER stress-related factors such as C/EBO homologous protein (CHOP) in vivo.	Zonisamide	0-10	DNA damage inducible transcript 3	Homo sapiens	197-201
25448036-5	2015	Adipogenesis proceeded in both normal and high glucose with concomitant activation of the UPR, but only high glucose was associated with increased levels of ER stress and mitochondrial stress as observed by parallel increases in CHOP and protein succination.	Glucose	109-116	DNA damage inducible transcript 3	Homo sapiens	229-233
25891535-2	2015	In this study we found the stress-regulated protein p8 was obviously increased after DHA treatment in several cancer cells, which further to induce autophagy by the upregulation of endoplasmic reticulum stress-related protein ATF4 and CHOP.	artenimol	85-88	DNA damage inducible transcript 3	Homo sapiens	235-239
24969101-7	2015	L-GPS based on systemic inflammatory indicators may be a useful clinical prognostic indicator for survival, and predicts the response for R-CHOP chemotherapy in patients with newly diagnosed DLBCL.	l-gps	0-5	DNA damage inducible transcript 3	Homo sapiens	140-144
26137775-13	2015	The most widely used and most effective is the combination Cyclophosphamide, Doxorubicin, Vincristine and Prednisone (CHOP).	Cyclophosphamide	59-75	DNA damage inducible transcript 3	Homo sapiens	118-122
26137775-13	2015	The most widely used and most effective is the combination Cyclophosphamide, Doxorubicin, Vincristine and Prednisone (CHOP).	Prednisone	106-116	DNA damage inducible transcript 3	Homo sapiens	118-122
25878913-3	2015	The patient received cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with rituximab and had excellent results.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	81-85
25878913-3	2015	The patient received cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with rituximab and had excellent results.	Prednisone	69-79	DNA damage inducible transcript 3	Homo sapiens	81-85
25295624-4	2015	RESULTS: Here we report that AMIO, but not iodine, significantly induced the expression of ER stress markers including Ig heavy chain-binding protein (BiP), phosphoeukaryotic translation initiation factor 2alpha (eIF2alpha), CCAAT/enhancer-binding protein homologous protein (CHOP) and spliced X-box binding protein-1 (XBP-1) in human thyroid ML-1 cells and human primary thyrocytes.	Amiodarone	29-33	DNA damage inducible transcript 3	Homo sapiens	225-274
26435723-4	2015	By treatment with PGE2, the chondrocytes apoptosis was significantly increased, the proapoptotic CHOP and JNK were upregulated, the prosurvival GRP78 and XBP1 were downregulated, and GSK-3beta was also upregulated.	Dinoprostone	18-22	DNA damage inducible transcript 3	Homo sapiens	97-101
25295624-4	2015	RESULTS: Here we report that AMIO, but not iodine, significantly induced the expression of ER stress markers including Ig heavy chain-binding protein (BiP), phosphoeukaryotic translation initiation factor 2alpha (eIF2alpha), CCAAT/enhancer-binding protein homologous protein (CHOP) and spliced X-box binding protein-1 (XBP-1) in human thyroid ML-1 cells and human primary thyrocytes.	Amiodarone	29-33	DNA damage inducible transcript 3	Homo sapiens	276-280
26090483-5	2015	Interestingly, we discovered that 4-phenylbutyric acid (4-PBA), a selective inhibitor of ERS, blocked the apoptosis of BM-MSCs from SLE patients and alleviated the level of Jun N-terminal kinase1/2 (JNK1/2) and CHOP.	4-phenylbutyric acid	34-54	DNA damage inducible transcript 3	Homo sapiens	211-215
26090483-5	2015	Interestingly, we discovered that 4-phenylbutyric acid (4-PBA), a selective inhibitor of ERS, blocked the apoptosis of BM-MSCs from SLE patients and alleviated the level of Jun N-terminal kinase1/2 (JNK1/2) and CHOP.	4-phenylbutyric acid	56-61	DNA damage inducible transcript 3	Homo sapiens	211-215
25653476-6	2015	Rapamycin attenuated PA-induced PERK and IRE1-associated UPR pathways, evidenced by decreased protein levels of eIF2alpha phosphorylation, ATF4, CHOP, and JNK phosphorylation.	Sirolimus	0-9	DNA damage inducible transcript 3	Homo sapiens	145-149
25686648-3	2015	The summary hazard ratios of low ALC/AMC ratio for overall survival were 2.00 (p = 0.000) in the population that received R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) and 1.12 (p = 0.479) in the population that received CHOP.	7-amino-4-methylcoumarin	37-40	DNA damage inducible transcript 3	Homo sapiens	124-128
25686648-3	2015	The summary hazard ratios of low ALC/AMC ratio for overall survival were 2.00 (p = 0.000) in the population that received R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) and 1.12 (p = 0.479) in the population that received CHOP.	7-amino-4-methylcoumarin	37-40	DNA damage inducible transcript 3	Homo sapiens	250-254
25653476-6	2015	Rapamycin attenuated PA-induced PERK and IRE1-associated UPR pathways, evidenced by decreased protein levels of eIF2alpha phosphorylation, ATF4, CHOP, and JNK phosphorylation.	Palmitates	21-23	DNA damage inducible transcript 3	Homo sapiens	145-149
25641142-8	2015	CR rate of the 26 patients received CHOP or CHOPE regimens as the first line chemotherapy was 19.2% (5/26).	Chromium	0-2	DNA damage inducible transcript 3	Homo sapiens	36-40
26334344-1	2015	INTRODUCTION: R-CHOP immunochemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is a standard first-line treatment for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	52-68	DNA damage inducible transcript 3	Homo sapiens	16-20
26334344-1	2015	INTRODUCTION: R-CHOP immunochemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is a standard first-line treatment for diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	70-81	DNA damage inducible transcript 3	Homo sapiens	16-20
26334344-1	2015	INTRODUCTION: R-CHOP immunochemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is a standard first-line treatment for diffuse large B-cell lymphoma (DLBCL).	Vincristine	83-94	DNA damage inducible transcript 3	Homo sapiens	16-20
26334344-1	2015	INTRODUCTION: R-CHOP immunochemotherapy (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) is a standard first-line treatment for diffuse large B-cell lymphoma (DLBCL).	Prednisone	96-106	DNA damage inducible transcript 3	Homo sapiens	16-20
25323748-7	2015	Specifically, LAC treatment increased the cisplatin-induced expression of PDI, GRP78, CHOP, cleaved caspase-4 and cleaved caspase-3.	Cisplatin	42-51	DNA damage inducible transcript 3	Homo sapiens	86-90
24723488-5	2014	RESULTS: Six courses of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) or cyclophosphamide, doxorubicin, vincristine, etoposide and prednisone (CHOEP) chemotherapy were recommended for first-line therapy of patients with nodal, intestinal or hepatosplenic T-cell lymphomas (evidence: low; recommendation: do, weak).	Prednisone	71-81	DNA damage inducible transcript 3	Homo sapiens	83-87
25527602-7	2014	Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy reduced the size of the tumor, and the symptoms thereafter improved.	Prednisolone	63-75	DNA damage inducible transcript 3	Homo sapiens	79-83
25251292-2	2014	Compared to oleate, palmitate treatment resulted in less intracellular accumulation of lipid droplets and more ER stress, as measured by upregulation of CHOP, ATF6 and GRP78 gene expression and phosphorylation of eukaryotic initiation factor 2a (EIF2a).	Palmitates	20-29	DNA damage inducible transcript 3	Homo sapiens	153-157
25459253-2	2014	We report the effect of a combined treatment of high-dose methotrexate, cyclophosphamide, doxorubicin, vincristine and prednisolone (M-CHOP) for immunocompetent patients with PCNSL.	Methotrexate	58-70	DNA damage inducible transcript 3	Homo sapiens	135-139
25459253-2	2014	We report the effect of a combined treatment of high-dose methotrexate, cyclophosphamide, doxorubicin, vincristine and prednisolone (M-CHOP) for immunocompetent patients with PCNSL.	Doxorubicin	90-101	DNA damage inducible transcript 3	Homo sapiens	135-139
25459253-2	2014	We report the effect of a combined treatment of high-dose methotrexate, cyclophosphamide, doxorubicin, vincristine and prednisolone (M-CHOP) for immunocompetent patients with PCNSL.	Prednisolone	119-131	DNA damage inducible transcript 3	Homo sapiens	135-139
24547705-7	2014	The ALC/AMC ratio during R-CHOP cycles predicts survival and provides a platform to develop therapeutic modalities to manipulate the ALC/AMC ratio during R-CHOP cycles to improve DLBCL clinical outcomes.	7-amino-4-methylcoumarin	8-11	DNA damage inducible transcript 3	Homo sapiens	27-31
25023940-0	2014	Piperlongumine induces cell death through ROS-mediated CHOP activation and potentiates TRAIL-induced cell death in breast cancer cells.	piperlonguminine	0-14	DNA damage inducible transcript 3	Homo sapiens	55-59
25023940-0	2014	Piperlongumine induces cell death through ROS-mediated CHOP activation and potentiates TRAIL-induced cell death in breast cancer cells.	Reactive Oxygen Species	42-45	DNA damage inducible transcript 3	Homo sapiens	55-59
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Reactive Oxygen Species	22-25	DNA damage inducible transcript 3	Homo sapiens	96-100
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Reactive Oxygen Species	22-25	DNA damage inducible transcript 3	Homo sapiens	174-178
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Acetylcysteine	36-53	DNA damage inducible transcript 3	Homo sapiens	96-100
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Acetylcysteine	36-53	DNA damage inducible transcript 3	Homo sapiens	174-178
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Reactive Oxygen Species	156-159	DNA damage inducible transcript 3	Homo sapiens	96-100
25023940-8	2014	Pretreatment with the ROS scavenger N-acetyl-cysteine abolishes the PL-induced up-regulation of CHOP and its target genes, suggesting an essential role for ROS in PL-induced CHOP activation.	Reactive Oxygen Species	156-159	DNA damage inducible transcript 3	Homo sapiens	174-178
25023940-11	2014	CONCLUSIONS: Overall, our data suggest a new mechanism for the PL-induced cell death in which ROS mediates CHOP activation, and combination treatment with PL and TRAIL could be a potential strategy for breast cancer therapy.	piperlonguminine	63-65	DNA damage inducible transcript 3	Homo sapiens	107-111
25023940-11	2014	CONCLUSIONS: Overall, our data suggest a new mechanism for the PL-induced cell death in which ROS mediates CHOP activation, and combination treatment with PL and TRAIL could be a potential strategy for breast cancer therapy.	Reactive Oxygen Species	94-97	DNA damage inducible transcript 3	Homo sapiens	107-111
25316096-8	2014	Five patients received cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP) chemotherapy.	Prednisolone	70-82	DNA damage inducible transcript 3	Homo sapiens	84-88
24547705-2	2014	Therefore, we studied the ALC/AMC ratio at each rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) cycle as a predictor for survival.	Acetyl-L-carnitine hydrochloride	26-29	DNA damage inducible transcript 3	Homo sapiens	120-124
24547705-7	2014	The ALC/AMC ratio during R-CHOP cycles predicts survival and provides a platform to develop therapeutic modalities to manipulate the ALC/AMC ratio during R-CHOP cycles to improve DLBCL clinical outcomes.	7-amino-4-methylcoumarin	8-11	DNA damage inducible transcript 3	Homo sapiens	156-160
24547705-7	2014	The ALC/AMC ratio during R-CHOP cycles predicts survival and provides a platform to develop therapeutic modalities to manipulate the ALC/AMC ratio during R-CHOP cycles to improve DLBCL clinical outcomes.	7-amino-4-methylcoumarin	137-140	DNA damage inducible transcript 3	Homo sapiens	27-31
24547705-7	2014	The ALC/AMC ratio during R-CHOP cycles predicts survival and provides a platform to develop therapeutic modalities to manipulate the ALC/AMC ratio during R-CHOP cycles to improve DLBCL clinical outcomes.	7-amino-4-methylcoumarin	137-140	DNA damage inducible transcript 3	Homo sapiens	156-160
25231320-6	2014	In human breast cancer MCF-7 cells, ER stress activator tunicamycin increased the expression of CCL5, STAT3 and CHOP in a time- and concentration-dependent manner.	Tunicamycin	56-67	DNA damage inducible transcript 3	Homo sapiens	112-116
25220073-5	2014	L-carnitine suppress the endoplasmic reticulum dilation and activation of ER stress-associated proteins including glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein-homologous protein (CHOP), JNK, Bax and Bim induced by H2O2 or TM.	Carnitine	0-11	DNA damage inducible transcript 3	Homo sapiens	152-201
25220073-5	2014	L-carnitine suppress the endoplasmic reticulum dilation and activation of ER stress-associated proteins including glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein-homologous protein (CHOP), JNK, Bax and Bim induced by H2O2 or TM.	Carnitine	0-11	DNA damage inducible transcript 3	Homo sapiens	203-207
25220073-5	2014	L-carnitine suppress the endoplasmic reticulum dilation and activation of ER stress-associated proteins including glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein-homologous protein (CHOP), JNK, Bax and Bim induced by H2O2 or TM.	Hydrogen Peroxide	238-242	DNA damage inducible transcript 3	Homo sapiens	152-201
25220073-6	2014	In addition, H2O2-induced cell apoptosis and activation of ER stress can also be attenuated by antioxidant N-acetylcysteine (NAC), CHOP siRNA and the inhibitor of ER stress 4-phenylbutyric acid (4-PBA).	Hydrogen Peroxide	13-17	DNA damage inducible transcript 3	Homo sapiens	131-135
25220073-8	2014	CHOP/Bim or JNK/Bim-dependent ER stress signaling pathways maybe related to the neuroprotective effects of L-carnitine against H2O2-induced apoptosis and oxidative injury.	Carnitine	107-118	DNA damage inducible transcript 3	Homo sapiens	0-4
25220073-8	2014	CHOP/Bim or JNK/Bim-dependent ER stress signaling pathways maybe related to the neuroprotective effects of L-carnitine against H2O2-induced apoptosis and oxidative injury.	Hydrogen Peroxide	127-131	DNA damage inducible transcript 3	Homo sapiens	0-4
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	166-170
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	226-230
25436452-7	2014	Additionally, RSV decreases radical oxygen species (ROS) generation in palmitate-treated cells but leads to enhanced X-box binding protein-1 (XBP1) splicing and C/EBP homologous protein (CHOP) expression.	Resveratrol	14-17	DNA damage inducible transcript 3	Homo sapiens	161-185
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Doxorubicin	125-136	DNA damage inducible transcript 3	Homo sapiens	166-170
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Doxorubicin	125-136	DNA damage inducible transcript 3	Homo sapiens	226-230
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Vincristine	138-149	DNA damage inducible transcript 3	Homo sapiens	226-230
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Prednisone	154-164	DNA damage inducible transcript 3	Homo sapiens	166-170
25323007-2	2014	Although patient outcomes have significantly improved to a greater than 40% cure rate by the combinatorial cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which is widely used, resistance to the CHOP regimen continues to pose a problem in managing or curing DLBCL.	Prednisone	154-164	DNA damage inducible transcript 3	Homo sapiens	226-230
25436452-7	2014	Additionally, RSV decreases radical oxygen species (ROS) generation in palmitate-treated cells but leads to enhanced X-box binding protein-1 (XBP1) splicing and C/EBP homologous protein (CHOP) expression.	Resveratrol	14-17	DNA damage inducible transcript 3	Homo sapiens	187-191
25360516-2	2014	Here, we show that induction in cell surface GRP78 by doxorubicin and tunicamycin was associated with CHOP/GADD153 upregulation and increase in apoptosis in triple negative breast cancer tumor cells.	Doxorubicin	54-65	DNA damage inducible transcript 3	Homo sapiens	102-106
25344211-7	2014	Diethylaminobenzaldehyde (DEAB) decreased the half maximal inhibitory concentration (IC50) of the CHOP regimen in Farage cells from 344.78 +- 65.75 to 183.88 +- 49.75 ng/ml (P = 0.004).	2-(Diethylamino)benzaldehyde	0-24	DNA damage inducible transcript 3	Homo sapiens	98-102
25344211-7	2014	Diethylaminobenzaldehyde (DEAB) decreased the half maximal inhibitory concentration (IC50) of the CHOP regimen in Farage cells from 344.78 +- 65.75 to 183.88 +- 49.75 ng/ml (P = 0.004).	DEAB	26-30	DNA damage inducible transcript 3	Homo sapiens	98-102
25360516-2	2014	Here, we show that induction in cell surface GRP78 by doxorubicin and tunicamycin was associated with CHOP/GADD153 upregulation and increase in apoptosis in triple negative breast cancer tumor cells.	Doxorubicin	54-65	DNA damage inducible transcript 3	Homo sapiens	107-114
25360516-2	2014	Here, we show that induction in cell surface GRP78 by doxorubicin and tunicamycin was associated with CHOP/GADD153 upregulation and increase in apoptosis in triple negative breast cancer tumor cells.	Tunicamycin	70-81	DNA damage inducible transcript 3	Homo sapiens	102-106
25360516-2	2014	Here, we show that induction in cell surface GRP78 by doxorubicin and tunicamycin was associated with CHOP/GADD153 upregulation and increase in apoptosis in triple negative breast cancer tumor cells.	Tunicamycin	70-81	DNA damage inducible transcript 3	Homo sapiens	107-114
25412307-7	2014	Our study demonstrates a pivotal role of ROS/VSOR in mediating ER stress and functional impairment of cardiomyocytes via the CHOP-Wnt pathway, and suggests the therapeutic values of VSOR Cl(-) channel blockers against ER stress-associated cardiac anomalies.	Reactive Oxygen Species	41-44	DNA damage inducible transcript 3	Homo sapiens	125-129
25937892-8	2014	Up-regulation of the ER stress-associated apoptosis promoting transcription factor CHOP and p-JNK suggested that the antitumor activity of ceramide is owing to activation of apoptotic ER stress.	Ceramides	139-147	DNA damage inducible transcript 3	Homo sapiens	83-87
25192658-0	2014	Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	DNA damage inducible transcript 3	Homo sapiens	103-107
25411799-8	2014	Modest differences with respect to passage number and response to DCVC exposure were observed in expression of three key proteins (Hsp27, GADD153, p53) involved in stress response.	S-(1,2-dichlorovinyl)cysteine	66-70	DNA damage inducible transcript 3	Homo sapiens	138-145
25192658-0	2014	Oroxylin A inhibits ATRA-induced IL-6 expression involved in retinoic acid syndrome by down-regulating CHOP.	Tretinoin	20-24	DNA damage inducible transcript 3	Homo sapiens	103-107
25192658-4	2014	Following treatment with ATRA, CHOP expression was increased and dimerized with LIP more preferentially than LAP to rescue function of LAP.	Tretinoin	25-29	DNA damage inducible transcript 3	Homo sapiens	31-35
25192658-5	2014	Oroxylin A has been reported to activate CHOP, a key mediator of unfolded protein response (UPR) pathway, and resulted in apoptosis.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	0-10	DNA damage inducible transcript 3	Homo sapiens	41-45
25192658-6	2014	Interestingly, we found that low concentration of oroxylin A (  40 muM) showed no apoptosis effect on NB4 and HL-60 cells and decreased the CHOP protein level via promoting its degradation.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	50-60	DNA damage inducible transcript 3	Homo sapiens	140-144
25192658-7	2014	MG132 was utilized to conform the effect of oroxylin A on degrading CHOP.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNA damage inducible transcript 3	Homo sapiens	68-72
24625454-10	2014	CONCLUSIONS: The future for new treatment options in DLBCL is promising with current clinical trials testing novel targeted agents such as bortezomib, lenalidomide, and ibrutinib as the "X" in R(X)CHOP.	Bortezomib	139-149	DNA damage inducible transcript 3	Homo sapiens	197-201
24625454-10	2014	CONCLUSIONS: The future for new treatment options in DLBCL is promising with current clinical trials testing novel targeted agents such as bortezomib, lenalidomide, and ibrutinib as the "X" in R(X)CHOP.	ibrutinib	169-178	DNA damage inducible transcript 3	Homo sapiens	197-201
24951124-4	2014	To evaluate the effects of bendamustine-rituximab and rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) on the recuperation of immune system, we analyze the distribution of CD4+ and CD8+ T cells, B cells, and NK cells in peripheral blood of 18 patients who received 4-6 cycles of rituximab-bendamustine (BR) or six R-CHOP before therapy and 6 months after completing treatment.	Bendamustine Hydrochloride	27-39	DNA damage inducible transcript 3	Homo sapiens	131-135
25192658-7	2014	MG132 was utilized to conform the effect of oroxylin A on degrading CHOP.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	44-54	DNA damage inducible transcript 3	Homo sapiens	68-72
25192658-9	2014	We conclude that oroxylin A possessed abilities of inhibiting the ATRA-induced IL-6 production via modulation of LAP/LIP/CHOP in leukemia cell lines, which could providing a therapeutic strategy for RAS.	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	17-27	DNA damage inducible transcript 3	Homo sapiens	121-125
25192658-9	2014	We conclude that oroxylin A possessed abilities of inhibiting the ATRA-induced IL-6 production via modulation of LAP/LIP/CHOP in leukemia cell lines, which could providing a therapeutic strategy for RAS.	Tretinoin	66-70	DNA damage inducible transcript 3	Homo sapiens	121-125
25530830-0	2014	Discovery of Sulfonamidebenzamides as Selective Apoptotic CHOP Pathway Activators of the Unfolded Protein Response.	sulfonamidebenzamides	13-34	DNA damage inducible transcript 3	Homo sapiens	58-62
25469343-0	2014	Rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy for diffuse large B-cell lymphoma in pregnancy may be associated with preterm birth.	Prednisone	59-69	DNA damage inducible transcript 3	Homo sapiens	73-77
25408580-1	2014	Febrile neutropenia (FN) is the major toxicity of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) regimen in the treatment of diffuse large B-cell lymphoma (DLBCL).	Prednisone	113-123	DNA damage inducible transcript 3	Homo sapiens	127-131
25229255-2	2014	Improvements in overall survival have been observed with the introduction of rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), however, prognostic markers are still needed.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	169-173
25229255-2	2014	Improvements in overall survival have been observed with the introduction of rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), however, prognostic markers are still needed.	Doxorubicin	125-136	DNA damage inducible transcript 3	Homo sapiens	169-173
25229255-2	2014	Improvements in overall survival have been observed with the introduction of rituximab in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), however, prognostic markers are still needed.	Prednisone	155-165	DNA damage inducible transcript 3	Homo sapiens	169-173
25530830-4	2014	A high throughput screen was performed directed at identifying compounds that selectively upregulate the apoptotic CHOP pathway while avoiding adaptive signaling cascades, resulting in a sulfonamidebenzamide chemotype that was optimized.	sulfonamidebenzamide	187-207	DNA damage inducible transcript 3	Homo sapiens	115-119
25182732-5	2014	The collective application of polyunsaturated fatty acids (PUFAs) and irradiation significantly changed the expression of EGR1, TNF-alpha, NOTCH1, c-MYC, TP53, HMOX1, AKR1C1, NQO1, while up-regulation of GADD45A, EGR1, GRP78, DDIT3, c-MYC, FOSL1 were recorded both in response to PUFA treatment or irradiation alone.	Fatty Acids, Unsaturated	30-57	DNA damage inducible transcript 3	Homo sapiens	226-231
25314137-2	2014	Palmitate loading of cells activates the endoplasmic reticulum stress response, including induction of the proapoptotic transcription factor C/EBP homologous protein (CHOP).	Palmitates	0-9	DNA damage inducible transcript 3	Homo sapiens	141-165
25314137-2	2014	Palmitate loading of cells activates the endoplasmic reticulum stress response, including induction of the proapoptotic transcription factor C/EBP homologous protein (CHOP).	Palmitates	0-9	DNA damage inducible transcript 3	Homo sapiens	167-171
25314137-9	2014	Augmentation of miR-615-3p levels, using a precursor molecule, repressed CHOP expression; and under these conditions palmitate- or tunicamycin-induced cell death were significantly reduced.	Tunicamycin	131-142	DNA damage inducible transcript 3	Homo sapiens	73-77
25314137-10	2014	Our results suggest that palmitate-induced apoptosis requires maximal expression of CHOP which is achieved via the downregulation of its repressive microRNA, miR-615-3p.	Palmitates	25-34	DNA damage inducible transcript 3	Homo sapiens	84-88
25004060-4	2014	We found that high-dose atorvastatin- and I-PostC significantly downregulated expression of glucose-regulating protein 78 and calreticulin (CRT; ER stress markers), expression of C/EBP homologous protein (CHOP), and caspase 12 (markers for ER stress-related apoptosis), and Bax (downstream molecule of CHOP), in the myocardial area at risk.	Atorvastatin	24-36	DNA damage inducible transcript 3	Homo sapiens	179-203
25004060-4	2014	We found that high-dose atorvastatin- and I-PostC significantly downregulated expression of glucose-regulating protein 78 and calreticulin (CRT; ER stress markers), expression of C/EBP homologous protein (CHOP), and caspase 12 (markers for ER stress-related apoptosis), and Bax (downstream molecule of CHOP), in the myocardial area at risk.	Atorvastatin	24-36	DNA damage inducible transcript 3	Homo sapiens	205-209
25004060-4	2014	We found that high-dose atorvastatin- and I-PostC significantly downregulated expression of glucose-regulating protein 78 and calreticulin (CRT; ER stress markers), expression of C/EBP homologous protein (CHOP), and caspase 12 (markers for ER stress-related apoptosis), and Bax (downstream molecule of CHOP), in the myocardial area at risk.	Atorvastatin	24-36	DNA damage inducible transcript 3	Homo sapiens	302-306
25238096-5	2014	Chop expression in MDSCs was induced by tumor-linked reactive oxygen and nitrogen species and regulated by the activating-transcription factor-4.	reactive oxygen and nitrogen species	53-89	DNA damage inducible transcript 3	Homo sapiens	0-4
25321472-9	2014	In conclusion, our results suggest that Med sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the upregulation of DR5 through activation of the ROS-JNK-CHOP pathway.	ros	163-166	DNA damage inducible transcript 3	Homo sapiens	171-175
25371707-5	2014	He received chemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R CHOP) for eight cycles followed by radiation to the residual mass and achieved complete remission.	Prednisolone	88-100	DNA damage inducible transcript 3	Homo sapiens	104-108
24928834-10	2014	Our results strongly support anti-infective prophylaxis with aciclovir and cotrimoxazole for all patients receiving R-CHOP.	Trimethoprim, Sulfamethoxazole Drug Combination	75-88	DNA damage inducible transcript 3	Homo sapiens	118-122
24188478-0	2014	Cariporide sensitizes leukemic cells to tumor necrosis factor related apoptosis-inducing ligand by up-regulation of death receptor 5 via endoplasmic reticulum stress-CCAAT/enhancer binding protein homologous protein dependent mechanism.	cariporide	0-10	DNA damage inducible transcript 3	Homo sapiens	166-215
25325035-1	2014	BACKGROUND: Although adding rituximab to the chemotherapy regimen of cyclophosphamide, vincristine, doxorubicin, and prednisone (R-CHOP) has improved clinical outcomes of patients with diffuse large B-cell lymphoma (DLBCL), several recent studies have shown that the effect of rituximab is dominantly in the non-germinal center (non-GC) subtype compared to the germinal center (GC) subtype.	Vincristine	87-98	DNA damage inducible transcript 3	Homo sapiens	131-135
25325035-1	2014	BACKGROUND: Although adding rituximab to the chemotherapy regimen of cyclophosphamide, vincristine, doxorubicin, and prednisone (R-CHOP) has improved clinical outcomes of patients with diffuse large B-cell lymphoma (DLBCL), several recent studies have shown that the effect of rituximab is dominantly in the non-germinal center (non-GC) subtype compared to the germinal center (GC) subtype.	Doxorubicin	100-111	DNA damage inducible transcript 3	Homo sapiens	131-135
25325035-1	2014	BACKGROUND: Although adding rituximab to the chemotherapy regimen of cyclophosphamide, vincristine, doxorubicin, and prednisone (R-CHOP) has improved clinical outcomes of patients with diffuse large B-cell lymphoma (DLBCL), several recent studies have shown that the effect of rituximab is dominantly in the non-germinal center (non-GC) subtype compared to the germinal center (GC) subtype.	Prednisone	117-127	DNA damage inducible transcript 3	Homo sapiens	131-135
24446069-5	2014	PA treatment induced increased expression of PRKR-like endoplasmic reticulum kinase, inositol-requiring kinase 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and C/EBP homologous protein (CHOP) mRNA.	Palmitic Acid	0-2	DNA damage inducible transcript 3	Homo sapiens	177-201
24446069-5	2014	PA treatment induced increased expression of PRKR-like endoplasmic reticulum kinase, inositol-requiring kinase 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and C/EBP homologous protein (CHOP) mRNA.	Palmitic Acid	0-2	DNA damage inducible transcript 3	Homo sapiens	203-207
25486962-0	2014	Expression of constitutively activated NF-kappaB/mTORC pathway proteins and response to CHOP with bortezomib in a patient with angioimmunoblastic peripheral T-cell lymphoma.	Bortezomib	98-108	DNA damage inducible transcript 3	Homo sapiens	88-92
24990631-7	2014	SPOP recognizes a Ser/Thr-rich degron in the transactivation domain of DDIT3 and triggers DDIT3 degradation via the ubiquitin-proteasome pathway.	Serine	18-21	DNA damage inducible transcript 3	Homo sapiens	71-76
24990631-7	2014	SPOP recognizes a Ser/Thr-rich degron in the transactivation domain of DDIT3 and triggers DDIT3 degradation via the ubiquitin-proteasome pathway.	Serine	18-21	DNA damage inducible transcript 3	Homo sapiens	90-95
24990631-7	2014	SPOP recognizes a Ser/Thr-rich degron in the transactivation domain of DDIT3 and triggers DDIT3 degradation via the ubiquitin-proteasome pathway.	Threonine	22-25	DNA damage inducible transcript 3	Homo sapiens	71-76
24990631-7	2014	SPOP recognizes a Ser/Thr-rich degron in the transactivation domain of DDIT3 and triggers DDIT3 degradation via the ubiquitin-proteasome pathway.	Threonine	22-25	DNA damage inducible transcript 3	Homo sapiens	90-95
24188478-4	2014	The present study showed that treatment with the NHE1 inhibitor cariporide led to ER stress-induced up-regulation of the death receptor 5 (DR5) which is mediated by CHOP at the transcriptional level.	cariporide	64-74	DNA damage inducible transcript 3	Homo sapiens	165-169
24930757-0	2014	Ilimaquinone induces death receptor expression and sensitizes human colon cancer cells to TRAIL-induced apoptosis through activation of ROS-ERK/p38 MAPK-CHOP signaling pathways.	ilimaquinone	0-12	DNA damage inducible transcript 3	Homo sapiens	153-157
24930757-7	2014	Induction of DR4 and DR5 by ilimaquinone was mediated through up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP).	ilimaquinone	28-40	DNA damage inducible transcript 3	Homo sapiens	79-128
24930757-7	2014	Induction of DR4 and DR5 by ilimaquinone was mediated through up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP).	ilimaquinone	28-40	DNA damage inducible transcript 3	Homo sapiens	130-134
24930757-9	2014	Finally, the generation of ROS was required for CHOP and DR5 up-regulation by ilimaquinone.	ros	27-30	DNA damage inducible transcript 3	Homo sapiens	48-52
24930757-9	2014	Finally, the generation of ROS was required for CHOP and DR5 up-regulation by ilimaquinone.	ilimaquinone	78-90	DNA damage inducible transcript 3	Homo sapiens	48-52
24930757-10	2014	These results demonstrate that ilimaquinone enhanced the sensitivity of human colon cancer cells to TRAIL-induced apoptosis through ROS-ERK/p38 MAPK-CHOP-mediated up-regulation of DR4 and DR5 expression, suggesting that ilimaquinone could be developed into an adjuvant chemotherapeutic drug.	ilimaquinone	31-43	DNA damage inducible transcript 3	Homo sapiens	149-153
25337586-9	2014	Furthermore, carnosic acid also induced expression of ER stress marker proteins, including activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-homologous protein (CHOP), in a dose- and time-dependent manner.	salvin	13-26	DNA damage inducible transcript 3	Homo sapiens	136-185
25337586-9	2014	Furthermore, carnosic acid also induced expression of ER stress marker proteins, including activating transcription factor 4 (ATF4) and CCAAT/enhancer-binding protein-homologous protein (CHOP), in a dose- and time-dependent manner.	salvin	13-26	DNA damage inducible transcript 3	Homo sapiens	187-191
25337586-10	2014	Down-regulation of ATF4 and CHOP by small interfering RNA (siRNA) markedly reduced carnosic acid-induced sub-G1 population and PARP cleavage.	salvin	83-96	DNA damage inducible transcript 3	Homo sapiens	28-32
24289107-4	2014	This exploratory study was designed to correlate the mRNA expression levels of candidate genes mainly involved in the doxorubicin pathway (ABCB1, GSTP1, TOPO2alpha, BCL2, PKCbetaII) with the outcome of 54 patients with DLBCL undergoing a dose-dense R-CHOP regimen.	Doxorubicin	118-129	DNA damage inducible transcript 3	Homo sapiens	251-255
24188478-6	2014	Combining cariporide with tumor necrosis factor related apoptosis-inducing ligand (TRAIL) led to a significantly enhanced level of apoptosis that was abrogated by siRNA silencing of CHOP.	cariporide	10-20	DNA damage inducible transcript 3	Homo sapiens	182-186
24961950-8	2014	Additionally, pretreatment with SB202190 and SP600125 also decreased the expression of CHOP.	4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole	32-40	DNA damage inducible transcript 3	Homo sapiens	87-91
24961950-8	2014	Additionally, pretreatment with SB202190 and SP600125 also decreased the expression of CHOP.	pyrazolanthrone	45-53	DNA damage inducible transcript 3	Homo sapiens	87-91
24962313-7	2014	Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP).	Propofol	0-8	DNA damage inducible transcript 3	Homo sapiens	74-98
25234470-7	2014	Additionally, overexpression of DDIT3 might induce oxidative stress via glutathione depletion as a result of overexpression of CHAC1.	Glutathione	72-83	DNA damage inducible transcript 3	Homo sapiens	32-37
24962313-10	2014	Knockdown endogenous BiP with siRNA abolished the suppression of propofol on tunicamycin-mediated activation of CHOP and caspase-3.	Propofol	65-73	DNA damage inducible transcript 3	Homo sapiens	112-116
24962313-7	2014	Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP).	Propofol	0-8	DNA damage inducible transcript 3	Homo sapiens	100-104
24962313-10	2014	Knockdown endogenous BiP with siRNA abolished the suppression of propofol on tunicamycin-mediated activation of CHOP and caspase-3.	Tunicamycin	77-88	DNA damage inducible transcript 3	Homo sapiens	112-116
24962313-7	2014	Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP).	Tunicamycin	37-48	DNA damage inducible transcript 3	Homo sapiens	74-98
24962313-7	2014	Propofol pretreatment also inhibited tunicamycin-induced up-regulation of C/EBP homologous protein (CHOP).	Tunicamycin	37-48	DNA damage inducible transcript 3	Homo sapiens	100-104
26331107-10	2014	We determined that DMC treatment displays a dose-dependent reduction in cell viability against a number of GBM cells, associated with ER stress induction, as shown by the up-regulation of glucose-regulated protein 78 (GRP78) and CCAAT/-enhancer-binding protein homologous protein (CHOP) in A172 and U87 cells.	2,5-dimethylcelecoxib	19-22	DNA damage inducible transcript 3	Homo sapiens	229-279
25177375-9	2014	CONCLUSIONS: In the current study, we identified the pre-treatment MTV measured by FDG-PET/CT as a potential predictor of survival in patients with DLBCL treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP), at least in Ann Arbor stage II and III disease.	Doxorubicin	196-207	DNA damage inducible transcript 3	Homo sapiens	242-246
25177375-9	2014	CONCLUSIONS: In the current study, we identified the pre-treatment MTV measured by FDG-PET/CT as a potential predictor of survival in patients with DLBCL treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP), at least in Ann Arbor stage II and III disease.	Vincristine	209-220	DNA damage inducible transcript 3	Homo sapiens	242-246
25177375-9	2014	CONCLUSIONS: In the current study, we identified the pre-treatment MTV measured by FDG-PET/CT as a potential predictor of survival in patients with DLBCL treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP), at least in Ann Arbor stage II and III disease.	Prednisolone	226-238	DNA damage inducible transcript 3	Homo sapiens	242-246
26331107-10	2014	We determined that DMC treatment displays a dose-dependent reduction in cell viability against a number of GBM cells, associated with ER stress induction, as shown by the up-regulation of glucose-regulated protein 78 (GRP78) and CCAAT/-enhancer-binding protein homologous protein (CHOP) in A172 and U87 cells.	2,5-dimethylcelecoxib	19-22	DNA damage inducible transcript 3	Homo sapiens	281-285
25068992-4	2014	Further, bufotalin induced endoplasmic reticulum (ER) stress activation in osteoblastoma cells, the latter was detected by the induction of C/EBP homologous protein (CHOP), phosphorylation of inositol-requiring enzyme 1 (IRE1) and PKR-like endoplasmic reticulum kinase (PERK), as well as caspase-12 activation.	bufotalin	9-18	DNA damage inducible transcript 3	Homo sapiens	140-164
25038520-7	2014	On the other hand, pioglitazone stimulated the expression of the unfolded protein response (UPR) marker DDIT3, with this effect occurring at early times and inhibitable by the PPARgamma antagonist GW9962.	Pioglitazone	19-31	DNA damage inducible transcript 3	Homo sapiens	104-109
25038520-7	2014	On the other hand, pioglitazone stimulated the expression of the unfolded protein response (UPR) marker DDIT3, with this effect occurring at early times and inhibitable by the PPARgamma antagonist GW9962.	gw9962	197-203	DNA damage inducible transcript 3	Homo sapiens	104-109
25038520-9	2014	Thus, pioglitazone promotes CYP11B2 expression but nevertheless inhibits aldosterone production in AngII-treated HAC15 cells, likely by blocking global protein translation initiation through DDIT3 and phospho-eIF2alpha.	Pioglitazone	6-18	DNA damage inducible transcript 3	Homo sapiens	191-196
25068992-4	2014	Further, bufotalin induced endoplasmic reticulum (ER) stress activation in osteoblastoma cells, the latter was detected by the induction of C/EBP homologous protein (CHOP), phosphorylation of inositol-requiring enzyme 1 (IRE1) and PKR-like endoplasmic reticulum kinase (PERK), as well as caspase-12 activation.	bufotalin	9-18	DNA damage inducible transcript 3	Homo sapiens	166-170
25068992-5	2014	Conversely, the ER stress inhibitor salubrinal, the caspase-12 inhibitor z-ATAD-fmk as well as CHOP depletion by shRNA significantly inhibited bufotalin-induced osteoblastoma cell death and apoptosis.	bufotalin	143-152	DNA damage inducible transcript 3	Homo sapiens	95-99
24982422-3	2014	Zymosan induced the mobilization of CHOP from the nuclear fractions to phagocytic vesicles.	Zymosan	0-7	DNA damage inducible transcript 3	Homo sapiens	36-40
24982422-9	2014	These data indicate the following: (i) zymosan decreases nuclear proapoptotic CHOP, most likely by promoting its accumulation in phagocytic vesicles; (ii) zymosan-induced il23a mRNA expression is best explained through coordinated kappaB- and ATF2-dependent transcription; and (iii) il23a expression relies on complementary phosphorylation of ATF2 on Thr-69 and Thr-71 dependent on PKC and MAPK activities.	Zymosan	39-46	DNA damage inducible transcript 3	Homo sapiens	78-82
24934808-9	2014	Importantly, TAS-117 enhanced bortezomib-induced cytotoxicity, associated with increased CHOP and PARP cleavage and blockade of bortezomib-induced p-Akt, suggesting that TAS-117 augments bortezomib-induced ER stress and apoptotic signaling.	3-amino-1-methyl-3-(4-(3-phenyl-5H- imidazo(1,2-c)pyrido(3,4-e)(1,3)oxazin-2-yl)phenyl)cyclobutanol	13-20	DNA damage inducible transcript 3	Homo sapiens	89-93
24982422-9	2014	These data indicate the following: (i) zymosan decreases nuclear proapoptotic CHOP, most likely by promoting its accumulation in phagocytic vesicles; (ii) zymosan-induced il23a mRNA expression is best explained through coordinated kappaB- and ATF2-dependent transcription; and (iii) il23a expression relies on complementary phosphorylation of ATF2 on Thr-69 and Thr-71 dependent on PKC and MAPK activities.	Zymosan	155-162	DNA damage inducible transcript 3	Homo sapiens	78-82
25337281-5	2014	The patient was treated with 6 courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone), which resulted in complete remission (CR).	Cyclophosphamide	56-72	DNA damage inducible transcript 3	Homo sapiens	42-46
25337281-5	2014	The patient was treated with 6 courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone), which resulted in complete remission (CR).	Doxorubicin	74-85	DNA damage inducible transcript 3	Homo sapiens	42-46
25337281-5	2014	The patient was treated with 6 courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone), which resulted in complete remission (CR).	Vincristine	87-98	DNA damage inducible transcript 3	Homo sapiens	42-46
25337281-5	2014	The patient was treated with 6 courses of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone), which resulted in complete remission (CR).	Prednisolone	104-116	DNA damage inducible transcript 3	Homo sapiens	42-46
25090026-8	2014	In univariate analysis, high MYC/BCL2 DHS, high MYC/BCL6 DHS and high THS were associated with inferior OS and PFS in both CHOP and R-CHOP cohorts (P&lt;0.05).	THYMIDINE-5'-(DITHIO)PHOSPHATE	70-73	DNA damage inducible transcript 3	Homo sapiens	123-127
24423982-2	2014	Here, we quantified the growth inhibition rate of a panel of clinically approved anticancer drugs in a patient-derived DLBCL cell line that is resistant to doxorubicin, a central component of the standard of care R-CHOP.	Doxorubicin	156-167	DNA damage inducible transcript 3	Homo sapiens	215-219
25090026-11	2014	These data together suggest that the immunohistochemical DHSs and THS defined a large subset of DLBCLs with double-hit biology and was strongly associated with poor outcome in patients treated with R-CHOP or CHOP.	THYMIDINE-5'-(DITHIO)PHOSPHATE	66-69	DNA damage inducible transcript 3	Homo sapiens	208-212
24815720-10	2014	Bortezomib treatment induced ER stress, evident by strong induction of Grp78, CHOP, PERK, and IRE1alpha (Western blot analysis) and the UPR (induction of hsp40, 70, and 90).	Bortezomib	0-10	DNA damage inducible transcript 3	Homo sapiens	78-82
24911634-8	2014	Pretreatment with irestatin 9389, salubrinal, or AEBSF also blocked ox-LDL-induced expression of CHOP and Bcl-2 and activation of caspase-12 activity, leading to an attenuation of endothelial cell apoptosis.	irestatin	18-27	DNA damage inducible transcript 3	Homo sapiens	97-101
24911634-8	2014	Pretreatment with irestatin 9389, salubrinal, or AEBSF also blocked ox-LDL-induced expression of CHOP and Bcl-2 and activation of caspase-12 activity, leading to an attenuation of endothelial cell apoptosis.	salubrinal	34-44	DNA damage inducible transcript 3	Homo sapiens	97-101
24911634-8	2014	Pretreatment with irestatin 9389, salubrinal, or AEBSF also blocked ox-LDL-induced expression of CHOP and Bcl-2 and activation of caspase-12 activity, leading to an attenuation of endothelial cell apoptosis.	4-(2-aminoethyl)benzenesulfonylfluoride	49-54	DNA damage inducible transcript 3	Homo sapiens	97-101
24931464-2	2014	We report here that low expression of miR-146b-5p and miR-320d is associated with poor prognosis of DLBCL patients treated with the standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen and that this is related to the inhibitory effect of these miRs on DLBCL cell proliferation.	Prednisone	189-199	DNA damage inducible transcript 3	Homo sapiens	201-205
24883150-0	2014	Risk Factors for Early-Onset Peripheral Neuropathy Caused by Vincristine in Patients With a First Administration of R-CHOP or R-CHOP-Like Chemotherapy.	Vincristine	61-72	DNA damage inducible transcript 3	Homo sapiens	118-122
24883150-0	2014	Risk Factors for Early-Onset Peripheral Neuropathy Caused by Vincristine in Patients With a First Administration of R-CHOP or R-CHOP-Like Chemotherapy.	Vincristine	61-72	DNA damage inducible transcript 3	Homo sapiens	128-132
24883150-1	2014	BACKGROUND: Peripheral neuropathy is a well-known side effect of vincristine (VCR), a microtubule inhibitor used for R-CHOP or R-CHOP-like (namely R-CVP and R-THP-COP) regimens.	Vincristine	65-76	DNA damage inducible transcript 3	Homo sapiens	119-123
24883150-1	2014	BACKGROUND: Peripheral neuropathy is a well-known side effect of vincristine (VCR), a microtubule inhibitor used for R-CHOP or R-CHOP-like (namely R-CVP and R-THP-COP) regimens.	Vincristine	65-76	DNA damage inducible transcript 3	Homo sapiens	129-133
24883150-1	2014	BACKGROUND: Peripheral neuropathy is a well-known side effect of vincristine (VCR), a microtubule inhibitor used for R-CHOP or R-CHOP-like (namely R-CVP and R-THP-COP) regimens.	r-cvp	147-152	DNA damage inducible transcript 3	Homo sapiens	129-133
25042202-0	2014	Combination of ibrutinib with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) for treatment-naive patients with CD20-positive B-cell non-Hodgkin lymphoma: a non-randomised, phase 1b study.	ibrutinib	15-24	DNA damage inducible transcript 3	Homo sapiens	103-107
25042202-0	2014	Combination of ibrutinib with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) for treatment-naive patients with CD20-positive B-cell non-Hodgkin lymphoma: a non-randomised, phase 1b study.	Prednisone	89-99	DNA damage inducible transcript 3	Homo sapiens	103-107
25042202-1	2014	BACKGROUND: Present first-line therapy for diffuse large B-cell lymphoma, a subtype of non-Hodgkin lymphoma, is rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Doxorubicin	141-152	DNA damage inducible transcript 3	Homo sapiens	185-189
25042202-21	2014	INTERPRETATION: Ibrutinib is well tolerated when added to R-CHOP, and could improve responses in patients with B-cell non-Hodgkin lymphoma, but our findings need confirmation in a phase 3 trial.	ibrutinib	16-25	DNA damage inducible transcript 3	Homo sapiens	60-64
24802810-8	2014	Western blot analysis showed that UA promoted the phosphorylation of PERK and eIF2alpha; this was followed by the upregulation of the downstream protein CHOP, implying the involvement of the ER stress-mediated PERK/eIF2alpha/CHOP pathway in glioma cells.	ursolic acid	34-36	DNA damage inducible transcript 3	Homo sapiens	153-157
24802810-8	2014	Western blot analysis showed that UA promoted the phosphorylation of PERK and eIF2alpha; this was followed by the upregulation of the downstream protein CHOP, implying the involvement of the ER stress-mediated PERK/eIF2alpha/CHOP pathway in glioma cells.	ursolic acid	34-36	DNA damage inducible transcript 3	Homo sapiens	225-229
25104093-5	2014	ROS, the expression levels of glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the combination of the two elements.	Reactive Oxygen Species	0-3	DNA damage inducible transcript 3	Homo sapiens	74-98
25197420-5	2014	The patient was treated with chemotherapeutic regimens-CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone).	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	55-59
25197420-5	2014	The patient was treated with chemotherapeutic regimens-CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone).	Doxorubicin	79-90	DNA damage inducible transcript 3	Homo sapiens	55-59
25197420-5	2014	The patient was treated with chemotherapeutic regimens-CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone).	Vincristine	92-103	DNA damage inducible transcript 3	Homo sapiens	55-59
25197420-5	2014	The patient was treated with chemotherapeutic regimens-CHOP (cyclophosphamide, doxorubicin, vincristine and prednisolone).	Prednisolone	108-120	DNA damage inducible transcript 3	Homo sapiens	55-59
24612334-1	2014	OBJECTIVES: Chemoimmunotherapy with cyclophosphamide, doxorubicin, vincristine, prednisolone, and rituximab (R-CHOP) is the standard of care for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	111-115
25054764-7	2014	R-CHOP chemotherapy regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) is the most widely accepted treatment.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	2-6
25054764-7	2014	R-CHOP chemotherapy regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) is the most widely accepted treatment.	Doxorubicin	58-69	DNA damage inducible transcript 3	Homo sapiens	2-6
25054764-7	2014	R-CHOP chemotherapy regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) is the most widely accepted treatment.	Vincristine	71-82	DNA damage inducible transcript 3	Homo sapiens	2-6
25054764-7	2014	R-CHOP chemotherapy regimen (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) is the most widely accepted treatment.	Prednisone	87-97	DNA damage inducible transcript 3	Homo sapiens	2-6
25104093-5	2014	ROS, the expression levels of glucose-regulated protein 78 (GRP78), IRE1, C/EBP homologous protein (CHOP), and spliced X-box-binding protein-1 (sXBP-1) were enhanced by fluoride or the combination of the two elements.	Fluorides	169-177	DNA damage inducible transcript 3	Homo sapiens	74-98
24752500-7	2014	Targeted RNA interference studies revealed that whereas ER stress signaling through inositol-requiring enzyme 1alpha (IRE1alpha) and activating transcription factor 6 (ATF6) acted cytoprotective, activation of the ER stress protein kinase PERK and subsequent expression of CHOP was pivotal for the onset of drug/TNFalpha-induced apoptosis.	Inositol	84-92	DNA damage inducible transcript 3	Homo sapiens	273-277
25286699-7	2014	The patients receiving HyperCVAD regimen had significantly longer overall survival (OS) (median 31.5 vs. 11 months, P = 0.012 7) and progression-free survival (PFS) time (median 16 vs. 5 months, P= 0.000 4) than those receiving CHOP regimen.	hypercvad	23-32	DNA damage inducible transcript 3	Homo sapiens	228-232
24180329-4	2014	Subanalysis of patients receiving cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) +- rituximab showed higher predictive power for both PFS (HR 2.75, 95% confidence interval [CI] 1.24-6.11, p = 0.01) and OS (HR 3.33, 95% CI 1.15-9.63, p = 0.02).	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
24180329-4	2014	Subanalysis of patients receiving cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) +- rituximab showed higher predictive power for both PFS (HR 2.75, 95% confidence interval [CI] 1.24-6.11, p = 0.01) and OS (HR 3.33, 95% CI 1.15-9.63, p = 0.02).	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
24768708-6	2014	Knockdown of C/EBP homologous protein (CHOP) with small interference RNA partially reversed erlotinib-induced apoptosis, production of IL-6 and down-regulation of E-cadherin in cultured intestinal epithelial cells.	Erlotinib Hydrochloride	92-101	DNA damage inducible transcript 3	Homo sapiens	13-37
24666891-6	2014	Quercetin administration modulated expression level of ER stress genes coding for glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP), and antioxidant enzymes such as superoxide dismutase and catalase, along with free radical generation assessed by malondialdehyde assay.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	123-147
24768708-6	2014	Knockdown of C/EBP homologous protein (CHOP) with small interference RNA partially reversed erlotinib-induced apoptosis, production of IL-6 and down-regulation of E-cadherin in cultured intestinal epithelial cells.	Erlotinib Hydrochloride	92-101	DNA damage inducible transcript 3	Homo sapiens	39-43
24530428-12	2014	CONCLUSIONS: The tellurium-containing compound DP41, in contrast to the corresponding selenium compound, induces O2(-) radical formation and oxidative and ER stress responses, including CHOP activation and finally apoptosis.	Tellurium	17-26	DNA damage inducible transcript 3	Homo sapiens	186-190
24530428-12	2014	CONCLUSIONS: The tellurium-containing compound DP41, in contrast to the corresponding selenium compound, induces O2(-) radical formation and oxidative and ER stress responses, including CHOP activation and finally apoptosis.	dp41	47-51	DNA damage inducible transcript 3	Homo sapiens	186-190
24963104-5	2014	The objective of the present study was to determine the contribution of the oxysterol-induced pro-apoptotic transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP) on the pathogenesis of CKD-dependent cardiovascular diseases through endoplasmic reticulum stress signaling.	Oxysterols	76-85	DNA damage inducible transcript 3	Homo sapiens	129-178
24963104-5	2014	The objective of the present study was to determine the contribution of the oxysterol-induced pro-apoptotic transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP) on the pathogenesis of CKD-dependent cardiovascular diseases through endoplasmic reticulum stress signaling.	Oxysterols	76-85	DNA damage inducible transcript 3	Homo sapiens	180-184
24963104-9	2014	The short hairpin RNA-mediated knockdown of CHOP and activating transcription factor-4 in vascular smooth muscle cells attenuated oxysterol-induced mineralization, osteogenic differentiation, and endoplasmic reticulum stress.	Oxysterols	130-139	DNA damage inducible transcript 3	Homo sapiens	44-48
24781973-9	2014	Within the anthracycline-treatment subgroup, the combined GRP78 and CHOP exhibited similar predictive significance.	Anthracyclines	11-24	DNA damage inducible transcript 3	Homo sapiens	68-72
24666891-6	2014	Quercetin administration modulated expression level of ER stress genes coding for glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP), and antioxidant enzymes such as superoxide dismutase and catalase, along with free radical generation assessed by malondialdehyde assay.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	149-153
24738922-11	2014	DDIT3 overexpression reduced HDPC proliferation, however, it increased their calcium nodule formation and expression of OSX, DSPP, DMP1 and OCN.	Calcium	77-84	DNA damage inducible transcript 3	Homo sapiens	0-5
24666891-8	2014	CONCLUSION: The current study indicates that quercetin modulated stress responsive genes GRP78 and CHOP, helping endothelial cells prevent TUN-induced ER stress.	Quercetin	45-54	DNA damage inducible transcript 3	Homo sapiens	99-103
24878898-10	2014	In particular, the JNK-specific inhibitor SP600125 blocked KIOM-C-induced ROS generation and CHOP expression almost completely, which consequently almost completely rescued cell death, indicating that JNK activation plays a critical role in KIOM-C-induced cell death.	pyrazolanthrone	42-50	DNA damage inducible transcript 3	Homo sapiens	93-97
24943970-0	2014	The relationship between anticancer effect of metformin and the transcriptional regulation of certain genes (CHOP, CAV-1, HO-1, SGK-1 and Par-4) on MCF-7 cell line.	Metformin	46-55	DNA damage inducible transcript 3	Homo sapiens	109-113
27708882-0	2014	Sjogren"s syndrome complicated with retroperitoneal Non-Hodgkin"s lymphoma: A case of an elderly woman during methotrexate treatment, treated with R-CHOP.	Methotrexate	110-122	DNA damage inducible transcript 3	Homo sapiens	149-153
25129083-6	2014	The incidence of FN in patients receiving the standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone(R-CHOP)regimen is approximately 20%.	Prednisone	114-124	DNA damage inducible transcript 3	Homo sapiens	127-131
24622883-5	2014	DFO and PHEN downregulated Grp78, Grp94, and MRP1 expressions and upregulated CHOP and HO-1 expressions.	Deferoxamine	0-3	DNA damage inducible transcript 3	Homo sapiens	78-82
24989286-9	2014	After 2 cycles of treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone(R-CHOP), the images of increasing metabolic activity in subcutaneous soft tissue gap disappeared, but the partial increasing metabolism focus could be observed in soft tissue of left knee hollow.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	106-110
24989286-9	2014	After 2 cycles of treatment with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone(R-CHOP), the images of increasing metabolic activity in subcutaneous soft tissue gap disappeared, but the partial increasing metabolism focus could be observed in soft tissue of left knee hollow.	Prednisolone	91-103	DNA damage inducible transcript 3	Homo sapiens	106-110
24706190-7	2014	Moreover, bortezomib-induced up-regulation of CHOP was readily enhanced by lenalidomide in contact with stromal cells.	Bortezomib	10-20	DNA damage inducible transcript 3	Homo sapiens	46-50
24706190-7	2014	Moreover, bortezomib-induced up-regulation of CHOP was readily enhanced by lenalidomide in contact with stromal cells.	Lenalidomide	75-87	DNA damage inducible transcript 3	Homo sapiens	46-50
24768635-8	2014	Moreover, when ATF3 knockdown cells were exposed to CsA, a prompt induction of CHOP was observed, which stimulated ROS production and induced cell death-related genes as compared to wild type.	Cyclosporine	52-55	DNA damage inducible transcript 3	Homo sapiens	79-83
24768635-8	2014	Moreover, when ATF3 knockdown cells were exposed to CsA, a prompt induction of CHOP was observed, which stimulated ROS production and induced cell death-related genes as compared to wild type.	ros	115-118	DNA damage inducible transcript 3	Homo sapiens	79-83
24768635-9	2014	Taken together, our data demonstrate that ATF3 plays a pivotal role in the attenuation of CsA-induced nephrotoxicity by downregulating CHOP and ROS production mediated by ER stress.	Cyclosporine	90-93	DNA damage inducible transcript 3	Homo sapiens	135-139
24859553-1	2014	Summary We report a case of a 56-year-old woman with a high-grade diffuse large B-cell lymphoma who unexpectedly developed toxic plasma levels of methotrexate (MTX) following the first cycle of rituximab-cyclophosphamide, hydroxydanorubicin, oncovin, prednisolone (R-CHOP) with a high-dose MTX chemotherapy protocol.	Methotrexate	146-158	DNA damage inducible transcript 3	Homo sapiens	267-271
24859553-1	2014	Summary We report a case of a 56-year-old woman with a high-grade diffuse large B-cell lymphoma who unexpectedly developed toxic plasma levels of methotrexate (MTX) following the first cycle of rituximab-cyclophosphamide, hydroxydanorubicin, oncovin, prednisolone (R-CHOP) with a high-dose MTX chemotherapy protocol.	Methotrexate	160-163	DNA damage inducible transcript 3	Homo sapiens	267-271
24556569-6	2014	In addition, NAC significantly attenuated MSG-induced endoplasmic reticulum (ER) stress markers, such as XBP1 splicing and CHOP, PERK, and GRP78 up-regulation.	Acetylcysteine	13-16	DNA damage inducible transcript 3	Homo sapiens	123-127
24078384-9	2014	By employing dithiothreitol as an UPR inducer, we observed that cells with silenced RHBDD2 showed increased expression of ATF6, IRE1, PERK, CRT, BiP, ATF4, and CHOP (p &lt;0.01).	Dithiothreitol	13-27	DNA damage inducible transcript 3	Homo sapiens	160-164
24053669-5	2014	Suppressing ER stress or inhibiting CHOP activation by pharmacological chaperones or genetic approaches attenuated hydroquinone-induced RPE cell apoptosis.	hydroquinone	115-127	DNA damage inducible transcript 3	Homo sapiens	36-40
24053669-6	2014	In contrast to enhanced CHOP activation, protein level of active X-box binding protein 1 (XBP1), a major regulator of the adaptive UPR, was reduced in hydroquinone-treated cells.	hydroquinone	151-163	DNA damage inducible transcript 3	Homo sapiens	24-28
24668805-0	2014	Ischemia-like oxygen and glucose deprivation mediates down-regulation of cell surface gamma-aminobutyric acidB receptors via the endoplasmic reticulum (ER) stress-induced transcription factor CCAAT/enhancer-binding protein (C/EBP)-homologous protein (CHOP).	Oxygen	14-20	DNA damage inducible transcript 3	Homo sapiens	251-255
24279877-8	2014	Expression of CHOP in SSc lung is accompanied by positive staining for the thrombin receptor, protease-activated receptor-1, and for terminal deoxynucleotidyl transferase dUTP nick end labeling, suggesting roles for both thrombin and CHOP in AEC apoptosis in SSc-ILD.	deoxyuridine triphosphate	171-175	DNA damage inducible transcript 3	Homo sapiens	14-18
24373849-7	2014	Acrolein (25-50muM) caused apoptotic cell death mediated by the ER after 2h, which was characterised by the induction of CHOP and activation of ER proteases calpain and caspase-4.	Acrolein	0-8	DNA damage inducible transcript 3	Homo sapiens	121-125
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	174-223
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	225-229
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Reactive Oxygen Species	135-158	DNA damage inducible transcript 3	Homo sapiens	174-223
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Reactive Oxygen Species	135-158	DNA damage inducible transcript 3	Homo sapiens	225-229
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Reactive Oxygen Species	160-163	DNA damage inducible transcript 3	Homo sapiens	174-223
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Reactive Oxygen Species	160-163	DNA damage inducible transcript 3	Homo sapiens	225-229
24612139-5	2014	The induction of DR5 was mediated through activation of JNK and through upregulation of a transcription factor CCAAT enhancer-binding protein homologous protein (CHOP); as silencing of these signaling molecules abrogated the effect of quercetin.	Quercetin	235-244	DNA damage inducible transcript 3	Homo sapiens	111-160
24612139-5	2014	The induction of DR5 was mediated through activation of JNK and through upregulation of a transcription factor CCAAT enhancer-binding protein homologous protein (CHOP); as silencing of these signaling molecules abrogated the effect of quercetin.	Quercetin	235-244	DNA damage inducible transcript 3	Homo sapiens	162-166
24612139-6	2014	Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins.	Reactive Oxygen Species	93-96	DNA damage inducible transcript 3	Homo sapiens	159-163
24612139-6	2014	Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins.	Quercetin	130-139	DNA damage inducible transcript 3	Homo sapiens	159-163
24612139-7	2014	Furthermore, quercetin enhances TRAIL mediated inhibition of tumor growth of human SKOV-3 xenograft was associated with induction of apoptosis, activation of caspase-3, CHOP and DR5.	Quercetin	13-22	DNA damage inducible transcript 3	Homo sapiens	169-173
24612139-8	2014	Overall, our data suggest that quercetin enhances apoptotic death of ovarian cancer cells to TRAIL through upregulation of CHOP-induced DR5 expression following ROS mediated endoplasmic reticulum-stress.	Quercetin	31-40	DNA damage inducible transcript 3	Homo sapiens	123-127
24612139-8	2014	Overall, our data suggest that quercetin enhances apoptotic death of ovarian cancer cells to TRAIL through upregulation of CHOP-induced DR5 expression following ROS mediated endoplasmic reticulum-stress.	Reactive Oxygen Species	161-164	DNA damage inducible transcript 3	Homo sapiens	123-127
24213373-7	2014	Induction of the DR5 by indomethacin was found to be p53 independent but dependent on the induction of CCAAT/enhancer-binding protein homologous protein (CHOP).	Indomethacin	24-36	DNA damage inducible transcript 3	Homo sapiens	103-152
24691439-8	2014	Dexamethasone induced the transcriptional factor CHOP, a marker for chronic ER stress, in the anterior segment tissues, and Chop deletion reduced ER stress in these tissues and prevented dexamethasone-induced ocular hypertension.	Dexamethasone	0-13	DNA damage inducible transcript 3	Homo sapiens	49-53
24691439-8	2014	Dexamethasone induced the transcriptional factor CHOP, a marker for chronic ER stress, in the anterior segment tissues, and Chop deletion reduced ER stress in these tissues and prevented dexamethasone-induced ocular hypertension.	Dexamethasone	187-200	DNA damage inducible transcript 3	Homo sapiens	124-128
24213373-7	2014	Induction of the DR5 by indomethacin was found to be p53 independent but dependent on the induction of CCAAT/enhancer-binding protein homologous protein (CHOP).	Indomethacin	24-36	DNA damage inducible transcript 3	Homo sapiens	154-158
24213373-8	2014	Knockdown of CHOP abolished indomethacin-induced DR5 expression and the associated potentiation of TRAIL-mediated cell death.	Indomethacin	28-40	DNA damage inducible transcript 3	Homo sapiens	13-17
24213373-9	2014	In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL.	Indomethacin	13-25	DNA damage inducible transcript 3	Homo sapiens	100-104
24213373-9	2014	In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL.	Reactive Oxygen Species	34-57	DNA damage inducible transcript 3	Homo sapiens	100-104
24213373-9	2014	In addition, indomethacin-induced reactive oxygen species (ROS) production preceded upregulation of CHOP and DR5, and consequent sensitization of cells to TRAIL.	Reactive Oxygen Species	59-62	DNA damage inducible transcript 3	Homo sapiens	100-104
24769598-2	2014	was diagnosed with non-Hodgkin lymphoma and underwent treatment with standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy.	Prednisone	137-147	DNA damage inducible transcript 3	Homo sapiens	151-155
24851895-7	2014	The high glucose with adiponectin group could reduce the podocyte apoptosis by 10% and down-regulated the mRNA and protein expressions of GRP78, CHOP and caspase 12 versus high glucose group (all P &lt; 0.05).	Glucose	9-16	DNA damage inducible transcript 3	Homo sapiens	145-149
24362844-9	2014	CONCLUSION: The results suggest a guideline for plasma glucose monitoring during CHOP chemotherapy in patients with no history of DM.	Glucose	55-62	DNA damage inducible transcript 3	Homo sapiens	81-85
24493716-1	2014	PURPOSE: R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard care for aggressive B-cell lymphoma.	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	11-15
24851895-6	2014	Compared with control group, the mRNA and protein expressions of GRP78, CHOP and caspase 12 were all up-regulated significantly in high glucose group (P &lt; 0.05).	Glucose	136-143	DNA damage inducible transcript 3	Homo sapiens	72-76
24493716-1	2014	PURPOSE: R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard care for aggressive B-cell lymphoma.	Doxorubicin	50-61	DNA damage inducible transcript 3	Homo sapiens	11-15
24493716-1	2014	PURPOSE: R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard care for aggressive B-cell lymphoma.	Vincristine	63-74	DNA damage inducible transcript 3	Homo sapiens	11-15
24493716-1	2014	PURPOSE: R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard care for aggressive B-cell lymphoma.	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	11-15
22431435-9	2014	Quercetin also stimulated the protein expression of ATF, GRP78, and GADD153 which is a hall marker of ER stress.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	68-75
24692703-3	2014	A 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay was performed to determine the change in growth inhibition by celecoxib after inhibition of the ER stress pathway by CHOP small-interfering RNA (siRNA).	Celecoxib	137-146	DNA damage inducible transcript 3	Homo sapiens	192-196
24692703-4	2014	RESULTS: Celecoxib triggered an ER stress response in this HNSCC cell line as shown by activation of CHOP, GRP78 and XBP1.	Celecoxib	9-18	DNA damage inducible transcript 3	Homo sapiens	101-105
24692703-5	2014	The inhibition of cell proliferation by celecoxib was effectively hindered with CHOP siRNA.	Celecoxib	40-49	DNA damage inducible transcript 3	Homo sapiens	80-84
24343359-6	2014	Polyphenon E  induced severe ERS in PC3 cells, causing a dramatic enlargement of the ER; persistent activation of UPR produced strong upregulation of GADD153/CHOP, a key protein of ERS-mediated cell death.	polyphenon E	0-12	DNA damage inducible transcript 3	Homo sapiens	158-162
24337903-5	2014	LicA also induced reactive oxygen species (ROS) accumulation and the anti-oxidant N-acetylcysteine reduced LicA-induced cell death and CHOP expression.	Acetylcysteine	82-98	DNA damage inducible transcript 3	Homo sapiens	135-139
25039189-7	2014	Curcumin could significantly increase the expression levels of GRP78 and CHOP in breast cancer cells.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	73-77
24525405-5	2014	Consequently, the integrated ER stress signals, such as eIF2alpha, ATF4, BiP, and CHOP are altered accordingly to induce ER-Ca2+ release, reactive oxygen species (ROS) overproduction, and cell death in HLECs treated with VPA.	Reactive Oxygen Species	138-161	DNA damage inducible transcript 3	Homo sapiens	82-86
24525405-5	2014	Consequently, the integrated ER stress signals, such as eIF2alpha, ATF4, BiP, and CHOP are altered accordingly to induce ER-Ca2+ release, reactive oxygen species (ROS) overproduction, and cell death in HLECs treated with VPA.	Reactive Oxygen Species	163-166	DNA damage inducible transcript 3	Homo sapiens	82-86
24525405-5	2014	Consequently, the integrated ER stress signals, such as eIF2alpha, ATF4, BiP, and CHOP are altered accordingly to induce ER-Ca2+ release, reactive oxygen species (ROS) overproduction, and cell death in HLECs treated with VPA.	Valproic Acid	221-224	DNA damage inducible transcript 3	Homo sapiens	82-86
24490819-5	2014	More importantly, ZnO NPs at noncytotoxic concentration, but not CeO2 NPs, can induce significant cellular ER stress response with higher expression of spliced xbp-1, chop, and caspase-12 at the mRNA level, and associated ER marker proteins including BiP, Chop, GADD34, p-PERK, p-eIF2alpha, and cleaved Caspase-12 at the protein levels.	Zinc Oxide	18-21	DNA damage inducible transcript 3	Homo sapiens	167-171
24490819-5	2014	More importantly, ZnO NPs at noncytotoxic concentration, but not CeO2 NPs, can induce significant cellular ER stress response with higher expression of spliced xbp-1, chop, and caspase-12 at the mRNA level, and associated ER marker proteins including BiP, Chop, GADD34, p-PERK, p-eIF2alpha, and cleaved Caspase-12 at the protein levels.	Zinc Oxide	18-21	DNA damage inducible transcript 3	Homo sapiens	256-260
24264887-7	2014	The proapoptotic effect of RSV was enhanced after suppression of autophagy by ATG7 siRNA or blocking the autophagic flux by bafilomycin A1, but that was not changed after targeted silence of IRE1 or CHOP by siRNA.	Resveratrol	27-30	DNA damage inducible transcript 3	Homo sapiens	199-203
24625971-0	2014	Stronger proteasomal inhibition and higher CHOP induction are responsible for more effective induction of paraptosis by dimethoxycurcumin than curcumin.	dimethoxycurcumin	120-137	DNA damage inducible transcript 3	Homo sapiens	43-47
24625971-0	2014	Stronger proteasomal inhibition and higher CHOP induction are responsible for more effective induction of paraptosis by dimethoxycurcumin than curcumin.	Curcumin	129-137	DNA damage inducible transcript 3	Homo sapiens	43-47
24625971-6	2014	DMC treatment upregulates the protein levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and Noxa, and the small interfering RNA-mediated suppression of CHOP, but not Noxa, markedly attenuates DMC-induced ER dilation and cell death.	dimethoxycurcumin	0-3	DNA damage inducible transcript 3	Homo sapiens	48-97
24625971-6	2014	DMC treatment upregulates the protein levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and Noxa, and the small interfering RNA-mediated suppression of CHOP, but not Noxa, markedly attenuates DMC-induced ER dilation and cell death.	dimethoxycurcumin	0-3	DNA damage inducible transcript 3	Homo sapiens	99-103
24625971-6	2014	DMC treatment upregulates the protein levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and Noxa, and the small interfering RNA-mediated suppression of CHOP, but not Noxa, markedly attenuates DMC-induced ER dilation and cell death.	dimethoxycurcumin	0-3	DNA damage inducible transcript 3	Homo sapiens	169-173
24625971-6	2014	DMC treatment upregulates the protein levels of CCAAT-enhancer-binding protein homologous protein (CHOP) and Noxa, and the small interfering RNA-mediated suppression of CHOP, but not Noxa, markedly attenuates DMC-induced ER dilation and cell death.	dimethoxycurcumin	209-212	DNA damage inducible transcript 3	Homo sapiens	169-173
24625971-8	2014	Taken together, these results suggest that DMC triggers a stronger proteasome inhibition and higher induction of CHOP compared with curcumin, giving it more potent anticancer effects on malignant breast cancer cells.	dimethoxycurcumin	43-46	DNA damage inducible transcript 3	Homo sapiens	113-117
24412303-12	2014	Soluble CaCO3 nanoparticles caused an increase in C/EBP-homologous protein (CHOP) expression and the activation of caspase-3.	Calcium Carbonate	8-13	DNA damage inducible transcript 3	Homo sapiens	50-74
24412303-12	2014	Soluble CaCO3 nanoparticles caused an increase in C/EBP-homologous protein (CHOP) expression and the activation of caspase-3.	Calcium Carbonate	8-13	DNA damage inducible transcript 3	Homo sapiens	76-80
24464048-10	2014	Furthermore, both OSU-CG5 and resveratrol induced dose-dependent energy restriction in the cells: they suppressed glucose uptake and Akt phosphorylation, decreased the levels of p-mTOR and p-p70S6K, increased the levels of ER stress response proteins GRP78 and GADD153, and increased the level of beta-TrCP, which led to the downregulation of cyclin D1 and Sp1.	OSU-CG5	18-25	DNA damage inducible transcript 3	Homo sapiens	261-268
24464048-10	2014	Furthermore, both OSU-CG5 and resveratrol induced dose-dependent energy restriction in the cells: they suppressed glucose uptake and Akt phosphorylation, decreased the levels of p-mTOR and p-p70S6K, increased the levels of ER stress response proteins GRP78 and GADD153, and increased the level of beta-TrCP, which led to the downregulation of cyclin D1 and Sp1.	Resveratrol	30-41	DNA damage inducible transcript 3	Homo sapiens	261-268
23734653-4	2014	In 80 patients chemotherapy was initiated; 70 patients received rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP).	Prednisolone	122-134	DNA damage inducible transcript 3	Homo sapiens	138-142
24373961-10	2014	In in vitro studies, increasing amounts of oxPAPC induced a dose-dependent increase in CHOP and apoptosis-related protein expression (p&lt;0.01) and a progressive decrease in Nrf2/ARE gene expression (p&lt;0.01).	oxidized-L-alpha-1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine	43-49	DNA damage inducible transcript 3	Homo sapiens	87-91
24724408-3	2014	The current standard of care for DLBCL is CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) combined with rituximab, anti-CD20 antibody, allowing many patients to achieve disease cure.	Doxorubicin	79-90	DNA damage inducible transcript 3	Homo sapiens	42-46
24469952-2	2014	Three hundred and eighty four DLBCL patients treated with rituximab, cyclophosphamide, doxorubicin/epirubicin, vincristine and prednisone (R-CHOP-like regimens) or CHOP-like regimens were included.	Prednisone	127-137	DNA damage inducible transcript 3	Homo sapiens	141-145
24394546-9	2014	NAC administration and shRNA ETFA conferred resistance to t-BHP-increased ETFA and CHOP expression via IRE1-alpha/TRAF2 complex formation, activation of JNK1/2 and p50.	tert-Butylhydroperoxide	58-63	DNA damage inducible transcript 3	Homo sapiens	83-87
24724408-3	2014	The current standard of care for DLBCL is CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) combined with rituximab, anti-CD20 antibody, allowing many patients to achieve disease cure.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	42-46
24525736-5	2014	Treatment of hepatoma cells with salubrinal, an inhibitor of eIF2alpha dephosphorylation, enhances TRAIL-induced eIF2alpha phosphorylation, CCAAT/enhancer-binding protein homologous protein (CHOP) expression and caspase activation.	salubrinal	33-43	DNA damage inducible transcript 3	Homo sapiens	140-189
23396363-8	2014	Finally, activation of GADD153, an AP-1 target gene, is also associated with a rapid increase in SUMOylation at the level of its TRE and c-Fos SUMOylation dampens its induction by TPA.	Tetradecanoylphorbol Acetate	180-183	DNA damage inducible transcript 3	Homo sapiens	23-30
24525736-5	2014	Treatment of hepatoma cells with salubrinal, an inhibitor of eIF2alpha dephosphorylation, enhances TRAIL-induced eIF2alpha phosphorylation, CCAAT/enhancer-binding protein homologous protein (CHOP) expression and caspase activation.	salubrinal	33-43	DNA damage inducible transcript 3	Homo sapiens	191-195
24525736-10	2014	Furthermore, the sensitization of hepatoma cells to TRAIL by salubrinal is dependent on CHOP.	salubrinal	61-71	DNA damage inducible transcript 3	Homo sapiens	88-92
24525736-11	2014	Knockdown of CHOP abrogates the stimulation of TRAIL-induced caspase activation and apoptosis by salubrinal.	salubrinal	97-107	DNA damage inducible transcript 3	Homo sapiens	13-17
24550689-7	2014	In addition, bufalin was also found to induce ER stress-mediated apoptosis, which was supported by the up- regulation of ER stress markers, CHOP and GRP78, and augmented phosphorylation of PERK and eIF2alpha as well as cleavage of caspase-4.	bufalin	13-20	DNA damage inducible transcript 3	Homo sapiens	140-144
24551210-6	2014	Furthermore, AMP was observed to activate endoplasmic reticulum (ER) stress, as evidenced by the up-regulation of ER stress-related proteins, including GRP78, p-PERK, p-elF2alpha, cleaved ATF6alpha and CHOP, while knockdown of ATF6alpha or PERK markedly down-regulated AMP-induced CHOP expression.	ampelopsin	13-16	DNA damage inducible transcript 3	Homo sapiens	202-206
24551210-6	2014	Furthermore, AMP was observed to activate endoplasmic reticulum (ER) stress, as evidenced by the up-regulation of ER stress-related proteins, including GRP78, p-PERK, p-elF2alpha, cleaved ATF6alpha and CHOP, while knockdown of ATF6alpha or PERK markedly down-regulated AMP-induced CHOP expression.	ampelopsin	13-16	DNA damage inducible transcript 3	Homo sapiens	281-285
24551210-7	2014	Blocking ER stress using 4-phenylbutyric acid not only down-regulated AMP-induced GRP78 and CHOP expression, but also significantly decreased AMP-induced cell growth inhibition and apoptosis, whereas ER stress inducer thapsigargin played opposing effects.	4-phenylbutyric acid	25-45	DNA damage inducible transcript 3	Homo sapiens	92-96
24551210-7	2014	Blocking ER stress using 4-phenylbutyric acid not only down-regulated AMP-induced GRP78 and CHOP expression, but also significantly decreased AMP-induced cell growth inhibition and apoptosis, whereas ER stress inducer thapsigargin played opposing effects.	ampelopsin	70-73	DNA damage inducible transcript 3	Homo sapiens	92-96
24707248-6	2014	RESULTS: The patient received six cycles of CHOP chemotherapy (vincristine, cyclophosphamide, doxorubicin, methylprednisolone) followed by a well-tolerated autologous bone marrow graft.	Vincristine	63-74	DNA damage inducible transcript 3	Homo sapiens	44-48
24551210-8	2014	Additionally, NAC inhibited AMP-induced ER stress by down-regulating GRP78 and CHOP expression.	ampelopsin	28-31	DNA damage inducible transcript 3	Homo sapiens	79-83
24551210-9	2014	Conversely, blocking ER stress using CHOP siRNA decreased AMP-induced ROS production and cell apoptosis.	ampelopsin	58-61	DNA damage inducible transcript 3	Homo sapiens	37-41
24551210-9	2014	Conversely, blocking ER stress using CHOP siRNA decreased AMP-induced ROS production and cell apoptosis.	Reactive Oxygen Species	70-73	DNA damage inducible transcript 3	Homo sapiens	37-41
24550689-11	2014	Furthermore, TUDC and silencing of eIF2alpha or CHOP partially blocked bufalin-induced accumulation of LC3-II, which indicated that ER stress preceded bufalin-induced autophagy and PERK/eIF2alpha/CHOP signaling pathway played a major part in the process.	bufalin	71-78	DNA damage inducible transcript 3	Homo sapiens	48-52
24550689-11	2014	Furthermore, TUDC and silencing of eIF2alpha or CHOP partially blocked bufalin-induced accumulation of LC3-II, which indicated that ER stress preceded bufalin-induced autophagy and PERK/eIF2alpha/CHOP signaling pathway played a major part in the process.	bufalin	71-78	DNA damage inducible transcript 3	Homo sapiens	196-200
24550689-11	2014	Furthermore, TUDC and silencing of eIF2alpha or CHOP partially blocked bufalin-induced accumulation of LC3-II, which indicated that ER stress preceded bufalin-induced autophagy and PERK/eIF2alpha/CHOP signaling pathway played a major part in the process.	bufalin	151-158	DNA damage inducible transcript 3	Homo sapiens	196-200
24275196-9	2014	Our results demonstrate that CAVI-b expression, which is increased through CHOP-signaling in response to unfolded protein stress, is also increased by oxygen-glucose deprivation (OGD).	oxygen-glucose	151-165	DNA damage inducible transcript 3	Homo sapiens	75-79
23880367-4	2014	The results showed that As2O3 increased the expression of GRP78, CHOP, phosphorylated eIF2alpha and ATF4, all of which are the molecule of ER stress.	Arsenic Trioxide	24-29	DNA damage inducible transcript 3	Homo sapiens	65-69
24300666-8	2014	Support of UPR induction was further obtained from the finding of increased protein levels of the ER stress markers DDIT3/CHOP and HSPA5 during ammonia treatment.	Ammonia	144-151	DNA damage inducible transcript 3	Homo sapiens	116-121
24300666-8	2014	Support of UPR induction was further obtained from the finding of increased protein levels of the ER stress markers DDIT3/CHOP and HSPA5 during ammonia treatment.	Ammonia	144-151	DNA damage inducible transcript 3	Homo sapiens	122-126
24395281-9	2014	Combination immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) regimen improved both MALT lymphoma and PLE, whereas rituximab monotherapy was not successful.	Cyclophosphamide	47-63	DNA damage inducible transcript 3	Homo sapiens	111-115
24395281-9	2014	Combination immunochemotherapy with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) regimen improved both MALT lymphoma and PLE, whereas rituximab monotherapy was not successful.	Prednisolone	95-107	DNA damage inducible transcript 3	Homo sapiens	111-115
24308372-5	2014	The relative efficacy of CHOP-R and CVP-R was estimated using an indirect treatment comparison similar to the original ScHARR approach.	r	30-31	DNA damage inducible transcript 3	Homo sapiens	25-29
24416259-0	2014	4-Phenylbutyrate inhibits tunicamycin-induced acute kidney injury via CHOP/GADD153 repression.	4-phenylbutyric acid	0-16	DNA damage inducible transcript 3	Homo sapiens	75-82
24416259-0	2014	4-Phenylbutyrate inhibits tunicamycin-induced acute kidney injury via CHOP/GADD153 repression.	Tunicamycin	26-37	DNA damage inducible transcript 3	Homo sapiens	75-82
24416259-8	2014	In vitro work showed that 4-PBA protected human proximal tubular cells from apoptosis and TM-induced CHOP expression, an ER stress inducible proapoptotic gene.	4-phenylbutyric acid	26-31	DNA damage inducible transcript 3	Homo sapiens	101-105
24416259-13	2014	When taken together, these results indicate that 4-PBA acts as an ER stress inhibitor, to partially protect the kidney from TM-induced AKI through the repression of ER stress-induced CHOP expression.	4-phenylbutyric acid	49-54	DNA damage inducible transcript 3	Homo sapiens	183-187
25610877-2	2014	The diabetogenic effect of palmitate is achieved by increasing beta cell death through induction of the endoplasmic reticulum (ER) stress markers including activating transcription factor 3 (Atf3) and CAAT/enhancer-binding protein homologous protein-10 (Chop).	Palmitates	27-36	DNA damage inducible transcript 3	Homo sapiens	201-252
24387758-11	2014	Knockdown of ATF4 and DDIT3 abrogated PTL-induced apoptosis, which suggested that PTL induced apoptosis in NSCLC cells through activation of endoplasmic reticulum stress pathway.	parthenolide	38-41	DNA damage inducible transcript 3	Homo sapiens	22-27
24387758-11	2014	Knockdown of ATF4 and DDIT3 abrogated PTL-induced apoptosis, which suggested that PTL induced apoptosis in NSCLC cells through activation of endoplasmic reticulum stress pathway.	parthenolide	82-85	DNA damage inducible transcript 3	Homo sapiens	22-27
24192382-10	2014	The addition of rituximab to CHOP seems to be helpful for the management of THRLBCL, as it is for DLBCL-NOS.	thrlbcl	76-83	DNA damage inducible transcript 3	Homo sapiens	29-33
24114361-6	2014	Our data supported the pro-survival role of bufalin-induced autophagy when the autophagy pathway was blocked with specific chemical inhibitors; the involvement of the IRE1 pathway in the ER stress-induced autophagy was also demonstrated when the expression of IRE1 and CHOP was silenced using siRNA.	bufalin	44-51	DNA damage inducible transcript 3	Homo sapiens	269-273
24141009-0	2014	High-dose etoposide plus granulocyte colony-stimulating factor as an effective chemomobilization regimen for autologous stem cell transplantation in patients with non-Hodgkin Lymphoma previously treated with CHOP-based chemotherapy: a study from the Consortium for Improving Survival of Lymphoma.	Etoposide	10-19	DNA damage inducible transcript 3	Homo sapiens	208-212
24872902-7	2014	The patient was able to complete six cycles of rituximab combined with cyclophosphamide, adriamycin, vincristine, and prednisone (R-CHOP) chemotherapy and achieved a complete response verified by positron emission tomography-computed tomography (PET-CT).	Prednisone	118-128	DNA damage inducible transcript 3	Homo sapiens	132-136
24451129-4	2014	We found that ADMA treatment activated the endoplasmic reticulum (ER) stress sensor proteins phosphorylated protein kinase RNA-activated-like ER kinase (PERK) and inositol requiring-1alpha (IRE1), which correspondingly induced C/EBP homologous protein (CHOP) expression and phosphorylated c-Jun N-terminal kinase (JNK) phosphorylation in glomerular endothelial cells (GEnCs).	N,N-dimethylarginine	14-18	DNA damage inducible transcript 3	Homo sapiens	227-251
24451129-4	2014	We found that ADMA treatment activated the endoplasmic reticulum (ER) stress sensor proteins phosphorylated protein kinase RNA-activated-like ER kinase (PERK) and inositol requiring-1alpha (IRE1), which correspondingly induced C/EBP homologous protein (CHOP) expression and phosphorylated c-Jun N-terminal kinase (JNK) phosphorylation in glomerular endothelial cells (GEnCs).	N,N-dimethylarginine	14-18	DNA damage inducible transcript 3	Homo sapiens	253-257
24451129-6	2014	SP600125, an inhibitor of JNK, and CHOP siRNA protected against ADMA-induced cell apoptosis and TGF-beta expression.	N,N-dimethylarginine	64-68	DNA damage inducible transcript 3	Homo sapiens	35-39
24451129-10	2014	Overall, these observations indicate that ADMA may induce GEnCs apoptosis and TGF-beta expression by targeting the PERK-CHOP and IRE1-JNK pathway.	N,N-dimethylarginine	42-46	DNA damage inducible transcript 3	Homo sapiens	120-124
25431671-11	2014	Phosphorylation of p53 and Chk1 and expression of ATF4 and CHOP genes were detected in IS-, PCS-, and PhS-treated cells, but not in IAA-treated cells.	phenylsulfate	102-105	DNA damage inducible transcript 3	Homo sapiens	59-63
25610877-2	2014	The diabetogenic effect of palmitate is achieved by increasing beta cell death through induction of the endoplasmic reticulum (ER) stress markers including activating transcription factor 3 (Atf3) and CAAT/enhancer-binding protein homologous protein-10 (Chop).	Palmitates	27-36	DNA damage inducible transcript 3	Homo sapiens	254-258
25610877-5	2014	The protective effect of MS-275 was associated with the attenuation of the expression of Atf3 and Chop.	entinostat	25-31	DNA damage inducible transcript 3	Homo sapiens	98-102
24068329-10	2014	H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus.	Hydrogen Peroxide	0-4	DNA damage inducible transcript 3	Homo sapiens	125-129
24028444-7	2014	Incremental cost-effectiveness ratios (ICERs) for PP vs SP for CHOP were $13,400 per FN event avoided, $29,500 per QALY gained, and $25,800 per LYS.	TFF2 protein, human	56-58	DNA damage inducible transcript 3	Homo sapiens	63-67
25374377-5	2014	Our results showed that the cadmium-induced increase in expression of the ER stress marker proteins, BiP and CHOP, was further enhanced by inhibiting FBXO6 expression.	Cadmium	28-35	DNA damage inducible transcript 3	Homo sapiens	109-113
24068329-10	2014	H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus.	Hydrogen Peroxide	0-4	DNA damage inducible transcript 3	Homo sapiens	154-158
24068329-10	2014	H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus.	MK-886	9-14	DNA damage inducible transcript 3	Homo sapiens	125-129
24068329-10	2014	H2O2 and MK886 both reduced the viability of HepG2 cells, increased oxidative stress and apoptosis, up-regulated the BiP and CHOP expression, and induced CHOP translocation from the cytoplasm to the nucleus.	MK-886	9-14	DNA damage inducible transcript 3	Homo sapiens	154-158
24068329-11	2014	Compared with cells treated with H2O2 alone, pre-administration of WY14643 increased cell viability, attenuated apoptosis, improved cell function, down-regulated BiP and CHOP expression and inhibited CHOP translocation.	pirinixic acid	67-74	DNA damage inducible transcript 3	Homo sapiens	170-174
24068329-11	2014	Compared with cells treated with H2O2 alone, pre-administration of WY14643 increased cell viability, attenuated apoptosis, improved cell function, down-regulated BiP and CHOP expression and inhibited CHOP translocation.	pirinixic acid	67-74	DNA damage inducible transcript 3	Homo sapiens	200-204
24339898-0	2013	CCAAT/enhancer-binding protein homologous (CHOP) protein promotes carcinogenesis in the DEN-induced hepatocellular carcinoma model.	Diethylnitrosamine	88-91	DNA damage inducible transcript 3	Homo sapiens	43-47
25138135-5	2014	DISCUSSION: Lymphomas are known to be steroid sensitive; the medication is an essential component of the common CHOP therapy.	Steroids	38-45	DNA damage inducible transcript 3	Homo sapiens	112-116
25402962-11	2014	Pretreatment with NAC attenuated the expression of 2 ER stress markers, especially CHOP in A2E and blue light-treated RPE cells.	Acetylcysteine	18-21	DNA damage inducible transcript 3	Homo sapiens	83-87
24368569-5	2013	Palmitic acid was the main compound responsible for this apoptotic effect by a ceramide-independent mechanism that involved endoplasmic reticulum (ER)-stress with upregulation of CCAAT/-enhancer-binding protein homologous protein (CHOP).	Palmitic Acid	0-13	DNA damage inducible transcript 3	Homo sapiens	179-229
24368569-5	2013	Palmitic acid was the main compound responsible for this apoptotic effect by a ceramide-independent mechanism that involved endoplasmic reticulum (ER)-stress with upregulation of CCAAT/-enhancer-binding protein homologous protein (CHOP).	Palmitic Acid	0-13	DNA damage inducible transcript 3	Homo sapiens	231-235
24359437-12	2013	Besides we found that PEE exposure to T24 cells could provoke intensive activation of procaspase-12 and enhance the expressions of CHOP and Bip, endoplasmic reticulum (ER) stress marker, suggesting that ER stress might be the cardinal apoptotic mechanism of PEE-induced inhibition of bladder cancer cell.	pee	22-25	DNA damage inducible transcript 3	Homo sapiens	131-135
24379257-6	2013	It was observed that in vitro treatment with ONC in combination with rituximab, mafosfamide, vincristine, doxorubicin, and dexamethasone (drugs corresponding with elements of R-CHOP regimen) resulted in increased cytotoxicity.	Dexamethasone	123-136	DNA damage inducible transcript 3	Homo sapiens	177-181
24286417-8	2013	In the HUVEC experiment, TUDCA significantly reduced apoptosis and the expressions of GRP78, CHOP and caspase12.	Taurodeoxycholic Acid	25-30	DNA damage inducible transcript 3	Homo sapiens	93-97
23973637-4	2013	We show here that LPV induces the most potent CHOP expression, ER stress marker, among the 9 Food and Drug Administration (FDA)-approved PIs in human peripheral blood mononuclear cells, several human epithelial cells, and mouse embryonic fibroblasts.	Lopinavir	18-21	DNA damage inducible transcript 3	Homo sapiens	46-50
23973637-4	2013	We show here that LPV induces the most potent CHOP expression, ER stress marker, among the 9 Food and Drug Administration (FDA)-approved PIs in human peripheral blood mononuclear cells, several human epithelial cells, and mouse embryonic fibroblasts.	Monothiopyrophosphoric acid	137-140	DNA damage inducible transcript 3	Homo sapiens	46-50
23975510-2	2013	METHODS: Four dose levels (2.5 to 10 mg) of everolimus from days 1 to 14 with CHOP (750 mg/m(2) cyclophosphamide, 50 mg/m(2) doxorubicin, and 1.4 mg/m(2) (maximum 2 mg) vincristine on day 1, and 100 mg/day prednisone on days 1 to 5) every 21 days were planned.	Everolimus	44-54	DNA damage inducible transcript 3	Homo sapiens	78-82
24335377-10	2013	She was successfully treated with 8 courses of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone(R-CHOP) chemotherapy, and maintains a complete remission.	Prednisone	110-120	DNA damage inducible transcript 3	Homo sapiens	123-127
24772975-0	2013	Effect of dexamethasone on unfolded protein response genes (MTJ1, Grp78, Grp94, CHOP, HMOX-1) in HEp2 cell line.	Dexamethasone	10-23	DNA damage inducible transcript 3	Homo sapiens	80-84
24772975-7	2013	CHOP expression, on the other hand, decreased with 0.1 microM dex.	Dexamethasone	62-65	DNA damage inducible transcript 3	Homo sapiens	0-4
24772975-10	2013	Dex in low dose (0.1 microM) caused a decrease in CHOP expression in HEp2 cells and an increase in Grp78 expression, in particular.	Dextromethorphan	0-3	DNA damage inducible transcript 3	Homo sapiens	50-54
24368982-11	2013	Treatment with quercetin also increased the expression of Grp78/Bip and GADD153/CHOP protein and induced mitochondrial dysfunction.	Quercetin	15-24	DNA damage inducible transcript 3	Homo sapiens	72-79
24368982-11	2013	Treatment with quercetin also increased the expression of Grp78/Bip and GADD153/CHOP protein and induced mitochondrial dysfunction.	Quercetin	15-24	DNA damage inducible transcript 3	Homo sapiens	80-84
23911414-1	2013	Among the non-carbohydrate components of glycans, the addition of phosphocholine (ChoP) to the glycans of pathogens occurs more rarely than acetylation or methylation, but it has far more potent biological consequences.	Carbohydrates	14-26	DNA damage inducible transcript 3	Homo sapiens	82-86
23749468-0	2013	CHOP-mediated hepcidin suppression modulates hepatic iron load.	Iron	53-57	DNA damage inducible transcript 3	Homo sapiens	0-4
23911414-1	2013	Among the non-carbohydrate components of glycans, the addition of phosphocholine (ChoP) to the glycans of pathogens occurs more rarely than acetylation or methylation, but it has far more potent biological consequences.	Polysaccharides	41-48	DNA damage inducible transcript 3	Homo sapiens	82-86
23911414-1	2013	Among the non-carbohydrate components of glycans, the addition of phosphocholine (ChoP) to the glycans of pathogens occurs more rarely than acetylation or methylation, but it has far more potent biological consequences.	Phosphorylcholine	66-80	DNA damage inducible transcript 3	Homo sapiens	82-86
23911414-1	2013	Among the non-carbohydrate components of glycans, the addition of phosphocholine (ChoP) to the glycans of pathogens occurs more rarely than acetylation or methylation, but it has far more potent biological consequences.	Polysaccharides	95-102	DNA damage inducible transcript 3	Homo sapiens	82-86
23911414-6	2013	We describe the biosynthesis of the ChoP modification, the structures of the pathogen glycans known to carry ChoP groups and the host proteins that recognize ChoP.	Polysaccharides	86-93	DNA damage inducible transcript 3	Homo sapiens	36-40
23911414-6	2013	We describe the biosynthesis of the ChoP modification, the structures of the pathogen glycans known to carry ChoP groups and the host proteins that recognize ChoP.	Polysaccharides	86-93	DNA damage inducible transcript 3	Homo sapiens	109-113
23911414-6	2013	We describe the biosynthesis of the ChoP modification, the structures of the pathogen glycans known to carry ChoP groups and the host proteins that recognize ChoP.	Polysaccharides	86-93	DNA damage inducible transcript 3	Homo sapiens	109-113
22548975-2	2013	The hypothesis of this retrospective study was that a 15-week dose intense CHOP protocol would have shorter treatment duration with similar efficacy to other doxorubicin-based multidrug protocols.	Doxorubicin	158-169	DNA damage inducible transcript 3	Homo sapiens	75-79
24062391-5	2013	Skeletal involvement was associated with a worse outcome after cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus rituximab (HREFS = 1.5, P = .048; HROS = 1.1; P = .828), but not after CHOP without rituximab (HREFS = 0.8, P = .181; HROS = 0.7, P = .083).	Prednisone	111-121	DNA damage inducible transcript 3	Homo sapiens	123-127
24177007-5	2013	These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition.	Glucose	142-149	DNA damage inducible transcript 3	Homo sapiens	131-135
24177007-5	2013	These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition.	trimethyloxamine	211-215	DNA damage inducible transcript 3	Homo sapiens	131-135
24278099-10	2013	TUDCA could attenuate the effect of ox-LDL on GRP78 and CHOP expressions and reduce visfatin and resistin at mRNA and protein level in dose-dependent manner.	ursodoxicoltaurine	0-5	DNA damage inducible transcript 3	Homo sapiens	56-60
24177007-5	2013	These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition.	trimethyloxamine	240-244	DNA damage inducible transcript 3	Homo sapiens	131-135
24177007-5	2013	These dual effects would be mediated through endoplasmic reticulum (ER) stress, because we observed (1) up-regulation of GRP78 and CHOP under glucose-deprived condition, which was inhibited by chemical chaperon TMAO, and (2) treatment with TMAO inhibited IL-6 production under glucose-deprived condition.	Glucose	277-284	DNA damage inducible transcript 3	Homo sapiens	131-135
24078627-5	2013	The induction of DRs was mediated through activation of ERK and through up-regulation of a transcription factor CCAAT enhancer-binding protein homologous protein (CHOP) as silencing of these signaling molecules abrogated the effect of azadirone.	azadirone	235-244	DNA damage inducible transcript 3	Homo sapiens	112-161
24078627-0	2013	Azadirone, a limonoid tetranortriterpene, induces death receptors and sensitizes human cancer cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) through a p53 protein-independent mechanism: evidence for the role of the ROS-ERK-CHOP-death receptor pathway.	azadirone	0-9	DNA damage inducible transcript 3	Homo sapiens	249-253
24078627-5	2013	The induction of DRs was mediated through activation of ERK and through up-regulation of a transcription factor CCAAT enhancer-binding protein homologous protein (CHOP) as silencing of these signaling molecules abrogated the effect of azadirone.	azadirone	235-244	DNA damage inducible transcript 3	Homo sapiens	163-167
24078627-7	2013	The CHOP binding site on the DR5 gene was required for induction of DR5 by azadirone.	azadirone	75-84	DNA damage inducible transcript 3	Homo sapiens	4-8
24078627-8	2013	Up-regulation of DRs was mediated through the generation of reactive oxygen species (ROS) as ROS scavengers reduced the effect of azadirone on ERK activation, CHOP up-regulation, DR induction, and TRAIL sensitization.	Reactive Oxygen Species	60-83	DNA damage inducible transcript 3	Homo sapiens	159-163
24078627-8	2013	Up-regulation of DRs was mediated through the generation of reactive oxygen species (ROS) as ROS scavengers reduced the effect of azadirone on ERK activation, CHOP up-regulation, DR induction, and TRAIL sensitization.	Reactive Oxygen Species	85-88	DNA damage inducible transcript 3	Homo sapiens	159-163
24078627-8	2013	Up-regulation of DRs was mediated through the generation of reactive oxygen species (ROS) as ROS scavengers reduced the effect of azadirone on ERK activation, CHOP up-regulation, DR induction, and TRAIL sensitization.	Reactive Oxygen Species	93-96	DNA damage inducible transcript 3	Homo sapiens	159-163
24078627-8	2013	Up-regulation of DRs was mediated through the generation of reactive oxygen species (ROS) as ROS scavengers reduced the effect of azadirone on ERK activation, CHOP up-regulation, DR induction, and TRAIL sensitization.	azadirone	130-139	DNA damage inducible transcript 3	Homo sapiens	159-163
24078627-12	2013	Overall, this study indicates that azadirone can sensitize cancer cells to TRAIL through ROS-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins, and up-regulation of proapoptotic proteins.	azadirone	35-44	DNA damage inducible transcript 3	Homo sapiens	97-101
24078627-12	2013	Overall, this study indicates that azadirone can sensitize cancer cells to TRAIL through ROS-ERK-CHOP-mediated up-regulation of DR5 and DR4 signaling, down-regulation of cell survival proteins, and up-regulation of proapoptotic proteins.	Reactive Oxygen Species	89-92	DNA damage inducible transcript 3	Homo sapiens	97-101
23881281-4	2013	Meanwhile, curcumin induced endoplasmic reticulum (ER) stress and mitochondrial dysfunction as evidenced by up-regulation of CCAAT/enhancer binding protein homologous protein (CHOP), phosphorylation of JNK and down-regulation of SERCA2ATPase, release of cytochrome c, decrease of Bcl-2 and reduction of mitochondrial membrane potential in both AGS and HT-29 cells.	Curcumin	11-19	DNA damage inducible transcript 3	Homo sapiens	125-174
23881281-4	2013	Meanwhile, curcumin induced endoplasmic reticulum (ER) stress and mitochondrial dysfunction as evidenced by up-regulation of CCAAT/enhancer binding protein homologous protein (CHOP), phosphorylation of JNK and down-regulation of SERCA2ATPase, release of cytochrome c, decrease of Bcl-2 and reduction of mitochondrial membrane potential in both AGS and HT-29 cells.	Curcumin	11-19	DNA damage inducible transcript 3	Homo sapiens	176-180
23881281-9	2013	siRNA to CHOP markedly reduced curcumin-induced apoptosis.	Curcumin	31-39	DNA damage inducible transcript 3	Homo sapiens	9-13
24428090-1	2013	OBJECTIVE: To determine the effectiveness and tolerability of the combination of chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) with the addition of etoposide (CHOEP-21) for newly diagnosed nodal peripheral T-cell lymphomas (PTCLs).	Doxorubicin	117-128	DNA damage inducible transcript 3	Homo sapiens	161-165
23775435-1	2013	BACKGROUND: High levels of cyclin E (CCNE) are accompanied by shorter survival in cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (CHOP)-treated diffuse large B-cell lymphomas (DLBCL), independent of the international prognostic index (IPI).	Prednisone	133-143	DNA damage inducible transcript 3	Homo sapiens	145-149
23775435-7	2013	We were able to reproduce data suggesting an IPI- and response to therapy independent, negative prognostic impact of CCNE in CHOP-treated DLBCL patients: CCNE-positive cases had a median survival of 16 months compared with 57 months in negative ones (p=0.012).	diprotin A	45-48	DNA damage inducible transcript 3	Homo sapiens	125-129
24428090-1	2013	OBJECTIVE: To determine the effectiveness and tolerability of the combination of chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) with the addition of etoposide (CHOEP-21) for newly diagnosed nodal peripheral T-cell lymphomas (PTCLs).	Prednisolone	147-159	DNA damage inducible transcript 3	Homo sapiens	161-165
23452117-1	2013	Rituximab combined with cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) is regarded as the first-line treatment for elderly patients with diffuse large B-cell lymphoma (DLBCL), but it is often necessary to reduce the dose or prolong the intervals between doses.	Prednisolone	71-83	DNA damage inducible transcript 3	Homo sapiens	87-91
23954561-4	2013	These impairments in macrophage functions are associated with ATO-induced unfolded protein response (UPR) signaling pathway characterized by the enhancement in proteins such as GRP78, p-PERK, p-eIF2alpha, ATF4 and CHOP.	Arsenic Trioxide	62-65	DNA damage inducible transcript 3	Homo sapiens	214-218
23879968-3	2013	gamma-T3 was necessary for endoplasmic reticulum stress markers CHOP and GRP78, whereas an intrinsic apoptotic marker, caspase 3 activation was induced only in the presence of statins.	gamma-t3	0-8	DNA damage inducible transcript 3	Homo sapiens	64-68
23636313-7	2013	Activation of the PI3K/AKT/mTOR pathway was related to poor disease outcome in DLBCL patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) but not in those treated with rituximab-CHOP.	Prednisone	155-165	DNA damage inducible transcript 3	Homo sapiens	167-171
24143112-1	2013	Fludarabine-based regimens and CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens with or without rituximab are the most common treatment modalities for indolent lymphoma.	Doxorubicin	37-48	DNA damage inducible transcript 3	Homo sapiens	31-35
24143112-1	2013	Fludarabine-based regimens and CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens with or without rituximab are the most common treatment modalities for indolent lymphoma.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	31-35
24143112-1	2013	Fludarabine-based regimens and CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens with or without rituximab are the most common treatment modalities for indolent lymphoma.	Vincristine	68-79	DNA damage inducible transcript 3	Homo sapiens	31-35
24143112-1	2013	Fludarabine-based regimens and CHOP (doxorubicin, cyclophosphamide, vincristine, prednisone)-like regimens with or without rituximab are the most common treatment modalities for indolent lymphoma.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	31-35
24143112-11	2013	In conclusion, the present study revealed that the use of fludarabine-based regimens could induce high rates of myelosuppression over CHOP-like regimens, in spite of significant increases in PFS.	fludarabine	58-69	DNA damage inducible transcript 3	Homo sapiens	134-138
23636313-7	2013	Activation of the PI3K/AKT/mTOR pathway was related to poor disease outcome in DLBCL patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) but not in those treated with rituximab-CHOP.	Cyclophosphamide	107-123	DNA damage inducible transcript 3	Homo sapiens	167-171
23636313-7	2013	Activation of the PI3K/AKT/mTOR pathway was related to poor disease outcome in DLBCL patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) but not in those treated with rituximab-CHOP.	Doxorubicin	125-136	DNA damage inducible transcript 3	Homo sapiens	167-171
24270384-3	2013	Further examination showed that Celergen enhanced expression of the p21(CIPl1WAF1), GADD153 genes and downregulated the c-myc gene.	celergen	32-40	DNA damage inducible transcript 3	Homo sapiens	84-91
23743301-5	2013	We found that 700nM TBT induced ER stress markers such as CHOP, GRP78, spliced XBP1 mRNA and phosphorylated eIF2alpha.	tributyltin	20-23	DNA damage inducible transcript 3	Homo sapiens	58-62
24313062-11	2013	Chemotherapy regimens using multi-agents combined with anthracycline i.e. CHOP have been playing the fundamental role in the therapeutic paradigm, but because of the poorer survival of 20-50% at the 5-year point, AITL is classified as a high-grade malignancy.	Anthracyclines	55-68	DNA damage inducible transcript 3	Homo sapiens	74-78
24086672-4	2013	We found that bortezomib induced up-regulation of the pro-survival and pro-death ER stress molecules BIP and CHOP and activated c-Jun NH2-terminal kinase (JNK), resulting in Bcl-2 phosphorylation and induction of autophagy.	Bortezomib	14-24	DNA damage inducible transcript 3	Homo sapiens	109-113
24490570-6	2013	Its mechanism may be related to down-regulation of ERS apoptosis-related signal molecules phosphorylated PERK, phosphorylated elF2alpha, cleaved Caspase-12, GRP78 and CHOP that maintain calcium homeostasis in endoplasmic reticulum.	Calcium	186-193	DNA damage inducible transcript 3	Homo sapiens	167-171
24167719-4	2013	Thapsigargin-induced ER-stress caused only apoptosis after ~2 hr with Ire1 phosphorylation, and Grp78, ATF4, and CHOP expressions.	Thapsigargin	0-12	DNA damage inducible transcript 3	Homo sapiens	113-117
24058556-6	2013	Gene ontology analysis revealed that response to stress and cell apoptosis dysfunction were ranked in the top 10 cellular events being affected, and that the major components of endoplasmic reticulum stress-mediated apoptosis pathway - CHOP and TRIB3- were up-regulated in a concentration- and time-dependent manner when cells were treated with clopidogrel.	Clopidogrel	345-356	DNA damage inducible transcript 3	Homo sapiens	236-240
24058556-7	2013	Pathway analysis demonstrated that multiple MAPK kinases were phosphorylated in clopidogrel-treated GES-1 cells, but that only SB-203580 (a p38-specific MAPK inhibitor) attenuated cell apoptosis and CHOP over-expression, both of which were induced by clopidogrel.	Clopidogrel	80-91	DNA damage inducible transcript 3	Homo sapiens	199-203
24058556-7	2013	Pathway analysis demonstrated that multiple MAPK kinases were phosphorylated in clopidogrel-treated GES-1 cells, but that only SB-203580 (a p38-specific MAPK inhibitor) attenuated cell apoptosis and CHOP over-expression, both of which were induced by clopidogrel.	SB 203580	127-136	DNA damage inducible transcript 3	Homo sapiens	199-203
23711089-0	2013	Melatonin reverses tunicamycin-induced endoplasmic reticulum stress in human hepatocellular carcinoma cells and improves cytotoxic response to doxorubicin by increasing CHOP and decreasing survivin.	Melatonin	0-9	DNA damage inducible transcript 3	Homo sapiens	169-173
23711089-0	2013	Melatonin reverses tunicamycin-induced endoplasmic reticulum stress in human hepatocellular carcinoma cells and improves cytotoxic response to doxorubicin by increasing CHOP and decreasing survivin.	Doxorubicin	143-154	DNA damage inducible transcript 3	Homo sapiens	169-173
23711089-9	2013	Furthermore, consistent with inhibition of AKT activation by using the PI3K inhibitor LY294002, melatonin elevated the levels of CHOP (C/EBP-homologous protein) and reduced the levels of Survivin (a member of the inhibitor of apoptosis protein family)suggesting that inhibition of the PI3K/AKT pathway by melatonin-reversed ER stress-induced resistance to doxorubicin in human hepatocellular carcinoma cells.	Melatonin	96-105	DNA damage inducible transcript 3	Homo sapiens	129-133
23711089-9	2013	Furthermore, consistent with inhibition of AKT activation by using the PI3K inhibitor LY294002, melatonin elevated the levels of CHOP (C/EBP-homologous protein) and reduced the levels of Survivin (a member of the inhibitor of apoptosis protein family)suggesting that inhibition of the PI3K/AKT pathway by melatonin-reversed ER stress-induced resistance to doxorubicin in human hepatocellular carcinoma cells.	Melatonin	96-105	DNA damage inducible transcript 3	Homo sapiens	135-159
23711089-10	2013	These results demonstrate that melatonin attenuates ER stress-induced resistance to doxorubicin in human hepatocellular carcinoma cells by down-regulating the PI3K/AKT pathway, increasing the levels of CHOP and decreasing the levels of Survivin.	Melatonin	31-40	DNA damage inducible transcript 3	Homo sapiens	202-206
23647505-11	2013	A full-dosage regimen of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) was successfully used in the patient with WAS and B-cell lymphoma; he was still in remission after 3 years.	Prednisone	88-98	DNA damage inducible transcript 3	Homo sapiens	102-106
23670255-2	2013	Previously, we identified GADD153 as a target of BRCA1 protein, which increases doxorubicin sensitivity in human p53 -/- PCa cells (PC3).	Doxorubicin	80-91	DNA damage inducible transcript 3	Homo sapiens	26-33
23670255-4	2013	METHODS: We performed reverse transcription quantitative PCR (RT-qPCR), western blot and luciferase assays to analyze GADD153 and/or BRCA1 expression in response to ultraviolet or doxorubicin exposure in PC3 p53 stable-transfected cells and LNCaP (p53+/+) cells.	Doxorubicin	180-191	DNA damage inducible transcript 3	Homo sapiens	118-125
23670255-8	2013	RESULTS: We found that GADD153 was highly induced by doxorubicin in PC3 cells; however, this response was totally abolished in LNCaP (p53wt) and in p53-restituted PC3 cells.	Doxorubicin	53-64	DNA damage inducible transcript 3	Homo sapiens	23-30
23916707-3	2013	In the present study we found that photo-oxidative (phox)-ER stress induced by hypericin-based photodynamic therapy is associated with activation of PERK (an ER sessile, stress sensor), robust induction of CHOP (a pro-apoptotic transcription factor) and induction of Bim and Noxa (accompanied by an eventual drop in Mcl-1 levels).	hypericin	79-88	DNA damage inducible transcript 3	Homo sapiens	206-210
24013954-6	2013	Meanwhile, intracellular calcium homeostasis was disturbed along with the alteration in the expressions of GRP78, CHOP and pro-caspase12.	Calcium	25-32	DNA damage inducible transcript 3	Homo sapiens	114-118
24023313-8	2013	Interestingly, by examining the upstream signaling pathway of REDD1, we found that ZOL can induce endoplasmic reticulum stress responses through activating the protein kinase R (PKR)-related ER kinase-eukaryotic initiation factor 2 alpha-CCAAT/enhancer binding protein homologous protein (PERK-eIF2alpha-CHOP) pathway.	Zoledronic Acid	83-86	DNA damage inducible transcript 3	Homo sapiens	304-308
24023313-9	2013	CONCLUSION: Taken together, these results indicated that ZOL-induced cell death was caused by endoplasmic reticulum stress activating PERK-eIF2alpha-CHOP pathway to induce REDD1 expression and inhibit the mTOR pathway.	Zoledronic Acid	57-60	DNA damage inducible transcript 3	Homo sapiens	149-153
24167719-6	2013	ATF4-siRNA completely inhibited the autophagy induced by NaF or tunicamycin with suppressed ATF4 protein and mRNA expressions, and also inhibited apoptosis by thapsigargin with suppression of both ATF4 and CHOP.	Sodium Fluoride	57-60	DNA damage inducible transcript 3	Homo sapiens	206-210
24167719-6	2013	ATF4-siRNA completely inhibited the autophagy induced by NaF or tunicamycin with suppressed ATF4 protein and mRNA expressions, and also inhibited apoptosis by thapsigargin with suppression of both ATF4 and CHOP.	Tunicamycin	64-75	DNA damage inducible transcript 3	Homo sapiens	206-210
24167719-6	2013	ATF4-siRNA completely inhibited the autophagy induced by NaF or tunicamycin with suppressed ATF4 protein and mRNA expressions, and also inhibited apoptosis by thapsigargin with suppression of both ATF4 and CHOP.	Thapsigargin	159-171	DNA damage inducible transcript 3	Homo sapiens	206-210
24167719-8	2013	On the other hand, CHOP-siRNA activated autophagy in thapsigargin-induced ER-stress with significant ATF4 expression, and suppressed apoptosis with CHOP suppression.	Thapsigargin	53-65	DNA damage inducible transcript 3	Homo sapiens	19-23
24167719-5	2013	On the other hand, NaF- and tunicamycin-induced ER-stress caused only autophagy in the early stage by ~8 hr with ATF4 expression and without CHOP expression.	Sodium Fluoride	19-22	DNA damage inducible transcript 3	Homo sapiens	141-145
24167719-5	2013	On the other hand, NaF- and tunicamycin-induced ER-stress caused only autophagy in the early stage by ~8 hr with ATF4 expression and without CHOP expression.	Tunicamycin	28-39	DNA damage inducible transcript 3	Homo sapiens	141-145
23951005-0	2013	Gadd153 and NF-kappaB crosstalk regulates 27-hydroxycholesterol-induced increase in BACE1 and beta-amyloid production in human neuroblastoma SH-SY5Y cells.	27-hydroxycholesterol	42-63	DNA damage inducible transcript 3	Homo sapiens	0-7
23973991-0	2013	Sinulariolide induced hepatocellular carcinoma apoptosis through activation of mitochondrial-related apoptotic and PERK/eIF2alpha/ATF4/CHOP pathway.	sinulariolide	0-13	DNA damage inducible transcript 3	Homo sapiens	135-139
23843497-4	2013	We also evaluated the influence of HLA polymorphisms on survival in those patients treated with curative intention using cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP)-like regimen without (n = 64, 26%) or with (n = 153, 61%) rituximab.	Prednisolone	169-181	DNA damage inducible transcript 3	Homo sapiens	183-187
24009772-3	2013	Metformin activated AMPK, down-regulated the unfolded protein response (UPR) demonstrated by significant decrease in the main UPR regulator GRP78, and led to UPR-mediated cell death via up-regulation of the ER stress/UPR cell death mediators IRE1alpha and CHOP.	Metformin	0-9	DNA damage inducible transcript 3	Homo sapiens	256-260
24009772-4	2013	Using shRNA, we demonstrate that metformin-induced apoptosis is AMPK-dependent since AMPK knock-down rescued ALL cells, which correlated with down-regulation of IRE1alpha and CHOP and restoration of the UPR/GRP78 function.	Metformin	33-42	DNA damage inducible transcript 3	Homo sapiens	175-179
24009772-5	2013	Additionally rapamycin, a known inhibitor of mTOR-dependent protein synthesis, rescued cells from metformin-induced apoptosis and down-regulated CHOP expression.	Sirolimus	13-22	DNA damage inducible transcript 3	Homo sapiens	145-149
23921690-5	2013	Follow-up after six courses of R-CHOP (rituximab, cyclophosphamide, vindesine, epirubicin and prednisone) regimen revealed complete resolution of symptoms.	Prednisone	94-104	DNA damage inducible transcript 3	Homo sapiens	33-37
23838288-0	2013	Inhibition of vacuolar H+ ATPase enhances sensitivity to tamoxifen via up-regulation of CHOP in breast cancer cells.	Tamoxifen	57-66	DNA damage inducible transcript 3	Homo sapiens	88-92
23838288-5	2013	Knock-down of CHOP by siRNA suppressed the cell death induced by bafilomycin A1 and tamoxifen, suggesting that bafilomycin A1-mediated CHOP activation sensitizes to tamoxifen.	bafilomycin	65-76	DNA damage inducible transcript 3	Homo sapiens	14-18
23838288-5	2013	Knock-down of CHOP by siRNA suppressed the cell death induced by bafilomycin A1 and tamoxifen, suggesting that bafilomycin A1-mediated CHOP activation sensitizes to tamoxifen.	bafilomycin	65-76	DNA damage inducible transcript 3	Homo sapiens	135-139
23838288-5	2013	Knock-down of CHOP by siRNA suppressed the cell death induced by bafilomycin A1 and tamoxifen, suggesting that bafilomycin A1-mediated CHOP activation sensitizes to tamoxifen.	Tamoxifen	84-93	DNA damage inducible transcript 3	Homo sapiens	14-18
23838288-5	2013	Knock-down of CHOP by siRNA suppressed the cell death induced by bafilomycin A1 and tamoxifen, suggesting that bafilomycin A1-mediated CHOP activation sensitizes to tamoxifen.	Tamoxifen	84-93	DNA damage inducible transcript 3	Homo sapiens	135-139
23838288-5	2013	Knock-down of CHOP by siRNA suppressed the cell death induced by bafilomycin A1 and tamoxifen, suggesting that bafilomycin A1-mediated CHOP activation sensitizes to tamoxifen.	Tamoxifen	165-174	DNA damage inducible transcript 3	Homo sapiens	14-18
23582047-5	2013	Depletion of calcium from reticulum was accompanied by increase in endoplasmic reticulum (ER) stress markers, such as X-box, CHOP and ATF4, thus pointing to the development of ER stress due to GYY4137 treatment.	Calcium	13-20	DNA damage inducible transcript 3	Homo sapiens	125-129
23838288-5	2013	Knock-down of CHOP by siRNA suppressed the cell death induced by bafilomycin A1 and tamoxifen, suggesting that bafilomycin A1-mediated CHOP activation sensitizes to tamoxifen.	Tamoxifen	165-174	DNA damage inducible transcript 3	Homo sapiens	135-139
23838288-8	2013	Overall, our results demonstrate that inhibition of vATPase can potentiate the apoptotic effects of tamoxifen through up-regulation of CHOP.	Tamoxifen	100-109	DNA damage inducible transcript 3	Homo sapiens	135-139
23582047-5	2013	Depletion of calcium from reticulum was accompanied by increase in endoplasmic reticulum (ER) stress markers, such as X-box, CHOP and ATF4, thus pointing to the development of ER stress due to GYY4137 treatment.	GYY 4137	193-200	DNA damage inducible transcript 3	Homo sapiens	125-129
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	polyether antibiotics	21-42	DNA damage inducible transcript 3	Homo sapiens	173-177
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	salinomycin	52-63	DNA damage inducible transcript 3	Homo sapiens	173-177
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	Nigericin	65-74	DNA damage inducible transcript 3	Homo sapiens	173-177
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	narasin	76-83	DNA damage inducible transcript 3	Homo sapiens	173-177
23615398-5	2013	Interestingly, other polyether antibiotics, such as salinomycin, nigericin, narasin and lasalocid A, also stimulated TRAIL-mediated apoptosis in glioma cells via ER stress, CHOP-mediated DR5 upregulation and c-FLIP downregulation.	Lasalocid	88-99	DNA damage inducible transcript 3	Homo sapiens	173-177
23984080-8	2013	To the best of our knowledge, this is the first study which investigated the impact of R-CHOP in the context of CoO and IPI in a relatively young cohort.	coo	112-115	DNA damage inducible transcript 3	Homo sapiens	89-93
23660295-6	2013	When stimulated with 12-O-tetradecanoylphorbol 13-acetate (TPA) or CD437, this TR3-TRAPgamma interaction not only induced Ca(2+) depletion in the endoplasmic reticulum (ER) but also promoted the expression of the proapoptotic transcriptional regulator CHOP.	Tetradecanoylphorbol Acetate	21-57	DNA damage inducible transcript 3	Homo sapiens	252-256
23660295-6	2013	When stimulated with 12-O-tetradecanoylphorbol 13-acetate (TPA) or CD437, this TR3-TRAPgamma interaction not only induced Ca(2+) depletion in the endoplasmic reticulum (ER) but also promoted the expression of the proapoptotic transcriptional regulator CHOP.	Tetradecanoylphorbol Acetate	59-62	DNA damage inducible transcript 3	Homo sapiens	252-256
23660295-6	2013	When stimulated with 12-O-tetradecanoylphorbol 13-acetate (TPA) or CD437, this TR3-TRAPgamma interaction not only induced Ca(2+) depletion in the endoplasmic reticulum (ER) but also promoted the expression of the proapoptotic transcriptional regulator CHOP.	CD 437	67-72	DNA damage inducible transcript 3	Homo sapiens	252-256
23780584-7	2013	Many hydroxyprolines (HOPs), such as 4-L-THOP and cis-4-hydroxy-L-proline (4-L-CHOP), are useful chiral building blocks for the organic synthesis of pharmaceuticals.	Hydroxyproline	5-20	DNA damage inducible transcript 3	Homo sapiens	79-83
23780584-7	2013	Many hydroxyprolines (HOPs), such as 4-L-THOP and cis-4-hydroxy-L-proline (4-L-CHOP), are useful chiral building blocks for the organic synthesis of pharmaceuticals.	Hydroxyproline	50-73	DNA damage inducible transcript 3	Homo sapiens	79-83
23846384-2	2013	The BM infiltration and the condition of the MF improved following CHOP therapy (cyclophosphamide hydrate, doxorubicin hydrochloride, vincristine sulfate, and prednisolone).	Cyclophosphamide	81-105	DNA damage inducible transcript 3	Homo sapiens	67-71
23846384-2	2013	The BM infiltration and the condition of the MF improved following CHOP therapy (cyclophosphamide hydrate, doxorubicin hydrochloride, vincristine sulfate, and prednisolone).	Doxorubicin	107-132	DNA damage inducible transcript 3	Homo sapiens	67-71
23846384-2	2013	The BM infiltration and the condition of the MF improved following CHOP therapy (cyclophosphamide hydrate, doxorubicin hydrochloride, vincristine sulfate, and prednisolone).	Vincristine	134-153	DNA damage inducible transcript 3	Homo sapiens	67-71
23551302-10	2013	IGL-1 + MEL + TMZ induced a significant decrease in GRP78, pPERK, and CHOP activation after reperfusion.	Temozolomide	14-17	DNA damage inducible transcript 3	Homo sapiens	70-74
23137070-3	2013	Patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) had significantly superior survival rates.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	94-98
23137070-3	2013	Patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) had significantly superior survival rates.	Doxorubicin	51-62	DNA damage inducible transcript 3	Homo sapiens	94-98
23137070-3	2013	Patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) had significantly superior survival rates.	Vincristine	64-75	DNA damage inducible transcript 3	Homo sapiens	94-98
23137070-3	2013	Patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) had significantly superior survival rates.	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	94-98
23984080-8	2013	To the best of our knowledge, this is the first study which investigated the impact of R-CHOP in the context of CoO and IPI in a relatively young cohort.	diprotin A	120-123	DNA damage inducible transcript 3	Homo sapiens	89-93
23692856-2	2013	Nonetheless, outcomes are suboptimal for patients failing rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	117-127	DNA damage inducible transcript 3	Homo sapiens	131-135
23512567-3	2013	For clinically fit patients younger than 60-65 years of age we recommend cytarabine-containing induction and conditioning regimens such as Rituximab (R)-CHOP alternating with R-DHAP followed by autologous SCT consolidation.	Cytarabine	73-83	DNA damage inducible transcript 3	Homo sapiens	153-157
23806691-9	2013	In addition, pre-treatment with BIX significantly attenuated the induction of CHOP and activated caspase 4 and caspase 3.	2-(3,4-dihydroxyphenyl)-2-oxoethyl thiocyanate	32-35	DNA damage inducible transcript 3	Homo sapiens	78-82
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	DNA damage inducible transcript 3	Homo sapiens	345-369
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	DNA damage inducible transcript 3	Homo sapiens	371-375
23684743-4	2013	In the early phase (up to 6h after proteasomal inhibition), MG132 induced time-dependent proteasomal inhibition which resulted in stimulation of the UPR, increased autophagic flux and stimulated heat shock protein response as determined by increased levels of phosphorylation of the eukaryotic translation initiation factor 2 alpha (eIF2alpha), C/EBP homologous protein (CHOP)/GADD153, turnover of autophagy related microtubule-associated protein 1 light chain 3 (LC3) and increased levels of Hsp70 respectively.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	60-65	DNA damage inducible transcript 3	Homo sapiens	377-384
23475945-8	2013	Additionally, BMJ decreased survivin and X-linked inhibitor of apoptosis protein but increased p21, CHOP and phosphorylated mitogen-activated protein kinases (extracellular signal-regulated kinase 1/2 and p38) levels.	(12R)-12-methyltetradecanoic acid	14-17	DNA damage inducible transcript 3	Homo sapiens	100-104
23673810-10	2013	Furthermore, GL63 induced an ER stress response, upregulation of CHOP, XBP-1 and ATF-4 expression, while the same concentration of curcumin had no effect on ER stress.	gl63	13-17	DNA damage inducible transcript 3	Homo sapiens	65-69
24356732-8	2013	In FL, the OR in patients treated with R-CHOP or R-CHOP-like was 85%) with 54% CR.	Chromium	79-81	DNA damage inducible transcript 3	Homo sapiens	41-45
24356732-8	2013	In FL, the OR in patients treated with R-CHOP or R-CHOP-like was 85%) with 54% CR.	Chromium	79-81	DNA damage inducible transcript 3	Homo sapiens	51-55
24356732-9	2013	With CHOP-like the OR was 59%&gt; with 18% CR.	Chromium	43-45	DNA damage inducible transcript 3	Homo sapiens	5-9
23761079-9	2013	Treatment with HCPT increased the expression of glucose-regulated protein 78 (GRP78), phospho-PERK, activating transcription factor 6 (ATF6), phosphoinositol-requiring kinase 1 (IRE1), C/EBP homologous protein (CHOP), Bax, and phospho-c-Jun N-terminal kinase (JNK) and decreased the expression of Bcl-2.	hydroxycamptothecinum	15-19	DNA damage inducible transcript 3	Homo sapiens	185-209
23761079-9	2013	Treatment with HCPT increased the expression of glucose-regulated protein 78 (GRP78), phospho-PERK, activating transcription factor 6 (ATF6), phosphoinositol-requiring kinase 1 (IRE1), C/EBP homologous protein (CHOP), Bax, and phospho-c-Jun N-terminal kinase (JNK) and decreased the expression of Bcl-2.	hydroxycamptothecinum	15-19	DNA damage inducible transcript 3	Homo sapiens	211-215
23861942-11	2013	Inhibition of CHOP expression significantly decreased sodium azide-induced neuronal death.	Sodium Azide	54-66	DNA damage inducible transcript 3	Homo sapiens	14-18
23670030-4	2013	Furthermore, we demonstrated that salinomycin stimulated endoplasmic reticulum stress and mediated autophagy via the ATF4-DDIT3/CHOP-TRIB3-AKT1-MTOR axis.	salinomycin	34-45	DNA damage inducible transcript 3	Homo sapiens	122-127
23670030-4	2013	Furthermore, we demonstrated that salinomycin stimulated endoplasmic reticulum stress and mediated autophagy via the ATF4-DDIT3/CHOP-TRIB3-AKT1-MTOR axis.	salinomycin	34-45	DNA damage inducible transcript 3	Homo sapiens	128-132
23674497-7	2013	This resulted in an unfolded protein response (UPR), which was required for the potentiating effect of IGF-I on bortezomib cytotoxicity as shown by siRNA-mediated inhibition of GADD153 expression.	Bortezomib	112-122	DNA damage inducible transcript 3	Homo sapiens	177-184
24649228-2	2013	The reported 5-year overall survival for patients with localized nasal NKTCL treated with cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (CHOP) is &lt;50%.	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	153-157
24649228-2	2013	The reported 5-year overall survival for patients with localized nasal NKTCL treated with cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (CHOP) is &lt;50%.	Doxorubicin	108-127	DNA damage inducible transcript 3	Homo sapiens	153-157
24649228-2	2013	The reported 5-year overall survival for patients with localized nasal NKTCL treated with cyclophosphamide, hydroxydaunorubicin, oncovin and prednisone (CHOP) is &lt;50%.	Prednisone	141-151	DNA damage inducible transcript 3	Homo sapiens	153-157
23512567-4	2013	Elderly patients benefit from R-bendamustine or R-CHOP with maintenance rituximab following induction therapy, especially after R-CHOP.	r-bendamustine	30-44	DNA damage inducible transcript 3	Homo sapiens	130-134
23612979-7	2013	Consistent with this notion, exogenously expressed c-MYC reversed the ability of rapamycin to prevent bortezomib-induced CHOP and ATF4 expression as well as apoptosis.	Bortezomib	102-112	DNA damage inducible transcript 3	Homo sapiens	121-125
23554101-3	2013	Further study showed that HDMC elevated cellular reactive oxygen species (ROS) levels, thus inducing expressions of ATF4 and C/EBP homologous protein (CHOP).	2'-hydroxy-4',5'-dimethoxychalcone	26-30	DNA damage inducible transcript 3	Homo sapiens	125-149
23554101-3	2013	Further study showed that HDMC elevated cellular reactive oxygen species (ROS) levels, thus inducing expressions of ATF4 and C/EBP homologous protein (CHOP).	2'-hydroxy-4',5'-dimethoxychalcone	26-30	DNA damage inducible transcript 3	Homo sapiens	151-155
23554101-6	2013	In conclusion, HDMC induces apoptosis in human nonsmall cell lung cancer cells via activation of DR5 signaling pathway, and ROS-mediated ATF4-CHOP axis is involved in the process.	Reactive Oxygen Species	124-127	DNA damage inducible transcript 3	Homo sapiens	142-146
23665024-9	2013	From a mechanistic stand point, fasudil inhibited expression of activating transcription factor (ATF)4 and subsequent C/EBP homologous protein (CHOP) induction by tunicamycin.	fasudil	32-39	DNA damage inducible transcript 3	Homo sapiens	118-142
23665024-9	2013	From a mechanistic stand point, fasudil inhibited expression of activating transcription factor (ATF)4 and subsequent C/EBP homologous protein (CHOP) induction by tunicamycin.	fasudil	32-39	DNA damage inducible transcript 3	Homo sapiens	144-148
23665024-9	2013	From a mechanistic stand point, fasudil inhibited expression of activating transcription factor (ATF)4 and subsequent C/EBP homologous protein (CHOP) induction by tunicamycin.	Tunicamycin	163-174	DNA damage inducible transcript 3	Homo sapiens	118-142
23665024-9	2013	From a mechanistic stand point, fasudil inhibited expression of activating transcription factor (ATF)4 and subsequent C/EBP homologous protein (CHOP) induction by tunicamycin.	Tunicamycin	163-174	DNA damage inducible transcript 3	Homo sapiens	144-148
23612979-8	2013	These findings indicate that the induction of ATF4/CHOP expression occurs via mTORC1 regulation of c-MYC and that this signaling pathway is a major determinant in the ability of bortezomib to induce apoptosis.	Bortezomib	178-188	DNA damage inducible transcript 3	Homo sapiens	51-55
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Cyclophosphamide	55-71	DNA damage inducible transcript 3	Homo sapiens	117-121
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Cyclophosphamide	55-71	DNA damage inducible transcript 3	Homo sapiens	236-240
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Doxorubicin	73-84	DNA damage inducible transcript 3	Homo sapiens	117-121
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Doxorubicin	73-84	DNA damage inducible transcript 3	Homo sapiens	236-240
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Vincristine	86-97	DNA damage inducible transcript 3	Homo sapiens	236-240
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Prednisolone	103-115	DNA damage inducible transcript 3	Homo sapiens	117-121
23615461-1	2013	BACKGROUND: Dose intensification with a combination of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) every 2 weeks improves outcomes in patients older than 60 years with diffuse large B-cell lymphoma compared with CHOP every 3 weeks.	Prednisolone	103-115	DNA damage inducible transcript 3	Homo sapiens	236-240
23658755-9	2013	However, co-pretreatment with tunicamycin and Pae decreased the expression of COX-2 and levels of activation of Akt as well as increasing the levels of CHOP in HCC cells.	Tunicamycin	30-41	DNA damage inducible transcript 3	Homo sapiens	152-156
24029486-6	2013	RESULTS: The expressions of GRP78, CHOP and cleaved-caspase 4 were induced significantly by cisplatin (6 mg/L) in SKOV3 cells.	Cisplatin	92-101	DNA damage inducible transcript 3	Homo sapiens	35-39
24029486-10	2013	Inhibition of GRP78 expression reduced the cisplatin-induced up-regulations of p-Akt and p-mTOR and induced XBP1 mRNA shear expression and CHOP mRNA expression.	Cisplatin	43-52	DNA damage inducible transcript 3	Homo sapiens	139-143
23658755-10	2013	CONCLUSIONS/SIGNIFICANCE: Our results demonstrate that Pae reverses ER stress-induced resistance to doxorubicin in human hepatocellular carcinoma cells by targeting COX-2 mediated inactivation of PI3K/AKT/CHOP.	paeonol	55-58	DNA damage inducible transcript 3	Homo sapiens	205-209
23598937-3	2013	We present a case of a 54-year-old man, diagnosed with non-Hodgkin lymphoma who received a first cycle of rituximab, cyclophosphamide, hydroxydaunorubicin (doxorubicin), oncovin (vincristine), prednisolone (R-CHOP) chemotherapy 10 days prior presenting.	Doxorubicin	156-167	DNA damage inducible transcript 3	Homo sapiens	209-213
23578722-1	2013	BACKGROUND: Immunochemotherapy with rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become the standard of care for elderly patients with diffuse large B-cell lymphoma.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	112-116
23578722-1	2013	BACKGROUND: Immunochemotherapy with rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become the standard of care for elderly patients with diffuse large B-cell lymphoma.	Doxorubicin	68-79	DNA damage inducible transcript 3	Homo sapiens	112-116
23578722-1	2013	BACKGROUND: Immunochemotherapy with rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become the standard of care for elderly patients with diffuse large B-cell lymphoma.	Vincristine	81-92	DNA damage inducible transcript 3	Homo sapiens	112-116
23578722-1	2013	BACKGROUND: Immunochemotherapy with rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has become the standard of care for elderly patients with diffuse large B-cell lymphoma.	Prednisone	98-108	DNA damage inducible transcript 3	Homo sapiens	112-116
23624402-3	2013	Forced expression of ATF4 and CHOP increased protein synthesis and caused ATP depletion, oxidative stress and cell death.	Adenosine Triphosphate	74-77	DNA damage inducible transcript 3	Homo sapiens	30-34
23750173-0	2013	Fatal Interstitial Pneumonitis Rapidly Developed after the First Cycle of CHOP with Etoposide Combination Chemotherapy in a Patient with Lymphoma.	Etoposide	84-93	DNA damage inducible transcript 3	Homo sapiens	74-78
23083489-5	2013	PDI inhibition by bacitracin potentiated ER stress (increased mRNA expression of CHOP and sXBP1) and apoptosis induced by oxLDLs.	Bacitracin	18-28	DNA damage inducible transcript 3	Homo sapiens	81-85
23460351-4	2013	We analyzed 122 newly diagnosed consecutive DLBCL patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemo-immunotherapy.	Prednisone	131-141	DNA damage inducible transcript 3	Homo sapiens	145-149
23333652-7	2013	Finally, we showed that CHOP induction by t10,c12 CLA was dependent on ROS production and that the anti-oxidant N-acetyl-cysteine reduced CHOP induction-dependent cell death.	Reactive Oxygen Species	71-74	DNA damage inducible transcript 3	Homo sapiens	24-28
23333652-7	2013	Finally, we showed that CHOP induction by t10,c12 CLA was dependent on ROS production and that the anti-oxidant N-acetyl-cysteine reduced CHOP induction-dependent cell death.	Acetylcysteine	112-129	DNA damage inducible transcript 3	Homo sapiens	138-142
23335369-8	2013	A combined immunohistochemical or FISH/immunohistochemical score predicts outcome in DLBCL patients independent of the IPI and identifies a subset of 15% of patients with dismal prognosis in the high-risk IPI group following treatment with R-CHOP.	diprotin A	205-208	DNA damage inducible transcript 3	Homo sapiens	242-246
23638338-10	2013	Although not routinely reported, high baseline TLG may be a useful index to identify patients with DLBCL who are at increased risk for relapse after conventional R-CHOP.	(5r)-3-Acetyl-4-Hydroxy-5-Methyl-5-[(1z)-2-Methylbuta-1,3-Dien-1-Yl]thiophen-2(5h)-One	47-50	DNA damage inducible transcript 3	Homo sapiens	164-168
23339126-5	2013	As standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy may cure the majority of patients, it must always be the first proposed option.	Prednisone	71-81	DNA damage inducible transcript 3	Homo sapiens	85-89
23352640-2	2013	The aim of this retrospective study is to compare characteristics, prognostic factors and outcomes of Asian and Western patients with DLBCL treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP).	Prednisone	211-221	DNA damage inducible transcript 3	Homo sapiens	225-229
22580614-5	2013	The induction of ER stress in glioma cells by CsA was evidenced by detection of unfolded protein response activation (phosphorylation of PERK, accumulation of IRE1alpha) and accumulation of ER stress-associated proteins (BIP and CHOP).	Cyclosporine	46-49	DNA damage inducible transcript 3	Homo sapiens	229-233
23333938-6	2013	GSK2656157 inhibits PERK activity in cells with an IC(50) in the range of 10-30 nmol/L as shown by inhibition of stress-induced PERK autophosphorylation, eIF2alpha substrate phosphorylation, together with corresponding decreases in ATF4 and CAAT/enhancer binding protein homologous protein (CHOP) in multiple cell lines.	GSK2656157	0-10	DNA damage inducible transcript 3	Homo sapiens	291-295
23083489-7	2013	These effects on PDI were mimicked by exogenous 4-HNE and prevented by the carbonyl-scavengers N-acetylcysteine and pyridoxamine, which reduced CHOP expression and toxicity by oxLDLs.	Acetylcysteine	95-111	DNA damage inducible transcript 3	Homo sapiens	144-148
23083489-7	2013	These effects on PDI were mimicked by exogenous 4-HNE and prevented by the carbonyl-scavengers N-acetylcysteine and pyridoxamine, which reduced CHOP expression and toxicity by oxLDLs.	Pyridoxamine	116-128	DNA damage inducible transcript 3	Homo sapiens	144-148
23415873-7	2013	Furthermore, curcumin increased the expression of the ER stress associated transcriptional factors XBP-1, cleaved p50ATF6alpha and C/EBP homologous protein (CHOP) in human CD4+ and Jurkat T cells.	Curcumin	13-21	DNA damage inducible transcript 3	Homo sapiens	131-155
24648941-8	2013	Sodium 4-phenylbutyrate (PBA), an ERS inhibitor, reduced CHOP and GRP78, as well as SNP-stimulated apoptosis of chondrocytes, without affecting the SNP-dependent generation of NO.	4-phenylbutyric acid	0-23	DNA damage inducible transcript 3	Homo sapiens	57-61
24648941-8	2013	Sodium 4-phenylbutyrate (PBA), an ERS inhibitor, reduced CHOP and GRP78, as well as SNP-stimulated apoptosis of chondrocytes, without affecting the SNP-dependent generation of NO.	4-phenylbutyric acid	25-28	DNA damage inducible transcript 3	Homo sapiens	57-61
23394581-1	2013	Diffuse large B-cell lymphoma primary of lung (DLBCL-PL) is a rare presentation of extranodal lymphoma, in most cases chemotherapy-based anthracyclines: CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) has been the treatment, with excellent outcome.	Doxorubicin	177-188	DNA damage inducible transcript 3	Homo sapiens	153-157
23394581-1	2013	Diffuse large B-cell lymphoma primary of lung (DLBCL-PL) is a rare presentation of extranodal lymphoma, in most cases chemotherapy-based anthracyclines: CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) has been the treatment, with excellent outcome.	Vincristine	190-201	DNA damage inducible transcript 3	Homo sapiens	153-157
23394581-1	2013	Diffuse large B-cell lymphoma primary of lung (DLBCL-PL) is a rare presentation of extranodal lymphoma, in most cases chemotherapy-based anthracyclines: CHOP (cyclophosphamide, doxorubicin, vincristine, and prednisone) has been the treatment, with excellent outcome.	Prednisone	207-217	DNA damage inducible transcript 3	Homo sapiens	153-157
23415873-7	2013	Furthermore, curcumin increased the expression of the ER stress associated transcriptional factors XBP-1, cleaved p50ATF6alpha and C/EBP homologous protein (CHOP) in human CD4+ and Jurkat T cells.	Curcumin	13-21	DNA damage inducible transcript 3	Homo sapiens	157-161
23415873-8	2013	In PHA-activated T cells, curcumin further enhanced PHA-induced CHOP expression and reduced the expression of the anti-apoptotic protein Bcl-2.	Curcumin	26-34	DNA damage inducible transcript 3	Homo sapiens	64-68
23415873-9	2013	Finally, curcumin treatment induced apoptotic cell death in activated T cells via eliciting an excessive ER stress response, which was reversed by the ER-stress inhibitor 4-phenylbutyric acid or transfection with CHOP-specific siRNA.	Curcumin	9-17	DNA damage inducible transcript 3	Homo sapiens	213-217
23400962-7	2013	Four patients were treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) alone: One was alive with no evidence of disease, and three were alive with disease.	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	92-96
23280445-9	2013	Although only CELE upregulates the expression of CHOP, it appears that CHOP induction could be associated with mitochondrial poisoning.	Celecoxib	14-18	DNA damage inducible transcript 3	Homo sapiens	49-53
22972488-1	2013	PURPOSE: Treatment of non-Hodgkin lymphoma (NHL) with cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) is known to be associated with a significant risk of febrile neutropenia (FN) of up to 50% [Osby et al.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	113-117
22972488-1	2013	PURPOSE: Treatment of non-Hodgkin lymphoma (NHL) with cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) is known to be associated with a significant risk of febrile neutropenia (FN) of up to 50% [Osby et al.	Vincristine	72-83	DNA damage inducible transcript 3	Homo sapiens	113-117
22972488-1	2013	PURPOSE: Treatment of non-Hodgkin lymphoma (NHL) with cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) is known to be associated with a significant risk of febrile neutropenia (FN) of up to 50% [Osby et al.	Doxorubicin	85-96	DNA damage inducible transcript 3	Homo sapiens	113-117
22972488-1	2013	PURPOSE: Treatment of non-Hodgkin lymphoma (NHL) with cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) is known to be associated with a significant risk of febrile neutropenia (FN) of up to 50% [Osby et al.	Prednisone	101-111	DNA damage inducible transcript 3	Homo sapiens	113-117
22676837-6	2013	And the antioxidant N-acetyl-l-cysteine inhibited induction of both GRP78 and CHOP by alpha-TOS transcriptionally and translationally.	Acetylcysteine	20-39	DNA damage inducible transcript 3	Homo sapiens	78-82
23123298-4	2013	We found that helenalin markedly induced endoplasmic reticulum (ER) stress-related genes, such as regulated in development and DNA damage responses (REDD) 1, activating transcription factor-4 (ATF4) and/or the CCAAT enhancer-binding protein-homologous protein (CHOP).	helenalin	14-23	DNA damage inducible transcript 3	Homo sapiens	210-259
23123298-4	2013	We found that helenalin markedly induced endoplasmic reticulum (ER) stress-related genes, such as regulated in development and DNA damage responses (REDD) 1, activating transcription factor-4 (ATF4) and/or the CCAAT enhancer-binding protein-homologous protein (CHOP).	helenalin	14-23	DNA damage inducible transcript 3	Homo sapiens	261-265
22676837-7	2013	Furthermore, knocking down CHOP by RNA interference decreased ROS generation, increased glutathione level and induced glutathione peroxidase mRNA expression in alpha-TOS-treated cells, whereas catalase and superoxide dismutases mRNA expression were not altered.	Reactive Oxygen Species	62-65	DNA damage inducible transcript 3	Homo sapiens	27-31
22676837-7	2013	Furthermore, knocking down CHOP by RNA interference decreased ROS generation, increased glutathione level and induced glutathione peroxidase mRNA expression in alpha-TOS-treated cells, whereas catalase and superoxide dismutases mRNA expression were not altered.	Glutathione	88-99	DNA damage inducible transcript 3	Homo sapiens	27-31
22676837-8	2013	The results imply that alpha-TOS induces ER stress response through ROS production, while CHOP perturbs the redox state of SGC-7901 cells treated with alpha-TOS.	alpha-Tocopherol	151-160	DNA damage inducible transcript 3	Homo sapiens	90-94
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	43-71	DNA damage inducible transcript 3	Homo sapiens	111-115
23321314-3	2013	In all three cell lines, treatments with nobiletin (100 muM) for 24 h resulted in more than 200% increases in the expression levels of five genes, including the endoplasmic reticulum stress-responsive genes Ddit3, Trib3, and Asns, and in less than 50% decreases in the expression levels of seven genes, including the cell cycle-regulating genes Ccna2, Ccne2, and E2f8 and the oxidative stress-promoting gene Txnip.	nobiletin	41-50	DNA damage inducible transcript 3	Homo sapiens	207-212
23261452-0	2013	Lipoxygenase inhibitor MK886 potentiates TRAIL-induced apoptosis through CHOP- and p38 MAPK-mediated up-regulation of death receptor 5 in malignant glioma.	MK-886	23-28	DNA damage inducible transcript 3	Homo sapiens	73-77
23281479-5	2013	We found that metabolic dysregulation was associated with induction of eIF2alpha signaling and CHOP up-regulation during challenge with tunicamycin or Velcade.	Tunicamycin	136-147	DNA damage inducible transcript 3	Homo sapiens	95-99
23281479-5	2013	We found that metabolic dysregulation was associated with induction of eIF2alpha signaling and CHOP up-regulation during challenge with tunicamycin or Velcade.	Bortezomib	151-158	DNA damage inducible transcript 3	Homo sapiens	95-99
22934693-4	2013	Our previous study revealed that DMI at the clinical relevant concentrations could induce CHOP-dependent apoptotic death in C6 glioma cells.	Desipramine	33-36	DNA damage inducible transcript 3	Homo sapiens	90-94
22960596-0	2013	Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway.	Simvastatin	0-11	DNA damage inducible transcript 3	Homo sapiens	114-118
22960596-0	2013	Simvastatin inhibition of mevalonate pathway induces apoptosis in human breast cancer cells via activation of JNK/CHOP/DR5 signaling pathway.	Mevalonic Acid	26-36	DNA damage inducible transcript 3	Homo sapiens	114-118
22960596-1	2013	Simvastatin (SVA) was shown to up-regulate expression of death receptor-5 (DR5), CCAAT/enhancer binding protein homologous protein (CHOP) and phosphorylated c-Jun N-terminal kinase (pJNK) in human breast cancer cell lines.	Simvastatin	0-11	DNA damage inducible transcript 3	Homo sapiens	81-130
22960596-1	2013	Simvastatin (SVA) was shown to up-regulate expression of death receptor-5 (DR5), CCAAT/enhancer binding protein homologous protein (CHOP) and phosphorylated c-Jun N-terminal kinase (pJNK) in human breast cancer cell lines.	Simvastatin	0-11	DNA damage inducible transcript 3	Homo sapiens	132-136
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	Mevalonic Acid	29-39	DNA damage inducible transcript 3	Homo sapiens	111-115
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	Mevalonic Acid	29-39	DNA damage inducible transcript 3	Homo sapiens	177-181
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	43-71	DNA damage inducible transcript 3	Homo sapiens	177-181
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	73-77	DNA damage inducible transcript 3	Homo sapiens	111-115
22960596-3	2013	Exogenous addition of either mevalonate or geranylgeranyl pyrophosphate (GGPP) inhibited SVA activation of JNK/CHOP/DR5 pro-apoptotic pathway, indicating that activation of JNK/CHOP/DR5 pro-apoptotic pathway is dependent on SVA inhibition of 3-hydroxy-3-methylglutaryl Coenzyme A (HMG-CoA) reductase and its intermediate GGPP.	geranylgeranyl pyrophosphate	73-77	DNA damage inducible transcript 3	Homo sapiens	177-181
23241730-7	2013	The expression of CHOP and caspase-3 in mesangial cells was also found to be significantly enhanced under high glucose conditions compared with the normal group (P&lt;0.01).	Glucose	111-118	DNA damage inducible transcript 3	Homo sapiens	18-22
23107612-0	2013	Eeyarestatin causes cervical cancer cell sensitization to bortezomib treatment by augmenting ER stress and CHOP expression.	eeyarestatin	0-12	DNA damage inducible transcript 3	Homo sapiens	107-111
23107612-0	2013	Eeyarestatin causes cervical cancer cell sensitization to bortezomib treatment by augmenting ER stress and CHOP expression.	Bortezomib	58-68	DNA damage inducible transcript 3	Homo sapiens	107-111
23107612-7	2013	Combination of bortezomib with eeyarestatin resulted in a massive induction of the endoplasmic reticulum stress reaction, small and large heat shock protein activation, autophagy, and upregulation of pro-apoptotic CHOP.	Bortezomib	15-25	DNA damage inducible transcript 3	Homo sapiens	214-218
23107612-7	2013	Combination of bortezomib with eeyarestatin resulted in a massive induction of the endoplasmic reticulum stress reaction, small and large heat shock protein activation, autophagy, and upregulation of pro-apoptotic CHOP.	eeyarestatin	31-43	DNA damage inducible transcript 3	Homo sapiens	214-218
23395946-6	2013	Furthermore, gene expression arrays revealed that metformin caused expression of stress markers DDIT3, CYP1A1,and GDF-15 and a concomitant reduction in PTGS1 expression.	Metformin	50-59	DNA damage inducible transcript 3	Homo sapiens	96-101
23335397-0	2013	Oligomycin A enhances apoptotic effect of TRAIL through CHOP-mediated death receptor 5 expression.	oligomycin A	0-12	DNA damage inducible transcript 3	Homo sapiens	56-60
23107915-8	2013	CONCLUSION: Our results suggest that use of non-CHOP induction regimen and early use of high dose therapy and SCT consolidation may translate to improved survival for pts with HSTCL.	hstcl	176-181	DNA damage inducible transcript 3	Homo sapiens	48-52
23275230-3	2013	Knockdown of miR-21 with antisense oligonucleotides significantly increased the cytotoxic effects of the CHOP regimen in CRL2631 cells.	Oligonucleotides	35-51	DNA damage inducible transcript 3	Homo sapiens	105-109
23243060-4	2013	Sorafenib inhibited platelet-derived growth factor receptor (PDGFR) alpha, TRKA and RON, caused decreases in total and phosphorylated amounts of several signaling molecules, and provoked caspase-3-independent cell death, most likely due to endoplasmic reticulum stress as indicated by upregulation of GADD34 and GADD153 and phosphorylation of PERK.	Sorafenib	0-9	DNA damage inducible transcript 3	Homo sapiens	312-319
23335397-6	2013	Collectively, our data suggest that OMA enhances apoptotic death of cervical cancer cells to TRAIL through upregulation of CHOP-mediated DR5 expression following ER-stress.	oligomycin A	36-39	DNA damage inducible transcript 3	Homo sapiens	123-127
23233035-6	2013	Western blot analysis demonstrated that Smh-3 increased the protein levels of caspase-4 and GADD153 that may lead to ER stress and consequently apoptosis in Hep3B cells.	smh-3	40-45	DNA damage inducible transcript 3	Homo sapiens	92-99
23166041-2	2013	The CHOP chemotherapy             regimen, which includes cyclophosphamide, doxorubicin, vincristine and prednisone,             has been used previously to treat other types of lymphomas.	Cyclophosphamide	58-74	DNA damage inducible transcript 3	Homo sapiens	4-8
23166041-2	2013	The CHOP chemotherapy             regimen, which includes cyclophosphamide, doxorubicin, vincristine and prednisone,             has been used previously to treat other types of lymphomas.	Doxorubicin	76-87	DNA damage inducible transcript 3	Homo sapiens	4-8
23166041-2	2013	The CHOP chemotherapy             regimen, which includes cyclophosphamide, doxorubicin, vincristine and prednisone,             has been used previously to treat other types of lymphomas.	Vincristine	89-100	DNA damage inducible transcript 3	Homo sapiens	4-8
23166041-2	2013	The CHOP chemotherapy             regimen, which includes cyclophosphamide, doxorubicin, vincristine and prednisone,             has been used previously to treat other types of lymphomas.	Prednisone	105-115	DNA damage inducible transcript 3	Homo sapiens	4-8
23339468-0	2013	Cadmium induces neuronal cell death through reactive oxygen species activated by GADD153.	Cadmium	0-7	DNA damage inducible transcript 3	Homo sapiens	81-88
22982206-0	2013	Verrucarin A sensitizes TRAIL-induced apoptosis via the upregulation of DR5 in an eIF2alpha/CHOP-dependent manner.	muconomycin A	0-12	DNA damage inducible transcript 3	Homo sapiens	92-96
22982206-5	2013	We first found that VA induces a major molecule of ER stress, CCAAT/enhancer binding protein homologous protein (CHOP)-dependent DR5 induction and subsequently increases TRAIL-induced cleavage of caspases and PARP in TRAIL-resistant Hep3B cells.	muconomycin A	20-22	DNA damage inducible transcript 3	Homo sapiens	62-111
22982206-5	2013	We first found that VA induces a major molecule of ER stress, CCAAT/enhancer binding protein homologous protein (CHOP)-dependent DR5 induction and subsequently increases TRAIL-induced cleavage of caspases and PARP in TRAIL-resistant Hep3B cells.	muconomycin A	20-22	DNA damage inducible transcript 3	Homo sapiens	113-117
22982206-10	2013	Therefore, VA-induced eIF2alpha phosphorylation seemed to be important for CHOP and DR5 upregulation and TRAIL-induced apoptosis.	muconomycin A	11-13	DNA damage inducible transcript 3	Homo sapiens	75-79
22982206-12	2013	We concluded that VA triggers TRAIL-induced apoptosis by eIF2alpha/CHOP-dependent DR5 induction via ROS generation.	Reactive Oxygen Species	100-103	DNA damage inducible transcript 3	Homo sapiens	67-71
23339468-0	2013	Cadmium induces neuronal cell death through reactive oxygen species activated by GADD153.	Reactive Oxygen Species	44-67	DNA damage inducible transcript 3	Homo sapiens	81-88
23339468-6	2013	The exposure of neuroblastoma cells to Cd led to increase in intracellular GADD153 and Bak levels in a doses and time dependent manner.	Cadmium	39-41	DNA damage inducible transcript 3	Homo sapiens	75-82
23339468-8	2013	Cd-induced apoptosis is decreased in GADD153 knockdown cells compared with normal cells.	Cadmium	0-2	DNA damage inducible transcript 3	Homo sapiens	37-44
23339468-9	2013	The effect of GADD153 on the binding of C/EBP to the Bak promoters were analyzed ChIP assay.	bakuchiol	53-56	DNA damage inducible transcript 3	Homo sapiens	14-21
23339468-10	2013	Basal constitutive GADD153 recruitment to the -3,398/-3,380 region of the Bak promoter is observed in SH-SY5Y cells.	bakuchiol	74-77	DNA damage inducible transcript 3	Homo sapiens	19-26
23339468-12	2013	The generation of ROS result in the induction of GADD153 is causative of cadmium-induced apoptosis.	Reactive Oxygen Species	18-21	DNA damage inducible transcript 3	Homo sapiens	49-56
23339468-12	2013	The generation of ROS result in the induction of GADD153 is causative of cadmium-induced apoptosis.	Cadmium	73-80	DNA damage inducible transcript 3	Homo sapiens	49-56
23339468-13	2013	GADD153 regulates Bak expression by its binding to promoter region (between -3,398 and -3,380).	bakuchiol	18-21	DNA damage inducible transcript 3	Homo sapiens	0-7
23339468-14	2013	Therefore, we conclude that GADD153 sensitizes cells to ROS through mechanisms that involve up-regulation of BAK and enhanced oxidant injury.	Reactive Oxygen Species	56-59	DNA damage inducible transcript 3	Homo sapiens	28-35
24080827-0	2013	ER stress activating ATF4/CHOP-TNF-alpha signaling pathway contributes to alcohol-induced disruption of osteogenic lineage of multipotential mesenchymal stem cell.	Alcohols	74-81	DNA damage inducible transcript 3	Homo sapiens	26-30
25374716-0	2013	Death from Liver Failure despite Lamivudine Prophylaxis during R-CHOP Chemotherapy due to Rapid Emergence M204 Mutations.	Lamivudine	33-43	DNA damage inducible transcript 3	Homo sapiens	65-69
23053189-1	2013	R-CHOP chemotherapy composed of rituximab, cyclophosphamide, adriamycin, vincristine, and prednisolone which might increase the risk of Pneumocystis pneumonia in patients with non-Hodgkin lymphoma.	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	2-6
23053189-1	2013	R-CHOP chemotherapy composed of rituximab, cyclophosphamide, adriamycin, vincristine, and prednisolone which might increase the risk of Pneumocystis pneumonia in patients with non-Hodgkin lymphoma.	Doxorubicin	61-71	DNA damage inducible transcript 3	Homo sapiens	2-6
23053189-1	2013	R-CHOP chemotherapy composed of rituximab, cyclophosphamide, adriamycin, vincristine, and prednisolone which might increase the risk of Pneumocystis pneumonia in patients with non-Hodgkin lymphoma.	Vincristine	73-84	DNA damage inducible transcript 3	Homo sapiens	2-6
23053189-1	2013	R-CHOP chemotherapy composed of rituximab, cyclophosphamide, adriamycin, vincristine, and prednisolone which might increase the risk of Pneumocystis pneumonia in patients with non-Hodgkin lymphoma.	Prednisolone	90-102	DNA damage inducible transcript 3	Homo sapiens	2-6
24351550-6	2013	In normal human chondrocytes, CHOP "gain of function" sensitized chondrocytes to IL-1beta induced nitric oxide (NO) and matrix metalloproteinase (MMP)-3 release without inducing these responses by itself.	Nitric Oxide	98-110	DNA damage inducible transcript 3	Homo sapiens	30-34
24351550-7	2013	Excess CHOP expression, by itself, induced superoxide production and apoptosis.	Superoxides	43-53	DNA damage inducible transcript 3	Homo sapiens	7-11
24351550-12	2013	Conversely, pharmacologic activation of AMPK by 5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) blunted chondrocyte CHOP expression in response to biomechanical injury.	AICA ribonucleotide	48-93	DNA damage inducible transcript 3	Homo sapiens	122-126
24371535-6	2013	The most common treatment is chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens, but the overall survival rate is poor despite its relative responsiveness to chemotherapy.	Prednisone	95-105	DNA damage inducible transcript 3	Homo sapiens	107-111
23984169-8	2013	Complete response of this PTLD was achieved with 6 cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy; however, 4 months off therapy he developed CNS PTLD (monomorphic CD20-, EBV+, lambda-restricted, plasmacytoid PTLD) of the brain and spine.	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	121-125
23000344-4	2013	Salubrinal inhibits ursolic acid-induced CHOP expression, Bim ER accumulation and caspase-3 activation in T24 cells.	salubrinal	0-10	DNA damage inducible transcript 3	Homo sapiens	41-45
23000344-4	2013	Salubrinal inhibits ursolic acid-induced CHOP expression, Bim ER accumulation and caspase-3 activation in T24 cells.	ursolic acid	20-32	DNA damage inducible transcript 3	Homo sapiens	41-45
23711492-6	2013	Similar results were observed using A549 cells for XBP-1s, BiP, and CHOP in response to thapsigargin.	Thapsigargin	88-100	DNA damage inducible transcript 3	Homo sapiens	68-72
24080827-9	2013	Alcohol induced ER stress, as reflected by increased expression of glucose-regulated proteins GRP78 and GRP94, and by increased expression of transcription factors activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP), and enhanced caspase 3 activity.	Alcohols	0-7	DNA damage inducible transcript 3	Homo sapiens	209-233
24080827-9	2013	Alcohol induced ER stress, as reflected by increased expression of glucose-regulated proteins GRP78 and GRP94, and by increased expression of transcription factors activating transcription factor 4 (ATF4) and C/EBP homologous protein (CHOP), and enhanced caspase 3 activity.	Alcohols	0-7	DNA damage inducible transcript 3	Homo sapiens	235-239
24080827-12	2013	Knockdown of either ATF4 and CHOP or TNF-alpha by their siRNAs was able to reverse the ethanol-induced adipogenesis.	Ethanol	87-94	DNA damage inducible transcript 3	Homo sapiens	29-33
24080827-13	2013	CONCLUSION: Our data therefore revealed a role of ER stress and ATF4/CHOP in the ethanol-induced inhibition of osteogenesis, and activation of TNF-alpha signaling by ATF4/CHOP linking ER stress to adipogenic lineage in response to alcohol stimulation.	Ethanol	81-88	DNA damage inducible transcript 3	Homo sapiens	69-73
24080827-14	2013	This work should establish a new signaling pathway linking alcohol, ER stress, and TNF-alpha to loss of bone formation: Ethanol   ER stress      ATF4 &amp; CHOP      TNF-alpha      Osteoblasts   .	Alcohols	59-66	DNA damage inducible transcript 3	Homo sapiens	156-160
24080827-14	2013	This work should establish a new signaling pathway linking alcohol, ER stress, and TNF-alpha to loss of bone formation: Ethanol   ER stress      ATF4 &amp; CHOP      TNF-alpha      Osteoblasts   .	Ethanol	120-127	DNA damage inducible transcript 3	Homo sapiens	156-160
24072968-8	2013	A recently performed large randomized study for elderly patients, however, has shown that R-CHOP (rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy followed by maintenance rituximab can result in a long progression-free survival.	Doxorubicin	131-142	DNA damage inducible transcript 3	Homo sapiens	92-96
23812398-6	2013	UPR markers such as GRP78, C/EBP homology protein (CHOP) and phosphorylated protein kinase RNA-activated (PKR)-like ER kinase (PERK) were significantly down-regulated with hydroxynaphthoic acids in western blot.	3-hydroxy-2-naphthoic acid	172-194	DNA damage inducible transcript 3	Homo sapiens	27-49
23812398-6	2013	UPR markers such as GRP78, C/EBP homology protein (CHOP) and phosphorylated protein kinase RNA-activated (PKR)-like ER kinase (PERK) were significantly down-regulated with hydroxynaphthoic acids in western blot.	3-hydroxy-2-naphthoic acid	172-194	DNA damage inducible transcript 3	Homo sapiens	51-55
24072968-8	2013	A recently performed large randomized study for elderly patients, however, has shown that R-CHOP (rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy followed by maintenance rituximab can result in a long progression-free survival.	Vincristine	144-155	DNA damage inducible transcript 3	Homo sapiens	92-96
24072968-8	2013	A recently performed large randomized study for elderly patients, however, has shown that R-CHOP (rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy followed by maintenance rituximab can result in a long progression-free survival.	Prednisone	161-171	DNA damage inducible transcript 3	Homo sapiens	92-96
23573140-4	2013	Additionally, subamolide B evoked cell death pathways mediated by FasL/Fas, mitochondria, and endoplasmic reticulum (ER) stress, as supported by subamolide B-induced FasL upregulation, BCL-2 suppression/cytosolic release of cytochrome c, and UPR activation/CHOP upregulation, respectively.	subamolide B	14-26	DNA damage inducible transcript 3	Homo sapiens	257-261
23781265-4	2013	Knockdown of growth arrest- and DNA damage-inducible gene 153 (GADD153), a marker of the endoplasmic-reticulum-stress- (ERS-) mediated apoptosis pathway, by specific siRNA attenuated capsaicin-induced apoptosis both in PANC-1 and SW1990 cells.	Capsaicin	183-192	DNA damage inducible transcript 3	Homo sapiens	13-61
23781265-4	2013	Knockdown of growth arrest- and DNA damage-inducible gene 153 (GADD153), a marker of the endoplasmic-reticulum-stress- (ERS-) mediated apoptosis pathway, by specific siRNA attenuated capsaicin-induced apoptosis both in PANC-1 and SW1990 cells.	Capsaicin	183-192	DNA damage inducible transcript 3	Homo sapiens	63-70
23781265-6	2013	Furthermore, capsaicin increased the expression of some key ERS markers, including glucose-regulated protein 78 (GRP78), phosphoprotein kinase-like endoplasmic reticulum kinase (phosphoPERK), and phosphoeukaryotic initiation factor-2 alpha (phospho-eIF2 alpha ), activating transcription factor 4 (ATF4) and GADD153 in tumor tissues.	Capsaicin	13-22	DNA damage inducible transcript 3	Homo sapiens	308-315
23573140-4	2013	Additionally, subamolide B evoked cell death pathways mediated by FasL/Fas, mitochondria, and endoplasmic reticulum (ER) stress, as supported by subamolide B-induced FasL upregulation, BCL-2 suppression/cytosolic release of cytochrome c, and UPR activation/CHOP upregulation, respectively.	subamolide B	145-157	DNA damage inducible transcript 3	Homo sapiens	257-261
23573140-6	2013	Collectively, these results underscored the central role of mitochondrial and CHOP-mediated cell death pathways in subamolide B-induced cytotoxicity.	subamolide B	115-127	DNA damage inducible transcript 3	Homo sapiens	78-82
22918703-9	2013	Compared to SU5416 treatment alone, cell viability was reduced with CHOP plasmid but it was unchanged with CHOP siRNA.	Semaxinib	12-18	DNA damage inducible transcript 3	Homo sapiens	68-72
22918703-0	2013	CCAAT/Enhancer-binding protein-homologous protein sensitizes to SU5416 by modulating p21 and PI3K/Akt signal pathway in FRO anaplastic thyroid carcinoma cells.	Semaxinib	64-70	DNA damage inducible transcript 3	Homo sapiens	0-49
22918703-12	2013	In conclusion, these results suggest that CHOP may sensitize FRO ATC cells to SU5416 thereby inhibiting cell survival by modulating p21 and PI3K/Akt signal pathway.	Semaxinib	78-84	DNA damage inducible transcript 3	Homo sapiens	42-46
22918703-13	2013	Furthermore, these findings imply that CHOP may be a possible candidate as the chemosensitizing factor for induction of cytotoxicity in ATC cells exposed to SU5416.	Semaxinib	157-163	DNA damage inducible transcript 3	Homo sapiens	39-43
23696740-3	2013	Among these pilin modifications, the presence of phosphorylcholine (ChoP) and a glycan on the pilin protein are phase-variable (subject to high frequency, reversible on/off switching of expression).	Phosphorylcholine	49-66	DNA damage inducible transcript 3	Homo sapiens	68-72
24200545-8	2013	The patient received R-CHOP therapy (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab) with good response.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	23-27
24200545-8	2013	The patient received R-CHOP therapy (cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab) with good response.	Doxorubicin	55-66	DNA damage inducible transcript 3	Homo sapiens	23-27
23065334-4	2013	SH-SY5Y cells treated with 100 muM 6-OHDA for 24 h showed reduced Wnt/beta-catenin activity, decreased mitochondrial transmembrane potential, elevated levels of reactive oxidative species (ROS) and phosphatidylserine (PS) extraversion, increased levels of Chop and Bip/GRP78 and reduced level of p-Akt (Ser473).	Oxidopamine	35-41	DNA damage inducible transcript 3	Homo sapiens	256-260
23533616-6	2013	MMC-induced apoptosis was correlated with elevation of 78-kDa glucose-regulated protein (GRP78) and C/EBP homologous protein (CHOP), which are hallmarks of ER stress.	Mitomycin	0-3	DNA damage inducible transcript 3	Homo sapiens	100-124
23533616-6	2013	MMC-induced apoptosis was correlated with elevation of 78-kDa glucose-regulated protein (GRP78) and C/EBP homologous protein (CHOP), which are hallmarks of ER stress.	Mitomycin	0-3	DNA damage inducible transcript 3	Homo sapiens	126-130
23533616-8	2013	Knockdown of CHOP attenuated MMC-induced apoptosis by increasing the ratio of BCL-2/BAX and decreasing BIM expression, suggesting that ER stress is involved in MMC-induced fibroblast apoptosis.	Mitomycin	29-32	DNA damage inducible transcript 3	Homo sapiens	13-17
23533616-10	2013	Reactive oxygen species (ROS) scavenging also decreased the expression of GRP78, phospho-PERK, CHOP, and BIM.	Reactive Oxygen Species	0-23	DNA damage inducible transcript 3	Homo sapiens	95-99
23533616-10	2013	Reactive oxygen species (ROS) scavenging also decreased the expression of GRP78, phospho-PERK, CHOP, and BIM.	Reactive Oxygen Species	25-28	DNA damage inducible transcript 3	Homo sapiens	95-99
24319235-3	2013	A randomized study from the Groupe d"Etude des Lymphomes de l"Adulte showed that R-ACVBP (rituximab plus doxorubicin, cyclophosphamide, vindesine, bleomycin, prednisone) was superior to rituximab plus CHOP (R-CHOP) in patients under 60 years of age, but toxicity limits its use to younger patients.	r-acvbp	81-88	DNA damage inducible transcript 3	Homo sapiens	207-213
24319235-4	2013	Studies also suggest that DA-EPOCH-R (dose-adjusted etoposide, prednisone, vincristine, cyclophosphamide, doxorubicin, rituximab) is more effective in some subtypes of diffuse large B-cell lymphoma and a randomized comparison with R-CHOP is now nearing completion.	da-epoch-r	26-36	DNA damage inducible transcript 3	Homo sapiens	231-237
23318862-5	2013	After undergoing rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) therapy, the patient was successfully treated with allogeneic hematopoietic transplantation, and no relapse was observed for three years.	Prednisolone	75-87	DNA damage inducible transcript 3	Homo sapiens	91-95
24039428-1	2013	We describe a case of a patient whose clozapine was discontinued after a "red result" following R-CHOP (rituximab with cyclophosphamide, hydroxydaunorubicin, Oncovin, and prednisolone) chemotherapy for large B-cell lymphoma.	Clozapine	38-47	DNA damage inducible transcript 3	Homo sapiens	98-102
24039428-10	2013	We managed to stabilize him with olanzapine and aripiprazole which enabled the heme-oncology group to resume R-CHOP therapy with filgrastim (granulocyte colony-stimulating factor).	Olanzapine	33-43	DNA damage inducible transcript 3	Homo sapiens	111-115
24039428-10	2013	We managed to stabilize him with olanzapine and aripiprazole which enabled the heme-oncology group to resume R-CHOP therapy with filgrastim (granulocyte colony-stimulating factor).	Aripiprazole	48-60	DNA damage inducible transcript 3	Homo sapiens	111-115
23536831-9	2013	Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production.	casticin	172-180	DNA damage inducible transcript 3	Homo sapiens	22-71
23536831-9	2013	Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production.	casticin	172-180	DNA damage inducible transcript 3	Homo sapiens	73-77
23536831-9	2013	Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production.	Reactive Oxygen Species	232-235	DNA damage inducible transcript 3	Homo sapiens	22-71
23536831-9	2013	Gene silencing of the CCAAT/enhancer binding protein homologous protein (CHOP) and pretreatment with salubrinal, an endoplasmic reticulum (ER) stress inhibitor, attenuated casticin-induced DR5 receptor expression, and apoptosis and ROS production.	Reactive Oxygen Species	232-235	DNA damage inducible transcript 3	Homo sapiens	73-77
23536831-12	2013	CONCLUSION/SIGNIFICANCE: Casticin enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-ER stress-CHOP pathway.	casticin	25-33	DNA damage inducible transcript 3	Homo sapiens	195-199
23536831-12	2013	CONCLUSION/SIGNIFICANCE: Casticin enhances TRAIL-induced apoptosis through the downregulation of cell survival proteins and the upregulation of DR5 receptors through actions on the ROS-ER stress-CHOP pathway.	Reactive Oxygen Species	181-184	DNA damage inducible transcript 3	Homo sapiens	195-199
23996885-4	2013	We describe a patient with follicular lymphoma treated with R-CHOP scheme (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) who had pulmonary symptoms during chemotherapy which were diagnosed as rituximab-induced interstitial pneumonia.	Cyclophosphamide	86-102	DNA damage inducible transcript 3	Homo sapiens	62-66
23996885-4	2013	We describe a patient with follicular lymphoma treated with R-CHOP scheme (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) who had pulmonary symptoms during chemotherapy which were diagnosed as rituximab-induced interstitial pneumonia.	Doxorubicin	104-115	DNA damage inducible transcript 3	Homo sapiens	62-66
23996885-4	2013	We describe a patient with follicular lymphoma treated with R-CHOP scheme (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) who had pulmonary symptoms during chemotherapy which were diagnosed as rituximab-induced interstitial pneumonia.	Vincristine	117-128	DNA damage inducible transcript 3	Homo sapiens	62-66
23996885-4	2013	We describe a patient with follicular lymphoma treated with R-CHOP scheme (rituximab, cyclophosphamide, doxorubicin, vincristine, prednisone) who had pulmonary symptoms during chemotherapy which were diagnosed as rituximab-induced interstitial pneumonia.	Prednisone	130-140	DNA damage inducible transcript 3	Homo sapiens	62-66
23696740-5	2013	We show that the surface accessibility of ChoP on pili is affected by phase variable changes to the structure of the pilin-linked glycan.	Polysaccharides	130-136	DNA damage inducible transcript 3	Homo sapiens	42-46
23065795-3	2012	siRNA knockdown of JNK, CHOP, or DR5 shows that gammaT-induced apoptosis is JNK/CHOP/DR5 signaling dependent, which is similar to gammaT3-mediated apoptotic signaling.	gamma-Tocopherol	48-54	DNA damage inducible transcript 3	Homo sapiens	24-28
23047912-6	2013	Nevertheless, low L-BMAA concentrations (>= 0.1mM, 48 h) increased protein ubiquitination, 20S proteasomal and caspase 12 activity, expression of the endoplasmic reticulum (ER) stress marker CHOP, and enhanced phosphorylation of elf2alpha in SH-SY5Y cells.	beta-N-methylamino-L-alanine	18-24	DNA damage inducible transcript 3	Homo sapiens	191-195
23814970-2	2012	Standard chemotherapy is CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).	Cyclophosphamide	39-55	DNA damage inducible transcript 3	Homo sapiens	25-29
23814970-2	2012	Standard chemotherapy is CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).	Doxorubicin	57-68	DNA damage inducible transcript 3	Homo sapiens	25-29
23814970-2	2012	Standard chemotherapy is CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).	Vincristine	70-81	DNA damage inducible transcript 3	Homo sapiens	25-29
23814970-2	2012	Standard chemotherapy is CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone).	Prednisone	86-96	DNA damage inducible transcript 3	Homo sapiens	25-29
22959511-2	2012	Arsenic trioxide exposure led to much significant induction of apoptosis in K562/ADM cells than the parental K562 cells, and the chaperone proteins glucose-regulated protein 78, CHOP/GADD153, X-box binding protein-1 and caspase-12 were activated to varying degrees.	Arsenic Trioxide	0-16	DNA damage inducible transcript 3	Homo sapiens	183-190
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	withaferin A	73-85	DNA damage inducible transcript 3	Homo sapiens	43-47
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	withaferin A	73-85	DNA damage inducible transcript 3	Homo sapiens	223-227
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	Thapsigargin	87-99	DNA damage inducible transcript 3	Homo sapiens	43-47
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	Thapsigargin	87-99	DNA damage inducible transcript 3	Homo sapiens	223-227
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	Brefeldin A	101-112	DNA damage inducible transcript 3	Homo sapiens	43-47
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	Brefeldin A	101-112	DNA damage inducible transcript 3	Homo sapiens	223-227
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	Silybin	118-125	DNA damage inducible transcript 3	Homo sapiens	43-47
22753273-4	2012	We found that treatment of Caki cells with CHOP-inducing drugs including withaferin A, thapsigargin, brefeldin A, and silybin led to a strong reduction in cFLIP(L) protein levels together with a concomitant increase in the CHOP protein.	Silybin	118-125	DNA damage inducible transcript 3	Homo sapiens	223-227
23065795-3	2012	siRNA knockdown of JNK, CHOP, or DR5 shows that gammaT-induced apoptosis is JNK/CHOP/DR5 signaling dependent, which is similar to gammaT3-mediated apoptotic signaling.	gamma-Tocopherol	48-54	DNA damage inducible transcript 3	Homo sapiens	80-84
23065795-5	2012	Inhibition of de novo ceramide synthesis using chemical inhibitors blocked the ability of gammaT and gammaT3 to induce apoptosis as detected by Annexin V-FITC/PI assay and to activate JNK/CHOP/DR5 pro-apoptotic signaling thereby demonstrating the involvement of de novo ceramide synthesis in gammaT- and gammaT3-induced apoptosis.	Ceramides	22-30	DNA damage inducible transcript 3	Homo sapiens	188-192
23065795-6	2012	CONCLUSION: Taken together, data show that both gammaT and gammaT3 induce apoptosis via de novo ceramide synthesis dependent activation of JNK/CHOP/DR5 pro-apoptotic signaling.	Ceramides	96-104	DNA damage inducible transcript 3	Homo sapiens	143-147
23171849-3	2012	Here we show in U937 cells that the ER stressors tunicamycin and thapsigargin cause increased expression of c-Jun N-terminal kinase 2 (JNK2), which allows regulation of the UPR, whose silencing or pharmacological inhibition delays BiP (immunoglobulin heavy-chain binding protein) upregulation, and causes earlier and greater expression of CCAAT/enhancer-binding protein-homologous protein (CHOP).	Tunicamycin	49-60	DNA damage inducible transcript 3	Homo sapiens	339-388
23036742-8	2012	These results suggest that phycocyanin might suppress d-galactose-induced hLEC apoptosis through two pathways: mitochondrial pathway, involving p53 and Bcl-2 family protein expression, and unfolded protein response pathway, involving GRP78 and CHOP expression.	Galactose	54-65	DNA damage inducible transcript 3	Homo sapiens	244-248
23171849-3	2012	Here we show in U937 cells that the ER stressors tunicamycin and thapsigargin cause increased expression of c-Jun N-terminal kinase 2 (JNK2), which allows regulation of the UPR, whose silencing or pharmacological inhibition delays BiP (immunoglobulin heavy-chain binding protein) upregulation, and causes earlier and greater expression of CCAAT/enhancer-binding protein-homologous protein (CHOP).	Thapsigargin	65-77	DNA damage inducible transcript 3	Homo sapiens	339-388
23171849-3	2012	Here we show in U937 cells that the ER stressors tunicamycin and thapsigargin cause increased expression of c-Jun N-terminal kinase 2 (JNK2), which allows regulation of the UPR, whose silencing or pharmacological inhibition delays BiP (immunoglobulin heavy-chain binding protein) upregulation, and causes earlier and greater expression of CCAAT/enhancer-binding protein-homologous protein (CHOP).	Thapsigargin	65-77	DNA damage inducible transcript 3	Homo sapiens	390-394
22972372-6	2012	Moreover, Abnobaviscum F treatment             led to both a reduction of cellular glutathione (GSH) and the induction of ER             stress (GRP78 and CHOP induction and eIF-2alpha phosphorylation).	abnobaviscum f	10-24	DNA damage inducible transcript 3	Homo sapiens	155-159
23171849-3	2012	Here we show in U937 cells that the ER stressors tunicamycin and thapsigargin cause increased expression of c-Jun N-terminal kinase 2 (JNK2), which allows regulation of the UPR, whose silencing or pharmacological inhibition delays BiP (immunoglobulin heavy-chain binding protein) upregulation, and causes earlier and greater expression of CCAAT/enhancer-binding protein-homologous protein (CHOP).	Tunicamycin	49-60	DNA damage inducible transcript 3	Homo sapiens	390-394
22922338-0	2012	Capsazepine, a TRPV1 antagonist, sensitizes colorectal cancer cells to apoptosis by TRAIL through ROS-JNK-CHOP-mediated upregulation of death receptors.	capsazepine	0-11	DNA damage inducible transcript 3	Homo sapiens	106-110
22922338-0	2012	Capsazepine, a TRPV1 antagonist, sensitizes colorectal cancer cells to apoptosis by TRAIL through ROS-JNK-CHOP-mediated upregulation of death receptors.	Reactive Oxygen Species	98-101	DNA damage inducible transcript 3	Homo sapiens	106-110
22922338-8	2012	Capsazepine"s effects appeared to be mediated via JNK, as shown by capsazepine"s ability to induce JNK and by the suppression of both CHOP and DR5 activation by inhibition of JNK.	capsazepine	0-11	DNA damage inducible transcript 3	Homo sapiens	134-138
22922338-6	2012	DR induction was dependent on CCAAT/enhancer-binding protein homologous protein (CHOP), as shown by (a) the induction of CHOP by capsazepine and (b) the abolition of DR- and potentiation of TRAIL-induced apoptosis by CHOP gene silencing.	capsazepine	129-140	DNA damage inducible transcript 3	Homo sapiens	30-79
22922338-11	2012	Together, our results indicate that capsazepine potentiates the apoptotic effects of TRAIL through downregulation of cell survival proteins and upregulation of death receptors via the ROS-JNK-CHOP-mediated pathway.	capsazepine	36-47	DNA damage inducible transcript 3	Homo sapiens	192-196
22922338-6	2012	DR induction was dependent on CCAAT/enhancer-binding protein homologous protein (CHOP), as shown by (a) the induction of CHOP by capsazepine and (b) the abolition of DR- and potentiation of TRAIL-induced apoptosis by CHOP gene silencing.	capsazepine	129-140	DNA damage inducible transcript 3	Homo sapiens	81-85
22922338-11	2012	Together, our results indicate that capsazepine potentiates the apoptotic effects of TRAIL through downregulation of cell survival proteins and upregulation of death receptors via the ROS-JNK-CHOP-mediated pathway.	Reactive Oxygen Species	184-187	DNA damage inducible transcript 3	Homo sapiens	192-196
22922338-6	2012	DR induction was dependent on CCAAT/enhancer-binding protein homologous protein (CHOP), as shown by (a) the induction of CHOP by capsazepine and (b) the abolition of DR- and potentiation of TRAIL-induced apoptosis by CHOP gene silencing.	capsazepine	129-140	DNA damage inducible transcript 3	Homo sapiens	121-125
22922338-6	2012	DR induction was dependent on CCAAT/enhancer-binding protein homologous protein (CHOP), as shown by (a) the induction of CHOP by capsazepine and (b) the abolition of DR- and potentiation of TRAIL-induced apoptosis by CHOP gene silencing.	capsazepine	129-140	DNA damage inducible transcript 3	Homo sapiens	121-125
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	24-47	DNA damage inducible transcript 3	Homo sapiens	0-4
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	24-47	DNA damage inducible transcript 3	Homo sapiens	206-210
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	49-52	DNA damage inducible transcript 3	Homo sapiens	0-4
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	49-52	DNA damage inducible transcript 3	Homo sapiens	206-210
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	capsazepine	77-88	DNA damage inducible transcript 3	Homo sapiens	0-4
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	capsazepine	77-88	DNA damage inducible transcript 3	Homo sapiens	206-210
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	109-112	DNA damage inducible transcript 3	Homo sapiens	0-4
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Reactive Oxygen Species	109-112	DNA damage inducible transcript 3	Homo sapiens	0-4
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Acetylcysteine	144-160	DNA damage inducible transcript 3	Homo sapiens	0-4
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Acetylcysteine	144-160	DNA damage inducible transcript 3	Homo sapiens	206-210
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Glutathione	164-175	DNA damage inducible transcript 3	Homo sapiens	0-4
22922338-7	2012	CHOP induction was also reactive oxygen species (ROS)-dependent, as shown by capsazepine"s ability to induce ROS and by the quenching of ROS by N-acetylcysteine or glutathione, which prevented induction of CHOP and DR5 and consequent sensitization to TRAIL.	Glutathione	164-175	DNA damage inducible transcript 3	Homo sapiens	206-210
22739576-3	2012	Two hundred sixty-three patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) were enrolled to this prospective cohort study, and their QoL was evaluated.	Prednisolone	105-117	DNA damage inducible transcript 3	Homo sapiens	121-125
22752193-1	2012	The combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) plus rituximab is the standard treatment for patients with primary gastric diffuse large B cell lymphoma (DLBCL).	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	96-100
22752193-1	2012	The combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) plus rituximab is the standard treatment for patients with primary gastric diffuse large B cell lymphoma (DLBCL).	Prednisolone	82-94	DNA damage inducible transcript 3	Homo sapiens	96-100
22752193-5	2012	The CR rates were 93.9% for patients receiving CHOP and 92.5% for patients receiving R-CHOP.	Chromium	4-6	DNA damage inducible transcript 3	Homo sapiens	47-51
22752193-5	2012	The CR rates were 93.9% for patients receiving CHOP and 92.5% for patients receiving R-CHOP.	Chromium	4-6	DNA damage inducible transcript 3	Homo sapiens	87-91
23320431-1	2012	OBJECTIVES: To report the case of a patient with diffuse large B-cell lymphoma (DLBCL) who developed vincristine (VCR)-induced seizure after R-CHOP chemotherapy.	Vincristine	101-112	DNA damage inducible transcript 3	Homo sapiens	143-147
23320431-1	2012	OBJECTIVES: To report the case of a patient with diffuse large B-cell lymphoma (DLBCL) who developed vincristine (VCR)-induced seizure after R-CHOP chemotherapy.	Vincristine	114-117	DNA damage inducible transcript 3	Homo sapiens	143-147
22935424-4	2012	Further, ceramide-induced cell death reduced significantly in stable SH-SY5Y cells expressing C/EBP homologous protein (CHOP) shRNA.	Ceramides	9-17	DNA damage inducible transcript 3	Homo sapiens	94-118
22898769-8	2012	Endoplasmic reticulum (ER) stress was increased in response to RSV, as indicated by increased phosphorylation of eukaryotic initiation factor 2alpha (eIF2alpha) and increased expression of CCAAT/enhancer binding protein homologous protein (CHOP).	Resveratrol	63-66	DNA damage inducible transcript 3	Homo sapiens	189-238
22898769-8	2012	Endoplasmic reticulum (ER) stress was increased in response to RSV, as indicated by increased phosphorylation of eukaryotic initiation factor 2alpha (eIF2alpha) and increased expression of CCAAT/enhancer binding protein homologous protein (CHOP).	Resveratrol	63-66	DNA damage inducible transcript 3	Homo sapiens	240-244
23267908-5	2012	The malignant lymphoma patient was treated by cyclophosphamide+doxorubicin+vincristine+prednisolone(CHOP) with rituximab.	Cyclophosphamide	46-62	DNA damage inducible transcript 3	Homo sapiens	100-104
23267908-5	2012	The malignant lymphoma patient was treated by cyclophosphamide+doxorubicin+vincristine+prednisolone(CHOP) with rituximab.	Prednisolone	87-99	DNA damage inducible transcript 3	Homo sapiens	100-104
23267962-13	2012	Cyclophosphamide+doxorubicin+vincristine+prednisolone(CHOP) with rituximab therapy was performed.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	54-58
23267962-13	2012	Cyclophosphamide+doxorubicin+vincristine+prednisolone(CHOP) with rituximab therapy was performed.	Prednisolone	41-53	DNA damage inducible transcript 3	Homo sapiens	54-58
22983648-0	2012	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in the treatment of stage IE/IIE extranodal natural killer/T cell lymphoma, nasal type: 13-year follow-up in 135 patients.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
22983648-0	2012	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in the treatment of stage IE/IIE extranodal natural killer/T cell lymphoma, nasal type: 13-year follow-up in 135 patients.	Prednisone	48-58	DNA damage inducible transcript 3	Homo sapiens	60-64
22935424-4	2012	Further, ceramide-induced cell death reduced significantly in stable SH-SY5Y cells expressing C/EBP homologous protein (CHOP) shRNA.	Ceramides	9-17	DNA damage inducible transcript 3	Homo sapiens	120-124
22959463-6	2012	LCL exposed to sodium arsenite for 8-days induced expression of UPR-activated genes, including CHOP and GRP78, at the RNA and the protein level.	sodium arsenite	15-30	DNA damage inducible transcript 3	Homo sapiens	95-99
22955275-7	2012	ChIP analysis of the Jmjd3, Atf3, and Chop genes in Atf4 knock-out cells documented that activation of the AAR in the presence of TSA led to specific changes in acetylation of histone H4.	trichostatin A	130-133	DNA damage inducible transcript 3	Homo sapiens	38-42
22843330-4	2012	Focused gene expression array analysis followed by immunoblot detection revealed that DP rapidly activates the cytotoxic unfolded protein response (UPR; involving phospho-PERK, phospho-eIF2alpha, Grp78, CHOP, and Hsp70) and the mitochondrial pathway of apoptosis with p53 upregulation and modulation of Bcl-2 family members (involving Noxa, Mcl-1, and Bcl-2).	dp	86-88	DNA damage inducible transcript 3	Homo sapiens	203-207
22415659-7	2012	CHOP was indirectly bound to the MICA/B promoter region by interacting with AP-1, leading to MICA/B transcription.	mica	33-37	DNA damage inducible transcript 3	Homo sapiens	0-4
22678742-6	2012	In addition, when PQ was exposed to L2 cells, the expressions of ER stress-related signaling genes (including Grp78, CHOP, and caspase-12 mRNA) and proteins (including phospho-eIF-2alpha, CHOP, Grp78, calpain I and -II, and caspase-12) were significantly increased.	Primaquine	18-20	DNA damage inducible transcript 3	Homo sapiens	117-121
22678742-6	2012	In addition, when PQ was exposed to L2 cells, the expressions of ER stress-related signaling genes (including Grp78, CHOP, and caspase-12 mRNA) and proteins (including phospho-eIF-2alpha, CHOP, Grp78, calpain I and -II, and caspase-12) were significantly increased.	Primaquine	18-20	DNA damage inducible transcript 3	Homo sapiens	188-192
22678742-10	2012	Cells transfected with Nrf-2 siRNA significantly reversed the PQ-induced toxicity, including depolarization of MMP, increased the Bax, Bak, p53 mRNAs expression, decreased the Bcl-2 mRNA expression, increased the caspase 3/7 activity,  Grp78, CHOP, and caspase-12 mRNAs and protein expression, and decreased that of pro-caspase-3.	Primaquine	62-64	DNA damage inducible transcript 3	Homo sapiens	243-247
22415659-7	2012	CHOP was indirectly bound to the MICA/B promoter region by interacting with AP-1, leading to MICA/B transcription.	mica	93-97	DNA damage inducible transcript 3	Homo sapiens	0-4
22828666-8	2012	At a higher dose, 20 mug/ml, carnosic acid activated the expression of antioxidant (AKR1C2, TNXRD1, HMOX1) and apoptosis (GDF15, PHLDA1, DDIT3) genes and suppressed the expression of inhibitor of transcription (ID3) and cell cycle (CDKN2C) genes.	salvin	29-42	DNA damage inducible transcript 3	Homo sapiens	137-142
22791333-9	2012	After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	DNA damage inducible transcript 3	Homo sapiens	91-115
22859272-10	2012	Western blot analysis confirmed that the expression of GRP78, cleaved caspase-4,             CHOP, NF-kappaB p65 and cleaved caspase-3 were upregulated in a dose-dependent manner             after adenosine treatment.	Adenosine	197-206	DNA damage inducible transcript 3	Homo sapiens	93-97
22859272-12	2012	This             is the first demonstration that adenosine inhibits cell proliferation, increases             GRP78 and NF-kappaB p65 expression and induces apoptosis by CHOP and caspase-4 pathways.	Adenosine	49-58	DNA damage inducible transcript 3	Homo sapiens	170-174
22448918-2	2012	For this reason we decided to explore the combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) given every 14 days with pegfilgrastim (Neulasta) and GM-CSF (Leukine).	Prednisone	115-125	DNA damage inducible transcript 3	Homo sapiens	129-133
22848091-5	2012	We discovered that PS-341 activated ER stress through elevating the expression of BiP, p-eIF2alpha, IRE1alpha, ATF4, ATF3, and CCAAT/enhancer-binding protein homologous protein (CHOP).	Bortezomib	19-25	DNA damage inducible transcript 3	Homo sapiens	127-176
22848091-5	2012	We discovered that PS-341 activated ER stress through elevating the expression of BiP, p-eIF2alpha, IRE1alpha, ATF4, ATF3, and CCAAT/enhancer-binding protein homologous protein (CHOP).	Bortezomib	19-25	DNA damage inducible transcript 3	Homo sapiens	178-182
22791333-9	2012	After proteasome inhibition with MG-132, Western blot analyses showed greater induction of C/EBP-homologous protein (CHOP) and more poly (ADP-ribose) polymerase (PARP) and caspase-3 cleavage, supporting ER stress-induced apoptosis.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	33-39	DNA damage inducible transcript 3	Homo sapiens	117-121
22759738-4	2012	SUMMARY: Rituximab administered as induction or maintenance therapy in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival.	Cyclophosphamide	88-104	DNA damage inducible transcript 3	Homo sapiens	148-152
22721383-1	2012	R (rituximab)-CHOP (cyclophosphamide, adriamycin, vincristin, and prednisone) is given to outpatients with CD20-positive lymphoma as a standard treatment.	Cyclophosphamide	20-36	DNA damage inducible transcript 3	Homo sapiens	14-18
22721383-1	2012	R (rituximab)-CHOP (cyclophosphamide, adriamycin, vincristin, and prednisone) is given to outpatients with CD20-positive lymphoma as a standard treatment.	Vincristine	50-60	DNA damage inducible transcript 3	Homo sapiens	14-18
22759738-4	2012	SUMMARY: Rituximab administered as induction or maintenance therapy in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival.	Doxorubicin	106-117	DNA damage inducible transcript 3	Homo sapiens	148-152
22759738-4	2012	SUMMARY: Rituximab administered as induction or maintenance therapy in combination with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly prolonged event-free survival.	Prednisone	136-146	DNA damage inducible transcript 3	Homo sapiens	148-152
23181121-4	2012	A multicentre retrospective analysis of DLBCL patients who were treated with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP)-like chemotherapy alone or chemotherapy plus rituximab (R-CHOP-like) was performed.	Prednisone	124-134	DNA damage inducible transcript 3	Homo sapiens	136-140
23181121-7	2012	Although the IPI remained predictive for the CHOP-like group, it failed to distinguish between the various prognostic categories in the R-CHOP-like group.	diprotin A	13-16	DNA damage inducible transcript 3	Homo sapiens	45-49
23181121-8	2012	Notably, redistribution of the IPI factors into R-IPI factors identified three discrete prognostic groups with significantly different outcomes in both the CHOP-like and R-CHOP-like groups.	diprotin A	31-34	DNA damage inducible transcript 3	Homo sapiens	156-160
23181121-8	2012	Notably, redistribution of the IPI factors into R-IPI factors identified three discrete prognostic groups with significantly different outcomes in both the CHOP-like and R-CHOP-like groups.	diprotin A	31-34	DNA damage inducible transcript 3	Homo sapiens	172-176
22851557-1	2012	PURPOSE: To test the hypothesis that consolidation therapy with yttrium-90 ((90)Y) -ibritumomab tiuxetan after brief initial therapy with four cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in patients with previously untreated mantle-cell lymphoma would be a well-tolerated regimen that would improve outcomes compared with historical R-CHOP data.	Yttrium-90	64-74	DNA damage inducible transcript 3	Homo sapiens	230-234
22684338-5	2012	We found that 5-FU profoundly induces             ER stress in Sk-Hep1 cells and upregulates p53 and activates CHOP/GADD153 and             caspase-12.	Fluorouracil	14-18	DNA damage inducible transcript 3	Homo sapiens	111-115
22684338-5	2012	We found that 5-FU profoundly induces             ER stress in Sk-Hep1 cells and upregulates p53 and activates CHOP/GADD153 and             caspase-12.	Fluorouracil	14-18	DNA damage inducible transcript 3	Homo sapiens	116-123
22851557-1	2012	PURPOSE: To test the hypothesis that consolidation therapy with yttrium-90 ((90)Y) -ibritumomab tiuxetan after brief initial therapy with four cycles of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in patients with previously untreated mantle-cell lymphoma would be a well-tolerated regimen that would improve outcomes compared with historical R-CHOP data.	Yttrium-90	64-74	DNA damage inducible transcript 3	Homo sapiens	384-388
22118157-7	2012	Furthermore, we found that silibinin enhances ER stress-mediated apoptosis in HaCaT cells by increasing the expression of CHOP protein.	Silybin	27-36	DNA damage inducible transcript 3	Homo sapiens	122-126
23213463-6	2012	CHOP induced by piceatannol or by permanent overexpression in LiSa-2 cells blocks adipocyte differentiation as characterized by inhibited fat droplet formation and vascular endothelial growth factor (VEGF) production.	3,3',4,5'-tetrahydroxystilbene	16-27	DNA damage inducible transcript 3	Homo sapiens	0-4
23213463-9	2012	Pulldowns and glycerol gradients reveal that CHOP interacts with a supercomplex consisting of the CSN, cullin 3 and Keap1.	Glycerol	14-22	DNA damage inducible transcript 3	Homo sapiens	45-49
22080215-4	2012	We found that taurine suppresses the up-regulation of caspase-12 and GADD153/CHOP induced by hypoxia/reoxygenation, suggesting that taurine may exert a protective function against hypoxia/reoxygenation by reducing the ER stress.	Taurine	14-21	DNA damage inducible transcript 3	Homo sapiens	69-76
22080215-4	2012	We found that taurine suppresses the up-regulation of caspase-12 and GADD153/CHOP induced by hypoxia/reoxygenation, suggesting that taurine may exert a protective function against hypoxia/reoxygenation by reducing the ER stress.	Taurine	14-21	DNA damage inducible transcript 3	Homo sapiens	77-81
22080215-4	2012	We found that taurine suppresses the up-regulation of caspase-12 and GADD153/CHOP induced by hypoxia/reoxygenation, suggesting that taurine may exert a protective function against hypoxia/reoxygenation by reducing the ER stress.	Taurine	132-139	DNA damage inducible transcript 3	Homo sapiens	69-76
22080215-4	2012	We found that taurine suppresses the up-regulation of caspase-12 and GADD153/CHOP induced by hypoxia/reoxygenation, suggesting that taurine may exert a protective function against hypoxia/reoxygenation by reducing the ER stress.	Taurine	132-139	DNA damage inducible transcript 3	Homo sapiens	77-81
22587388-1	2012	Rituximab (R) plus doxorubicin, cyclophosphamide, vincristine, and prednisolone (CHOP) chemotherapy (R-CHOP) is widely accepted as standard care for diffuse large B-cell lymphoma (DLBCL) patients.	Prednisolone	67-79	DNA damage inducible transcript 3	Homo sapiens	81-85
22865806-4	2012	A brain biopsy confirmed the diagnosis of intravascular B-cell lymphoma and he was treated with CHOP chemotherapy (cyclophosphamide, hydroxydaunorubicin, vincristine and prednisolone).	Cyclophosphamide	115-131	DNA damage inducible transcript 3	Homo sapiens	96-100
22865806-4	2012	A brain biopsy confirmed the diagnosis of intravascular B-cell lymphoma and he was treated with CHOP chemotherapy (cyclophosphamide, hydroxydaunorubicin, vincristine and prednisolone).	Doxorubicin	133-152	DNA damage inducible transcript 3	Homo sapiens	96-100
22587388-1	2012	Rituximab (R) plus doxorubicin, cyclophosphamide, vincristine, and prednisolone (CHOP) chemotherapy (R-CHOP) is widely accepted as standard care for diffuse large B-cell lymphoma (DLBCL) patients.	Prednisolone	67-79	DNA damage inducible transcript 3	Homo sapiens	103-107
23015779-7	2012	Immunoblotting data displayed up-regulations of PERK/eIF2alpha/ATF4/CHOP and ATF6/CHOP coupling with elevation of ER stress chaperones GRP78, GRP94, calnexin, calreticulin and PDI, implicating the involvement of these factors in ER stress-mediated apoptosis induced by 11-dehydrosinulariolide.	11-dehydrosinulariolide	269-292	DNA damage inducible transcript 3	Homo sapiens	68-72
22440390-10	2012	Excellent results have been reported with a variety of anthracycline-based chemotherapy regimens including CHOP, CHOEP or MACOP-B.	Anthracyclines	55-68	DNA damage inducible transcript 3	Homo sapiens	107-111
21547369-5	2012	Expression array analysis revealed DHA-induced upregulation of oxidative and genotoxic stress response genes (GADD45A, GADD153, CDKN1A, PMAIP1, HMOX1, EGR1) in A375 cells.	artenimol	35-38	DNA damage inducible transcript 3	Homo sapiens	119-126
22289049-4	2012	Cotreatment with melatonin (1mm) and TG (50nm) induced approximately 10-fold expression levels of CCAAT-enhancer-binding proteins homologous protein (CHOP) compared with that of TG (50nm) alone.	Melatonin	17-26	DNA damage inducible transcript 3	Homo sapiens	150-154
22289049-4	2012	Cotreatment with melatonin (1mm) and TG (50nm) induced approximately 10-fold expression levels of CCAAT-enhancer-binding proteins homologous protein (CHOP) compared with that of TG (50nm) alone.	Thapsigargin	37-39	DNA damage inducible transcript 3	Homo sapiens	150-154
22289049-5	2012	Downregulation of CHOP expression using small interfering RNAs markedly attenuated melatonin plus TG-mediated apoptosis.	Melatonin	83-92	DNA damage inducible transcript 3	Homo sapiens	18-22
22289049-5	2012	Downregulation of CHOP expression using small interfering RNAs markedly attenuated melatonin plus TG-mediated apoptosis.	Thapsigargin	98-100	DNA damage inducible transcript 3	Homo sapiens	18-22
22289049-6	2012	In addition, cotreatment with TG- and melatonin-induced CHOP upregulation likely relates to melatonin"s antioxidant capacity because we proved that this CHOP upregulation is melatonin receptor independent.	Thapsigargin	30-32	DNA damage inducible transcript 3	Homo sapiens	56-60
22289049-6	2012	In addition, cotreatment with TG- and melatonin-induced CHOP upregulation likely relates to melatonin"s antioxidant capacity because we proved that this CHOP upregulation is melatonin receptor independent.	Thapsigargin	30-32	DNA damage inducible transcript 3	Homo sapiens	153-157
22289049-6	2012	In addition, cotreatment with TG- and melatonin-induced CHOP upregulation likely relates to melatonin"s antioxidant capacity because we proved that this CHOP upregulation is melatonin receptor independent.	Melatonin	38-47	DNA damage inducible transcript 3	Homo sapiens	56-60
22289049-6	2012	In addition, cotreatment with TG- and melatonin-induced CHOP upregulation likely relates to melatonin"s antioxidant capacity because we proved that this CHOP upregulation is melatonin receptor independent.	Melatonin	38-47	DNA damage inducible transcript 3	Homo sapiens	153-157
22289049-6	2012	In addition, cotreatment with TG- and melatonin-induced CHOP upregulation likely relates to melatonin"s antioxidant capacity because we proved that this CHOP upregulation is melatonin receptor independent.	Melatonin	92-101	DNA damage inducible transcript 3	Homo sapiens	56-60
22289049-6	2012	In addition, cotreatment with TG- and melatonin-induced CHOP upregulation likely relates to melatonin"s antioxidant capacity because we proved that this CHOP upregulation is melatonin receptor independent.	Melatonin	92-101	DNA damage inducible transcript 3	Homo sapiens	153-157
22289049-7	2012	Our results collectively demonstrate that the upregulation of CHOP contributes to the enhancing effect of melatonin plus TG on apoptosis in cancer cells.	Melatonin	106-115	DNA damage inducible transcript 3	Homo sapiens	62-66
21678129-9	2012	Activation of the general control nonderepressible-2 (GCN2) kinase stress responsive pathway and induction of CHOP protein was significantly higher in ALL cell lines treated with borrelidin.	borrelidin	179-189	DNA damage inducible transcript 3	Homo sapiens	110-114
22628618-6	2012	Either stearate or the SCD inhibitor but not oleate or other fatty acid treatments also increased ER stress as determined by the expression of p-eIF2alpha, CHOP, and the spliced form of XBP-1, which were directly correlated with ER stearate levels.	Stearates	7-15	DNA damage inducible transcript 3	Homo sapiens	156-160
23015779-7	2012	Immunoblotting data displayed up-regulations of PERK/eIF2alpha/ATF4/CHOP and ATF6/CHOP coupling with elevation of ER stress chaperones GRP78, GRP94, calnexin, calreticulin and PDI, implicating the involvement of these factors in ER stress-mediated apoptosis induced by 11-dehydrosinulariolide.	11-dehydrosinulariolide	269-292	DNA damage inducible transcript 3	Homo sapiens	82-86
22445861-4	2012	The results showed that treatment of HK-2 cells (a human proximal tubular epithelial cell line) with AAI caused an increase in eukaryotic initiation factor-2alpha (eIF2alpha) phosphorylation, X-box binding protein 1 (XBP1) mRNA splicing and the expression of glucose-regulated protein (GRP) 78 and CAAT/enhancer-binding protein-homologous protein (CHOP).	aristolochic acid I	101-104	DNA damage inducible transcript 3	Homo sapiens	298-346
22445861-4	2012	The results showed that treatment of HK-2 cells (a human proximal tubular epithelial cell line) with AAI caused an increase in eukaryotic initiation factor-2alpha (eIF2alpha) phosphorylation, X-box binding protein 1 (XBP1) mRNA splicing and the expression of glucose-regulated protein (GRP) 78 and CAAT/enhancer-binding protein-homologous protein (CHOP).	aristolochic acid I	101-104	DNA damage inducible transcript 3	Homo sapiens	348-352
21801305-10	2012	We demonstrate that salermide induces expression of ATF4, and ATF4 up-regulates ATF3 and subsequently modulates CHOP.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	20-29	DNA damage inducible transcript 3	Homo sapiens	112-116
22609744-4	2012	In HepG2 but not L02 cells, oroxylin A induced substantial production of intracellular H2O2 and inordinate activation of the PERK-eIF2alpha-ATF4-CHOP branch of the unfolded protein response (UPR) pathway, which resulted in the induction of TRB3 and causal reduction of p-AKT1/2/3 (Ser473).	5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one	28-38	DNA damage inducible transcript 3	Homo sapiens	145-149
22609744-5	2012	Moreover, these effects were eliminated by either the stable knockdown of CHOP or the pretreatment and then co-incubation with the specific H2O2 scavenger catalase.	Hydrogen Peroxide	140-144	DNA damage inducible transcript 3	Homo sapiens	74-78
22825471-9	2012	Pretreatment with the protein synthesis inhibitor, cycloheximide, decreased levels of ubiquitinated proteins, ATF3, CHOP, and the overall total cell death, suggesting that inhibition of protein synthesis increases cell survival by relieving proteotoxic stress.	Cycloheximide	51-64	DNA damage inducible transcript 3	Homo sapiens	116-120
21801305-0	2012	Salermide up-regulates death receptor 5 expression through the ATF4-ATF3-CHOP axis and leads to apoptosis in human cancer cells.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	0-9	DNA damage inducible transcript 3	Homo sapiens	73-77
21801305-7	2012	We discovered that IRE-1alpha, Bip, activating transcription factor 3 (ATF4), activating transcription factor 3 (ATF3) and C/EBP homologous protein (CHOP) are induced by salermide, which suggests that DR5-dependent apoptosis is induced by endoplasmic reticulum stress.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	170-179	DNA damage inducible transcript 3	Homo sapiens	123-147
22535574-2	2012	A phase 1 study of bortezomib combined with rituximab, cyclophosphamide, doxorubicin, modified vincristine, and prednisone (R-CHOP) was conducted in patients with untreated follicular lymphoma (FL) and other indolent NHLs.	Bortezomib	19-29	DNA damage inducible transcript 3	Homo sapiens	126-130
22535574-7	2012	RESULTS: The maximum tolerated dose (MTD) of bortezomib with modified R-CHOP was reached at 1.6 mg/m(2).	Bortezomib	45-55	DNA damage inducible transcript 3	Homo sapiens	72-76
22753726-4	2012	RESULTS: ATF3 protein expression was up-regulated after cytotoxic doses of cisplatin treatment and it directly bound to the CHOP gene promoter, increasing this pro-apoptotic protein"s expression.	Cisplatin	75-84	DNA damage inducible transcript 3	Homo sapiens	124-128
21801305-7	2012	We discovered that IRE-1alpha, Bip, activating transcription factor 3 (ATF4), activating transcription factor 3 (ATF3) and C/EBP homologous protein (CHOP) are induced by salermide, which suggests that DR5-dependent apoptosis is induced by endoplasmic reticulum stress.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	170-179	DNA damage inducible transcript 3	Homo sapiens	149-153
21801305-11	2012	This suggests that DR5 is modulated by the ATF4-ATF3-CHOP axis in NSCLC after Sirt1/2 inhibition or salermide treatment.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	100-109	DNA damage inducible transcript 3	Homo sapiens	53-57
21801305-9	2012	Transfected NSCLC cells with ATF4, ATF3 or CHOP siRNA results in a decline in pro-apoptotic proteins (such as caspase-8, caspase-9, caspase-3 and PARP) despite salermide treatment.	N-(3-((2-hydroxynaphthalen-1-ylmethylene)amino)phenyl)-2-phenylpropionamide	160-169	DNA damage inducible transcript 3	Homo sapiens	43-47
22160255-1	2012	The purpose of the study is to evaluate the 10 years follow-up of the efficacy in Chinese patients receiving cyclophosphamide, doxorubicin/epirubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) regimen as the initial treatment for diffuse large B cell lymphoma (DLBCL).	Doxorubicin	127-138	DNA damage inducible transcript 3	Homo sapiens	180-184
22692960-6	2012	2-DG-treated ALL cells exhibit upregulation of P-AMPK, P-Akt, and induction of ER stress/UPR markers (IRE1alpha, GRP78, P-eIF2alpha, and CHOP), which correlate with PARP cleavage and apoptosis.	Deoxyglucose	0-4	DNA damage inducible transcript 3	Homo sapiens	137-141
22516760-7	2012	According to immunoblotting analyses chloropicrin increased the amount of the ER-stress related proteins, Bip (about 3-fold compared to the controls), IRE1alpha (2.5-fold) and Gadd 153/Chop (2.5-fold), evidence for accumulation of misfolded proteins in the ER.	chloropicrin	37-49	DNA damage inducible transcript 3	Homo sapiens	176-184
22516760-7	2012	According to immunoblotting analyses chloropicrin increased the amount of the ER-stress related proteins, Bip (about 3-fold compared to the controls), IRE1alpha (2.5-fold) and Gadd 153/Chop (2.5-fold), evidence for accumulation of misfolded proteins in the ER.	chloropicrin	37-49	DNA damage inducible transcript 3	Homo sapiens	185-189
22160255-1	2012	The purpose of the study is to evaluate the 10 years follow-up of the efficacy in Chinese patients receiving cyclophosphamide, doxorubicin/epirubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) regimen as the initial treatment for diffuse large B cell lymphoma (DLBCL).	Epirubicin	139-149	DNA damage inducible transcript 3	Homo sapiens	180-184
22012966-2	2012	The GOELAMS (Groupe Ouest-Est des Leucemies Aigues et Maladies du Sang) group previously developed the (R)VAD+C regimen (rituximab, vincristine, doxorubicin, dexamethasone and chlorambucil), which appeared as efficient as R-CHOP (rituximab, cyclophosphamide, doxorubicine, vincristine, prednisone) while less toxic.	(r)vad+c	103-111	DNA damage inducible transcript 3	Homo sapiens	224-228
22160255-1	2012	The purpose of the study is to evaluate the 10 years follow-up of the efficacy in Chinese patients receiving cyclophosphamide, doxorubicin/epirubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) regimen as the initial treatment for diffuse large B cell lymphoma (DLBCL).	Prednisone	168-178	DNA damage inducible transcript 3	Homo sapiens	180-184
22160255-6	2012	But in the CHOP group, IPI still distinguished four risk groups.	diprotin A	23-26	DNA damage inducible transcript 3	Homo sapiens	11-15
22489671-10	2012	Nicotine induced ER stress, as evidenced by survival molecules, such as phosphorylated protein kinase-like ER-resident kinase, phosphorylated eukaryotic initiation factor-2alpha and glucose-regulated protein-78, and apoptotic molecules, such as CAAT/enhancer binding protein homologous protein (CHOP).	Nicotine	0-8	DNA damage inducible transcript 3	Homo sapiens	295-299
22687457-3	2012	The efficacy of CHOP as induction therapy before ASCT in MCL is questioned and there is now evidence that as pretreatment before ASCT, AraC + rituximab leads to deeper remission and prolongs progression-free survival compared to rituximab + CHOP.	Cytarabine	135-139	DNA damage inducible transcript 3	Homo sapiens	16-20
22687457-3	2012	The efficacy of CHOP as induction therapy before ASCT in MCL is questioned and there is now evidence that as pretreatment before ASCT, AraC + rituximab leads to deeper remission and prolongs progression-free survival compared to rituximab + CHOP.	Cytarabine	135-139	DNA damage inducible transcript 3	Homo sapiens	241-245
22489671-12	2012	Inhibition of ER stress by salubrinal and transfection of CHOP small interfering RNA attenuated the nicotine-induced cell death, ECM degradation and production of MMPs.	Nicotine	100-108	DNA damage inducible transcript 3	Homo sapiens	58-62
22475637-5	2012	The notable exception is NK/T-cell lymphoma of nasal type where radiotherapy is critically important and recommended to a higher dose, partly because of poor response to anthracycline-based chemotherapy regimens like CHOP.	Anthracyclines	170-183	DNA damage inducible transcript 3	Homo sapiens	217-221
21859781-5	2012	Capsaicin treatment triggered ER stress by promoting the production of reactive oxygen species (ROS), increasing levels of inositol-requiring 1 enzyme (IRE1), growth arrest and DNA-damage-inducible 153 (GADD153) and glucose-regulated protein 78 (GRP78).	Capsaicin	0-9	DNA damage inducible transcript 3	Homo sapiens	159-201
21859781-5	2012	Capsaicin treatment triggered ER stress by promoting the production of reactive oxygen species (ROS), increasing levels of inositol-requiring 1 enzyme (IRE1), growth arrest and DNA-damage-inducible 153 (GADD153) and glucose-regulated protein 78 (GRP78).	Capsaicin	0-9	DNA damage inducible transcript 3	Homo sapiens	203-210
22489671-13	2012	Salubrinal and CHOP small interfering RNA inhibited the effects of nicotine on the activation of Akt, JNK and nuclear factor-kappaB.	Nicotine	67-75	DNA damage inducible transcript 3	Homo sapiens	15-19
21986940-7	2012	2DG also induced GADD153/CHOP expression, a marker of endoplasmic reticulum (ER) stress and a known activator of Bim.	Deoxyglucose	0-3	DNA damage inducible transcript 3	Homo sapiens	17-24
22707267-4	2012	Chemical inhibitors of caspase-8 and -9 and small interfering RNAs (siRNAs) show DHA to induce ERS/CHOP/DR5-mediated caspase-8 and -9 dependent apoptosis.	Docosahexaenoic Acids	81-84	DNA damage inducible transcript 3	Homo sapiens	99-103
22707267-7	2012	CONCLUSION: Data, for the first time, demonstrate that DHA induces apoptosis in TNBC cells via activation of ERS/CHOP/DR5-mediated caspase-8 and -9 dependent pro-apoptotic events, and that different forms of vitamin E exhibit distinct effects on DHA-induced apoptosis; namely, inhibition by alphaT and enhancement by gammaT3.	Docosahexaenoic Acids	55-58	DNA damage inducible transcript 3	Homo sapiens	113-117
21986940-7	2012	2DG also induced GADD153/CHOP expression, a marker of endoplasmic reticulum (ER) stress and a known activator of Bim.	Deoxyglucose	0-3	DNA damage inducible transcript 3	Homo sapiens	25-29
22433868-8	2012	3-MA also blocked induction of GRP78 and CHOP, suggesting that PI3-kinase, which is known to mediate ER stress-induced autophagy, also plays a role in initiating apoptosis in response to ER stress.	3-methyladenine	0-4	DNA damage inducible transcript 3	Homo sapiens	41-45
22266985-11	2012	Bortezomib induces mitochondrial             damage in native cells and also activates the UPR by splicing of Xbp-1 and induction             of CHOP, which is significantly reduced by silencing of MUC4.	Bortezomib	0-10	DNA damage inducible transcript 3	Homo sapiens	145-149
22593445-8	2012	Furthermore, safrole promoted the expression of glucose-regulated protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153) and of activating transcription factor 6alpha (ATF-6alpha).	Safrole	13-20	DNA damage inducible transcript 3	Homo sapiens	86-134
22593445-8	2012	Furthermore, safrole promoted the expression of glucose-regulated protein 78 (GRP78), growth arrest- and DNA damage-inducible gene 153 (GADD153) and of activating transcription factor 6alpha (ATF-6alpha).	Safrole	13-20	DNA damage inducible transcript 3	Homo sapiens	136-143
22328338-8	2012	Moreover,             orlistat induced reactive oxygen species (ROS), and a ROS scavenger diminished             the sensitivity to TRAIL through the suppression of CHOP and DR5 expression in             both cell lines.	Reactive Oxygen Species	76-79	DNA damage inducible transcript 3	Homo sapiens	165-169
22328338-9	2012	These results suggest that there are two pathways of upregulation             of DR5 by orlistat, which are the ROS-CHOP pathway and the ROS-direct pathway.	Reactive Oxygen Species	112-115	DNA damage inducible transcript 3	Homo sapiens	116-120
21799120-4	2012	In contrast, the ER stress inducer thapsigargin (THP) increased CHOP.	Thapsigargin	35-47	DNA damage inducible transcript 3	Homo sapiens	64-68
21799120-4	2012	In contrast, the ER stress inducer thapsigargin (THP) increased CHOP.	Thapsigargin	49-52	DNA damage inducible transcript 3	Homo sapiens	64-68
21948810-5	2012	RESULTS: Only 46% of patients received the standard therapy [aggressive chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP)-like chemotherapy].	Prednisone	137-147	DNA damage inducible transcript 3	Homo sapiens	149-153
20925121-10	2012	Confocal laser microscope examination also showed that capsaicin induced the releases of AIF, ATF-4, and GADD153 from mitochondria of SCC-4 cells.	Capsaicin	55-64	DNA damage inducible transcript 3	Homo sapiens	105-112
22200786-0	2012	Clarithromycin enhances bortezomib-induced cytotoxicity via endoplasmic             reticulum stress-mediated CHOP (GADD153) induction and autophagy in breast cancer             cells.	Clarithromycin	0-14	DNA damage inducible transcript 3	Homo sapiens	110-114
22228470-6	2012	PKR/eIF2alpha activation-induced growth arrest and DNA damage-inducible gene 153 (GADD153) and heat shock protein 27 (Hsp27) expression contribute to cell cycle arrest in response to DHT.	Dihydrotestosterone	183-186	DNA damage inducible transcript 3	Homo sapiens	33-80
22228470-6	2012	PKR/eIF2alpha activation-induced growth arrest and DNA damage-inducible gene 153 (GADD153) and heat shock protein 27 (Hsp27) expression contribute to cell cycle arrest in response to DHT.	Dihydrotestosterone	183-186	DNA damage inducible transcript 3	Homo sapiens	82-89
22228470-7	2012	It is notable that DHT administration results in androgen-sensitive liver cells apoptosis, at least in part, through PKR/eIF2alpha/GADD153 cascades.	Dihydrotestosterone	19-22	DNA damage inducible transcript 3	Homo sapiens	131-138
22446330-5	2012	Additionally, up-regulation of CHOP mRNA and cathepsin D protein expression, following retinoid treatment, suggests involvement of the endoplasmatic reticulum (ER) and lysosomes, respectively.	Retinoids	87-95	DNA damage inducible transcript 3	Homo sapiens	31-35
22035416-1	2012	The prognosis of patients with peripheral T-cell lymphoma (PTCL) treated with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) is poor, but their laboratory prognostic parameters had not previously been evaluated.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	136-140
22035416-1	2012	The prognosis of patients with peripheral T-cell lymphoma (PTCL) treated with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) is poor, but their laboratory prognostic parameters had not previously been evaluated.	Doxorubicin	96-106	DNA damage inducible transcript 3	Homo sapiens	136-140
22035416-1	2012	The prognosis of patients with peripheral T-cell lymphoma (PTCL) treated with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP) is poor, but their laboratory prognostic parameters had not previously been evaluated.	Prednisone	124-134	DNA damage inducible transcript 3	Homo sapiens	136-140
22035417-9	2012	Thus, (90)Y-ibritumomab tiuxetan consolidation following six cycles of R-CHOP resulted in an acceptable response with tolerable toxicity in patients with limited-stage and bulky DLBCL.	y-ibritumomab tiuxetan	10-32	DNA damage inducible transcript 3	Homo sapiens	73-77
22246806-0	2012	Saturated fatty acid induction of endoplasmic reticulum stress and apoptosis in human liver cells via the PERK/ATF4/CHOP signaling pathway.	Fatty Acids	0-20	DNA damage inducible transcript 3	Homo sapiens	116-120
22246806-9	2012	Knockdown of PERK gene expression suppressed the PERK/ATF4/CHOP signaling pathway during sodium palmitate-induced ER stress and significantly inhibited sodium palmitate-induced apoptosis in L02 and HepG2 cells.	Palmitic Acid	89-105	DNA damage inducible transcript 3	Homo sapiens	59-63
22246806-10	2012	Saturated fatty acid-induced ER stress and apoptosis in these human liver cells were enacted through the PERK/ATF4/CHOP signaling pathway.	Fatty Acids	0-20	DNA damage inducible transcript 3	Homo sapiens	115-119
22410117-6	2012	We also observed that CHOP protein levels were significantly increased by rottlerin, but CHOP siRNA did not affect rottlerin-induced NAG-1 expression.	rottlerin	74-83	DNA damage inducible transcript 3	Homo sapiens	22-26
22400995-0	2012	Isoobtusilactone A sensitizes human hepatoma Hep G2 cells to TRAIL-induced apoptosis via ROS and CHOP-mediated up-regulation of DR5.	isoobtusilactone A	0-18	DNA damage inducible transcript 3	Homo sapiens	97-101
22507791-2	2012	Immunochemotherapy, R-CHOP (rituximab, cyclophosphamide, adriamycin, vincristine, and prednisone) is the standard of care.	Prednisone	86-96	DNA damage inducible transcript 3	Homo sapiens	22-26
22200786-0	2012	Clarithromycin enhances bortezomib-induced cytotoxicity via endoplasmic             reticulum stress-mediated CHOP (GADD153) induction and autophagy in breast cancer             cells.	Clarithromycin	0-14	DNA damage inducible transcript 3	Homo sapiens	116-123
22200786-0	2012	Clarithromycin enhances bortezomib-induced cytotoxicity via endoplasmic             reticulum stress-mediated CHOP (GADD153) induction and autophagy in breast cancer             cells.	Bortezomib	24-34	DNA damage inducible transcript 3	Homo sapiens	110-114
22200786-0	2012	Clarithromycin enhances bortezomib-induced cytotoxicity via endoplasmic             reticulum stress-mediated CHOP (GADD153) induction and autophagy in breast cancer             cells.	Bortezomib	24-34	DNA damage inducible transcript 3	Homo sapiens	116-123
22200786-7	2012	Knockdown of CHOP by siRNA attenuated the death-promoting effect of BZ             in MDA-MB-231 cells.	Bortezomib	68-70	DNA damage inducible transcript 3	Homo sapiens	13-17
22225575-7	2012	Interestingly, co-treatment with tunicamycin and melatonin also decreased the expression of COX-2 and significantly increased the rate of apoptosis by elevating the levels of CHOP and reducing the Bcl-2/Bax ratio.	Tunicamycin	33-44	DNA damage inducible transcript 3	Homo sapiens	175-179
22225575-7	2012	Interestingly, co-treatment with tunicamycin and melatonin also decreased the expression of COX-2 and significantly increased the rate of apoptosis by elevating the levels of CHOP and reducing the Bcl-2/Bax ratio.	Melatonin	49-58	DNA damage inducible transcript 3	Homo sapiens	175-179
22225575-6	2012	Furthermore, down-regulation of COX-2 expression using the COX-2 inhibitor, celecoxib, increased tunicamycin-induced apoptosis concomitant with the up-regulation of pro-apoptotic transcription factor CHOP (GADD153) and down-regulation of B-cell lymphoma 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, suggesting that inhibition of COX-2 sensitized human hepatoma cells to ER stress-induced apoptosis.	Celecoxib	76-85	DNA damage inducible transcript 3	Homo sapiens	200-204
22225575-6	2012	Furthermore, down-regulation of COX-2 expression using the COX-2 inhibitor, celecoxib, increased tunicamycin-induced apoptosis concomitant with the up-regulation of pro-apoptotic transcription factor CHOP (GADD153) and down-regulation of B-cell lymphoma 2/Bcl-2-associated X protein (Bcl-2/Bax) ratio, suggesting that inhibition of COX-2 sensitized human hepatoma cells to ER stress-induced apoptosis.	Celecoxib	76-85	DNA damage inducible transcript 3	Homo sapiens	206-213
22225575-8	2012	These results demonstrate that melatonin sensitizes human hepatoma cells to ER stress-induced apoptosis by down-regulating COX-2 expression, increasing the levels of CHOP and decreasing the Bcl-2/Bax ratio.	Melatonin	31-40	DNA damage inducible transcript 3	Homo sapiens	166-170
22203419-7	2012	Pretreatment with sodium hydrosulfide (NaHS, a H(2)S donor) before DOX exposure markedly suppressed DOX-induced overexpressions of GRP78 and CHOP, cytotoxicity and oxidative stress.	sodium bisulfide	18-37	DNA damage inducible transcript 3	Homo sapiens	141-145
22203419-7	2012	Pretreatment with sodium hydrosulfide (NaHS, a H(2)S donor) before DOX exposure markedly suppressed DOX-induced overexpressions of GRP78 and CHOP, cytotoxicity and oxidative stress.	sodium bisulfide	39-43	DNA damage inducible transcript 3	Homo sapiens	141-145
22203419-7	2012	Pretreatment with sodium hydrosulfide (NaHS, a H(2)S donor) before DOX exposure markedly suppressed DOX-induced overexpressions of GRP78 and CHOP, cytotoxicity and oxidative stress.	Hydrogen Sulfide	47-52	DNA damage inducible transcript 3	Homo sapiens	141-145
22203419-7	2012	Pretreatment with sodium hydrosulfide (NaHS, a H(2)S donor) before DOX exposure markedly suppressed DOX-induced overexpressions of GRP78 and CHOP, cytotoxicity and oxidative stress.	Doxorubicin	100-103	DNA damage inducible transcript 3	Homo sapiens	141-145
22781712-8	2012	CR rate for R-CHOP group and CHOP group was 77.01% and 71.43%, respectively.	Chromium	0-2	DNA damage inducible transcript 3	Homo sapiens	12-18
22781712-8	2012	CR rate for R-CHOP group and CHOP group was 77.01% and 71.43%, respectively.	Chromium	0-2	DNA damage inducible transcript 3	Homo sapiens	14-18
22126515-12	2012	Conversely, in patients with a high MTV (&gt;160.1 cm(3)), survival was longer in those who underwent surgery plus R-CHOP than in those treated with R-CHOP alone (P &lt; 0.001 for PFS; P &lt; 0.001 for OS).	mtv	36-39	DNA damage inducible transcript 3	Homo sapiens	117-121
21850390-13	2012	We conclude that replacing conventional doxorubicin with PLD in polychemotherapy regimens such as CHOP is an efficient alternative in the treatment of patients with preexisting cardiac dysfunction.	Doxorubicin	40-51	DNA damage inducible transcript 3	Homo sapiens	98-102
22004570-0	2012	Zyflamend sensitizes tumor cells to TRAIL-induced apoptosis through up-regulation of death receptors and down-regulation of survival proteins: role of ROS-dependent CCAAT/enhancer-binding protein-homologous protein pathway.	Reactive Oxygen Species	151-154	DNA damage inducible transcript 3	Homo sapiens	165-214
22004570-13	2012	CONCLUSION: Zyflamend potentiates TRAIL-induced apoptosis through the ROS-CHOP-mediated up-regulation of DRs, increase in pro-apoptotic protein and down-regulation of cell survival proteins.	Reactive Oxygen Species	70-73	DNA damage inducible transcript 3	Homo sapiens	74-78
22126515-12	2012	Conversely, in patients with a high MTV (&gt;160.1 cm(3)), survival was longer in those who underwent surgery plus R-CHOP than in those treated with R-CHOP alone (P &lt; 0.001 for PFS; P &lt; 0.001 for OS).	mtv	36-39	DNA damage inducible transcript 3	Homo sapiens	151-155
22008998-11	2012	Taken together, RU486 enhances TRAIL-mediated apoptosis through down-regulation of Bcl-2 and c-FLIP(L) as well as CHOP-mediated DR5 up-regulation.	Mifepristone	16-21	DNA damage inducible transcript 3	Homo sapiens	114-118
22210905-6	2012	Recent studies by the Gotoh group have shown that the CHOP pathway is also involved in ER stress-induced cytokine production in macrophages.	gotoh	22-27	DNA damage inducible transcript 3	Homo sapiens	54-58
22107872-5	2012	We found that metformin activates the PERK-ATF4 but not the ATF6 or IRE1-XBP1 branch in ERSS and leads to a strong upregulation of CHOP mRNA and protein.	Metformin	14-23	DNA damage inducible transcript 3	Homo sapiens	131-135
22107872-6	2012	Surprisingly, long-term induction of CHOP by metformin is not accompanied by apoptosis even though CHOP is regarded to be a mediator of ER-stress-induced apoptosis.	Metformin	45-54	DNA damage inducible transcript 3	Homo sapiens	37-41
22333190-12	2012	The patient was treated with chemotherapy (CHOP: cyclophosphamide, hydroxydaunorbicin, vincristine, and predonisone), and the lung tumor disappeared.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	43-47
22479278-2	2012	We evaluated the safety and efficacy of bortezomib treatment with dose-dense cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) every 2 weeks (CHOP-14).	Bortezomib	40-50	DNA damage inducible transcript 3	Homo sapiens	137-141
22310719-3	2012	The treatment of MDA-MB-231 cells with MG132 induced endoplasmic reticulum stress through the induction of ATF6a, PERK phosphorylation, and CHOP, and apoptosis through the cleavage of Bax and procaspase-3.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	39-44	DNA damage inducible transcript 3	Homo sapiens	140-144
22281495-6	2012	Aldo promoted tubular epithelial cell apoptosis, increased intracellular ROS production and induced ER stress, as evidenced by increased expression of glucose-regulated protein 78 (GRP78) and CAAT/enhancer-binding protein homologous protein (CHOP) in a dose- and time-dependent manner.	Aldosterone	0-4	DNA damage inducible transcript 3	Homo sapiens	242-246
22281495-9	2012	Altogether, these observations suggest that Aldo induces apoptosis via ROS-mediated, CHOP-dependent activation in renal tubular epithelial cells.	Aldosterone	44-48	DNA damage inducible transcript 3	Homo sapiens	85-89
22281495-9	2012	Altogether, these observations suggest that Aldo induces apoptosis via ROS-mediated, CHOP-dependent activation in renal tubular epithelial cells.	Reactive Oxygen Species	71-74	DNA damage inducible transcript 3	Homo sapiens	85-89
21365646-5	2012	The level of GADD153 was gradually elevated as the effect of AFP was counteracted by increasing dose or prolonging treatment time with ATRA in HepG2 cells.	Tretinoin	135-139	DNA damage inducible transcript 3	Homo sapiens	13-20
22333190-12	2012	The patient was treated with chemotherapy (CHOP: cyclophosphamide, hydroxydaunorbicin, vincristine, and predonisone), and the lung tumor disappeared.	hydroxydaunorbicin	67-85	DNA damage inducible transcript 3	Homo sapiens	43-47
22333190-12	2012	The patient was treated with chemotherapy (CHOP: cyclophosphamide, hydroxydaunorbicin, vincristine, and predonisone), and the lung tumor disappeared.	Vincristine	87-98	DNA damage inducible transcript 3	Homo sapiens	43-47
22333190-12	2012	The patient was treated with chemotherapy (CHOP: cyclophosphamide, hydroxydaunorbicin, vincristine, and predonisone), and the lung tumor disappeared.	predonisone	104-115	DNA damage inducible transcript 3	Homo sapiens	43-47
21983012-6	2012	We demonstrate that 27-OHC-induced ER stress attenuates leptin expression by activating C/EBP Homologous Protein (CHOP) which negatively regulates C/EBPalpha, a transcription factor required for leptin expression.	27-hydroxycholesterol	20-26	DNA damage inducible transcript 3	Homo sapiens	88-112
21797841-13	2012	CONCLUSIONS AND IMPLICATIONS: Cardamonin potentiates TRAIL-induced apoptosis through ROS-CHOP-mediated up-regulation of DRs, decreased expression of decoy receptor and cell survival proteins.	Reactive Oxygen Species	85-88	DNA damage inducible transcript 3	Homo sapiens	89-93
21983012-0	2012	Endoplasmic reticulum stress-induced CHOP activation mediates the down-regulation of leptin in human neuroblastoma SH-SY5Y cells treated with the oxysterol 27-hydroxycholesterol.	Oxysterols	146-155	DNA damage inducible transcript 3	Homo sapiens	37-41
22325198-5	2012	Importantly, such differential activations of CHOP and XBP-1 and their distinct effects on neuronal cell death are also observed in RGCs with other types of axonal insults, such as vincristine treatment and intraocular pressure elevation, suggesting a new protective strategy for neurodegeneration associated with axonal damage.	Vincristine	181-192	DNA damage inducible transcript 3	Homo sapiens	46-50
21983012-6	2012	We demonstrate that 27-OHC-induced ER stress attenuates leptin expression by activating C/EBP Homologous Protein (CHOP) which negatively regulates C/EBPalpha, a transcription factor required for leptin expression.	27-hydroxycholesterol	20-26	DNA damage inducible transcript 3	Homo sapiens	114-118
21983012-0	2012	Endoplasmic reticulum stress-induced CHOP activation mediates the down-regulation of leptin in human neuroblastoma SH-SY5Y cells treated with the oxysterol 27-hydroxycholesterol.	27-hydroxycholesterol	156-177	DNA damage inducible transcript 3	Homo sapiens	37-41
22450587-10	2012	We had previously experienced successful treatment with ABVD chemotherapy for interdigitating dendritic cell sarcoma after ineffective CHOP chemotherapy.	ABVD protocol	56-60	DNA damage inducible transcript 3	Homo sapiens	135-139
22969886-1	2012	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine and prednisone [CHOP (i.e., R-CHOP)] is considered to be the standard regimen for treating localized, primary gastric diffuse large B-cell lymphoma (PG-DLBCL).	Prednisone	76-86	DNA damage inducible transcript 3	Homo sapiens	88-92
22969886-2	2012	However, few studies have reported the long-term efficacy of R-CHOP therapy in the management of localized PG-DLBCL.	pg-dlbcl	107-115	DNA damage inducible transcript 3	Homo sapiens	63-67
22969886-13	2012	Our data suggest the feasibility and effectiveness of the addition of rituximab to conventional CHOP therapy in the management of localized PG-DLBCL.	pg-dlbcl	140-148	DNA damage inducible transcript 3	Homo sapiens	96-100
21460380-3	2012	The combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) with addition of etoposide (CHOEP) has in other patient groups been shown to be effective.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
22260632-4	2012	The patient initially received 6 cycles of chemotherapy with CHOP regimen (cyclophosphamide, vincristine, adriamycin, prednisone), but his symptoms did not disappear.	Cyclophosphamide	75-91	DNA damage inducible transcript 3	Homo sapiens	61-65
22260632-4	2012	The patient initially received 6 cycles of chemotherapy with CHOP regimen (cyclophosphamide, vincristine, adriamycin, prednisone), but his symptoms did not disappear.	Vincristine	93-104	DNA damage inducible transcript 3	Homo sapiens	61-65
22260632-4	2012	The patient initially received 6 cycles of chemotherapy with CHOP regimen (cyclophosphamide, vincristine, adriamycin, prednisone), but his symptoms did not disappear.	Doxorubicin	106-116	DNA damage inducible transcript 3	Homo sapiens	61-65
22260632-4	2012	The patient initially received 6 cycles of chemotherapy with CHOP regimen (cyclophosphamide, vincristine, adriamycin, prednisone), but his symptoms did not disappear.	Prednisone	118-128	DNA damage inducible transcript 3	Homo sapiens	61-65
22260632-9	2012	CHOP-R chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab) was then administered, resulting in partial response of the disease with pancytopenia and suppression of cellular immunity.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	0-4
22260632-9	2012	CHOP-R chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab) was then administered, resulting in partial response of the disease with pancytopenia and suppression of cellular immunity.	Doxorubicin	39-50	DNA damage inducible transcript 3	Homo sapiens	0-4
22260632-9	2012	CHOP-R chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab) was then administered, resulting in partial response of the disease with pancytopenia and suppression of cellular immunity.	Vincristine	52-63	DNA damage inducible transcript 3	Homo sapiens	0-4
22260632-9	2012	CHOP-R chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone and rituximab) was then administered, resulting in partial response of the disease with pancytopenia and suppression of cellular immunity.	Prednisone	65-75	DNA damage inducible transcript 3	Homo sapiens	0-4
22178955-6	2012	The incidence of treatment-related respiratory infections was higher in patients receiving R-CHOP-14.	r	91-92	DNA damage inducible transcript 3	Homo sapiens	93-97
22178955-10	2012	Trimethoprim/sulfamethoxazole prophylaxis is found to be highly efficient in preventing this life-threatening complication and, therefore, should be recommended for patients receiving the R-CHOP-14 regimen.	Trimethoprim, Sulfamethoxazole Drug Combination	0-29	DNA damage inducible transcript 3	Homo sapiens	190-194
21949157-3	2012	The TRPV1 agonist nonivamide induced GADD153 expression and caused cytotoxicity in immortalized and primary human bronchial, bronchiolar/alveolar, and microvascular endothelial cells, proportional to TRPV1 mRNA expression.	nonivamide	18-28	DNA damage inducible transcript 3	Homo sapiens	37-44
22223138-9	2012	CpdA+BZ blocked activation of glucocorticoid-responsive pro-survival genes, including SGK1, but activated BZ-induced ERS-related genes BIP/HSPA5 and CHOP /GADD153.	CPDA	0-4	DNA damage inducible transcript 3	Homo sapiens	149-153
22223138-9	2012	CpdA+BZ blocked activation of glucocorticoid-responsive pro-survival genes, including SGK1, but activated BZ-induced ERS-related genes BIP/HSPA5 and CHOP /GADD153.	CPDA	0-4	DNA damage inducible transcript 3	Homo sapiens	155-162
22223138-9	2012	CpdA+BZ blocked activation of glucocorticoid-responsive pro-survival genes, including SGK1, but activated BZ-induced ERS-related genes BIP/HSPA5 and CHOP /GADD153.	Bortezomib	5-7	DNA damage inducible transcript 3	Homo sapiens	149-153
22223138-9	2012	CpdA+BZ blocked activation of glucocorticoid-responsive pro-survival genes, including SGK1, but activated BZ-induced ERS-related genes BIP/HSPA5 and CHOP /GADD153.	Bortezomib	5-7	DNA damage inducible transcript 3	Homo sapiens	155-162
22223138-9	2012	CpdA+BZ blocked activation of glucocorticoid-responsive pro-survival genes, including SGK1, but activated BZ-induced ERS-related genes BIP/HSPA5 and CHOP /GADD153.	Bortezomib	106-108	DNA damage inducible transcript 3	Homo sapiens	149-153
22223138-10	2012	Using ChIP, we showed that SGK1, BIP/HSPA5 and CHOP regulation was due to effects of CpdA and CpdA+BZ on GR loading on their promoters.	CPDA	85-89	DNA damage inducible transcript 3	Homo sapiens	47-51
22223138-10	2012	Using ChIP, we showed that SGK1, BIP/HSPA5 and CHOP regulation was due to effects of CpdA and CpdA+BZ on GR loading on their promoters.	cpda+bz	94-101	DNA damage inducible transcript 3	Homo sapiens	47-51
22792112-8	2012	Preliminary data regarding the role of lenalidomide in addition to chemoimmunotherapy (R-CHOP) in first line clinical trials were discussed; data of safety, feasibility and efficacy were promising.	Lenalidomide	39-51	DNA damage inducible transcript 3	Homo sapiens	89-93
21460380-3	2012	The combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) with addition of etoposide (CHOEP) has in other patient groups been shown to be effective.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
21460380-3	2012	The combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) with addition of etoposide (CHOEP) has in other patient groups been shown to be effective.	Doxorubicin	52-63	DNA damage inducible transcript 3	Homo sapiens	93-97
21809093-6	2012	On the other hand, CdCl(2)-induced expression of C/EBP homologous protein (CHOP) was reduced by salubrinal treatment.	Cadmium Chloride	19-26	DNA damage inducible transcript 3	Homo sapiens	49-73
21809093-6	2012	On the other hand, CdCl(2)-induced expression of C/EBP homologous protein (CHOP) was reduced by salubrinal treatment.	Cadmium Chloride	19-26	DNA damage inducible transcript 3	Homo sapiens	75-79
21809093-6	2012	On the other hand, CdCl(2)-induced expression of C/EBP homologous protein (CHOP) was reduced by salubrinal treatment.	salubrinal	96-106	DNA damage inducible transcript 3	Homo sapiens	49-73
21809093-6	2012	On the other hand, CdCl(2)-induced expression of C/EBP homologous protein (CHOP) was reduced by salubrinal treatment.	salubrinal	96-106	DNA damage inducible transcript 3	Homo sapiens	75-79
21809093-7	2012	Expression of ATF4, an upstream regulator of GRP78 and CHOP, appeared to be a prerequisite for full protection by salubrinal against cadmium cytotoxicity, because CdCl(2)-induced cellular damage was not fully suppressed in ATF4-deficient cells.	salubrinal	114-124	DNA damage inducible transcript 3	Homo sapiens	55-59
21660448-8	2012	RESULTS: Our results demonstrated subtoxic concentrations of DMF sensitize HCC cells to TRAIL-induced apoptosis and induce the death receptor 5 (DR5) expression level, accompanying the generation of reactive oxygen species (ROS) and the upregulation of CHOP, GPR78, and ATF4 protein expression.	Dimethylformamide	61-64	DNA damage inducible transcript 3	Homo sapiens	253-257
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	18-34	DNA damage inducible transcript 3	Homo sapiens	84-88
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Acetylcysteine	36-39	DNA damage inducible transcript 3	Homo sapiens	84-88
22319522-6	2012	In real-time PCR and western blotting analysis, PTX decreased MCD-diet-induced TNF-alpha mRNA expression and proapoptotic unfolded protein response by ER stress (GRP78, p-eIF2, ATF4, IRE1alpha, CHOP, and p-JNK activation) in vivo.	Pentoxifylline	48-51	DNA damage inducible transcript 3	Homo sapiens	194-198
21660448-9	2012	Pretreatment with N-acetylcysteine (NAC) inhibited DMF-induced upregulation of DR5, CHOP, GPR78, and ATF4 protein expression and blocked the cotreatment-induced apoptosis.	Dimethylformamide	51-54	DNA damage inducible transcript 3	Homo sapiens	84-88
21660448-10	2012	Furthermore, DMF-mediated sensitization of HCC cells to TRAIL was reduced by administration of a blocking antibody or small interfering RNAs for DR5, salubrinal, an inhibitor of ER stress, and the small interfering RNAs for CHOP.	Dimethylformamide	13-16	DNA damage inducible transcript 3	Homo sapiens	224-228
21660448-12	2012	CONCLUSION: The present study demonstrates that DMF selectively enhances TRAIL-induced apoptosis by ROS-stimulated ER-stress triggering CHOP-mediated DR5 upregulation in HCC.	Dimethylformamide	48-51	DNA damage inducible transcript 3	Homo sapiens	136-140
21660448-12	2012	CONCLUSION: The present study demonstrates that DMF selectively enhances TRAIL-induced apoptosis by ROS-stimulated ER-stress triggering CHOP-mediated DR5 upregulation in HCC.	Reactive Oxygen Species	100-103	DNA damage inducible transcript 3	Homo sapiens	136-140
22997596-2	2012	We present the results of a long-term followup of two patients who were diagnosed with PRL and treated with cyclophosphamide, adriamycin, vincristine, prednisolone and rituximab (CHOP + R) regimen.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	179-183
22927878-4	2012	FUR significantly inhibited colony formation in A549 and 95-D cells and upregulated both the mRNA and protein expression levels of binding immunoglobulin protein (BIP) and C/EBP homologous protein (CHOP), indicating that endoplasmic reticulum (ER) stress is induced.	furanodiene	0-3	DNA damage inducible transcript 3	Homo sapiens	172-196
22927878-4	2012	FUR significantly inhibited colony formation in A549 and 95-D cells and upregulated both the mRNA and protein expression levels of binding immunoglobulin protein (BIP) and C/EBP homologous protein (CHOP), indicating that endoplasmic reticulum (ER) stress is induced.	furanodiene	0-3	DNA damage inducible transcript 3	Homo sapiens	198-202
22927878-5	2012	FUR treatment led to the accumulation of CHOP in the nucleus, which further confirms induction of ER stress.	furanodiene	0-3	DNA damage inducible transcript 3	Homo sapiens	41-45
22550476-5	2012	Cells subjected to either glucolipotoxicity or tunicamycin exhibited increased ROS generation, gene and protein (PERK, GRP-78, IRE1alpha, and CHOP) expression of ER stress markers.	Tunicamycin	47-58	DNA damage inducible transcript 3	Homo sapiens	142-146
22319522-7	2012	PTX (1 mM) reduced TNF-alpha-induced activation of GRP78, p-eIF2, ATF4, IRE1alpha, and CHOP in vitro.	Pentoxifylline	0-3	DNA damage inducible transcript 3	Homo sapiens	87-91
22864129-5	2012	Combination chemotherapy composed of cyclophosphamide, vincristine, doxorubicin and prednisolone (CHOP) was effective for polyneuropathy as well as for lymphoma.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	98-102
23095791-10	2012	CONCLUSION: These results show that amifostine can be added to the standard CHOP treatment schedule with less acute toxicity and without influencing the outcome.	Amifostine	36-46	DNA damage inducible transcript 3	Homo sapiens	76-80
22864129-5	2012	Combination chemotherapy composed of cyclophosphamide, vincristine, doxorubicin and prednisolone (CHOP) was effective for polyneuropathy as well as for lymphoma.	Prednisolone	84-96	DNA damage inducible transcript 3	Homo sapiens	98-102
23226467-7	2012	Furthermore, numerous dilated endoplasmic reticula (ER) were present in oxaliplatin-treated Caco-2 cells, and blocking ER stress by RNA interference against candidate of metastasis-1 (P8) and C/EBP-homologous protein (CHOP) decreased autophagy and ROS production.	Oxaliplatin	72-83	DNA damage inducible transcript 3	Homo sapiens	218-222
22906294-4	2012	The patient received two cycles of cyclophosphamide + epirubicin + vincristine + prednisone (CHOP) chemo therapy, which was ineffective.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
21864040-1	2012	In the rituximab era, several large studies have suggested that full-dose rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) might be the best treatment for patients with diffuse large B-cell lymphoma (DLBCL) aged 60 years and older.	Cyclophosphamide	89-105	DNA damage inducible transcript 3	Homo sapiens	150-154
21864040-1	2012	In the rituximab era, several large studies have suggested that full-dose rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) might be the best treatment for patients with diffuse large B-cell lymphoma (DLBCL) aged 60 years and older.	Doxorubicin	107-118	DNA damage inducible transcript 3	Homo sapiens	150-154
21864040-1	2012	In the rituximab era, several large studies have suggested that full-dose rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) might be the best treatment for patients with diffuse large B-cell lymphoma (DLBCL) aged 60 years and older.	Vincristine	120-131	DNA damage inducible transcript 3	Homo sapiens	150-154
21864040-1	2012	In the rituximab era, several large studies have suggested that full-dose rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) might be the best treatment for patients with diffuse large B-cell lymphoma (DLBCL) aged 60 years and older.	Prednisone	136-146	DNA damage inducible transcript 3	Homo sapiens	150-154
22519436-7	2012	Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2+ mobilization, upregulation of Bip/GRP78 and CHOP/GADD153, and activation of caspase-4.	diallyl trisulfide	12-16	DNA damage inducible transcript 3	Homo sapiens	153-157
22519436-7	2012	Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2+ mobilization, upregulation of Bip/GRP78 and CHOP/GADD153, and activation of caspase-4.	diallyl trisulfide	12-16	DNA damage inducible transcript 3	Homo sapiens	158-165
22905241-4	2012	METHODOLOGY/PRINCIPAL FINDINGS: Analysis of gene expression microarray data and subsequent confirmation by quantitative real-time PCR, showed that CTet is able to induce up-regulation of key signaling molecules involved in endoplasmic reticulum (ER) stress response (e.g. DDIT3/CHOP, CHAC1, ATF3, HSPA5/BiP/GRP78, CEBPB, ASNS) and autophagy (e.g. MAP1LC3B), in both MCF-7 and MDA-MB-231 cell lines.	ctet	147-151	DNA damage inducible transcript 3	Homo sapiens	272-277
23133576-6	2012	We have observed that 2OHOA treatments induced augments in the expression of important ER stress/UPR markers, such as phosphorylated eIF2alpha, IRE1alpha, CHOP, ATF4 and the spliced form of XBP1 in human glioma cells.	2-hydroxyoleic acid	22-27	DNA damage inducible transcript 3	Homo sapiens	155-159
22905241-4	2012	METHODOLOGY/PRINCIPAL FINDINGS: Analysis of gene expression microarray data and subsequent confirmation by quantitative real-time PCR, showed that CTet is able to induce up-regulation of key signaling molecules involved in endoplasmic reticulum (ER) stress response (e.g. DDIT3/CHOP, CHAC1, ATF3, HSPA5/BiP/GRP78, CEBPB, ASNS) and autophagy (e.g. MAP1LC3B), in both MCF-7 and MDA-MB-231 cell lines.	ctet	147-151	DNA damage inducible transcript 3	Homo sapiens	278-282
22745676-6	2012	TMZ treatment triggered ER stress with increased expression of GADD153 and GRP78 proteins, and deceased pro-caspase 12 protein.	Temozolomide	0-3	DNA damage inducible transcript 3	Homo sapiens	63-70
22496745-4	2012	By analyzing cells carrying tamoxifen inducible DDIT3 expression constructs we show distinct gene expression profiles for cells with cytoplasmic and nuclear localized DDIT3.	Tamoxifen	28-37	DNA damage inducible transcript 3	Homo sapiens	48-53
22496745-4	2012	By analyzing cells carrying tamoxifen inducible DDIT3 expression constructs we show distinct gene expression profiles for cells with cytoplasmic and nuclear localized DDIT3.	Tamoxifen	28-37	DNA damage inducible transcript 3	Homo sapiens	167-172
22496840-0	2012	Free cysteine modulates the conformation of human C/EBP homologous protein.	Cysteine	5-13	DNA damage inducible transcript 3	Homo sapiens	50-74
22438966-7	2012	Celecoxib possessed the ability to activate ER stress-related chaperones (IRE-1alpha and GRP78), caspase-4, and CCAAT/enhancer binding protein homologous protein (CHOP), which were involved in UC cell apoptosis.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	112-161
22496840-4	2012	Using circular dichroism, differential scanning calorimetry and nuclear magnetic resonance, we investigated the global conformation and secondary structure of CHOP and demonstrated, for the first time, that conformational changes in this protein can be induced by the free amino acid L-cysteine.	amino acid l-cysteine	273-294	DNA damage inducible transcript 3	Homo sapiens	159-163
22496840-6	2012	Furthermore, the presence of small amounts of free amino acid (80 microM, an 8:1 cysteine:CHOP ratio) during CHOP thermal denaturation altered the molecular mechanism of its melting process, leading to a complex, multi-step transition.	Cysteine	81-89	DNA damage inducible transcript 3	Homo sapiens	109-113
22496840-8	2012	These results suggested a potential regulatory function of L-cysteine which may lead to changes in global conformation of CHOP in response to the cellular redox state and/or endoplasmic reticulum stress.	Cysteine	59-69	DNA damage inducible transcript 3	Homo sapiens	122-126
22438966-7	2012	Celecoxib possessed the ability to activate ER stress-related chaperones (IRE-1alpha and GRP78), caspase-4, and CCAAT/enhancer binding protein homologous protein (CHOP), which were involved in UC cell apoptosis.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	163-167
22470469-10	2012	Furthermore, blockage of JNK1/2 signaling by JNK siRNA resulted in decreased expression of IRE1-alpha and GADD153/CHOP genes, implicating that BP-induced ER stress may be elicited via JNK1/2 signaling in prostate cancer cells.	butylidenephthalide	143-145	DNA damage inducible transcript 3	Homo sapiens	106-113
22470469-10	2012	Furthermore, blockage of JNK1/2 signaling by JNK siRNA resulted in decreased expression of IRE1-alpha and GADD153/CHOP genes, implicating that BP-induced ER stress may be elicited via JNK1/2 signaling in prostate cancer cells.	butylidenephthalide	143-145	DNA damage inducible transcript 3	Homo sapiens	114-118
22470469-7	2012	Several BP-induced genes, including the GADD153/CHOP, an endoplasmic reticulum stress (ER stress)-regulated gene, were identified.	butylidenephthalide	8-10	DNA damage inducible transcript 3	Homo sapiens	40-47
22470469-7	2012	Several BP-induced genes, including the GADD153/CHOP, an endoplasmic reticulum stress (ER stress)-regulated gene, were identified.	butylidenephthalide	8-10	DNA damage inducible transcript 3	Homo sapiens	48-52
22470469-8	2012	BP-induced ER stress was evidenced by increased expression of the downstream molecules GRP78/BiP, IRE1-alpha and GADD153/CHOP in both cell lines.	butylidenephthalide	0-2	DNA damage inducible transcript 3	Homo sapiens	113-120
22470469-8	2012	BP-induced ER stress was evidenced by increased expression of the downstream molecules GRP78/BiP, IRE1-alpha and GADD153/CHOP in both cell lines.	butylidenephthalide	0-2	DNA damage inducible transcript 3	Homo sapiens	121-125
22470469-9	2012	Blockage of IRE1-alpha or GADD153/CHOP expression by siRNA significantly reduced BP-induced cell death in LNCaP cells.	butylidenephthalide	81-83	DNA damage inducible transcript 3	Homo sapiens	26-33
22470469-9	2012	Blockage of IRE1-alpha or GADD153/CHOP expression by siRNA significantly reduced BP-induced cell death in LNCaP cells.	butylidenephthalide	81-83	DNA damage inducible transcript 3	Homo sapiens	34-38
21875624-6	2011	Longer exposure (1-3h) to H(2)O(2) induced ER-mediated apoptosis, whereby CHOP expression increased, and enzymatic activity of calpain, caspase-7, -4, -12 and -9 also increased.	1-3h	17-21	DNA damage inducible transcript 3	Homo sapiens	74-78
23323070-8	2012	The association of this antibody to the cyclophosphamide, hydroxydaunorubicin, oncovin and prednisolone (CHOP) regimen has increased overall survival of diffuse large B-Cell lymphoma and follicular lymphoma patients by 20%.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	105-109
23323070-8	2012	The association of this antibody to the cyclophosphamide, hydroxydaunorubicin, oncovin and prednisolone (CHOP) regimen has increased overall survival of diffuse large B-Cell lymphoma and follicular lymphoma patients by 20%.	Doxorubicin	58-77	DNA damage inducible transcript 3	Homo sapiens	105-109
23323070-8	2012	The association of this antibody to the cyclophosphamide, hydroxydaunorubicin, oncovin and prednisolone (CHOP) regimen has increased overall survival of diffuse large B-Cell lymphoma and follicular lymphoma patients by 20%.	Prednisolone	91-103	DNA damage inducible transcript 3	Homo sapiens	105-109
22052592-7	2011	The chiral phosphate anion (O-P*) controls the enantioselectivity through formation of a loose ion pair with the metal center and establishes a C-H   O-P* hydrogen bond with the substrate.	phosphate anion	11-26	DNA damage inducible transcript 3	Homo sapiens	144-153
22052592-7	2011	The chiral phosphate anion (O-P*) controls the enantioselectivity through formation of a loose ion pair with the metal center and establishes a C-H   O-P* hydrogen bond with the substrate.	Metals	113-118	DNA damage inducible transcript 3	Homo sapiens	144-153
22052592-7	2011	The chiral phosphate anion (O-P*) controls the enantioselectivity through formation of a loose ion pair with the metal center and establishes a C-H   O-P* hydrogen bond with the substrate.	Hydrogen	155-163	DNA damage inducible transcript 3	Homo sapiens	144-153
21903093-0	2011	Guggulsterone sensitizes hepatoma cells to TRAIL-induced apoptosis through the induction of CHOP-dependent DR5: involvement of ROS-dependent ER-stress.	pregna-4,17-diene-3,16-dione	0-13	DNA damage inducible transcript 3	Homo sapiens	92-96
21903093-11	2011	Pretreatment with N-acetyl-L-cysteine and glutathione inhibited GGS-induced ER-stress, and CHOP and DR5 upregulation and almost completely blocked GGS/TRAIL-induced apoptosis.	Acetylcysteine	18-37	DNA damage inducible transcript 3	Homo sapiens	91-95
21875624-6	2011	Longer exposure (1-3h) to H(2)O(2) induced ER-mediated apoptosis, whereby CHOP expression increased, and enzymatic activity of calpain, caspase-7, -4, -12 and -9 also increased.	Hydrogen Peroxide	26-34	DNA damage inducible transcript 3	Homo sapiens	74-78
21903093-11	2011	Pretreatment with N-acetyl-L-cysteine and glutathione inhibited GGS-induced ER-stress, and CHOP and DR5 upregulation and almost completely blocked GGS/TRAIL-induced apoptosis.	Glutathione	42-53	DNA damage inducible transcript 3	Homo sapiens	91-95
22175899-15	2011	All of these patients were treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP), and this was followed by clinical remission (CR).	Prednisone	99-109	DNA damage inducible transcript 3	Homo sapiens	113-117
22175899-18	2011	Treatment with R-CHOP usually leads to CR.	Chromium	39-41	DNA damage inducible transcript 3	Homo sapiens	17-21
20607588-5	2011	Further study demonstrated that DHA enhanced expression of GRP78 as well as growth arrest and DNA-damage-inducible gene 153 (GADD153, another ER stress-associated molecule) at both mRNA and protein levels.	artenimol	32-35	DNA damage inducible transcript 3	Homo sapiens	76-123
22057509-5	2011	The patient underwent one course of idarubicin and cytosine arabinose therapy combined with imatinib followed by daunorubicin/cyclophosphamide plus vincristine and prednisone/L: -asparaginase (DNR/COP/L: -ASP) therapy, high-dose cytosine arabinose, and CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone).	Idarubicin	36-46	DNA damage inducible transcript 3	Homo sapiens	253-257
20607588-5	2011	Further study demonstrated that DHA enhanced expression of GRP78 as well as growth arrest and DNA-damage-inducible gene 153 (GADD153, another ER stress-associated molecule) at both mRNA and protein levels.	artenimol	32-35	DNA damage inducible transcript 3	Homo sapiens	125-132
20607588-6	2011	DHA treatment also led to accumulation of GADD153 in cell nucleus.	artenimol	0-3	DNA damage inducible transcript 3	Homo sapiens	42-49
20607588-7	2011	Moreover, pretreatment of HCT116 cells with the iron chelator deferoxamine mesylate salt (DFO) abrogated induction of GRP78 and GADD153 upon DHA treatment, indicating iron is required for DHA-induced ER stress.	Iron	48-52	DNA damage inducible transcript 3	Homo sapiens	128-135
20607588-7	2011	Moreover, pretreatment of HCT116 cells with the iron chelator deferoxamine mesylate salt (DFO) abrogated induction of GRP78 and GADD153 upon DHA treatment, indicating iron is required for DHA-induced ER stress.	Deferoxamine mesylate	62-88	DNA damage inducible transcript 3	Homo sapiens	128-135
20607588-7	2011	Moreover, pretreatment of HCT116 cells with the iron chelator deferoxamine mesylate salt (DFO) abrogated induction of GRP78 and GADD153 upon DHA treatment, indicating iron is required for DHA-induced ER stress.	Deferoxamine	90-93	DNA damage inducible transcript 3	Homo sapiens	128-135
20607588-7	2011	Moreover, pretreatment of HCT116 cells with the iron chelator deferoxamine mesylate salt (DFO) abrogated induction of GRP78 and GADD153 upon DHA treatment, indicating iron is required for DHA-induced ER stress.	artenimol	141-144	DNA damage inducible transcript 3	Homo sapiens	128-135
21109616-8	2011	R-CHOP patients experienced numerically more CRS (65.5% vs. 42.9%, p=0.0517) and significantly more chills/rigors (p=0.0376).	3-cresol	45-48	DNA damage inducible transcript 3	Homo sapiens	0-6
21815196-5	2011	In addition, polydatin triggered endoplasmic reticulum (ER) stress and down-regulated the phosphorylation of Akt in CNE cells, while knock-down of CCAAT/enhancer-binding protein homologous protein (CHOP) dramatically abrogated the inactivation of Akt and reversed the pro-apoptotic effect of polydatin.	polydatin	292-301	DNA damage inducible transcript 3	Homo sapiens	147-196
21815196-5	2011	In addition, polydatin triggered endoplasmic reticulum (ER) stress and down-regulated the phosphorylation of Akt in CNE cells, while knock-down of CCAAT/enhancer-binding protein homologous protein (CHOP) dramatically abrogated the inactivation of Akt and reversed the pro-apoptotic effect of polydatin.	polydatin	292-301	DNA damage inducible transcript 3	Homo sapiens	198-202
21109616-9	2011	Maximum and minimum oxygen (O(2)) saturations were significantly lower in the R-CHOP group (p=0.0444 and 0.0165, respectively).	Oxygen	20-26	DNA damage inducible transcript 3	Homo sapiens	78-84
21109616-9	2011	Maximum and minimum oxygen (O(2)) saturations were significantly lower in the R-CHOP group (p=0.0444 and 0.0165, respectively).	Oxygen	28-33	DNA damage inducible transcript 3	Homo sapiens	78-84
22259636-5	2011	The patient was treated using cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP), and achieved complete response (CR) at the first response assessment conducted after 3 CHOP cycles.	Prednisolone	77-89	DNA damage inducible transcript 3	Homo sapiens	91-95
21907693-8	2011	R-CHOP with bortezomib (R-CHOP-BZ) reduces BiP/GRP78 expression and overcomes bortezomib resistance, mimicking the small-interfering RNA silencing of BiP/GRP78.	Bortezomib	12-22	DNA damage inducible transcript 3	Homo sapiens	2-6
21851218-7	2011	In the current study generation, the addition of high-dose Ara-C to a rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP)-like regimen followed by myeloablative consolidation achieved a significant improvement of progression-free survival.	Cytarabine	59-64	DNA damage inducible transcript 3	Homo sapiens	142-146
21851218-7	2011	In the current study generation, the addition of high-dose Ara-C to a rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP)-like regimen followed by myeloablative consolidation achieved a significant improvement of progression-free survival.	Doxorubicin	99-110	DNA damage inducible transcript 3	Homo sapiens	142-146
21851218-7	2011	In the current study generation, the addition of high-dose Ara-C to a rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP)-like regimen followed by myeloablative consolidation achieved a significant improvement of progression-free survival.	Prednisone	128-138	DNA damage inducible transcript 3	Homo sapiens	142-146
23556105-7	2011	A prospective, multicenter, international phase II trial evaluating sequential treatment with rituximab and CHOP-based chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) is ongoing and preliminary results have been promising.	Cyclophosphamide	133-149	DNA damage inducible transcript 3	Homo sapiens	108-112
21907693-1	2011	Activation of the endoplasmic reticulum (ER) stress pathway is associated with poor response to doxorubicin-containing regimens, such as rituximab, cyclophosphamide, hydroxydaunorubicin (doxorubicin), vincristine and prednisone (R-CHOP), in patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	96-107	DNA damage inducible transcript 3	Homo sapiens	231-235
21907693-8	2011	R-CHOP with bortezomib (R-CHOP-BZ) reduces BiP/GRP78 expression and overcomes bortezomib resistance, mimicking the small-interfering RNA silencing of BiP/GRP78.	Bortezomib	12-22	DNA damage inducible transcript 3	Homo sapiens	26-30
21907693-8	2011	R-CHOP with bortezomib (R-CHOP-BZ) reduces BiP/GRP78 expression and overcomes bortezomib resistance, mimicking the small-interfering RNA silencing of BiP/GRP78.	Bortezomib	78-88	DNA damage inducible transcript 3	Homo sapiens	2-6
21907693-8	2011	R-CHOP with bortezomib (R-CHOP-BZ) reduces BiP/GRP78 expression and overcomes bortezomib resistance, mimicking the small-interfering RNA silencing of BiP/GRP78.	Bortezomib	78-88	DNA damage inducible transcript 3	Homo sapiens	26-30
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	DNA damage inducible transcript 3	Homo sapiens	100-104
21819973-1	2011	Exposure of human Jurkat T cells to MG132 caused apoptosis along with upregulation of Grp78/BiP and CHOP/GADD153, activation of JNK and p38MAPK, activation of Bak, mitochondrial membrane potential (Deltapsim) loss, cytochrome c release, activation of caspase-12, -9, -3, -7, and -8, cleavage of Bid and PARP, and DNA fragmentation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	36-41	DNA damage inducible transcript 3	Homo sapiens	105-112
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNA damage inducible transcript 3	Homo sapiens	73-77
21819973-6	2011	MG132-induced apoptotic changes, including upregulation of Grp78/BiP and CHOP/GADD153 levels, activation of caspase-12, p38MAPK and Bak, and mitochondria-dependent activation of caspase cascade were more significant in p56(lck)-stable transfectant JCaM1.6/lck than in p56(lck)-deficient JCaM1.6/vector.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	0-5	DNA damage inducible transcript 3	Homo sapiens	78-85
22586509-2	2011	The cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) treatment regimen has been the standard of care for more than 20 years.	Cyclophosphamide	4-20	DNA damage inducible transcript 3	Homo sapiens	64-68
21726997-8	2011	In addition, silencing of C/EBP homologous protein (CHOP) expression reduced DR5 expression, demonstrating that the transcriptional factor CHOP has a pivotal role on DR5 up-regulation following pemetrexed treatment.	Pemetrexed	194-204	DNA damage inducible transcript 3	Homo sapiens	26-50
21726997-8	2011	In addition, silencing of C/EBP homologous protein (CHOP) expression reduced DR5 expression, demonstrating that the transcriptional factor CHOP has a pivotal role on DR5 up-regulation following pemetrexed treatment.	Pemetrexed	194-204	DNA damage inducible transcript 3	Homo sapiens	52-56
21726997-8	2011	In addition, silencing of C/EBP homologous protein (CHOP) expression reduced DR5 expression, demonstrating that the transcriptional factor CHOP has a pivotal role on DR5 up-regulation following pemetrexed treatment.	Pemetrexed	194-204	DNA damage inducible transcript 3	Homo sapiens	139-143
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	49-65	DNA damage inducible transcript 3	Homo sapiens	92-96
21854768-8	2011	Interestingly, pretreatment with an antioxidant, N-acetylcysteine (NAC), inhibited not only CHOP and DR5 up-regulation but also the cell death induced by acrolein plus TRAIL.	Acetylcysteine	67-70	DNA damage inducible transcript 3	Homo sapiens	92-96
22099782-4	2011	The grafts were saved by treatments with rituximab, cyclophosphamide, hydroxydaunorubicin, and prednisone-based chemotherapy (R-CHOP) after reduction of immunosuppression (IR).	Prednisone	95-105	DNA damage inducible transcript 3	Homo sapiens	128-132
22322845-10	2011	An increase in GADD153 and Bax expression and a decrease in Bcl-2 were observed in DHA-treated cells.	artenimol	83-86	DNA damage inducible transcript 3	Homo sapiens	15-22
22322845-12	2011	CONCLUSION: DHA could inhibit proliferation and induce apoptosis in HepG2 cell lines through increasing the intracellular production of ROS and [Ca2+]i. Endoplasmic reticulum stress-induced apoptosis may contribute to this effect by regulating the expression of GADD153, proapoptotic Bax, and antiapoptotic Bcl-2.	artenimol	12-15	DNA damage inducible transcript 3	Homo sapiens	262-269
22586509-2	2011	The cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) treatment regimen has been the standard of care for more than 20 years.	Doxorubicin	22-33	DNA damage inducible transcript 3	Homo sapiens	64-68
22586509-2	2011	The cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) treatment regimen has been the standard of care for more than 20 years.	Prednisone	52-62	DNA damage inducible transcript 3	Homo sapiens	64-68
22586511-1	2011	Chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has long been a standard treatment for lymphoma.	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	78-82
22586511-1	2011	Chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has long been a standard treatment for lymphoma.	Doxorubicin	36-47	DNA damage inducible transcript 3	Homo sapiens	78-82
22586511-1	2011	Chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has long been a standard treatment for lymphoma.	Prednisone	66-76	DNA damage inducible transcript 3	Homo sapiens	78-82
22586511-2	2011	Improvements to the efficacy of this regimen can be made by increasing the doses of doxorubicin and cyclophosphamide, as in the chemotherapeutic regimen of doxorubicin, cyclophosphamide, vindesine, bleomycin, and prednisone (ACVBP), and by reducing the standard dosing interval, as seen with the CHOP-14 regimen.	Doxorubicin	84-95	DNA damage inducible transcript 3	Homo sapiens	296-300
22586511-2	2011	Improvements to the efficacy of this regimen can be made by increasing the doses of doxorubicin and cyclophosphamide, as in the chemotherapeutic regimen of doxorubicin, cyclophosphamide, vindesine, bleomycin, and prednisone (ACVBP), and by reducing the standard dosing interval, as seen with the CHOP-14 regimen.	Cyclophosphamide	100-116	DNA damage inducible transcript 3	Homo sapiens	296-300
22586513-3	2011	To date, the most widely used regimen seems to be rituximab combined with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	122-132	DNA damage inducible transcript 3	Homo sapiens	136-140
21959050-0	2011	Cyclosporine, prednisone, and high-dose immunoglobulin treatment of angioimmunoblastic T-cell lymphoma refractory to prior CHOP or CHOP-like regimen.	Cyclosporine	0-12	DNA damage inducible transcript 3	Homo sapiens	123-127
21931035-1	2011	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat indolent B-cell lymphoma.	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	86-90
21931035-1	2011	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat indolent B-cell lymphoma.	Doxorubicin	42-53	DNA damage inducible transcript 3	Homo sapiens	86-90
21931035-1	2011	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is one of the most effective front-line therapies to treat indolent B-cell lymphoma.	Prednisone	72-82	DNA damage inducible transcript 3	Homo sapiens	86-90
21693187-13	2011	Our data suggest that the iNOS/NO signaling can modulate Akt/survivin and p38MAPK/CHOP pathways to mediate the GCDC-induced the apoptosis in hepatocytes.	Glycochenodeoxycholic Acid	111-115	DNA damage inducible transcript 3	Homo sapiens	82-86
21667023-0	2011	Involvement of endoplasmic reticulum stress-mediated CHOP (GADD153) induction in the cytotoxicity of 2-aminophenoxazine-3-one in cancer cells.	3-aminophenoxazone	101-125	DNA damage inducible transcript 3	Homo sapiens	53-57
22563154-3	2011	We report a patient with primary ovarian diffuse large B-cell lymphoma (DLBCL) and associated auto-immune hemolytic anemia (AIHA) who achieved complete remission after treatment with Rituximab-cyclophosphamide-doxorubicin-vincristine and prednisolone (R-CHOP) chemotherapy.	Cyclophosphamide	193-209	DNA damage inducible transcript 3	Homo sapiens	254-258
21667023-2	2011	Comparison of the expression profiles of endoplasmic reticulum (ER) stress-related genes in U266 multiple myeloma cells after treatment with Phx-3 and the ER stress inducers tunicamycin (TNM) and thapsigargin (TPG) indicated that although TNM and TPG potently induced pro-apoptotic transcription factor CHOP (GADD153) within 8 h of treatment, Phx-3 induced almost no CHOP within 48 h of treatment in U266 cells.	Thapsigargin	196-208	DNA damage inducible transcript 3	Homo sapiens	303-307
21667023-2	2011	Comparison of the expression profiles of endoplasmic reticulum (ER) stress-related genes in U266 multiple myeloma cells after treatment with Phx-3 and the ER stress inducers tunicamycin (TNM) and thapsigargin (TPG) indicated that although TNM and TPG potently induced pro-apoptotic transcription factor CHOP (GADD153) within 8 h of treatment, Phx-3 induced almost no CHOP within 48 h of treatment in U266 cells.	Thapsigargin	196-208	DNA damage inducible transcript 3	Homo sapiens	309-316
21667023-0	2011	Involvement of endoplasmic reticulum stress-mediated CHOP (GADD153) induction in the cytotoxicity of 2-aminophenoxazine-3-one in cancer cells.	3-aminophenoxazone	101-125	DNA damage inducible transcript 3	Homo sapiens	59-66
21667023-2	2011	Comparison of the expression profiles of endoplasmic reticulum (ER) stress-related genes in U266 multiple myeloma cells after treatment with Phx-3 and the ER stress inducers tunicamycin (TNM) and thapsigargin (TPG) indicated that although TNM and TPG potently induced pro-apoptotic transcription factor CHOP (GADD153) within 8 h of treatment, Phx-3 induced almost no CHOP within 48 h of treatment in U266 cells.	Thapsigargin	196-208	DNA damage inducible transcript 3	Homo sapiens	367-371
21703327-14	2011	These results suggest that O(2)(-) and ONOO(-) are selectively involved in CSE-triggered induction of CHOP and that the PERK-eIF2alpha pathway plays a crucial role in the induction of CHOP and apoptosis downstream of the particular reactive oxygen species.	Superoxides	27-31	DNA damage inducible transcript 3	Homo sapiens	102-106
21718130-6	2011	The revised IPI better predicted survival than did the standard IPI in patients with DLBCL treated with R-CHOP.	diprotin A	12-15	DNA damage inducible transcript 3	Homo sapiens	106-110
22117311-5	2011	Both patients were successfully treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	104-114	DNA damage inducible transcript 3	Homo sapiens	118-122
21703327-14	2011	These results suggest that O(2)(-) and ONOO(-) are selectively involved in CSE-triggered induction of CHOP and that the PERK-eIF2alpha pathway plays a crucial role in the induction of CHOP and apoptosis downstream of the particular reactive oxygen species.	onoo	39-43	DNA damage inducible transcript 3	Homo sapiens	102-106
21703327-6	2011	We investigated roles of individual reactive oxygen/nitrogen species in the transcriptional induction of CHOP by cigarette smoke.	reactive oxygen/nitrogen species	36-68	DNA damage inducible transcript 3	Homo sapiens	105-109
21703327-7	2011	Exposure of bronchial epithelial cells to O(2)(-), ONOO(-) or H(2)O(2) induced expression of CHOP, whereas NO alone did not.	Superoxides	42-46	DNA damage inducible transcript 3	Homo sapiens	93-97
21703327-14	2011	These results suggest that O(2)(-) and ONOO(-) are selectively involved in CSE-triggered induction of CHOP and that the PERK-eIF2alpha pathway plays a crucial role in the induction of CHOP and apoptosis downstream of the particular reactive oxygen species.	Reactive Oxygen Species	232-255	DNA damage inducible transcript 3	Homo sapiens	184-188
21703327-7	2011	Exposure of bronchial epithelial cells to O(2)(-), ONOO(-) or H(2)O(2) induced expression of CHOP, whereas NO alone did not.	onoo	51-55	DNA damage inducible transcript 3	Homo sapiens	93-97
21703327-7	2011	Exposure of bronchial epithelial cells to O(2)(-), ONOO(-) or H(2)O(2) induced expression of CHOP, whereas NO alone did not.	Water	62-67	DNA damage inducible transcript 3	Homo sapiens	93-97
21571032-2	2011	The addition of DL-PDMP caused massive autophagy with an increase of CAAT/enhancer binding protein homologous protein (CHOP) expression as the marker of endoplasmic reticulum (ER) stress, lactate dehydrogenase (LDH) release without caspase 3 activation and many autophagic vacuoles/devoid of a cell membrane on morphology.	RV 538	16-23	DNA damage inducible transcript 3	Homo sapiens	119-123
21703327-8	2011	Induction of CHOP mRNA by cigarette smoke extract (CSE) was attenuated by scavengers for O(2)(-), ONOO(-) or NO, whereas scavenging H(2)O(2) did not affect the induction of CHOP.	Superoxides	89-93	DNA damage inducible transcript 3	Homo sapiens	13-17
21703327-8	2011	Induction of CHOP mRNA by cigarette smoke extract (CSE) was attenuated by scavengers for O(2)(-), ONOO(-) or NO, whereas scavenging H(2)O(2) did not affect the induction of CHOP.	onoo	98-102	DNA damage inducible transcript 3	Homo sapiens	13-17
21703327-9	2011	Like CSE, O(2)(-) and ONOO(-) caused activation of the CHOP gene promoter.	Superoxides	10-14	DNA damage inducible transcript 3	Homo sapiens	55-59
21703327-9	2011	Like CSE, O(2)(-) and ONOO(-) caused activation of the CHOP gene promoter.	onoo	22-26	DNA damage inducible transcript 3	Homo sapiens	55-59
21703327-10	2011	Scavengers for O(2)(-), ONOO(-) or NO attenuated CSE-triggered activation of the CHOP gene promoter.	Superoxides	15-19	DNA damage inducible transcript 3	Homo sapiens	81-85
21703327-10	2011	Scavengers for O(2)(-), ONOO(-) or NO attenuated CSE-triggered activation of the CHOP gene promoter.	onoo	24-28	DNA damage inducible transcript 3	Homo sapiens	81-85
21159733-7	2011	However, tunicamycin (a potent stimulator of ER stress) changed the ER stress response from protective to cytotoxic, as tunicamycin induced the proapoptotic ER stress gene, C/EBP homologous protein-10, and exacerbated apoptosis in GECs adherent to plastic, but not collagen.	Tunicamycin	9-20	DNA damage inducible transcript 3	Homo sapiens	173-200
21159733-7	2011	However, tunicamycin (a potent stimulator of ER stress) changed the ER stress response from protective to cytotoxic, as tunicamycin induced the proapoptotic ER stress gene, C/EBP homologous protein-10, and exacerbated apoptosis in GECs adherent to plastic, but not collagen.	Tunicamycin	120-131	DNA damage inducible transcript 3	Homo sapiens	173-200
21709020-4	2011	Loss-of-function studies show that ECM detachment activates a canonical PERK-eukaryotic translation initiation factor 2alpha (eIF2alpha)-ATF4-CHOP pathway that coordinately induces the autophagy regulators ATG6 and ATG8, sustains ATP levels, and reduces ROS levels to delay anoikis.	Adenosine Triphosphate	230-233	DNA damage inducible transcript 3	Homo sapiens	142-146
21844328-6	2011	The mycotoxin methoxycitrinin was isolated from a natural extract and found to selectively activate the CHOP-luciferase reporter at 80 microM.	methoxycitrinin	14-29	DNA damage inducible transcript 3	Homo sapiens	104-108
21669190-5	2011	Moreover, helenalin induces an atypical form of cell death with necrotic features in Bcl-2 overexpressing cells, neither activating classical mediators of apoptosis (caspases, AIF, Omi/HtrA2, Apaf/apoptosome) nor ER-stress mediators (BiP/GRP78 and CHOP/GADD153), nor autophagy pathways (LC3 conversion).	helenalin	10-19	DNA damage inducible transcript 3	Homo sapiens	253-260
21597379-7	2011	In addition, C-DIMs inhibited cell proliferation and induced PARP cleavage through death receptor 5 and CHOP in HEp-2 and HN22 cells.	c-dims	13-19	DNA damage inducible transcript 3	Homo sapiens	104-108
21472389-3	2011	She was treated with 4 cycles of CHOP chemotherapy consisting of doxorubicin, cyclophosphamide, vincristine, and prednisolone at 4-week intervals.	Doxorubicin	65-76	DNA damage inducible transcript 3	Homo sapiens	33-37
21709020-4	2011	Loss-of-function studies show that ECM detachment activates a canonical PERK-eukaryotic translation initiation factor 2alpha (eIF2alpha)-ATF4-CHOP pathway that coordinately induces the autophagy regulators ATG6 and ATG8, sustains ATP levels, and reduces ROS levels to delay anoikis.	Reactive Oxygen Species	254-257	DNA damage inducible transcript 3	Homo sapiens	142-146
21257672-1	2011	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is widely recommended for the treatment of aggressive B-cell lymphomas.	Cyclophosphamide	57-73	DNA damage inducible transcript 3	Homo sapiens	119-123
21697087-0	2011	Modulation of CCAAT/enhancer binding protein homologous protein (CHOP)-dependent DR5 expression by nelfinavir sensitizes glioblastoma multiforme cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Nelfinavir	99-109	DNA damage inducible transcript 3	Homo sapiens	14-63
21697087-0	2011	Modulation of CCAAT/enhancer binding protein homologous protein (CHOP)-dependent DR5 expression by nelfinavir sensitizes glioblastoma multiforme cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Nelfinavir	99-109	DNA damage inducible transcript 3	Homo sapiens	65-69
21471847-6	2011	PGE2-treated astroglioma cells showed a marked upregulation of IL-8, C/EBP-beta, and CHOP, as well as increased proliferation and decreased apoptosis compared with untreated cells.	Dinoprostone	0-4	DNA damage inducible transcript 3	Homo sapiens	85-89
21471847-10	2011	(2) C/EBP-beta and CHOP may be involved in mediating PGE2-induced IL-8 activation in these tumors.	Dinoprostone	53-57	DNA damage inducible transcript 3	Homo sapiens	19-23
21257672-1	2011	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is widely recommended for the treatment of aggressive B-cell lymphomas.	Doxorubicin	75-86	DNA damage inducible transcript 3	Homo sapiens	119-123
21257672-1	2011	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is widely recommended for the treatment of aggressive B-cell lymphomas.	Vincristine	88-99	DNA damage inducible transcript 3	Homo sapiens	119-123
21257672-1	2011	BACKGROUND: Rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is widely recommended for the treatment of aggressive B-cell lymphomas.	Prednisone	105-115	DNA damage inducible transcript 3	Homo sapiens	119-123
21257672-11	2011	All other grade 3 and 4 hematotoxicities and non-hematological toxic effects ranged between 2% and 11% CONCLUSIONS: Because of its efficacy and low toxicity, bendamustine in combination with rituximab may be an alternative treatment for aggressive lymphomas in old patients not eligible for R-CHOP.	Bendamustine Hydrochloride	158-170	DNA damage inducible transcript 3	Homo sapiens	293-297
21601561-7	2011	We further found that Redd1-induced mTOR down-regulation and ATF4/CHOP-induced expression of the TRAIL receptor DR5 associated with sorafenib treatment helped sensitize cells to TRAIL-induced apoptosis.	Sorafenib	132-141	DNA damage inducible transcript 3	Homo sapiens	66-70
21700680-0	2011	BRCA1 loss induces GADD153-mediated doxorubicin resistance in prostate cancer.	Doxorubicin	36-47	DNA damage inducible transcript 3	Homo sapiens	19-26
21294793-7	2011	Tunicamycin dose dependently increased CHOP expression and apoptosis of cultured chondrocytes.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	39-43
21700680-8	2011	Finally, GADD153 depletion significantly abrogates BRCA1 influence on cell-cycle progression and cell death in response to doxorubicin treatment.	Doxorubicin	123-134	DNA damage inducible transcript 3	Homo sapiens	9-16
21567098-9	2011	CHOP, a marker of ERS involved in apoptosis, was also increased by celecoxib.	Celecoxib	67-76	DNA damage inducible transcript 3	Homo sapiens	0-4
21727211-12	2011	The clinical significance of these findings was supported by the evidence that celecoxib, a nonsteroidal anti-inflammatory drug known to induce GADD153-mediated apoptosis, strongly increases both type I and type II PCD in HGG cells when combined with another inducer of GADD153.	Celecoxib	79-88	DNA damage inducible transcript 3	Homo sapiens	144-151
21181164-8	2011	Four patients received cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP)-like chemotherapy, and their median survival was 13 months.	Prednisolone	70-82	DNA damage inducible transcript 3	Homo sapiens	84-88
21727211-12	2011	The clinical significance of these findings was supported by the evidence that celecoxib, a nonsteroidal anti-inflammatory drug known to induce GADD153-mediated apoptosis, strongly increases both type I and type II PCD in HGG cells when combined with another inducer of GADD153.	Celecoxib	79-88	DNA damage inducible transcript 3	Homo sapiens	270-277
21447826-7	2011	Bortezomib also induces the unfolded protein response (UPR), as evidenced by increases in ATF4, CHOP10, and XBP1s and cleavage of ATF6.	Bortezomib	0-10	DNA damage inducible transcript 3	Homo sapiens	96-102
21479362-9	2011	The immunofluorescence assay demonstrated that adenosine induced the translocation of CHOP and of caspase-3 from the cytoplasm to the nucleus.	Adenosine	47-56	DNA damage inducible transcript 3	Homo sapiens	86-90
21479362-10	2011	Western blotting confirmed that CHOP, caspase-4 and caspase-3 were up-regulated in HepG2 cells after treatment with adenosine.	Adenosine	116-125	DNA damage inducible transcript 3	Homo sapiens	32-36
21782063-4	2011	The regimen most commonly used is rituximab combined with an anthracycline-combination therapy, ie, R-CHOP.	Anthracyclines	61-74	DNA damage inducible transcript 3	Homo sapiens	102-106
22093624-14	2011	In the melanoma cells after exposure to tunicamycin (3 micromol/L) for 6, 12, 24, and 36 hours the transcription factor CHOP at mRNA level were significantly increased and the expressions at protein level were also up-regulated.	Tunicamycin	40-51	DNA damage inducible transcript 3	Homo sapiens	120-124
21489796-6	2011	A diagnosis of a grade III LYG was made and chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was administered.	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	121-125
21504179-4	2011	In this study, we found that only compound 19 [(1E,4E)-1,5-bis(2,3-dimethoxyphenyl)penta-1,4-dien-3-one] can induce C/EBP-homologous protein (CHOP) expression in human lung cancer H460 cells.	(1e,4e)-1,5-bis(2,3-dimethoxyphenyl)penta-1,4-dien-3-one	47-103	DNA damage inducible transcript 3	Homo sapiens	116-140
21504179-4	2011	In this study, we found that only compound 19 [(1E,4E)-1,5-bis(2,3-dimethoxyphenyl)penta-1,4-dien-3-one] can induce C/EBP-homologous protein (CHOP) expression in human lung cancer H460 cells.	(1e,4e)-1,5-bis(2,3-dimethoxyphenyl)penta-1,4-dien-3-one	47-103	DNA damage inducible transcript 3	Homo sapiens	142-146
21573892-1	2011	We describe MR-CHOP therapy, a novel treatment regimen consisting of high-dose methotrexate and R-CHOP that provides systemic anti-tumor activity with penetration of the blood-brain barrier in patients with newly diagnosed primary central nervous system lymphoma.	Methotrexate	79-91	DNA damage inducible transcript 3	Homo sapiens	15-19
22096849-1	2011	OBJECTIVE: To investigate the effects of the cadmium chloride on the DNA damage and the expression of the gadd153 and gadd45beta promoter and mRNA in HepG2 cells.	Cadmium Chloride	45-61	DNA damage inducible transcript 3	Homo sapiens	106-113
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	101-105
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	123-127
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	59-70	DNA damage inducible transcript 3	Homo sapiens	101-105
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	59-70	DNA damage inducible transcript 3	Homo sapiens	123-127
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Vincristine	72-83	DNA damage inducible transcript 3	Homo sapiens	123-127
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Prednisone	89-99	DNA damage inducible transcript 3	Homo sapiens	101-105
21747882-1	2011	BACKGROUND: The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP) has significantly improved clinical outcomes for patients with diffuse large B-cell lymphoma (DLBCL).	Prednisone	89-99	DNA damage inducible transcript 3	Homo sapiens	123-127
22096849-9	2011	The expression levels of gadd153 mRNA induced by cadmium chloride at the doses of 1, 5, 10 micromol/L and the expression levels of gadd45beta mRNA induced at the doses of 5, 10 micromol/L were significantly higher than thoae in control group (P &lt; 0.05).	Cadmium Chloride	49-65	DNA damage inducible transcript 3	Homo sapiens	25-32
22096849-10	2011	CONCLUSION: The cadmium chloride can induce the DNA damage and increase the expression levels of the gadd153 and gadd45beta promoters in HepG2 cells.	Cadmium Chloride	16-32	DNA damage inducible transcript 3	Homo sapiens	101-108
20501519-5	2011	We found that ATO induced the expression of the proapoptotic GADD153 protein, a key player involved in ER stress-induced apoptosis, activated nuclear nuclear factor kappaB (NF-kappaB) DNA binding activities, and increased prostaglandine E2 (PGE2) production.	Arsenic Trioxide	14-17	DNA damage inducible transcript 3	Homo sapiens	61-68
21276850-0	2011	Proteasome inhibitor-I enhances tunicamycin-induced chemosensitization of prostate cancer cells through regulation of NF-kappaB and CHOP expression.	Tunicamycin	32-43	DNA damage inducible transcript 3	Homo sapiens	132-136
21324313-5	2011	Using a cell line-based model for CHOP resistant DLBCL, we show that treatment with simvastatin, which inhibits protein farnesylation and geranylgeranylation, sensitizes DLBCL cells to cytotoxic treatment.	Simvastatin	84-95	DNA damage inducible transcript 3	Homo sapiens	34-38
21944785-4	2011	Chemotherapy  in the form of R-CHOP (rituximab, cyclophosphamide, hydroxydaunorubicin, Oncovin and prednisolone) is considered to be the first line of treatment for these lymphomas.	Doxorubicin	66-85	DNA damage inducible transcript 3	Homo sapiens	31-35
21944785-4	2011	Chemotherapy  in the form of R-CHOP (rituximab, cyclophosphamide, hydroxydaunorubicin, Oncovin and prednisolone) is considered to be the first line of treatment for these lymphomas.	Prednisolone	99-111	DNA damage inducible transcript 3	Homo sapiens	31-35
20625822-0	2011	Genotoxic evaluation of the insecticide endosulfan based on the induced GADD153-GFP reporter gene expression.	Endosulfan	40-50	DNA damage inducible transcript 3	Homo sapiens	72-79
20625822-4	2011	Methyl methanesulfonate, a known carcinogenic and genotoxic agent, was used to test the effects of damage dose and post-treatment incubation time on GADD153-GFP expression.	Methyl Methanesulfonate	0-23	DNA damage inducible transcript 3	Homo sapiens	149-156
20625822-6	2011	Endosulfan was able to cause the increase of GADD153-GFP expression at a sublethal dose (0.02-20 mg/L).	Endosulfan	0-10	DNA damage inducible transcript 3	Homo sapiens	45-52
20501519-5	2011	We found that ATO induced the expression of the proapoptotic GADD153 protein, a key player involved in ER stress-induced apoptosis, activated nuclear nuclear factor kappaB (NF-kappaB) DNA binding activities, and increased prostaglandine E2 (PGE2) production.	prostaglandine e2	222-239	DNA damage inducible transcript 3	Homo sapiens	61-68
20501519-5	2011	We found that ATO induced the expression of the proapoptotic GADD153 protein, a key player involved in ER stress-induced apoptosis, activated nuclear nuclear factor kappaB (NF-kappaB) DNA binding activities, and increased prostaglandine E2 (PGE2) production.	Dinoprostone	241-245	DNA damage inducible transcript 3	Homo sapiens	61-68
21168266-6	2011	Celastrol"s ability to modulate the expression of pro-inflammatory cytokines, MHC II, HO-1, iNOS, NF-kappaB, Notch-1, AKT/mTOR, CXCR4, TRAIL receptors DR4 and DR5, CHOP, JNK, VEGF, adhesion molecules, proteasome activity, topoisomerase II, potassium channels, and heat shock response has been reported.	celastrol	0-9	DNA damage inducible transcript 3	Homo sapiens	164-168
21343315-3	2011	In this study, chemical variants of the capsaicin analog nonivamide were synthesized and used to probe the relationship between TRPV1 receptor binding, ER calcium release, GADD153 expression, and cell death in TRPV1-overexpressing BEAS-2B, normal BEAS-2B, and primary normal human bronchial epithelial lung cells.	nonivamide	57-67	DNA damage inducible transcript 3	Homo sapiens	172-179
21482186-3	2011	We aimed to investigate the efficacy and safety of a decreased dose of CHOP (doxorubicin, cyclophosphamide, vincristine, and prednisone) chemotherapy with a conventional dose of rituximab in elderly patients with diffuse large B-cell lymphoma.	Doxorubicin	77-88	DNA damage inducible transcript 3	Homo sapiens	71-75
21482186-3	2011	We aimed to investigate the efficacy and safety of a decreased dose of CHOP (doxorubicin, cyclophosphamide, vincristine, and prednisone) chemotherapy with a conventional dose of rituximab in elderly patients with diffuse large B-cell lymphoma.	Cyclophosphamide	90-106	DNA damage inducible transcript 3	Homo sapiens	71-75
21482186-3	2011	We aimed to investigate the efficacy and safety of a decreased dose of CHOP (doxorubicin, cyclophosphamide, vincristine, and prednisone) chemotherapy with a conventional dose of rituximab in elderly patients with diffuse large B-cell lymphoma.	Vincristine	108-119	DNA damage inducible transcript 3	Homo sapiens	71-75
21482186-3	2011	We aimed to investigate the efficacy and safety of a decreased dose of CHOP (doxorubicin, cyclophosphamide, vincristine, and prednisone) chemotherapy with a conventional dose of rituximab in elderly patients with diffuse large B-cell lymphoma.	Prednisone	125-135	DNA damage inducible transcript 3	Homo sapiens	71-75
21498532-1	2011	UNLABELLED: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone)-like chemotherapy is the standard therapy in aggressive B-cell lymphoma.	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	14-18
21498532-1	2011	UNLABELLED: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone)-like chemotherapy is the standard therapy in aggressive B-cell lymphoma.	Doxorubicin	49-60	DNA damage inducible transcript 3	Homo sapiens	14-18
21498532-1	2011	UNLABELLED: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone)-like chemotherapy is the standard therapy in aggressive B-cell lymphoma.	Vincristine	62-73	DNA damage inducible transcript 3	Homo sapiens	14-18
21498532-1	2011	UNLABELLED: R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone)-like chemotherapy is the standard therapy in aggressive B-cell lymphoma.	Prednisone	79-89	DNA damage inducible transcript 3	Homo sapiens	14-18
21498532-3	2011	Here, we present the results of a prospective study correlating the initial uptake of the in vivo proliferation marker 3"-deoxy-3"-(18)F-fluorothymidine ((18)F-FLT) with the clinical outcome of patients with aggressive non-Hodgkin lymphoma treated with R-CHOP.	alovudine	137-152	DNA damage inducible transcript 3	Homo sapiens	255-259
21323512-1	2011	Development of resistance to the CHOP chemotherapeutic regimen (cyclophosphamide, doxorubicin, vincristine, prednisone) remains a major cause of treatment failure and mortality in approximately 40% of patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	33-37
21323512-1	2011	Development of resistance to the CHOP chemotherapeutic regimen (cyclophosphamide, doxorubicin, vincristine, prednisone) remains a major cause of treatment failure and mortality in approximately 40% of patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	82-93	DNA damage inducible transcript 3	Homo sapiens	33-37
21323512-1	2011	Development of resistance to the CHOP chemotherapeutic regimen (cyclophosphamide, doxorubicin, vincristine, prednisone) remains a major cause of treatment failure and mortality in approximately 40% of patients with diffuse large B-cell lymphoma (DLBCL).	Vincristine	95-106	DNA damage inducible transcript 3	Homo sapiens	33-37
21323512-1	2011	Development of resistance to the CHOP chemotherapeutic regimen (cyclophosphamide, doxorubicin, vincristine, prednisone) remains a major cause of treatment failure and mortality in approximately 40% of patients with diffuse large B-cell lymphoma (DLBCL).	Prednisone	108-118	DNA damage inducible transcript 3	Homo sapiens	33-37
21323512-8	2011	Knockdown of vimentin by siRNA or withaferin A repressed the invasiveness of CHOP-resistant cells in collagen matrices.	withaferin A	34-46	DNA damage inducible transcript 3	Homo sapiens	77-81
20521053-2	2011	CHOP and CVP represent untargeted combination chemotherapy comprised of cyclophosphamide, vincristine and prednisone with or without doxorubicin, commonly used in the treatment of NHL.	Prednisone	106-116	DNA damage inducible transcript 3	Homo sapiens	0-4
21266189-0	2011	Hexahydro-beta-acids induce apoptosis through mitochondrial pathway, GADD153 expression, and caspase activation in human leukemia cells.	hexahydro-beta-acids	0-20	DNA damage inducible transcript 3	Homo sapiens	69-76
21559001-4	2011	The standard management for PTCL patients is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or CHOP-like regimens.	Prednisone	93-103	DNA damage inducible transcript 3	Homo sapiens	105-109
21401896-8	2011	The Western blot showed that increasing the concentration of HCPT resulted in a higher expression level of p-JNK, P53, ubiquitin, GADD 153 and Grp78/Bip in the Ufd1 knockdown cells than that in the control cells.	hydroxycamptothecinum	61-65	DNA damage inducible transcript 3	Homo sapiens	130-138
20619923-6	2011	Bortezomib treatment activated endoplasmic reticulum (ER) stress-mediated apoptosis, as demonstrated by the induction of GADD153, an ER stress-inducible transcription factor, and of the death receptor DR5, in EGFR inhibitor-resistant cells, but not in parental cells.	Bortezomib	0-10	DNA damage inducible transcript 3	Homo sapiens	121-128
22087145-4	2011	The patient was treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) without surgical resection with a favorable response.	Prednisone	95-105	DNA damage inducible transcript 3	Homo sapiens	31-35
21174067-7	2011	BAF treatment also induced ER stress, but the kinetics of inductions of ER stress-related genes [e.g. CHOP (GADD153) and GRP78] completely differed between BZ- and BAF-treatments: BZ induced these ER stress markers within 8 h, whereas treatment with BAF required more than 48 h in U266 cells.	Bortezomib	156-158	DNA damage inducible transcript 3	Homo sapiens	102-106
21174067-7	2011	BAF treatment also induced ER stress, but the kinetics of inductions of ER stress-related genes [e.g. CHOP (GADD153) and GRP78] completely differed between BZ- and BAF-treatments: BZ induced these ER stress markers within 8 h, whereas treatment with BAF required more than 48 h in U266 cells.	Bortezomib	180-182	DNA damage inducible transcript 3	Homo sapiens	102-106
21174067-7	2011	BAF treatment also induced ER stress, but the kinetics of inductions of ER stress-related genes [e.g. CHOP (GADD153) and GRP78] completely differed between BZ- and BAF-treatments: BZ induced these ER stress markers within 8 h, whereas treatment with BAF required more than 48 h in U266 cells.	Bortezomib	180-182	DNA damage inducible transcript 3	Homo sapiens	108-115
22099932-7	2011	AIM: The aim of the study was to evaluate the clinical risk stratification models including the age adjusted International prognostic index (aaIPI), patients profile and dose intensity (DI) of Cyclophosphamide and Doxorubicin as effective tools for predicting the outcome and prognosis of our DLBCL patients treated with first line CHOP regimen.	Cyclophosphamide	193-209	DNA damage inducible transcript 3	Homo sapiens	332-336
22099932-7	2011	AIM: The aim of the study was to evaluate the clinical risk stratification models including the age adjusted International prognostic index (aaIPI), patients profile and dose intensity (DI) of Cyclophosphamide and Doxorubicin as effective tools for predicting the outcome and prognosis of our DLBCL patients treated with first line CHOP regimen.	Doxorubicin	214-225	DNA damage inducible transcript 3	Homo sapiens	332-336
21146245-7	2011	Indeed, in CYP2E1-expressing HepG2 cells exposed to ethanol, the expression of ISR target genes (HMOX-1, GCLC, AsnS, IGFBP-1, GADD34,CHOP, ATF3, CHAC1) was induced.	Ethanol	52-59	DNA damage inducible transcript 3	Homo sapiens	133-137
21266191-6	2011	In addition, withaferin A caused up-regulation of CAAT/enhancer-binding protein-homologous protein (CHOP), suggesting the induction of ER stress.	withaferin A	13-25	DNA damage inducible transcript 3	Homo sapiens	50-98
21266191-6	2011	In addition, withaferin A caused up-regulation of CAAT/enhancer-binding protein-homologous protein (CHOP), suggesting the induction of ER stress.	withaferin A	13-25	DNA damage inducible transcript 3	Homo sapiens	100-104
21266191-8	2011	Furthermore, CHOP siRNA or inhibition of caspase-4 activity attenuated withaferin A-induced apoptosis.	withaferin A	71-83	DNA damage inducible transcript 3	Homo sapiens	13-17
20354901-4	2011	The patient was treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with rituximab, and a dramatic improvement of renal function was noticed after two weeks of treatment.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
20354901-4	2011	The patient was treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with rituximab, and a dramatic improvement of renal function was noticed after two weeks of treatment.	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	89-93
21189393-12	2011	CONCLUSION: Bortezomib with R-CHOP-21 can be safely administered and may enhance outcomes, particularly in non-GCB DLBCL, justifying randomized studies.	Bortezomib	12-22	DNA damage inducible transcript 3	Homo sapiens	30-34
21282356-5	2011	Curcumin-mediated ER stress via inhibiting the activity of SERCA2 caused increasing expressions of CHOP and its transcription target death receptor 5 (TRAIL-R2), leading to a caspase-3 and caspase-8 cascade-dependent apoptosis in SW872 cells in vitro and in vivo.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	99-103
21292685-0	2011	Amiodarone sensitizes human glioma cells but not astrocytes to TRAIL-induced apoptosis via CHOP-mediated DR5 upregulation.	Amiodarone	0-10	DNA damage inducible transcript 3	Homo sapiens	91-95
21292685-3	2011	Treatment of U251MG glioma cells with amiodarone increased intracellular Ca(2+) levels and enhanced the expression of the endoplasmic reticulum (ER) stress-inducible transcription factor C/EBP homologous protein (CHOP).	Amiodarone	38-48	DNA damage inducible transcript 3	Homo sapiens	187-211
21292685-3	2011	Treatment of U251MG glioma cells with amiodarone increased intracellular Ca(2+) levels and enhanced the expression of the endoplasmic reticulum (ER) stress-inducible transcription factor C/EBP homologous protein (CHOP).	Amiodarone	38-48	DNA damage inducible transcript 3	Homo sapiens	213-217
21292685-6	2011	siRNA-mediated CHOP suppression reduced amiodarone-induced DR5 upregulation and attenuated the cell death induced by amiodarone plus TRAIL.	Amiodarone	40-50	DNA damage inducible transcript 3	Homo sapiens	15-19
21292685-6	2011	siRNA-mediated CHOP suppression reduced amiodarone-induced DR5 upregulation and attenuated the cell death induced by amiodarone plus TRAIL.	Amiodarone	117-127	DNA damage inducible transcript 3	Homo sapiens	15-19
21292685-7	2011	In addition, omitting Ca(2+) from the external medium using ethylene glycol tetraacetic acid markedly inhibited this cell death, reducing the protein levels of CHOP and DR5.	Egtazic Acid	60-92	DNA damage inducible transcript 3	Homo sapiens	160-164
21292685-8	2011	These results suggest that amiodarone-induced influx of Ca(2+) plays an important role in sensitizing U251MG cells to TRAIL-mediated apoptosis through CHOP-mediated DR5 upregulation.	Amiodarone	27-37	DNA damage inducible transcript 3	Homo sapiens	151-155
21292685-9	2011	Furthermore, subtoxic doses of bepridil and cibenzoline, two other anti-arrhythmic drugs with NCX-inhibitor activity, also sensitized glioma cells to TRAIL-mediated apoptosis, via the upregulation of both CHOP and DR5.	Bepridil	31-39	DNA damage inducible transcript 3	Homo sapiens	205-209
21292685-9	2011	Furthermore, subtoxic doses of bepridil and cibenzoline, two other anti-arrhythmic drugs with NCX-inhibitor activity, also sensitized glioma cells to TRAIL-mediated apoptosis, via the upregulation of both CHOP and DR5.	cifenline	44-55	DNA damage inducible transcript 3	Homo sapiens	205-209
21268086-4	2011	Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), suggesting the induction of ER stress.	1-(3-chlorophenyl)piperazine	51-55	DNA damage inducible transcript 3	Homo sapiens	162-211
21168844-9	2011	Nicorandil significantly reduced the expression levels of endoplasmic reticulum stress markers, C/EBP homologous protein (CHOP) and glucose regulated protein/BiP (GRP78) in atherosclerotic lesions.	Nicorandil	0-10	DNA damage inducible transcript 3	Homo sapiens	96-120
21168844-9	2011	Nicorandil significantly reduced the expression levels of endoplasmic reticulum stress markers, C/EBP homologous protein (CHOP) and glucose regulated protein/BiP (GRP78) in atherosclerotic lesions.	Nicorandil	0-10	DNA damage inducible transcript 3	Homo sapiens	122-126
21168844-10	2011	Nicorandil significantly attenuated tunicamycin-induced CHOP upregulation in cultured THP-1 macrophages.	Nicorandil	0-10	DNA damage inducible transcript 3	Homo sapiens	56-60
21168844-10	2011	Nicorandil significantly attenuated tunicamycin-induced CHOP upregulation in cultured THP-1 macrophages.	Tunicamycin	36-47	DNA damage inducible transcript 3	Homo sapiens	56-60
21148334-6	2011	When rituximab was used with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP), there was no improvement of the outcomes in patients treated with primary surgical resection.	Prednisolone	77-89	DNA damage inducible transcript 3	Homo sapiens	91-95
21199169-7	2011	The synergistic enhancements of apoptosis and GADD153 gene expression in human non-small cell lung cancer cells by the combination of EGCG and celecoxib were mediated through the activation of the MAPK signaling pathway.	epigallocatechin gallate	134-138	DNA damage inducible transcript 3	Homo sapiens	46-53
21199169-7	2011	The synergistic enhancements of apoptosis and GADD153 gene expression in human non-small cell lung cancer cells by the combination of EGCG and celecoxib were mediated through the activation of the MAPK signaling pathway.	Celecoxib	143-152	DNA damage inducible transcript 3	Homo sapiens	46-53
21268086-4	2011	Treatment of HCT-116 human colon cancer cells with MCPP was found to induce a number of signature endoplasmic reticulum (ER) stress markers; and up-regulation of CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein (GRP)-78, phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), suggesting the induction of ER stress.	1-(3-chlorophenyl)piperazine	51-55	DNA damage inducible transcript 3	Homo sapiens	213-217
21268086-6	2011	Transfection of cells with GRP78 or CHOP siRNA, or treatment of GSK3 inhibitor SB216163 reduced MCPP-mediated cell apoptosis.	1-(3-chlorophenyl)piperazine	96-100	DNA damage inducible transcript 3	Homo sapiens	36-40
21268086-9	2011	Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation.	SB 216763	41-49	DNA damage inducible transcript 3	Homo sapiens	98-102
21268086-9	2011	Furthermore, treatment of GSK3 inhibitor SB216763 also dramatically reversed MCPP-induced GRP and CHOP up-regulation, and pro-caspase-3 and pro-caspase-9 degradation.	1-(3-chlorophenyl)piperazine	77-81	DNA damage inducible transcript 3	Homo sapiens	98-102
21268086-10	2011	Taken together, the present study provides evidences to support that GRP78 and CHOP expression, and GSK3alpha/beta activation in mediating the MCPP-induced human colon cancer cell apoptosis.	1-(3-chlorophenyl)piperazine	143-147	DNA damage inducible transcript 3	Homo sapiens	79-83
21067863-4	2011	In addition, combined niflumic acid-ciglitazone treatment significantly induced ER stress responses, and suppression of CHOP expression significantly attenuated the combined niflumic acid-ciglitazone treatment-induced activation of caspase-8 and caspase-3, and the subsequent apoptotic cell death, indicating a role of ER stress in caspase-8 activation and apoptosis.	Niflumic Acid	174-187	DNA damage inducible transcript 3	Homo sapiens	120-124
21078775-5	2011	PA induced ER stress, as determined by phosphorylation of PERK, eIF2alpha, and JNK, as well as induction of CHOP in macrophage-like THP-1 cells.	Palmitic Acid	0-2	DNA damage inducible transcript 3	Homo sapiens	108-112
21067863-4	2011	In addition, combined niflumic acid-ciglitazone treatment significantly induced ER stress responses, and suppression of CHOP expression significantly attenuated the combined niflumic acid-ciglitazone treatment-induced activation of caspase-8 and caspase-3, and the subsequent apoptotic cell death, indicating a role of ER stress in caspase-8 activation and apoptosis.	ciglitazone	188-199	DNA damage inducible transcript 3	Homo sapiens	120-124
21127198-0	2011	ROS and CHOP are critical for dibenzylideneacetone to sensitize tumor cells to TRAIL through induction of death receptors and downregulation of cell survival proteins.	dibenzylidene acetone	30-50	DNA damage inducible transcript 3	Homo sapiens	8-12
21127198-9	2011	In addition, DBA increased the expression of CHOP proteins.	dibenzylidene acetone	13-16	DNA damage inducible transcript 3	Homo sapiens	45-49
21127198-13	2011	Overall, our results show that DBA potentiates TRAIL-induced apoptosis through downregulation of cell survival proteins and upregulation of death receptors via activation of ROS and CHOP mediated pathways.	dibenzylidene acetone	31-34	DNA damage inducible transcript 3	Homo sapiens	182-186
21127198-10	2011	Knockdown of CHOP by siRNA decreased the induction of DBA-induced DR5 expression and apoptosis.	dibenzylidene acetone	54-57	DNA damage inducible transcript 3	Homo sapiens	13-17
21307594-3	2011	Furthermore, we also found that quinotrierixin inhibited the ER stress-induced increases of unfolded protein response-related genes such as GRP78, CHOP, EDEM, ERdj4, and p58(IPK).	quinotrierixin	32-46	DNA damage inducible transcript 3	Homo sapiens	147-151
20735367-0	2011	Mephedrone, new kid for the chop?	mephedrone	0-10	DNA damage inducible transcript 3	Homo sapiens	28-32
21901118-9	2011	Furthermore, with GRP78 synthesis inhibitor momitoxin (VT) and PKR inhibitor 2-aminopurine (2-AP) treatment for blocking GRP78 expression and eIF2alpha phosphorylation, PKR/PERK may involve in eIF2alpha phosphorylation/CHOP upregulation pathway that enhances the downstream regulators Bcl-2 family proteins expression and increased cell survival.	momitoxin	44-53	DNA damage inducible transcript 3	Homo sapiens	219-223
21274285-4	2011	DHTS was able to induce ER stress as evidenced by the upregulation of glucose regulation protein 78 (GRP78/Bip) and CAAT/enhancer binding protein homologous protein/growth arrest- and DNA damage-inducible gene 153 (CHOP/GADD153), as well as increases in phosphorylated eukaryotic initiation factor 2alpha (eIF2alpha), c-jun N-terminal kinase (JNK), and X-box-binding protein 1 (XBP1) mRNA splicing forms.	dhts	0-4	DNA damage inducible transcript 3	Homo sapiens	215-219
21274285-4	2011	DHTS was able to induce ER stress as evidenced by the upregulation of glucose regulation protein 78 (GRP78/Bip) and CAAT/enhancer binding protein homologous protein/growth arrest- and DNA damage-inducible gene 153 (CHOP/GADD153), as well as increases in phosphorylated eukaryotic initiation factor 2alpha (eIF2alpha), c-jun N-terminal kinase (JNK), and X-box-binding protein 1 (XBP1) mRNA splicing forms.	dhts	0-4	DNA damage inducible transcript 3	Homo sapiens	220-227
22454706-5	2011	He received chemotherapy with CHOP regimen (cyclophosphamide, adriamycin, vincristine and prednisolone) resulting in reduction in lesion size leaving a phthysical eyeball and a ptotic lid.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	30-34
22454706-5	2011	He received chemotherapy with CHOP regimen (cyclophosphamide, adriamycin, vincristine and prednisolone) resulting in reduction in lesion size leaving a phthysical eyeball and a ptotic lid.	Doxorubicin	62-72	DNA damage inducible transcript 3	Homo sapiens	30-34
22454706-5	2011	He received chemotherapy with CHOP regimen (cyclophosphamide, adriamycin, vincristine and prednisolone) resulting in reduction in lesion size leaving a phthysical eyeball and a ptotic lid.	Vincristine	74-85	DNA damage inducible transcript 3	Homo sapiens	30-34
22454706-5	2011	He received chemotherapy with CHOP regimen (cyclophosphamide, adriamycin, vincristine and prednisolone) resulting in reduction in lesion size leaving a phthysical eyeball and a ptotic lid.	Prednisolone	90-102	DNA damage inducible transcript 3	Homo sapiens	30-34
21966325-8	2011	Diclofenac, as well as indomethacin, is able to activate efficiently only the PERK pathway of the UPR, which induces the expression of the proapoptotic GADD153/CHOP protein.	Diclofenac	0-10	DNA damage inducible transcript 3	Homo sapiens	152-159
21966325-8	2011	Diclofenac, as well as indomethacin, is able to activate efficiently only the PERK pathway of the UPR, which induces the expression of the proapoptotic GADD153/CHOP protein.	Diclofenac	0-10	DNA damage inducible transcript 3	Homo sapiens	160-164
21966325-8	2011	Diclofenac, as well as indomethacin, is able to activate efficiently only the PERK pathway of the UPR, which induces the expression of the proapoptotic GADD153/CHOP protein.	Indomethacin	23-35	DNA damage inducible transcript 3	Homo sapiens	152-159
21966325-8	2011	Diclofenac, as well as indomethacin, is able to activate efficiently only the PERK pathway of the UPR, which induces the expression of the proapoptotic GADD153/CHOP protein.	Indomethacin	23-35	DNA damage inducible transcript 3	Homo sapiens	160-164
22046282-0	2011	Silencing GADD153/CHOP gene expression protects against Alzheimer"s disease-like pathology induced by 27-hydroxycholesterol in rabbit hippocampus.	27-hydroxycholesterol	102-123	DNA damage inducible transcript 3	Homo sapiens	10-17
22046282-0	2011	Silencing GADD153/CHOP gene expression protects against Alzheimer"s disease-like pathology induced by 27-hydroxycholesterol in rabbit hippocampus.	27-hydroxycholesterol	102-123	DNA damage inducible transcript 3	Homo sapiens	18-22
22046282-2	2011	Sustained ER stress leads to activation of the growth arrest and leucine zipper transcription factor, DNA damage inducible gene 153 (gadd153; also called CHOP).	Leucine	65-72	DNA damage inducible transcript 3	Homo sapiens	133-140
22046282-2	2011	Sustained ER stress leads to activation of the growth arrest and leucine zipper transcription factor, DNA damage inducible gene 153 (gadd153; also called CHOP).	Leucine	65-72	DNA damage inducible transcript 3	Homo sapiens	154-158
22046282-3	2011	Activated gadd153 can generate oxidative damage and reactive oxygen species (ROS), increase beta-amyloid (Abeta) levels, disturb iron homeostasis and induce inflammation as well as cell death, which are all pathological hallmarks of AD.	Reactive Oxygen Species	52-75	DNA damage inducible transcript 3	Homo sapiens	10-17
22046282-3	2011	Activated gadd153 can generate oxidative damage and reactive oxygen species (ROS), increase beta-amyloid (Abeta) levels, disturb iron homeostasis and induce inflammation as well as cell death, which are all pathological hallmarks of AD.	Reactive Oxygen Species	77-80	DNA damage inducible transcript 3	Homo sapiens	10-17
22046282-3	2011	Activated gadd153 can generate oxidative damage and reactive oxygen species (ROS), increase beta-amyloid (Abeta) levels, disturb iron homeostasis and induce inflammation as well as cell death, which are all pathological hallmarks of AD.	Iron	129-133	DNA damage inducible transcript 3	Homo sapiens	10-17
22046282-6	2011	However, the extent to which gadd153 mediates 27-OHC effects has not been determined.	27-hydroxycholesterol	46-52	DNA damage inducible transcript 3	Homo sapiens	29-36
22046282-9	2011	Additionally, 27-OHC-induced tau phosphorylation, ROS generation, TNF-alpha activation, and iron and apoptosis-regulatory protein levels alteration were also markedly reduced by siRNA to gadd153.	Reactive Oxygen Species	50-53	DNA damage inducible transcript 3	Homo sapiens	187-194
22046282-9	2011	Additionally, 27-OHC-induced tau phosphorylation, ROS generation, TNF-alpha activation, and iron and apoptosis-regulatory protein levels alteration were also markedly reduced by siRNA to gadd153.	Iron	92-96	DNA damage inducible transcript 3	Homo sapiens	187-194
22046282-10	2011	These data suggest that ER stress-mediated gadd153 activation plays a central role in the triggering of AD pathological hallmarks that result from incubation of hippocampal slices with 27-OHC.	-ohc	187-191	DNA damage inducible transcript 3	Homo sapiens	43-50
22046282-11	2011	Our results add important insights into cellular mechanisms that underlie the potential contribution of cholesterol metabolism in AD pathology, and suggest that preventing gadd153 activation protects against AD related to cholesterol oxidized products.	Cholesterol	104-115	DNA damage inducible transcript 3	Homo sapiens	172-179
22046282-11	2011	Our results add important insights into cellular mechanisms that underlie the potential contribution of cholesterol metabolism in AD pathology, and suggest that preventing gadd153 activation protects against AD related to cholesterol oxidized products.	Cholesterol	222-233	DNA damage inducible transcript 3	Homo sapiens	172-179
22115051-8	2011	alpha-TEA disrupted cholesterol-rich microdomains, acted cooperatively with TAM to reduce prosurvival mediators, and induced DR5-mediated mitochondria-dependent apoptosis via an endoplasmic reticulum stress-triggered pro-death pJNK/CHOP/DR5 amplification loop.	alpha-TEA	0-9	DNA damage inducible transcript 3	Homo sapiens	232-236
21863214-9	2011	Candesartan was associated with maintenance of XBP-1 expression and attenuated ATF4, cATF6 and CHOP protein expression.	candesartan	0-11	DNA damage inducible transcript 3	Homo sapiens	95-99
21895401-0	2011	Metformin induces apoptosis of lung cancer cells through activating JNK/p38 MAPK pathway and GADD153.	Metformin	0-9	DNA damage inducible transcript 3	Homo sapiens	93-100
21895401-4	2011	We also found that metformin treatment can activate AMP-activated protein kinase, JNK/p38 MAPK signaling pathway and caspases, as well as upregulate the expression of growth arrest and DNA damage inducible gene 153 (GADD153).	Metformin	19-28	DNA damage inducible transcript 3	Homo sapiens	167-214
21895401-4	2011	We also found that metformin treatment can activate AMP-activated protein kinase, JNK/p38 MAPK signaling pathway and caspases, as well as upregulate the expression of growth arrest and DNA damage inducible gene 153 (GADD153).	Metformin	19-28	DNA damage inducible transcript 3	Homo sapiens	216-223
21895401-5	2011	Either blockade of JNK/p38 MAPK pathway or knockdown of GADD153 gene abrogated the apoptosis-inducing effect of metformin.	Metformin	112-121	DNA damage inducible transcript 3	Homo sapiens	56-63
21895401-6	2011	Taken together, our data suggest that metformin inhibits the growth of lung cancer cells and induces apoptosis through activating JNK/p38 MAPK pathway and GADD153.	Metformin	38-47	DNA damage inducible transcript 3	Homo sapiens	155-162
21957486-9	2011	In contrast, CHOP (C/EBP homologous protein); the penultimate protein that leads to ER stress-related cell death was significantly decreased by exendin-4 in hepatocytes loaded with fatty acids.	Fatty Acids	181-192	DNA damage inducible transcript 3	Homo sapiens	13-17
21957486-9	2011	In contrast, CHOP (C/EBP homologous protein); the penultimate protein that leads to ER stress-related cell death was significantly decreased by exendin-4 in hepatocytes loaded with fatty acids.	Fatty Acids	181-192	DNA damage inducible transcript 3	Homo sapiens	19-43
21901118-9	2011	Furthermore, with GRP78 synthesis inhibitor momitoxin (VT) and PKR inhibitor 2-aminopurine (2-AP) treatment for blocking GRP78 expression and eIF2alpha phosphorylation, PKR/PERK may involve in eIF2alpha phosphorylation/CHOP upregulation pathway that enhances the downstream regulators Bcl-2 family proteins expression and increased cell survival.	2-Aminopurine	77-90	DNA damage inducible transcript 3	Homo sapiens	219-223
21901118-9	2011	Furthermore, with GRP78 synthesis inhibitor momitoxin (VT) and PKR inhibitor 2-aminopurine (2-AP) treatment for blocking GRP78 expression and eIF2alpha phosphorylation, PKR/PERK may involve in eIF2alpha phosphorylation/CHOP upregulation pathway that enhances the downstream regulators Bcl-2 family proteins expression and increased cell survival.	2-Aminopurine	92-96	DNA damage inducible transcript 3	Homo sapiens	219-223
21044953-4	2010	Both C/EBP homologous protein (CHOP) and Elk1 are required for celecoxib-induced DR5 expression based on promoter deletion and mutation analysis and siRNA-mediated gene silencing results.	Celecoxib	63-72	DNA damage inducible transcript 3	Homo sapiens	5-29
21044953-11	2010	Collectively, we conclude that small molecules such as celecoxib induce DR5 expression through activating ERK/RSK signaling and subsequent Elk1 activation and ATF4-dependent CHOP induction.	Celecoxib	55-64	DNA damage inducible transcript 3	Homo sapiens	174-178
21044953-4	2010	Both C/EBP homologous protein (CHOP) and Elk1 are required for celecoxib-induced DR5 expression based on promoter deletion and mutation analysis and siRNA-mediated gene silencing results.	Celecoxib	63-72	DNA damage inducible transcript 3	Homo sapiens	31-35
21044953-8	2010	Moreover, these inhibitions suppressed celecoxib-induced CHOP up-regulation.	Celecoxib	39-48	DNA damage inducible transcript 3	Homo sapiens	57-61
21044953-10	2010	Additionally, celecoxib increased CHOP promoter activity in an ATF4-dependent manner, and siRNA-mediated blockade of ATF4 abrogated both CHOP induction and DR5 up-regulation, indicating that ATF4 is involved in celecoxib-induced CHOP and DR5 expression.	Celecoxib	14-23	DNA damage inducible transcript 3	Homo sapiens	34-38
20970436-6	2010	KEY FINDINGS: Pa led to cytotoxicity and apoptosis in HepG2 cells in a dose-dependent pattern and also induced ER stress indicated by increased phosphorylation of eIF2alpha, upregulation of IRE1alpha and CHOP.	Palmitates	14-16	DNA damage inducible transcript 3	Homo sapiens	204-208
20920558-11	2010	Furthermore, PDTC/Cu complex could trigger the expressions of ER stress-associated signaling molecules including Grp78, Grp94, caspase-12, ATF4, and CHOP, which could be reversed by SP600125.	Copper	18-20	DNA damage inducible transcript 3	Homo sapiens	149-153
20920558-11	2010	Furthermore, PDTC/Cu complex could trigger the expressions of ER stress-associated signaling molecules including Grp78, Grp94, caspase-12, ATF4, and CHOP, which could be reversed by SP600125.	pyrazolanthrone	182-190	DNA damage inducible transcript 3	Homo sapiens	149-153
20851775-8	2010	T98G cells transfected with a dominant-negative PERK construct exhibited an attenuated response to neuro-steroid treatment in terms of decreases in: eIF2alpha activation; CHOP expression; the incidence of autophagy; and cytotoxicity.	Steroids	105-112	DNA damage inducible transcript 3	Homo sapiens	171-175
21151603-8	2010	GlcN had only minor effects on the expression of Hsp90, Grp78, and transcription factor CHOP/GADD 153 markers of nonspecific stress in the endoplasmic reticulum.	Glucosamine	0-4	DNA damage inducible transcript 3	Homo sapiens	88-92
20665890-2	2010	A phase 1 evaluation was conducted of bortezomib with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) in patients with untreated diffuse large B-cell lymphoma (DLBCL) or mantle cell lymphoma (MCL).	Bortezomib	38-48	DNA damage inducible transcript 3	Homo sapiens	131-135
20665890-6	2010	RESULTS: The maximum tolerated dose of bortezomib with R-CHOP was not reached, and the 1.3-mg/m2 dose level had acceptable tolerability.	Bortezomib	39-49	DNA damage inducible transcript 3	Homo sapiens	57-61
20665890-12	2010	CONCLUSIONS: Bortezomib at a dose of 1.3 mg/m2 twice per cycle can be added to R-CHOP chemotherapy with acceptable toxicity.	Bortezomib	13-23	DNA damage inducible transcript 3	Homo sapiens	81-85
21776480-4	2010	Overall, garcinol activated not only the death receptor and the mitochondrial apoptosis pathways but also the ER stress modulator GADD153.	garcinol	9-17	DNA damage inducible transcript 3	Homo sapiens	130-137
21776480-5	2010	Garcinol treatment led to the accumulation of reactive oxygen species (ROS), increased GADD153 expression, and reduced mitochondrial membrane potential.	garcinol	0-8	DNA damage inducible transcript 3	Homo sapiens	87-94
21115923-6	2010	RT-PCR analysis confirmed the presence of EWS-CHOP chimeric transcript type 1, in which exon 7 of EWS was in-frame fused to exon 2 of CHOP with a serine (AGT) to methionine (ATG) transition at the junction.	Serine	146-152	DNA damage inducible transcript 3	Homo sapiens	46-50
20837473-0	2010	Gossypol induces death receptor-5 through activation of the ROS-ERK-CHOP pathway and sensitizes colon cancer cells to TRAIL.	Gossypol	0-8	DNA damage inducible transcript 3	Homo sapiens	68-72
20837473-0	2010	Gossypol induces death receptor-5 through activation of the ROS-ERK-CHOP pathway and sensitizes colon cancer cells to TRAIL.	Reactive Oxygen Species	60-63	DNA damage inducible transcript 3	Homo sapiens	68-72
20837473-8	2010	Gossypol induction of the death receptor required the induction of CHOP, and thus, gene silencing of CHOP abolished gossypol-induced DR5 expression and associated potentiation of apoptosis.	Gossypol	0-8	DNA damage inducible transcript 3	Homo sapiens	67-71
20837473-8	2010	Gossypol induction of the death receptor required the induction of CHOP, and thus, gene silencing of CHOP abolished gossypol-induced DR5 expression and associated potentiation of apoptosis.	Gossypol	116-124	DNA damage inducible transcript 3	Homo sapiens	67-71
20837473-8	2010	Gossypol induction of the death receptor required the induction of CHOP, and thus, gene silencing of CHOP abolished gossypol-induced DR5 expression and associated potentiation of apoptosis.	Gossypol	116-124	DNA damage inducible transcript 3	Homo sapiens	101-105
20837473-11	2010	Overall, our results show that gossypol enhances TRAIL-induced apoptosis through the down-regulation of cell survival proteins and the up-regulation of TRAIL death receptors through the ROS-ERK-CHOP-DR5 pathway.	Gossypol	31-39	DNA damage inducible transcript 3	Homo sapiens	194-198
21037108-8	2010	Tubacin induces the expression of DDIT3 (CHOP/GADD153), a transcription factor up-regulated in response to cellular stress.	tubacin	0-7	DNA damage inducible transcript 3	Homo sapiens	34-39
21037108-8	2010	Tubacin induces the expression of DDIT3 (CHOP/GADD153), a transcription factor up-regulated in response to cellular stress.	tubacin	0-7	DNA damage inducible transcript 3	Homo sapiens	41-45
21037108-8	2010	Tubacin induces the expression of DDIT3 (CHOP/GADD153), a transcription factor up-regulated in response to cellular stress.	tubacin	0-7	DNA damage inducible transcript 3	Homo sapiens	46-53
21037108-9	2010	DDIT3 induction is further increased when tubacin is combined with SAHA.	tubacin	42-49	DNA damage inducible transcript 3	Homo sapiens	0-5
21037108-9	2010	DDIT3 induction is further increased when tubacin is combined with SAHA.	Vorinostat	67-71	DNA damage inducible transcript 3	Homo sapiens	0-5
21115923-6	2010	RT-PCR analysis confirmed the presence of EWS-CHOP chimeric transcript type 1, in which exon 7 of EWS was in-frame fused to exon 2 of CHOP with a serine (AGT) to methionine (ATG) transition at the junction.	Serine	146-152	DNA damage inducible transcript 3	Homo sapiens	134-138
21115923-6	2010	RT-PCR analysis confirmed the presence of EWS-CHOP chimeric transcript type 1, in which exon 7 of EWS was in-frame fused to exon 2 of CHOP with a serine (AGT) to methionine (ATG) transition at the junction.	Methionine	162-172	DNA damage inducible transcript 3	Homo sapiens	46-50
21115923-6	2010	RT-PCR analysis confirmed the presence of EWS-CHOP chimeric transcript type 1, in which exon 7 of EWS was in-frame fused to exon 2 of CHOP with a serine (AGT) to methionine (ATG) transition at the junction.	Methionine	162-172	DNA damage inducible transcript 3	Homo sapiens	134-138
20506110-11	2010	Furthermore, PA decreased GRP78 expression and induced increases in the endoplasmic reticulum (ER) stress signaling pathways p-PERK, p-eIF2alpha, p-ATF4, and CHOP, which were blocked by AM251 treatment.	Palmitic Acid	13-15	DNA damage inducible transcript 3	Homo sapiens	158-162
21030533-3	2010	DLBCL is associated with an aggressive natural history, but it can be cured with combination chemotherapy regimens like cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), which has been the mainstay of therapy for several decades.	Cyclophosphamide	120-136	DNA damage inducible transcript 3	Homo sapiens	180-184
21030533-3	2010	DLBCL is associated with an aggressive natural history, but it can be cured with combination chemotherapy regimens like cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), which has been the mainstay of therapy for several decades.	Doxorubicin	138-149	DNA damage inducible transcript 3	Homo sapiens	180-184
21050687-8	2010	The classic CHOP protocol (combination of doxorubicin-cyclophosphamide-vincristine-prednisone) does not have satisfactory results and survival remains poor, especially in patients with underlying RCD.	Doxorubicin	42-53	DNA damage inducible transcript 3	Homo sapiens	12-16
21050687-8	2010	The classic CHOP protocol (combination of doxorubicin-cyclophosphamide-vincristine-prednisone) does not have satisfactory results and survival remains poor, especially in patients with underlying RCD.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	12-16
21050687-8	2010	The classic CHOP protocol (combination of doxorubicin-cyclophosphamide-vincristine-prednisone) does not have satisfactory results and survival remains poor, especially in patients with underlying RCD.	Vincristine	71-82	DNA damage inducible transcript 3	Homo sapiens	12-16
21050687-8	2010	The classic CHOP protocol (combination of doxorubicin-cyclophosphamide-vincristine-prednisone) does not have satisfactory results and survival remains poor, especially in patients with underlying RCD.	Prednisone	83-93	DNA damage inducible transcript 3	Homo sapiens	12-16
20878089-11	2010	Curcumin induces the GADD153 expression by cleaving caspase-12 and ATF6, and then by translocating ATF6 to the nucleus.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	21-28
21103206-3	2010	We describe a 51-year-old man with jejunal B-cell lymphoma who developed recurrent episodes of ischemic colitis following chemotherapy with cyclophosphamide, vincristine, doxorubicine and prednisolone plus rituximab (R-CHOP).	Cyclophosphamide	140-156	DNA damage inducible transcript 3	Homo sapiens	219-223
20719828-11	2010	CONCLUSIONS: These results suggest that up-regulation of ORP150 in thyroid cancer cells inhibits MG132-induced apoptosis via suppression of CHOP induction, thereby decreasing the potential antitumor activity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	97-102	DNA damage inducible transcript 3	Homo sapiens	140-144
20889551-3	2010	Several representative ribotoxic agents (deoxynivalenol, anisomycin, and 15-acetyldeoxynivalenol) enhanced CHOP expression and its nuclear translocation in human intestinal epithelial cells.	deoxynivalenol	41-55	DNA damage inducible transcript 3	Homo sapiens	107-111
20889551-3	2010	Several representative ribotoxic agents (deoxynivalenol, anisomycin, and 15-acetyldeoxynivalenol) enhanced CHOP expression and its nuclear translocation in human intestinal epithelial cells.	Anisomycin	57-67	DNA damage inducible transcript 3	Homo sapiens	107-111
20889551-3	2010	Several representative ribotoxic agents (deoxynivalenol, anisomycin, and 15-acetyldeoxynivalenol) enhanced CHOP expression and its nuclear translocation in human intestinal epithelial cells.	15-acetyldeoxynivalenol	73-96	DNA damage inducible transcript 3	Homo sapiens	107-111
20889551-8	2010	Taken together, the results indicate that ribotoxin-induced CHOP protein is positively associated with production of proinflammatory cytokine IL-8, but it downregulates PPARgamma action, subsequently allowing the cytosolic translocation of HuR protein and stabilization of IL-8 mRNA in gut epithelial cells.	ribotoxin	42-51	DNA damage inducible transcript 3	Homo sapiens	60-64
20719828-11	2010	CONCLUSIONS: These results suggest that up-regulation of ORP150 in thyroid cancer cells inhibits MG132-induced apoptosis via suppression of CHOP induction, thereby decreasing the potential antitumor activity of MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	211-216	DNA damage inducible transcript 3	Homo sapiens	140-144
20647473-7	2010	Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells.	Panobinostat	49-61	DNA damage inducible transcript 3	Homo sapiens	105-109
20449747-8	2010	Chlorambucil alone and cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) or CHOP-like combination chemotherapy was frequently used as a first-line treatment, and a fludarabine-based regimen was commonly used as salvage therapy.	Chlorambucil	0-12	DNA damage inducible transcript 3	Homo sapiens	85-89
21046477-5	2010	Finally, the pro-apoptotic molecules CHOP and BIM are only induced in the presence of tunicamycin in the culture medium.	Tunicamycin	86-97	DNA damage inducible transcript 3	Homo sapiens	37-41
20668104-5	2010	Palmitic acid induces podocyte ER stress, leading to an unfolded protein response as reflected by the induction of the ER chaperone immunoglobulin heavy chain binding protein (BiP) and proapoptotic C/EBP homologous protein (CHOP) transcription factor.	Palmitic Acid	0-13	DNA damage inducible transcript 3	Homo sapiens	198-222
20668104-5	2010	Palmitic acid induces podocyte ER stress, leading to an unfolded protein response as reflected by the induction of the ER chaperone immunoglobulin heavy chain binding protein (BiP) and proapoptotic C/EBP homologous protein (CHOP) transcription factor.	Palmitic Acid	0-13	DNA damage inducible transcript 3	Homo sapiens	224-228
20668104-6	2010	Of note, the monounsaturated palmitoleic and oleic acid can attenuate the palmitic acid-induced upregulation of CHOP, thereby preventing cell death.	monounsaturated palmitoleic	13-40	DNA damage inducible transcript 3	Homo sapiens	112-116
20668104-6	2010	Of note, the monounsaturated palmitoleic and oleic acid can attenuate the palmitic acid-induced upregulation of CHOP, thereby preventing cell death.	Oleic Acid	45-55	DNA damage inducible transcript 3	Homo sapiens	112-116
20668104-6	2010	Of note, the monounsaturated palmitoleic and oleic acid can attenuate the palmitic acid-induced upregulation of CHOP, thereby preventing cell death.	Palmitic Acid	74-87	DNA damage inducible transcript 3	Homo sapiens	112-116
20668104-7	2010	Similarly, gene silencing of CHOP protects against palmitic acid-induced podocyte apoptosis.	Palmitic Acid	51-64	DNA damage inducible transcript 3	Homo sapiens	29-33
20647473-7	2010	Compared with each agent alone, cotreatment with panobinostat increased bortezomib-induced expression of CHOP and NOXA, as well as increased bortezomib-induced UPR and apoptosis of cultured and primary MCL cells.	Bortezomib	72-82	DNA damage inducible transcript 3	Homo sapiens	105-109
20647473-9	2010	CONCLUSION: These findings suggest that increased UPR and induction of CHOP are involved in enhanced anti-MCL activity of the combination of panobinostat and bortezomib.	Panobinostat	141-153	DNA damage inducible transcript 3	Homo sapiens	71-75
20647473-9	2010	CONCLUSION: These findings suggest that increased UPR and induction of CHOP are involved in enhanced anti-MCL activity of the combination of panobinostat and bortezomib.	Bortezomib	158-168	DNA damage inducible transcript 3	Homo sapiens	71-75
20863376-7	2010	In contrast, inhibition of the nuclear factor-kappaB pathway, which is regulated by the FUS-DDIT3 fusion product, in myxoid liposarcoma cells using casein kinase 2 inhibitor 4,5,6,7-tetrabromobenzotriazole (TBB) showed a significant decrease in cell viability, decreased phosphorylation of nuclear factor-kappaB pathway proteins, and caspase 3 mediated apoptosis.	4,5,6,7-tetrabromobenzotriazole	174-205	DNA damage inducible transcript 3	Homo sapiens	92-97
20359814-3	2010	In addition, cirsimaritin triggered endoplasmic reticulum (ER) stress and down-regulated the phosphorylation of Akt, while knock-down of CHOP dramatically abrogated the inactivation of Akt and reversed the pro-apoptotic effect of cirsimaritin.	cirsimaritin	230-242	DNA damage inducible transcript 3	Homo sapiens	137-141
20548096-1	2010	We report the outcome of patients included in the LNH-98.5 study, which compared cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) to rituximab plus CHOP (R-CHOP) therapy in 399 patients with diffuse large B-cell lymphoma (DLBCL) aged 60 to 80 years, with a median follow-up time of 10 years.	Prednisone	129-139	DNA damage inducible transcript 3	Homo sapiens	141-145
20564149-13	2010	CONCLUSIONS: Intravenous methotrexate can be safely administered concurrently with R-CHOP and is associated with a low risk of CNS recurrence in high-risk patients.	Methotrexate	25-37	DNA damage inducible transcript 3	Homo sapiens	85-89
20830228-1	2010	BACKGROUND/AIMS: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy (R-CHOP) has improved survival in patients with diffuse large B-cell lymphoma (DLBCL) and weakened the prognostic power of the international prognostic index (IPI).	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	107-111
20842604-8	2010	TREATMENT AND COURSE: After 6 cycles of rituximab, cyclophosphamide, doxorubicin, vincristin and prednisolone (R-CHOP), an early relapse developed which was treated with rituximab, ifosphamid, methotrexate and etoposide.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	113-117
20830228-1	2010	BACKGROUND/AIMS: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy (R-CHOP) has improved survival in patients with diffuse large B-cell lymphoma (DLBCL) and weakened the prognostic power of the international prognostic index (IPI).	Doxorubicin	50-61	DNA damage inducible transcript 3	Homo sapiens	107-111
20830228-1	2010	BACKGROUND/AIMS: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone chemotherapy (R-CHOP) has improved survival in patients with diffuse large B-cell lymphoma (DLBCL) and weakened the prognostic power of the international prognostic index (IPI).	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	107-111
20830228-11	2010	All three indices were predictive, but only the E-IPI identified the high-risk group of R-CHOP-treated Korean patients with disseminated DLBCL.	e-ipi	48-53	DNA damage inducible transcript 3	Homo sapiens	90-94
20803121-10	2010	Moreover, quercetin increased the AIF protein released from mitochondria to nuclei and the GADD153 protein translocation from endoplasmic reticulum to the nuclei.	Quercetin	10-19	DNA damage inducible transcript 3	Homo sapiens	91-98
20804592-5	2010	Furthermore, taurine exerted its protective effect through down-regulation of expression of GRP 78, CHOP, Bim and caspase 12.	Taurine	13-20	DNA damage inducible transcript 3	Homo sapiens	100-104
20809973-10	2010	In vivo, ML120B was effective by itself and enhanced CHOP anti-tumor activity significantly (P = 0.001) in the WSU-DLCL2-SCID model but did not prevent CNS lymphoma in the WSU-FSCCL-SCID model.	N-(6-chloro-7-methoxy-9H-beta-carbolin-8-yl)-2-methylnicotinamide	9-15	DNA damage inducible transcript 3	Homo sapiens	53-57
20561333-1	2010	BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) has primarily been treated with cyclophosphamide, doxorubicin, vincristine, and predisone (CHOP) chemotherapy since the 1970s.	Doxorubicin	100-111	DNA damage inducible transcript 3	Homo sapiens	141-145
20654631-5	2010	We also studied the effect of ATF5 knockdown on arsenite-induced CHOP protein expression and arsenite-induced cell death of HepG2 cells.	arsenite	48-56	DNA damage inducible transcript 3	Homo sapiens	65-69
20654631-8	2010	Furthermore, the existence of either AARE1 or activating protein-1 (AP-1) site is sufficient for transcriptional activation of the CHOP gene promoter by arsenite exposure, although complete induction requires the existence of both elements.	arsenite	153-161	DNA damage inducible transcript 3	Homo sapiens	131-135
20654631-9	2010	We also demonstrated that knockdown of ATF5 reduced arsenite-induced CHOP protein expression and arsenite-induced cell death of HepG2 cells.	arsenite	52-60	DNA damage inducible transcript 3	Homo sapiens	69-73
20654631-10	2010	SIGNIFICANCE: These results suggested that the CHOP gene is a potential target for ATF5, and that ATF5 raises the arsenite-induced CHOP gene expression level via the AARE1 site in HepG2 cells.	arsenite	114-122	DNA damage inducible transcript 3	Homo sapiens	47-51
20654631-10	2010	SIGNIFICANCE: These results suggested that the CHOP gene is a potential target for ATF5, and that ATF5 raises the arsenite-induced CHOP gene expression level via the AARE1 site in HepG2 cells.	arsenite	114-122	DNA damage inducible transcript 3	Homo sapiens	131-135
20686688-3	2010	METHODOLOGY/PRINCIPAL FINDINGS: alpha-TEA induces endoplasmic reticulum (ER) stress as indicated by increased expression of CCAAT/enhancer binding protein homologous protein (CHOP) as well as by enhanced expression or activation of specific markers of ER stress such as glucose regulated protein (GRP78), phosphorylated alpha subunit of eukaryotic initiation factor 2 (peIF-2alpha), and spliced XBP-1 mRNA.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	32-41	DNA damage inducible transcript 3	Homo sapiens	124-173
20606042-7	2010	Treatments of PC-9 cells with c-Jun-NH(2)-kinase inhibitor SP600125, with p38 mitogen-activated protein kinase inhibitor SB202190 and with PD98059 (extracellular signal-regulated kinase 1/2 inhibitor) all increased the upregulation of GADD153 and GADD45 genes by the combination.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	139-146	DNA damage inducible transcript 3	Homo sapiens	235-242
20606042-7	2010	Treatments of PC-9 cells with c-Jun-NH(2)-kinase inhibitor SP600125, with p38 mitogen-activated protein kinase inhibitor SB202190 and with PD98059 (extracellular signal-regulated kinase 1/2 inhibitor) all increased the upregulation of GADD153 and GADD45 genes by the combination.	gadd45	247-253	DNA damage inducible transcript 3	Homo sapiens	235-242
20555361-4	2010	The accumulation of polyubiquitinated proteins was reduced in bortezomib-resistant cells compared with the parental cells, associated with avoidance of catastrophic ER stress as assessed by downregulation of CHOP expression.	Bortezomib	62-72	DNA damage inducible transcript 3	Homo sapiens	208-212
20542986-1	2010	PURPOSE: This study aimed to evaluate the efficacy and safety of the treatment with (90)Y-ibritumomab tiuxetan following a short-course of rituximab with cyclophosphamide-adriamycin-vincristine-prednisone (R-CHOP) in high-risk elderly patients with previously untreated diffuse large B-cell lymphoma (DLBCL).	ibritumomab tiuxetan	90-110	DNA damage inducible transcript 3	Homo sapiens	208-212
20542986-1	2010	PURPOSE: This study aimed to evaluate the efficacy and safety of the treatment with (90)Y-ibritumomab tiuxetan following a short-course of rituximab with cyclophosphamide-adriamycin-vincristine-prednisone (R-CHOP) in high-risk elderly patients with previously untreated diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	171-181	DNA damage inducible transcript 3	Homo sapiens	208-212
20542986-5	2010	Eight (50%) of the 16 patients who achieved less than a complete response with CHOP improved their remission status after (90)Y-ibritumomab tiuxetan administration.	ibritumomab tiuxetan	128-139	DNA damage inducible transcript 3	Homo sapiens	79-83
20542986-5	2010	Eight (50%) of the 16 patients who achieved less than a complete response with CHOP improved their remission status after (90)Y-ibritumomab tiuxetan administration.	tiuxetan	140-148	DNA damage inducible transcript 3	Homo sapiens	79-83
21132068-4	2010	In contrast, the addition of HMG sensitizes LNCaP or PC3 prostate cancer cells harboring an active Akt to apoptosis, in which ROS is upregulated to induce the UPR and GADD153 expression.	ros	126-129	DNA damage inducible transcript 3	Homo sapiens	167-174
20686688-3	2010	METHODOLOGY/PRINCIPAL FINDINGS: alpha-TEA induces endoplasmic reticulum (ER) stress as indicated by increased expression of CCAAT/enhancer binding protein homologous protein (CHOP) as well as by enhanced expression or activation of specific markers of ER stress such as glucose regulated protein (GRP78), phosphorylated alpha subunit of eukaryotic initiation factor 2 (peIF-2alpha), and spliced XBP-1 mRNA.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	32-41	DNA damage inducible transcript 3	Homo sapiens	175-179
20686688-5	2010	CONCLUSION: Taken together, ER stress plays an important role in alpha-TEA induced apoptosis by enhancing DR5/caspase-8 pro-apoptotic signaling and suppressing anti-apoptotic factors c-FLIP and Bcl-2 via ER stress mediated JNK/CHOP/DR5/caspase-8 signaling.	2,5,7,8-tetramethyl-2R-(4R,8R,12-trimethyltridecyl)chroman-6-yloxy acetic acid	65-74	DNA damage inducible transcript 3	Homo sapiens	227-231
20448044-6	2010	Rather, CHOP deletion enhanced neuronal susceptibility to both hypoxic and thapsigargin-mediated injury and attenuated brain-derived neurotrophic factor-induced neuroprotection.	Thapsigargin	75-87	DNA damage inducible transcript 3	Homo sapiens	8-12
20504773-10	2010	GADD153 was also elevated in cells treated with 1-deoxySa.	spisulosine	48-57	DNA damage inducible transcript 3	Homo sapiens	0-7
20398749-0	2010	Flavokawain B, a novel chalcone from Alpinia pricei Hayata with potent apoptotic activity: Involvement of ROS and GADD153 upstream of mitochondria-dependent apoptosis in HCT116 cells.	flavokawain B	0-13	DNA damage inducible transcript 3	Homo sapiens	114-121
20398749-4	2010	Flavokawain B exerts its apoptotic action through ROS generation and GADD153 up-regulation, which lead to mitochondria-dependent apoptosis characterized by release of cytochrome c and translocation of Bak.	flavokawain B	0-13	DNA damage inducible transcript 3	Homo sapiens	69-76
20398749-5	2010	The up-regulation of GADD153 in flavokawain B-treated HCT116 cells is associated with mitochondrial dysfunction and altered expression of Bcl-2 family members.	flavokawain B	32-45	DNA damage inducible transcript 3	Homo sapiens	21-28
20398749-6	2010	Moreover, pretreatment with the ROS scavenger N-acetylcysteine abolishes flavokawain B-induced ROS generation, GADD153 up-regulation, and apoptosis.	ros	32-35	DNA damage inducible transcript 3	Homo sapiens	111-118
20398749-6	2010	Moreover, pretreatment with the ROS scavenger N-acetylcysteine abolishes flavokawain B-induced ROS generation, GADD153 up-regulation, and apoptosis.	Acetylcysteine	46-62	DNA damage inducible transcript 3	Homo sapiens	111-118
20398749-6	2010	Moreover, pretreatment with the ROS scavenger N-acetylcysteine abolishes flavokawain B-induced ROS generation, GADD153 up-regulation, and apoptosis.	flavokawain B	73-86	DNA damage inducible transcript 3	Homo sapiens	111-118
20398749-7	2010	Similarly, RNAi-mediated gene silencing reduced flavokawain B-enhanced expression of GADD153 and apoptotic Bim, leading to diminished apoptosis.	flavokawain B	48-61	DNA damage inducible transcript 3	Homo sapiens	85-92
20398749-9	2010	Taken together, our data provide evidence for a molecular mechanism to explain the apoptotic activity of Alpinia plants, showing that flavokawain B acts through ROS generation and GADD153 up-regulation to regulate the expression of Bcl-2 family members, thereby inducing mitochondrial dysfunction and apoptosis in HCT116 cells.	flavokawain B	134-147	DNA damage inducible transcript 3	Homo sapiens	180-187
20430872-5	2010	Our results demonstrate that short-hairpin RNA-targeted knockdown of CHOP attenuates palmitate-induced apoptosis in Huh-7 cells.	Palmitates	85-94	DNA damage inducible transcript 3	Homo sapiens	69-73
20651361-9	2010	Curcumin-induced apoptosis was also stimulated through the FAS/caspase-8 (extrinsic) pathway and ER stress proteins, growth arrest- and DNA damage-inducible gene 153 (GADD153) and glucose-regulated protein 78 (GRP78) were activated in the NCI-H460 cells.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	117-165
20439934-5	2010	NAC also affected the elevation of GRP78 and CHOP/GADD153 expression by butyric acid.	Butyric Acid	72-84	DNA damage inducible transcript 3	Homo sapiens	45-49
20439934-5	2010	NAC also affected the elevation of GRP78 and CHOP/GADD153 expression by butyric acid.	Butyric Acid	72-84	DNA damage inducible transcript 3	Homo sapiens	50-57
20371669-4	2010	In MCF-7 and MDA-MB-231 cells, capsaicin induced endoplasmic reticulum (ER) stress via inositol-requiring 1 and Chop and induced autophagy, as demonstrated by microtubule-associated protein 1 light chain-3 (LC3) conversion.	Capsaicin	31-40	DNA damage inducible transcript 3	Homo sapiens	112-116
21472292-7	2010	The protein expression of GADD153 and Caspase-3 was increased, but the proto-oncogene bcl-2 was notably decreased in H146 cells treated with Tan-IIA (5 microg/ml) for 24 h. FACS showed that Tan-IIA may increase the production of ROS and Ca2+, but decreases MMP.	Reactive Oxygen Species	229-232	DNA damage inducible transcript 3	Homo sapiens	26-33
20424162-5	2010	In addition, prolonged exposure to high glucose further increases IL-1beta-triggered CHOP expression.	Glucose	40-47	DNA damage inducible transcript 3	Homo sapiens	85-89
20559423-5	2010	Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153).	Reactive Oxygen Species	94-117	DNA damage inducible transcript 3	Homo sapiens	239-286
20559423-5	2010	Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153).	Reactive Oxygen Species	94-117	DNA damage inducible transcript 3	Homo sapiens	288-295
20559423-5	2010	Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153).	Reactive Oxygen Species	119-122	DNA damage inducible transcript 3	Homo sapiens	239-286
20559423-5	2010	Oxidative stress was found to be dependent on the upregulation of NAD(P)H oxidase 4 (Nox4), a reactive oxygen species (ROS) Nox homologue, triggering endoplasmic reticulum (ER) stress, as assessed by the ER stress-induced apoptosis marker Growth Arrest and DNA Damage-inducible gene 153 (GADD153).	Reactive Oxygen Species	119-122	DNA damage inducible transcript 3	Homo sapiens	288-295
20559423-6	2010	We demonstrated that 3DG-collagen activated GADD153 via phosphorylation of p38 mitogen activated protein kinase (MAPK), and this was dependent on upstream ROS.	Reactive Oxygen Species	155-158	DNA damage inducible transcript 3	Homo sapiens	44-51
20651361-9	2010	Curcumin-induced apoptosis was also stimulated through the FAS/caspase-8 (extrinsic) pathway and ER stress proteins, growth arrest- and DNA damage-inducible gene 153 (GADD153) and glucose-regulated protein 78 (GRP78) were activated in the NCI-H460 cells.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	167-174
20558856-6	2010	The patient was successfully treated with systemic R-CHOP with intrathecal methotrexate and achieved complete remission after six cycles of chemotherapy.	Methotrexate	75-87	DNA damage inducible transcript 3	Homo sapiens	53-57
20177729-8	2010	High-dose steroid therapy followed by six courses of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) therapy improved his symptoms.	Prednisolone	101-113	DNA damage inducible transcript 3	Homo sapiens	115-119
20038265-5	2010	Metformin also blocked the induction of ER stress proteins (GRP78, Chop, Cleaved ATF-6, p-eIF2 alpha and XBP-1) and regulated serine phosphorylation of IRS-1.	Metformin	0-9	DNA damage inducible transcript 3	Homo sapiens	67-71
20610938-1	2010	We report the case of a patient with non-Hodgkin"s lymphoma who, during chemotherapy according to the r-CHOP schedule (rituximab-cyclophosphamide-doxorubicin-vincristine and prednisone), showed a hepatic flare with jaundice.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	104-108
20610938-1	2010	We report the case of a patient with non-Hodgkin"s lymphoma who, during chemotherapy according to the r-CHOP schedule (rituximab-cyclophosphamide-doxorubicin-vincristine and prednisone), showed a hepatic flare with jaundice.	Doxorubicin	146-157	DNA damage inducible transcript 3	Homo sapiens	104-108
20610938-1	2010	We report the case of a patient with non-Hodgkin"s lymphoma who, during chemotherapy according to the r-CHOP schedule (rituximab-cyclophosphamide-doxorubicin-vincristine and prednisone), showed a hepatic flare with jaundice.	Vincristine	158-169	DNA damage inducible transcript 3	Homo sapiens	104-108
19700217-4	2010	DHE triggered endoplasmic reticulum (ER) stress, as indicated by changes in cytosol-calcium levels, PKR-like ER kinase (PERK) phosphorylation, inositol requiring protein 1 (IRE1) and CHOP/GADD153 upregulation, X-box transcription factor-1 (XBP-1) mRNA splicing, and caspase-4 activation.	dehydrocostus lactone	0-3	DNA damage inducible transcript 3	Homo sapiens	183-187
20459685-10	2010	Cd2+ also induced reactive oxygen species dependent expression of the pro-apoptotic ER stress marker and Wnt suppressor CHOP/GADD153 which, however, did not abolish Wnt response and cell viability.	Reactive Oxygen Species	18-41	DNA damage inducible transcript 3	Homo sapiens	120-124
20385988-2	2010	The introduction of rituximab has markedly improved outcome, and R-CHOP (rituximab + cyclophosphamide, doxorubicin, vincristine, prednisone) has become the standard treatment for CD20(+) diffuse large B-cell lymphoma.	Prednisone	129-139	DNA damage inducible transcript 3	Homo sapiens	67-71
20385988-11	2010	These results demonstrate that the IPI is still valid in the R-CHOP era.	diprotin A	35-38	DNA damage inducible transcript 3	Homo sapiens	63-67
20459685-10	2010	Cd2+ also induced reactive oxygen species dependent expression of the pro-apoptotic ER stress marker and Wnt suppressor CHOP/GADD153 which, however, did not abolish Wnt response and cell viability.	Reactive Oxygen Species	18-41	DNA damage inducible transcript 3	Homo sapiens	125-132
20372861-9	2010	Furthermore, GL63 induced the ER stress response, up-regulation of CHOP, XBP-1, ATF-4 and GRP78 expression in a dose-dependent, while curcumin had no effect on ER stress.	gl63	13-17	DNA damage inducible transcript 3	Homo sapiens	67-71
19850640-2	2010	cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is recognized as the standard chemotherapy regimen and the addition of rituximab to B-cell subtypes has been shown to significantly improve treatment outcomes.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	59-63
19850640-2	2010	cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is recognized as the standard chemotherapy regimen and the addition of rituximab to B-cell subtypes has been shown to significantly improve treatment outcomes.	Doxorubicin	18-29	DNA damage inducible transcript 3	Homo sapiens	59-63
19850640-2	2010	cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) is recognized as the standard chemotherapy regimen and the addition of rituximab to B-cell subtypes has been shown to significantly improve treatment outcomes.	Prednisone	47-57	DNA damage inducible transcript 3	Homo sapiens	59-63
19861575-1	2010	BACKGROUND: The addition of rituximab to CHOP (R-CHOP; CHOP, cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy improves outcome in patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	41-45
20495315-9	2010	6%, and 5-year OS was 100% for patients receiving the CHOP-like therapy.	Osmium	15-17	DNA damage inducible transcript 3	Homo sapiens	54-58
19647953-6	2010	RESULTS: The 5-year overall survival (OS) and disease-specific survival (DSS) improved with IFRT in both the R-CHOP (p = 0.006 and 0.02, respectively) and CHOP (p = 0.02 and p = 0.04, respectively) groups.	dss	73-76	DNA damage inducible transcript 3	Homo sapiens	111-115
19647953-6	2010	RESULTS: The 5-year overall survival (OS) and disease-specific survival (DSS) improved with IFRT in both the R-CHOP (p = 0.006 and 0.02, respectively) and CHOP (p = 0.02 and p = 0.04, respectively) groups.	dss	73-76	DNA damage inducible transcript 3	Homo sapiens	155-159
20367135-2	2010	PCP is uncommon with classical (3-weekly) R-CHOP, but the risk may be higher with biweekly R-CHOP (R-CHOP-14) due to the increased frequency of prednisolone pulses.	Prednisolone	144-156	DNA damage inducible transcript 3	Homo sapiens	93-97
20367135-2	2010	PCP is uncommon with classical (3-weekly) R-CHOP, but the risk may be higher with biweekly R-CHOP (R-CHOP-14) due to the increased frequency of prednisolone pulses.	Prednisolone	144-156	DNA damage inducible transcript 3	Homo sapiens	93-97
20367136-2	2010	Adding rituximab (R) to the initial therapy has improved outcomes; however, the benefit of ASCT for chemosensitive patients who fail R-CHOP (rituximab, cyclophosphamide, adriamycin, vincristine, prednisone) is unclear.	asct	91-95	DNA damage inducible transcript 3	Homo sapiens	135-139
20154087-7	2010	Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis.	triterpenoid TP-222	39-51	DNA damage inducible transcript 3	Homo sapiens	164-168
20154087-8	2010	We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL.	Reactive Oxygen Species	83-86	DNA damage inducible transcript 3	Homo sapiens	143-147
20154087-8	2010	We found that celastrol also induced reactive oxygen species (ROS) generation, and ROS sequestration inhibited celastrol-induced expression of CHOP and DR5, and consequent sensitization to TRAIL.	celastrol	111-120	DNA damage inducible transcript 3	Homo sapiens	143-147
20154087-7	2010	Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis.	triterpenoid TP-222	39-51	DNA damage inducible transcript 3	Homo sapiens	201-205
20154087-9	2010	Overall, our results demonstrate that celastrol can potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and up-regulation of death receptors via the ROS-mediated up-regulation of CHOP pathway.	celastrol	38-47	DNA damage inducible transcript 3	Homo sapiens	219-223
20154087-9	2010	Overall, our results demonstrate that celastrol can potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and up-regulation of death receptors via the ROS-mediated up-regulation of CHOP pathway.	Reactive Oxygen Species	189-192	DNA damage inducible transcript 3	Homo sapiens	219-223
20154087-7	2010	Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis.	celastrol	251-260	DNA damage inducible transcript 3	Homo sapiens	164-168
20154087-7	2010	Induction of the death receptor by the triterpenoid was found to be p53-independent but required the induction of CAAT/enhancer-binding protein homologous protein (CHOP), inasmuch as gene silencing of CHOP abolished the induction of DR5 expression by celastrol and associated enhancement of TRAIL-induced apoptosis.	celastrol	251-260	DNA damage inducible transcript 3	Homo sapiens	201-205
20130018-5	2010	ER stress markers such as glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and activating transcription factor (ATF)-3 were enhanced by sulindac sulfide in colon cancer cells.	sulindac sulfide	157-173	DNA damage inducible transcript 3	Homo sapiens	64-88
20032083-0	2010	Nitric oxide reduces SLC29A1 promoter activity and adenosine transport involving transcription factor complex hCHOP-C/EBPalpha in human umbilical vein endothelial cells from gestational diabetes.	Nitric Oxide	0-12	DNA damage inducible transcript 3	Homo sapiens	110-115
20032083-0	2010	Nitric oxide reduces SLC29A1 promoter activity and adenosine transport involving transcription factor complex hCHOP-C/EBPalpha in human umbilical vein endothelial cells from gestational diabetes.	Adenosine	51-60	DNA damage inducible transcript 3	Homo sapiens	110-115
19922526-5	2010	Furthermore, we analysed the expression of the ATF-4 target gene GADD153 as a function of oxygen concentration.	Oxygen	90-96	DNA damage inducible transcript 3	Homo sapiens	65-72
19922526-10	2010	CONCLUSION: Our results demonstrate the involvement of oxygen-dependent proteasomal degradation of ATF-4 in the hypoxia-induced expression of GADD153.	Oxygen	55-61	DNA damage inducible transcript 3	Homo sapiens	142-149
20130018-5	2010	ER stress markers such as glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and activating transcription factor (ATF)-3 were enhanced by sulindac sulfide in colon cancer cells.	sulindac sulfide	157-173	DNA damage inducible transcript 3	Homo sapiens	90-94
20539272-3	2010	Traditional treatments for MCL rely on conventional chemotherapy agents, including cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Prednisone	131-141	DNA damage inducible transcript 3	Homo sapiens	143-147
20305374-7	2010	Celecoxib and MG132, both alone and synergistically in combination, induced expression of the endoplasmic reticulum (ER) stress genes ATF4, CHOP, TRB3 and promoted the splicing of XBP1 mRNA.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	140-144
20305374-7	2010	Celecoxib and MG132, both alone and synergistically in combination, induced expression of the endoplasmic reticulum (ER) stress genes ATF4, CHOP, TRB3 and promoted the splicing of XBP1 mRNA.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	14-19	DNA damage inducible transcript 3	Homo sapiens	140-144
20371444-2	2010	PATIENTS AND METHODS: We retrospectively analyzed 46 patients all treated with standard chemotherapy ([CHOP] cyclophosphamide/doxorubicin/vincristine/prednisone-like); of these, 16 received rituximab.	Cyclophosphamide	109-125	DNA damage inducible transcript 3	Homo sapiens	103-107
20552750-3	2010	Traditional treatments for MCLrely on conventional chemotherapy agents, including cyclophosphamide, doxorubicin, vincristine, and prednisone(CHOP).	Prednisone	130-140	DNA damage inducible transcript 3	Homo sapiens	141-145
20198460-1	2010	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) improved the outcome of patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	88-92
19995374-0	2010	Serum concentration of L-kynurenine predicts the clinical outcome of patients with diffuse large B-cell lymphoma treated with R-CHOP.	Kynurenine	23-35	DNA damage inducible transcript 3	Homo sapiens	128-132
19995374-13	2010	CONCLUSIONS: Serum L-kynurenine might be a novel prognostic factor to determine the treatment outcome of DLBCL with the R-CHOP regimen.	Kynurenine	19-31	DNA damage inducible transcript 3	Homo sapiens	122-126
20198347-4	2010	The induction of CCAAT/enhancer-binding protein-homologous protein (CHOP) and glucose-regulated protein (GRP)-78, and ER stress-specific XBP1 splicing were found in HT29 human colon carcinoma cells treated with resveratrol.	Resveratrol	211-222	DNA damage inducible transcript 3	Homo sapiens	17-66
20198322-7	2010	ROS induced by 9-HPbD-PDT directly led to downregulated expression of Bcl-2, loss of mitochondrial membrane potential, release of cytochrome c from mitochondria, elevation of intracellular calcium due to ER stress, as well as induction of CHOP and activation of caspase-3, -8, -9 and -12.	Reactive Oxygen Species	0-3	DNA damage inducible transcript 3	Homo sapiens	239-243
20198460-1	2010	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) improved the outcome of patients with diffuse large B-cell lymphoma (DLBCL).	Prednisone	76-86	DNA damage inducible transcript 3	Homo sapiens	88-92
20198460-8	2010	In conclusion, our comparison suggests that R-CHOP may increase response and reduce relapse resulting in prolongation of progression-free survival of patients with PMBCL.	4-Methoxybenzyl chloride	164-169	DNA damage inducible transcript 3	Homo sapiens	46-50
20350662-2	2010	Until then, a combination of cyclophosphamide, vincristine, doxorubicin, and prednisone (CHOP) had been the standard of treatment for aggressive B-cell lymphoma for more than 25 years.	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	89-93
19919955-6	2010	The induction of CHOP by LPS was delayed and weak, in comparison with CHOP induction by ER stress-inducer thapsigargin.	Thapsigargin	106-118	DNA damage inducible transcript 3	Homo sapiens	70-74
19919955-9	2010	Treatment with the NO donor, SNAP (S-nitro-N-acetyl-dl-penicillamine), induces CHOP at an earlier period than LPS treatment.	snap	29-33	DNA damage inducible transcript 3	Homo sapiens	79-83
19919955-9	2010	Treatment with the NO donor, SNAP (S-nitro-N-acetyl-dl-penicillamine), induces CHOP at an earlier period than LPS treatment.	N-Acetyl-3-(nitrosulfanyl)-L-valine	35-68	DNA damage inducible transcript 3	Homo sapiens	79-83
20371724-6	2010	Treatment with panobinostat increased the levels of phosphorylated-eukaryotic translation initiation factor (p-eIF2alpha), ATF4, and CAAT/enhancer binding protein homologous protein (CHOP).	Panobinostat	15-27	DNA damage inducible transcript 3	Homo sapiens	183-187
20020442-5	2010	Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect.	Thapsigargin	18-30	DNA damage inducible transcript 3	Homo sapiens	120-124
20175544-1	2010	Rate constants for the reactions of OH radicals with isopropyl methyl methylphosphonate [(CH(3))(2)CHOP(O)(CH(3))OCH(3); IMMP] and dimethyl N,N-dimethylphosphoroamidate [(CH(3)O)(2)P(O)N(CH(3))(2); DMDMPA] have been measured over the temperature range 283-350 K and atmospheric pressure of air using a relative rate method.	oh radicals	36-47	DNA damage inducible transcript 3	Homo sapiens	99-103
20175544-1	2010	Rate constants for the reactions of OH radicals with isopropyl methyl methylphosphonate [(CH(3))(2)CHOP(O)(CH(3))OCH(3); IMMP] and dimethyl N,N-dimethylphosphoroamidate [(CH(3)O)(2)P(O)N(CH(3))(2); DMDMPA] have been measured over the temperature range 283-350 K and atmospheric pressure of air using a relative rate method.	Isopropyl methyl methylphosphonate	53-87	DNA damage inducible transcript 3	Homo sapiens	99-103
20175544-1	2010	Rate constants for the reactions of OH radicals with isopropyl methyl methylphosphonate [(CH(3))(2)CHOP(O)(CH(3))OCH(3); IMMP] and dimethyl N,N-dimethylphosphoroamidate [(CH(3)O)(2)P(O)N(CH(3))(2); DMDMPA] have been measured over the temperature range 283-350 K and atmospheric pressure of air using a relative rate method.	dmdmpa	198-204	DNA damage inducible transcript 3	Homo sapiens	99-103
20214520-1	2010	For more than 25 years, the combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was considered the "gold standard" for the treatment of aggressive lymphomas, 90% of which are diffuse large B-cell lymphomas (DLBCLs).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	102-106
20214520-1	2010	For more than 25 years, the combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was considered the "gold standard" for the treatment of aggressive lymphomas, 90% of which are diffuse large B-cell lymphomas (DLBCLs).	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	102-106
20020442-5	2010	Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect.	Tunicamycin	35-46	DNA damage inducible transcript 3	Homo sapiens	120-124
20020442-5	2010	Interestingly, in thapsigargin and tunicamycin-stressed chondrocytes induction of the proapoptotic transcription factor CHOP preceded that of the anti-apoptotic BiP by 12 h. Although both of these agents caused sustained Akt and ERK phosphorylation; inhibition of Akt phosphorylation sensitized chondrocytes to ER stress, while blocking ERK signaling by U0126 had no effect.	U 0126	354-359	DNA damage inducible transcript 3	Homo sapiens	120-124
20195409-0	2010	Severe pulmonary adverse effects in lymphoma patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen plus rituximab.	Cyclophosphamide	67-83	DNA damage inducible transcript 3	Homo sapiens	127-131
20195409-0	2010	Severe pulmonary adverse effects in lymphoma patients treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen plus rituximab.	Prednisone	115-125	DNA damage inducible transcript 3	Homo sapiens	127-131
20195409-1	2010	BACKGROUND/AIMS: The aim of our study was to determine the incidence and clinical features of severe pulmonary complications in patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) as the initial treatment for lymphoma.	Cyclophosphamide	147-163	DNA damage inducible transcript 3	Homo sapiens	207-211
20195409-1	2010	BACKGROUND/AIMS: The aim of our study was to determine the incidence and clinical features of severe pulmonary complications in patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) as the initial treatment for lymphoma.	Cyclophosphamide	147-163	DNA damage inducible transcript 3	Homo sapiens	237-243
20195409-1	2010	BACKGROUND/AIMS: The aim of our study was to determine the incidence and clinical features of severe pulmonary complications in patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or rituximab plus CHOP (R-CHOP) as the initial treatment for lymphoma.	Prednisone	195-205	DNA damage inducible transcript 3	Homo sapiens	207-211
20195409-5	2010	DIIP occurred in five patients in the R-CHOP arm (7%) and in one in the CHOP arm (3%).	diip	0-4	DNA damage inducible transcript 3	Homo sapiens	38-44
20195409-5	2010	DIIP occurred in five patients in the R-CHOP arm (7%) and in one in the CHOP arm (3%).	diip	0-4	DNA damage inducible transcript 3	Homo sapiens	40-44
19931551-5	2010	ER redox alterations and early ER-stress-related signaling events induced by acetaminophen, such as ER glutathione depletion, phosphorylation of eIF2alpha and JNK and induction of the transcription factor GADD153, were not counteracted by co-treatment with BGP-15.	Acetaminophen	77-90	DNA damage inducible transcript 3	Homo sapiens	205-212
19782747-12	2010	Indeed, a reduction in PKCdelta protein levels reduced thapsigargin-stimulated CHOP induction, a hallmark of the UPR, but not BiP/GRP78 induction, suggesting that PKCdelta does not globally regulate the UPR.	Thapsigargin	55-67	DNA damage inducible transcript 3	Homo sapiens	79-83
19878647-5	2010	Several key players of the unfolded protein response, including GRP78, GADD153, ATF6, XBP1 and eIF2alpha are expressed and activated in PMNs treated with ATO or other ER stress inducers.	Arsenic Trioxide	154-157	DNA damage inducible transcript 3	Homo sapiens	71-78
20154500-13	2010	The reason why CHOP-resistant ATLL responded dramatically to SBZ alone is not clear, but the plasma concentration of the metabolite of SBZ was possibly very high because of renal failure.	sobuzoxane	61-64	DNA damage inducible transcript 3	Homo sapiens	15-19
20154500-13	2010	The reason why CHOP-resistant ATLL responded dramatically to SBZ alone is not clear, but the plasma concentration of the metabolite of SBZ was possibly very high because of renal failure.	sobuzoxane	135-138	DNA damage inducible transcript 3	Homo sapiens	15-19
20141329-7	2010	Knockdown of CHOP by siRNA significantly reduced the HSA-induced apoptosis of HKC.	Altretamine	53-56	DNA damage inducible transcript 3	Homo sapiens	13-17
20141329-9	2010	Furthermore, knockdown of PERK significantly inhibited HSA-induced CHOP expression, suppressing apoptosis in HKCs by 2.48-fold compared to controls.	Altretamine	55-58	DNA damage inducible transcript 3	Homo sapiens	67-71
20023394-0	2010	Phospho-DeltaNp63alpha/NF-Y protein complex transcriptionally regulates DDIT3 expression in squamous cell carcinoma cells upon cisplatin exposure.	Cisplatin	127-136	DNA damage inducible transcript 3	Homo sapiens	72-77
20023394-7	2010	In contrast to the non-phosphorylated DeltaNp63alpha-S385G, the phospho-DeltaNp63alpha forms protein-protein complexes with NF-YA transcription factor and regulates the transcription of DDIT3 gene implicated in the programmed cell death of HNSCC cells upon cisplatin exposure.	Cisplatin	257-266	DNA damage inducible transcript 3	Homo sapiens	186-191
20122151-7	2010	Thapsigargin, a Ca2+-ATPase inhibitor, did not change the expression of GRP78, an ER chaperone in OASF and RASF, but induced another ER stress protein, CCAAT/enhancer binding protein (C/EBP) homologous protein (CHOP) differently, showing high levels in OASF and low levels in RASF.	Thapsigargin	0-12	DNA damage inducible transcript 3	Homo sapiens	211-215
21096927-4	2010	CO(2) is provided by a cylinder that delivers a stable flux, which is converted to a pulsatile mode through a high frequency solenoid valve that can chop it up to 1 kHz.	co(2)	0-5	DNA damage inducible transcript 3	Homo sapiens	149-153
20110775-9	2010	Further, bortezomib-treated breast cancer cells showed induction of the unfolded protein response, with upregulation of CH OP and GRP78.	Bortezomib	9-19	DNA damage inducible transcript 3	Homo sapiens	120-125
20110775-11	2010	Knockdown of CH OP and/or BNIP3 expression via RNAi targeting significantly attenuated the death-promoting effects of bortezomib.	Bortezomib	118-128	DNA damage inducible transcript 3	Homo sapiens	13-18
19723703-0	2010	Antiapoptotic roles of ceramide-synthase-6-generated C16-ceramide via selective regulation of the ATF6/CHOP arm of ER-stress-response pathways.	N-palmitoylsphingosine	53-65	DNA damage inducible transcript 3	Homo sapiens	103-107
19723703-6	2010	Mechanistically, regulation of ER-stress-induced apoptosis by CerS6/C(16)-ceramide was linked to the activation of a specific arm, ATF6/CHOP, of the unfolded protein response pathway.	Ceramides	74-82	DNA damage inducible transcript 3	Homo sapiens	136-140
20930302-4	2010	NaHS also significantly attenuated Abeta-induced LDH release and the up-regulation of protein expression of growth arrest DNA damage (GADD 153).	sodium bisulfide	0-4	DNA damage inducible transcript 3	Homo sapiens	134-142
19773801-8	2010	ER stress agent tunicamycin induced ARMET and CHOP expressions in the primary cultured neurons.	Tunicamycin	16-27	DNA damage inducible transcript 3	Homo sapiens	46-50
19722195-6	2010	Furthermore, the PERK-ATF4 pathway, which also induces the expression of CHOP, was activated in NAC-treated cells.	Acetylcysteine	96-99	DNA damage inducible transcript 3	Homo sapiens	73-77
19722195-7	2010	The role of the ER stress pathway was further confirmed through the small interfering RNA (siRNA)-mediated knockdown of CHOP, which attenuated NAC and PEN-induced apoptosis.	Acetylcysteine	143-146	DNA damage inducible transcript 3	Homo sapiens	120-124
19722195-7	2010	The role of the ER stress pathway was further confirmed through the small interfering RNA (siRNA)-mediated knockdown of CHOP, which attenuated NAC and PEN-induced apoptosis.	Penicillamine	151-154	DNA damage inducible transcript 3	Homo sapiens	120-124
20043261-0	2010	Selenium decreases thyroid cancer cell growth by increasing expression of GADD153 and GADD34.	Selenium	0-8	DNA damage inducible transcript 3	Homo sapiens	74-81
19835916-9	2010	The unfolded protein response (UPR) study showed that thapsigargin increased eIF2alpha phosphorylation and nuclear GADD153/CHOP induction under alpha-synuclein overexpressed conditions.	Thapsigargin	54-66	DNA damage inducible transcript 3	Homo sapiens	115-122
19835916-9	2010	The unfolded protein response (UPR) study showed that thapsigargin increased eIF2alpha phosphorylation and nuclear GADD153/CHOP induction under alpha-synuclein overexpressed conditions.	Thapsigargin	54-66	DNA damage inducible transcript 3	Homo sapiens	123-127
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	27-31
20302754-12	2010	Ten patients received adjuvant chemotherapy with the regimen of CHOP (cyclophosphamide + epirubicin + vincristine + prednisone) after the operation.	Cyclophosphamide	70-86	DNA damage inducible transcript 3	Homo sapiens	64-68
19934253-3	2010	Low concentration of anisomycin induces CHOP expression at both transcriptional and translational levels.	Anisomycin	21-31	DNA damage inducible transcript 3	Homo sapiens	40-44
19934253-5	2010	Here we show that anisomycin-induced CHOP expression depends on phosphorylated eIF4E/S209 and eIF2alpha/S51.	Anisomycin	18-28	DNA damage inducible transcript 3	Homo sapiens	37-41
19934253-9	2010	Furthermore, mutating the uORF sequence abolished the anisomycin-induced association of chop mRNA with phospho-eIF4E and polysomes, thus demonstrating the significance of this cis-regulatory element in conferring on the transcript a stress-responsive translational inducibility.	Anisomycin	54-64	DNA damage inducible transcript 3	Homo sapiens	88-92
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	131-135
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Doxorubicin	51-62	DNA damage inducible transcript 3	Homo sapiens	27-31
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Vincristine	64-75	DNA damage inducible transcript 3	Homo sapiens	131-135
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	27-31
20016232-2	2009	Conventional chemotherapy (CHOP: cyclophosphamide, doxorubicin, vincristine, prednisone) seems unsatisfactory, so modifications of CHOP are used to improve the efficacy.	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	131-135
20068280-1	2009	Here we report three cases of hepatitis B virus (HBV) reactivation after cessation of preemptive lamivudine therapy in B-cell lymphoma patients treated with rituximab plus CHOP (R-CHOP).	Lamivudine	97-107	DNA damage inducible transcript 3	Homo sapiens	178-184
19017364-6	2009	Moreover, our studies reveal that HSP70 knockdown or quercetin induces other typical components of the UPR, including CHOP expression, eIF2alpha and JNK phosphorylation, caspases activation and XBP-1 splicing.	Quercetin	53-62	DNA damage inducible transcript 3	Homo sapiens	118-122
19699254-6	2009	Capsaicin treatment triggered ER stress by increasing levels of IRE1, GADD153/Chop, GRP78/Bip, and activated caspase-4.	Capsaicin	0-9	DNA damage inducible transcript 3	Homo sapiens	78-82
19861288-1	2009	Treatment with cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been considered as the standard therapy for diffuse large B-cell lymphoma (DLBCL) for more than 20 years.	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	76-80
19861288-1	2009	Treatment with cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been considered as the standard therapy for diffuse large B-cell lymphoma (DLBCL) for more than 20 years.	Doxorubicin	33-44	DNA damage inducible transcript 3	Homo sapiens	76-80
19861288-1	2009	Treatment with cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been considered as the standard therapy for diffuse large B-cell lymphoma (DLBCL) for more than 20 years.	Prednisolone	62-74	DNA damage inducible transcript 3	Homo sapiens	76-80
19699254-6	2009	Capsaicin treatment triggered ER stress by increasing levels of IRE1, GADD153/Chop, GRP78/Bip, and activated caspase-4.	Capsaicin	0-9	DNA damage inducible transcript 3	Homo sapiens	70-77
19757311-4	2009	PKC-beta II expression correlated with inferior overall survival (OS) and progression-free survival (PFS) in CHOP-treated patients with low-risk International Prognostic Index (IPI) disease (0-2 adverse factors), but not in the overall patient group unstratified by IPI.	diprotin A	177-180	DNA damage inducible transcript 3	Homo sapiens	109-113
19593797-12	2009	CONCLUSIONS: R-CHOP + bortezomib was an effective regimen and produced an 84% CR rate.	Chromium	78-80	DNA damage inducible transcript 3	Homo sapiens	15-19
19381687-0	2009	Serum soluble Fas level determines clinical outcome of patients with diffuse large B-cell lymphoma treated with CHOP and R-CHOP.	ammonium ferrous sulfate	14-17	DNA damage inducible transcript 3	Homo sapiens	112-116
19381687-0	2009	Serum soluble Fas level determines clinical outcome of patients with diffuse large B-cell lymphoma treated with CHOP and R-CHOP.	ammonium ferrous sulfate	14-17	DNA damage inducible transcript 3	Homo sapiens	123-127
19381687-1	2009	INTRODUCTION: We previously reported that serum concentrations of soluble Fas (sFas) predict the clinical outcome of patients with diffuse large B cell lymphoma (DLBCL) after treatment with CHOP but without rituximab (R).	ammonium ferrous sulfate	74-77	DNA damage inducible transcript 3	Homo sapiens	190-194
19442655-11	2009	After Cd exposure, GADD153, a hallmark of ER stress, was upregulated (at 4h of exposure), followed by activation of ER-specific caspase-12 and its downstream molecule caspase-3 (at 16h of exposure).	Cadmium	6-8	DNA damage inducible transcript 3	Homo sapiens	19-26
19395464-3	2009	METHODS: Tumor specimens from 23 patients with previously untreated NK/T-cell lymphoma initially treated with cyclophosphamide, vincristine, doxorubicin and prednisone (CHOP) or CHOP-based chemotherapy were examined by immunohistochemistry for three NF-kappaB subunits (p65, p50 and p52), which are involved in either the canonical or alternative pathway.	Prednisone	157-167	DNA damage inducible transcript 3	Homo sapiens	169-173
19205655-8	2009	IPI is still important in predicting the prognosis in the R-CHOP era in DLBCL; however, obtaining CR after four cycles of R-CHOP and presence of bulky disease should be considered together.	diprotin A	0-3	DNA damage inducible transcript 3	Homo sapiens	60-64
19776000-1	2009	BACKGROUND: The results of CHOP-21 (cyclophosphamide, doxorubicin, vincristine and prednisone given every 21 days) for the treatment of aggressive B-cell lymphoma have recently been improved by the addition of rituximab and by increasing the dose density.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	27-31
19407336-5	2009	PFOA concentrations of 30 microM and above caused cell injury characterized by the expression of Ddit3.	perfluorooctanoic acid	0-4	DNA damage inducible transcript 3	Homo sapiens	97-102
19671747-7	2009	Importantly, knockdown of CHOP by small interference RNA antagonizes the TZD18-induced apoptosis, indicating a crucial role of CHOP in the apoptotic process triggered by TZD18.	5-(3-(3-(4-phenoxy-2-propylphenoxy)propoxy)phenyl)-2,4-thiazolidinedione	73-78	DNA damage inducible transcript 3	Homo sapiens	26-30
19671747-7	2009	Importantly, knockdown of CHOP by small interference RNA antagonizes the TZD18-induced apoptosis, indicating a crucial role of CHOP in the apoptotic process triggered by TZD18.	5-(3-(3-(4-phenoxy-2-propylphenoxy)propoxy)phenyl)-2,4-thiazolidinedione	73-78	DNA damage inducible transcript 3	Homo sapiens	127-131
19525224-1	2009	Patients presenting with diffuse large B cell lymphoma (DLBCL) are treated with a standard anthracycline-based chemotherapeutic mixture consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Anthracyclines	91-104	DNA damage inducible transcript 3	Homo sapiens	210-214
19153735-4	2009	Low concentrations of selenite elicited mild endoplasmic reticulum (ER) stress and mediated cell survival by activating unfolded protein response signaling, whereas high concentrations of selenite induced severe ER stress and caused cell death by activation of the pro-apoptotic transcription factors GADD153.	Selenious Acid	188-196	DNA damage inducible transcript 3	Homo sapiens	301-308
19461054-8	2009	Moreover, DHMEQ induced the expression of genes involved in the endoplasmic reticulum stress response (GRP78, CHOP, TRB3) and promoted the splicing of XBP1 mRNA in a dose-dependent fashion in both cell lines, which was reversed in the presence of NAC.	dehydroxymethylepoxyquinomicin	10-15	DNA damage inducible transcript 3	Homo sapiens	110-114
19496708-2	2009	Association of rituximab with chemotherapy (mostly the cyclophosphamide, doxorubicin, vincristine and prednisolone [CHOP] regimen) in diffuse large B-cell lymphoma (DLBCL) represents an extraordinary revolution in the prognosis of DLBCL, and is the new standard of therapy in elderly and young, low-risk patients.	Prednisolone	102-114	DNA damage inducible transcript 3	Homo sapiens	116-120
19345731-5	2009	Interestingly, a Wit A-induced increase in ROS levels preceded the up-regulation of CHOP and DR5.	Reactive Oxygen Species	43-46	DNA damage inducible transcript 3	Homo sapiens	84-88
19345731-6	2009	The involvement of ROS in CHOP-mediated DR5 up-regulation was confirmed by the result that pretreatment with an antioxidant, NAC or catalase, inhibited Wit A-induced up-regulation of both CHOP and DR5.	Reactive Oxygen Species	19-22	DNA damage inducible transcript 3	Homo sapiens	26-30
19345731-6	2009	The involvement of ROS in CHOP-mediated DR5 up-regulation was confirmed by the result that pretreatment with an antioxidant, NAC or catalase, inhibited Wit A-induced up-regulation of both CHOP and DR5.	Reactive Oxygen Species	19-22	DNA damage inducible transcript 3	Homo sapiens	188-192
19707509-10	2009	Cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) were administered for a total of 4 cycles.	Prednisone	47-57	DNA damage inducible transcript 3	Homo sapiens	59-63
19188481-4	2009	DHE triggered endoplasmic reticulum (ER) stress, as indicated by changes in cytosol-calcium levels, double-stranded RNA-activated protein kinase-like endoplasmic reticulum kinase phosphorylation, inositol-requiring protein 1 (IRE1) and CHOP/GADD153 up-regulation, X-box transcription factor-1 mRNA splicing, and caspase-4 activation.	Dihydroergotamine	0-3	DNA damage inducible transcript 3	Homo sapiens	236-240
19627200-7	2009	Isoflavones also suppressed ER stress as determined by decreased expressions of the immunoglobulin binding protein (BiP) mRNA, spliced X-box binding protein-1 (Xbp-1) mRNAs, and C/EBP homologous protein (CHOP).	Isoflavones	0-11	DNA damage inducible transcript 3	Homo sapiens	178-202
19627200-7	2009	Isoflavones also suppressed ER stress as determined by decreased expressions of the immunoglobulin binding protein (BiP) mRNA, spliced X-box binding protein-1 (Xbp-1) mRNAs, and C/EBP homologous protein (CHOP).	Isoflavones	0-11	DNA damage inducible transcript 3	Homo sapiens	204-208
19420259-5	2009	In Tsc2-deficient neurons, the expression of stress markers such as CHOP and HO-1 is increased, and this increase is completely reversed by the mTOR inhibitor rapamycin both in vitro and in vivo.	Sirolimus	159-168	DNA damage inducible transcript 3	Homo sapiens	68-72
19476545-7	2009	The mRNA and protein levels of CHOP, an ER stress-responsive gene, were remarkably increased by APP over-expression, which was attenuated by treatment with DAPT.	dapt	156-160	DNA damage inducible transcript 3	Homo sapiens	31-35
19391038-2	2009	Here, we have demonstrated that bortezomib targets the prototypical expression of unfolded protein response (UPR) genes BiP, CHOP and XBP-1 at the mRNA and protein levels, resulting in induction of proapoptotic UPR outputs and suppression of cytoprotective UPR components, leading to caspase-dependent apoptosis in human MM H929 and 8226/S cell lines.	Bortezomib	32-42	DNA damage inducible transcript 3	Homo sapiens	125-129
19037087-0	2009	Rottlerin induces apoptosis via death receptor 5 (DR5) upregulation through CHOP-dependent and PKC delta-independent mechanism in human malignant tumor cells.	rottlerin	0-9	DNA damage inducible transcript 3	Homo sapiens	76-80
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	0-9	DNA damage inducible transcript 3	Homo sapiens	54-103
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	0-9	DNA damage inducible transcript 3	Homo sapiens	105-109
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	0-9	DNA damage inducible transcript 3	Homo sapiens	218-222
19037087-5	2009	Rottlerin-induced DR5 upregulation was accompanied by CCAAT/enhancer-binding protein-homologous protein (CHOP) protein expression and rottlerin-induced increase of DR5 promoter activity was diminished by mutation of a CHOP-binding site of DR5 promoter.	rottlerin	134-143	DNA damage inducible transcript 3	Homo sapiens	218-222
19188481-4	2009	DHE triggered endoplasmic reticulum (ER) stress, as indicated by changes in cytosol-calcium levels, double-stranded RNA-activated protein kinase-like endoplasmic reticulum kinase phosphorylation, inositol-requiring protein 1 (IRE1) and CHOP/GADD153 up-regulation, X-box transcription factor-1 mRNA splicing, and caspase-4 activation.	Dihydroergotamine	0-3	DNA damage inducible transcript 3	Homo sapiens	241-248
19233273-5	2009	The same doses of rotenone that reduced ATP production also induced dose-dependent increases in PERK and eIF2alpha phosphorylation as well as activated the ISR stress genes, ATF4 and CHOP.	Rotenone	18-26	DNA damage inducible transcript 3	Homo sapiens	183-187
19386233-4	2009	Exposure of human dopaminergic cell line SH-SY5Y to the ER stressor brefeldin A led to Golgi disassembly, activation of the unfolded protein response (UPR), and subsequent expression of the proapoptotic mediator GADD153/CHOP.	Brefeldin A	68-79	DNA damage inducible transcript 3	Homo sapiens	212-219
19386233-4	2009	Exposure of human dopaminergic cell line SH-SY5Y to the ER stressor brefeldin A led to Golgi disassembly, activation of the unfolded protein response (UPR), and subsequent expression of the proapoptotic mediator GADD153/CHOP.	Brefeldin A	68-79	DNA damage inducible transcript 3	Homo sapiens	220-224
19386233-5	2009	In this context, PF9601N pretreatment prevented brefeldin A-induced UPR responses, thus blocking the expression of GADD153/CHOP and resulting apoptotic features.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	17-24	DNA damage inducible transcript 3	Homo sapiens	115-122
19386233-5	2009	In this context, PF9601N pretreatment prevented brefeldin A-induced UPR responses, thus blocking the expression of GADD153/CHOP and resulting apoptotic features.	N-(2-propynyl)-2-(5-benzyloxy-indolyl) methylamine	17-24	DNA damage inducible transcript 3	Homo sapiens	123-127
19386233-5	2009	In this context, PF9601N pretreatment prevented brefeldin A-induced UPR responses, thus blocking the expression of GADD153/CHOP and resulting apoptotic features.	Brefeldin A	48-59	DNA damage inducible transcript 3	Homo sapiens	115-122
19386233-5	2009	In this context, PF9601N pretreatment prevented brefeldin A-induced UPR responses, thus blocking the expression of GADD153/CHOP and resulting apoptotic features.	Brefeldin A	48-59	DNA damage inducible transcript 3	Homo sapiens	123-127
19233273-5	2009	The same doses of rotenone that reduced ATP production also induced dose-dependent increases in PERK and eIF2alpha phosphorylation as well as activated the ISR stress genes, ATF4 and CHOP.	Adenosine Triphosphate	40-43	DNA damage inducible transcript 3	Homo sapiens	183-187
19302589-6	2009	HMA dose-dependently increased the transcription of the ER stress genes GADD153 and GADD34 and rapidly depleted [Ca(2+)](ER), mimicking the effects of the sarco/endoplasmic reticulum ATPase (SERCA) inhibitor thapsigargin.	5-(N,N-hexamethylene)amiloride	0-3	DNA damage inducible transcript 3	Homo sapiens	72-79
19414399-7	2009	EGCG decreased the protein levels of Bcl-2, Bcl-xl, xIAP, cIAP, Hsp70 and Hsp90, but increased the protein expression of Bad, Bax, Fas/CD95, cytochrome c, Apaf-1, AIF, GADD153, GRP78, and caspase-3, -7,-8 and -9 as observed by Western blotting examination.	epigallocatechin gallate	0-4	DNA damage inducible transcript 3	Homo sapiens	168-175
19096011-3	2009	Strikingly, the early transcriptional response of cells treated with pristimerin closely resembles cellular responses elicited by proteosome inhibitors, with rapid induction of heat shock proteins, activating transcription factor 3 (ATF3), and CHOP.	pristimerin	69-80	DNA damage inducible transcript 3	Homo sapiens	244-248
19029441-6	2009	The latter had a markedly inferior survival when treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or rituximab-CHOP (R-CHOP; median survival of 1.2 and 3.0 years vs not reached for the others, P &lt; .001 and P = .001), independent of the International Prognostic Index.	Prednisone	110-120	DNA damage inducible transcript 3	Homo sapiens	122-126
19190324-6	2009	Mechanism analysis revealed that bortezomib-surviving quiescent cells attenuate eIF2alpha phosphorylation and induction of the ER stress proapoptotic gene GADD153.	Bortezomib	33-43	DNA damage inducible transcript 3	Homo sapiens	155-162
19326060-1	2009	We conducted a retrospective analysis to evaluate the impact on clinical outcomes of adding rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) treatment for diffuse large B-cell lymphoma (DLBCL) patients in Japan.	Prednisone	153-163	DNA damage inducible transcript 3	Homo sapiens	165-169
19309523-7	2009	However for overall response (CR+Partial response, PR), R-CHOP was superior, with odds ratios of 5.45 (95% CI: 2.51 - 11.83) and 5.54 (95% CI: 2.69 - 11.40), for the first and second analyses, respectively.	Chromium	30-32	DNA damage inducible transcript 3	Homo sapiens	58-62
19074749-1	2009	BACKGROUND: Soluble interleukin-2 receptor (SIL-2R) is known to be a prognostic parameter in patients with diffuse large B-cell lymphoma (DLBCL) receiving cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy.	Doxorubicin	173-184	DNA damage inducible transcript 3	Homo sapiens	214-218
19074749-1	2009	BACKGROUND: Soluble interleukin-2 receptor (SIL-2R) is known to be a prognostic parameter in patients with diffuse large B-cell lymphoma (DLBCL) receiving cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy.	Vincristine	186-197	DNA damage inducible transcript 3	Homo sapiens	214-218
19074749-1	2009	BACKGROUND: Soluble interleukin-2 receptor (SIL-2R) is known to be a prognostic parameter in patients with diffuse large B-cell lymphoma (DLBCL) receiving cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy.	Prednisone	202-212	DNA damage inducible transcript 3	Homo sapiens	214-218
19669383-0	2009	A case of lamivudine-sensitive de novo acute hepatitis B induced by rituximab with the CHOP regimen for diffuse large B cell lymphoma.	Lamivudine	10-20	DNA damage inducible transcript 3	Homo sapiens	87-91
19139269-7	2009	DHC induced ER stress by the action of heavy chain-binding protein, IRE1, Chop, eukaryotic initiation factor 2alpha, and caspase-4 and, to a lesser level, by capsaicin treatment.	dihydrocapsaicin	0-3	DNA damage inducible transcript 3	Homo sapiens	74-78
19139269-10	2009	Knockdown of Ire1 down-regulated the DHC-induced Chop and LC3II and enhanced caspase-3 activation.	dihydrocapsaicin	37-40	DNA damage inducible transcript 3	Homo sapiens	49-53
19139269-12	2009	The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal].	pyrazolanthrone	18-26	DNA damage inducible transcript 3	Homo sapiens	66-70
19139269-12	2009	The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal].	dihydrocapsaicin	93-96	DNA damage inducible transcript 3	Homo sapiens	66-70
19139269-12	2009	The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal].	Thapsigargin	98-110	DNA damage inducible transcript 3	Homo sapiens	66-70
19139269-12	2009	The JNK inhibitor SP600125 down-regulated the expression of IRE1, Chop, and LC3II induced by DHC, thapsigargin, and MG132 [N-benzoyloxycarbonyl (Z)-Leu-Leu-leucinal].	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	116-121	DNA damage inducible transcript 3	Homo sapiens	66-70
19107326-5	2009	Up regulation of GADD-153, GRP-78, with more pronounced expression in PGN vs. NPGN (P &lt; 0.05) and down regulation of Bcl-2 proteins was observed in the GN (PGD excluding MCD) as compared to MCD (P &lt; 0.05).	pgn	70-73	DNA damage inducible transcript 3	Homo sapiens	17-25
19276283-7	2009	This group showed a better FFS (P = 0.01) and a lower probability of progression (P = 0.004) compared with other genotype groups when treated with R-CHOP chemotherapy.	CHEMBL1198227	27-30	DNA damage inducible transcript 3	Homo sapiens	147-153
19023330-4	2009	We also show that loss of HtrA2 results in the accumulation of unfolded proteins in the mitochondria, defective mitochondrial respiration and enhanced production of reactive oxygen species that contribute to the induction of CHOP expression and to neuronal cell death.	Oxygen	174-180	DNA damage inducible transcript 3	Homo sapiens	225-229
19007793-5	2009	Furthermore, PACT-induced PKR activation is essential for tunicamycin-induced apoptosis, since PACT as well as PKR null cells are markedly resistant to tunicamycin and show defective eIF2alpha phosphorylation and C/EBP homologous protein (CHOP, also known as GADD153) induction especially at low concentrations of tunicamycin.	Tunicamycin	58-69	DNA damage inducible transcript 3	Homo sapiens	213-237
19036081-10	2009	In conclusion, high-dose Ara-C and BEAM with stem cell rescue in newly diagnosed MCL patients responsive to R-CHOP is a manageable treatment with respect to toxicity.	Cytarabine	25-30	DNA damage inducible transcript 3	Homo sapiens	110-114
19130236-4	2009	siRNA was used to detect the effect of GADD153 on selenite-induced cell apoptosis.	Selenious Acid	50-58	DNA damage inducible transcript 3	Homo sapiens	39-46
19007793-5	2009	Furthermore, PACT-induced PKR activation is essential for tunicamycin-induced apoptosis, since PACT as well as PKR null cells are markedly resistant to tunicamycin and show defective eIF2alpha phosphorylation and C/EBP homologous protein (CHOP, also known as GADD153) induction especially at low concentrations of tunicamycin.	Tunicamycin	58-69	DNA damage inducible transcript 3	Homo sapiens	239-243
19007793-5	2009	Furthermore, PACT-induced PKR activation is essential for tunicamycin-induced apoptosis, since PACT as well as PKR null cells are markedly resistant to tunicamycin and show defective eIF2alpha phosphorylation and C/EBP homologous protein (CHOP, also known as GADD153) induction especially at low concentrations of tunicamycin.	Tunicamycin	58-69	DNA damage inducible transcript 3	Homo sapiens	259-266
18992716-0	2009	Retinoic acid modulates retinaldehyde dehydrogenase 1 gene expression through the induction of GADD153-C/EBPbeta interaction.	Tretinoin	0-13	DNA damage inducible transcript 3	Homo sapiens	95-102
18992716-7	2009	Treatment with RA increases GADD153 and GADD153-C/EBPbeta interaction resulting in a decreased cellular availability of C/EBPbeta for binding to the Raldh1 CCAAT box.	Tretinoin	15-17	DNA damage inducible transcript 3	Homo sapiens	28-35
18992716-7	2009	Treatment with RA increases GADD153 and GADD153-C/EBPbeta interaction resulting in a decreased cellular availability of C/EBPbeta for binding to the Raldh1 CCAAT box.	Tretinoin	15-17	DNA damage inducible transcript 3	Homo sapiens	40-47
18992716-8	2009	These data support a model in which high RA levels inhibit Raldh1 gene expression by sequestering C/EBPbeta through its interaction to GADD153.	Tretinoin	41-43	DNA damage inducible transcript 3	Homo sapiens	135-142
19331147-7	2009	Immunostaining and confocal microscopic analysis also showed that capsaicin promoted cytoplasmic GADD153 expression and GRP78 nuclear translocation.	Capsaicin	66-75	DNA damage inducible transcript 3	Homo sapiens	97-104
18620786-2	2009	In phase 3 clinical trials, giving rituximab with cyclophosphamide, vincristine, doxorubicin, and prednisone (CHOP) every 3 weeks (R-CHOP-21) has been associated with improved survival, without increased toxicity, in all patient groups studied.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	110-114
18620786-2	2009	In phase 3 clinical trials, giving rituximab with cyclophosphamide, vincristine, doxorubicin, and prednisone (CHOP) every 3 weeks (R-CHOP-21) has been associated with improved survival, without increased toxicity, in all patient groups studied.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	133-137
18620786-2	2009	In phase 3 clinical trials, giving rituximab with cyclophosphamide, vincristine, doxorubicin, and prednisone (CHOP) every 3 weeks (R-CHOP-21) has been associated with improved survival, without increased toxicity, in all patient groups studied.	Prednisone	98-108	DNA damage inducible transcript 3	Homo sapiens	110-114
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	15-26	DNA damage inducible transcript 3	Homo sapiens	63-111
19903162-4	2009	The transcription of genes is affected in cancer cells treated with polyisoprenylated benzophenones; the oncogene c-Myb is down-regulated and endoplasmatic stress genes XBP1, ATF4, and DDIT3/CHOP are turned on.	Benzophenones	86-99	DNA damage inducible transcript 3	Homo sapiens	185-190
19903162-4	2009	The transcription of genes is affected in cancer cells treated with polyisoprenylated benzophenones; the oncogene c-Myb is down-regulated and endoplasmatic stress genes XBP1, ATF4, and DDIT3/CHOP are turned on.	Benzophenones	86-99	DNA damage inducible transcript 3	Homo sapiens	191-195
19182512-14	2009	Knocking down GADD153 by siRNA also reduced the cell killing effect of MSA/taxane.	methylselenic acid	71-74	DNA damage inducible transcript 3	Homo sapiens	14-21
19182512-14	2009	Knocking down GADD153 by siRNA also reduced the cell killing effect of MSA/taxane.	taxane	75-81	DNA damage inducible transcript 3	Homo sapiens	14-21
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	15-26	DNA damage inducible transcript 3	Homo sapiens	113-120
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	15-26	DNA damage inducible transcript 3	Homo sapiens	135-159
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	15-26	DNA damage inducible transcript 3	Homo sapiens	161-165
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	28-31	DNA damage inducible transcript 3	Homo sapiens	63-111
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	28-31	DNA damage inducible transcript 3	Homo sapiens	113-120
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	28-31	DNA damage inducible transcript 3	Homo sapiens	135-159
21783934-1	2009	The effects of tributyltin (TBT) exposure on the expression of growth arrest- and DNA damage-inducible gene 153 (GADD153), also called C/EBP homologous protein (CHOP), were examined in SH-SY5Y human neuroblastoma cells.	tributyltin	28-31	DNA damage inducible transcript 3	Homo sapiens	161-165
21783934-2	2009	In response to TBT exposure, the levels of both GADD153 mRNA and GADD153 protein increased significantly.	tributyltin	15-18	DNA damage inducible transcript 3	Homo sapiens	48-55
21783934-2	2009	In response to TBT exposure, the levels of both GADD153 mRNA and GADD153 protein increased significantly.	tributyltin	15-18	DNA damage inducible transcript 3	Homo sapiens	65-72
21783934-4	2009	Treatment with the JNK inhibitor, SP600125, markedly suppressed TBT-induced GADD153 expression.	pyrazolanthrone	34-42	DNA damage inducible transcript 3	Homo sapiens	76-83
21783934-4	2009	Treatment with the JNK inhibitor, SP600125, markedly suppressed TBT-induced GADD153 expression.	tributyltin	64-67	DNA damage inducible transcript 3	Homo sapiens	76-83
21783934-5	2009	TBT may induce the expression of GADD153, a gene highly responsive to endoplasmic reticulum (ER) stress, in a manner at least partially dependent upon the JNK pathway in SH-SY5Y cells.	tributyltin	0-3	DNA damage inducible transcript 3	Homo sapiens	33-40
19114067-4	2009	Moreover, pranoprofen inhibited ER stress-induced CCAAT/enhancer-binding protein homologous protein (CHOP) expression, an apoptotic transcription factor.	pyranoprofen	10-21	DNA damage inducible transcript 3	Homo sapiens	50-99
19293492-7	2009	Treatment with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus etoposide established complete remission.	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	75-79
19293492-7	2009	Treatment with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus etoposide established complete remission.	Prednisone	63-73	DNA damage inducible transcript 3	Homo sapiens	75-79
19204436-5	2009	There was significant improvement in response to the first 4 cycles of CHOP chemotherapy (consisting of cyclophosphamide, doxorubicin, vincristine and prednisolone) instituted, but then there were features of relapse.	Cyclophosphamide	104-120	DNA damage inducible transcript 3	Homo sapiens	71-75
19204436-5	2009	There was significant improvement in response to the first 4 cycles of CHOP chemotherapy (consisting of cyclophosphamide, doxorubicin, vincristine and prednisolone) instituted, but then there were features of relapse.	Doxorubicin	122-133	DNA damage inducible transcript 3	Homo sapiens	71-75
19204436-5	2009	There was significant improvement in response to the first 4 cycles of CHOP chemotherapy (consisting of cyclophosphamide, doxorubicin, vincristine and prednisolone) instituted, but then there were features of relapse.	Vincristine	135-146	DNA damage inducible transcript 3	Homo sapiens	71-75
19204436-5	2009	There was significant improvement in response to the first 4 cycles of CHOP chemotherapy (consisting of cyclophosphamide, doxorubicin, vincristine and prednisolone) instituted, but then there were features of relapse.	Prednisolone	151-163	DNA damage inducible transcript 3	Homo sapiens	71-75
19114067-4	2009	Moreover, pranoprofen inhibited ER stress-induced CCAAT/enhancer-binding protein homologous protein (CHOP) expression, an apoptotic transcription factor.	pyranoprofen	10-21	DNA damage inducible transcript 3	Homo sapiens	101-105
19114067-8	2009	Thus, the inhibitory effect of pranoprofen on ER stress-related genes (GRP78 and CHOP) would be mediated through the inhibition of XBP-1 splicing.	pyranoprofen	31-42	DNA damage inducible transcript 3	Homo sapiens	81-85
19129918-9	2009	Salubrinal further aggravated ER-stress and proteotoxicity inflicted by the proteasome inhibitors on the leukemic cells since characteristic ER stress responses, such as ATF4 and CHOP synthesis, XBP1 splicing, activation of MAP kinases and eventually apoptosis were efficiently abrogated by the translational inhibitor cycloheximide.	salubrinal	0-10	DNA damage inducible transcript 3	Homo sapiens	179-183
18679584-2	2008	RT-PCR analyses showed up-regulation of CHOP/GADD153 and splicing of XBP-1 mRNA in brefeldin A-treated cells.	Brefeldin A	83-94	DNA damage inducible transcript 3	Homo sapiens	40-44
18701210-5	2008	GADD153 and GRP78 were increased by curcumin which was indicative of ER stress.	Curcumin	36-44	DNA damage inducible transcript 3	Homo sapiens	0-7
19018773-9	2008	Overexpression of CHOP in AsPC-1 cells increased radiation sensitivity by IGF-II simulation under hypoxic conditions, whereas suppression of CHOP expression levels with small hairpin RNA or a dominant negative form of a proline-rich extensin-like receptor protein kinase in hypoxia decreased IGF-induced radiosensitivity.	Proline	220-227	DNA damage inducible transcript 3	Homo sapiens	141-145
18679584-2	2008	RT-PCR analyses showed up-regulation of CHOP/GADD153 and splicing of XBP-1 mRNA in brefeldin A-treated cells.	Brefeldin A	83-94	DNA damage inducible transcript 3	Homo sapiens	45-52
18679584-3	2008	CHOP promoter-luciferase reporter assays demonstrated activation of AARE, ERSE, and AP-1 elements of CHOP promoter by brefeldin A treatment.	Brefeldin A	118-129	DNA damage inducible transcript 3	Homo sapiens	0-4
18679584-3	2008	CHOP promoter-luciferase reporter assays demonstrated activation of AARE, ERSE, and AP-1 elements of CHOP promoter by brefeldin A treatment.	Brefeldin A	118-129	DNA damage inducible transcript 3	Homo sapiens	101-105
18679584-6	2008	Our results suggest that although CHOP is up-regulated by brefeldin A, it is not a major mediator of brefeldin A-induced apoptosis.	Brefeldin A	58-69	DNA damage inducible transcript 3	Homo sapiens	34-38
18807195-3	2008	Treatment of HT29 human colon carcinoma cells with rottlerin was found to induce a number of signature ER stress markers; phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), ER stress-specific XBP1 splicing, and up-regulation of glucose-regulated protein (GRP)-78 and CCAAT/enhancer-binding protein-homologous protein (CHOP).	rottlerin	51-60	DNA damage inducible transcript 3	Homo sapiens	285-334
19074830-10	2008	DR5 promoter activity induced by allopurinol was diminished by a mutation of a CAAT/enhancer binding protein homologous protein (CHOP)-binding site.	Allopurinol	33-44	DNA damage inducible transcript 3	Homo sapiens	129-133
19074830-11	2008	In addition, allopurinol also increased CHOP expression, suggesting that allopurinol induced DR5 expression via CHOP.	Allopurinol	13-24	DNA damage inducible transcript 3	Homo sapiens	40-44
19074830-11	2008	In addition, allopurinol also increased CHOP expression, suggesting that allopurinol induced DR5 expression via CHOP.	Allopurinol	13-24	DNA damage inducible transcript 3	Homo sapiens	112-116
19074830-11	2008	In addition, allopurinol also increased CHOP expression, suggesting that allopurinol induced DR5 expression via CHOP.	Allopurinol	73-84	DNA damage inducible transcript 3	Homo sapiens	40-44
19074830-11	2008	In addition, allopurinol also increased CHOP expression, suggesting that allopurinol induced DR5 expression via CHOP.	Allopurinol	73-84	DNA damage inducible transcript 3	Homo sapiens	112-116
18807195-3	2008	Treatment of HT29 human colon carcinoma cells with rottlerin was found to induce a number of signature ER stress markers; phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), ER stress-specific XBP1 splicing, and up-regulation of glucose-regulated protein (GRP)-78 and CCAAT/enhancer-binding protein-homologous protein (CHOP).	rottlerin	51-60	DNA damage inducible transcript 3	Homo sapiens	336-340
18807195-5	2008	These results suggest that rottlerin induces up-regulation of CHOP via PKC delta-independent pathway.	rottlerin	27-36	DNA damage inducible transcript 3	Homo sapiens	62-66
18807195-6	2008	Furthermore, down-regulation of CHOP expression using CHOP siRNA attenuated rottlerin-induced apoptosis.	rottlerin	76-85	DNA damage inducible transcript 3	Homo sapiens	32-36
18807195-6	2008	Furthermore, down-regulation of CHOP expression using CHOP siRNA attenuated rottlerin-induced apoptosis.	rottlerin	76-85	DNA damage inducible transcript 3	Homo sapiens	54-58
18664592-7	2008	Growth arrest and DNA damage inducible (GADD) 153, an ER stress-response gene, is up-regulated after treatment with BG plus cisplatin compared with cisplatin alone in SQ20b and SKOV-3x cells, but not in A549 cells.	O(6)-benzylguanine	116-118	DNA damage inducible transcript 3	Homo sapiens	0-49
18767967-6	2008	U0126, a selective inhibitor of upstream MEK, had a similar effect as PD98059 on butyrate-induced GADD153 mRNA upregulation.	U 0126	0-5	DNA damage inducible transcript 3	Homo sapiens	98-105
18767967-6	2008	U0126, a selective inhibitor of upstream MEK, had a similar effect as PD98059 on butyrate-induced GADD153 mRNA upregulation.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	70-77	DNA damage inducible transcript 3	Homo sapiens	98-105
18767967-6	2008	U0126, a selective inhibitor of upstream MEK, had a similar effect as PD98059 on butyrate-induced GADD153 mRNA upregulation.	Butyrates	81-89	DNA damage inducible transcript 3	Homo sapiens	98-105
18767967-7	2008	Collectively, these findings suggest that butyrate caused activation of the GADD153 gene at the level of transcription involving mainly the MEK/ERK branch of the MAPK signal transduction pathway.	Butyrates	42-50	DNA damage inducible transcript 3	Homo sapiens	76-83
18767967-0	2008	Upregulation of GADD153 by butyrate: involvement of MAPK.	Butyrates	27-35	DNA damage inducible transcript 3	Homo sapiens	16-23
18767967-2	2008	Herein, butyrate is shown to affect the growth arrest and DNA damage-inducible gene 153 (GADD153) in HCT-116 human colon adenocarcinoma cells.	Butyrates	8-16	DNA damage inducible transcript 3	Homo sapiens	40-87
18767967-2	2008	Herein, butyrate is shown to affect the growth arrest and DNA damage-inducible gene 153 (GADD153) in HCT-116 human colon adenocarcinoma cells.	Butyrates	8-16	DNA damage inducible transcript 3	Homo sapiens	89-96
18767967-4	2008	Butyrate-induced upregulation of GADD153 mRNA was attenuated by actinomycin D, but apparently not by cycloheximide.	Butyrates	0-8	DNA damage inducible transcript 3	Homo sapiens	33-40
18767967-4	2008	Butyrate-induced upregulation of GADD153 mRNA was attenuated by actinomycin D, but apparently not by cycloheximide.	Dactinomycin	64-77	DNA damage inducible transcript 3	Homo sapiens	33-40
18767967-5	2008	In investigating possible involvement of MAPK in mediating the effect of butyrate on GADD153 mRNA expression, the extracellular regulated kinase (ERK) inhibitor PD98059, but neither the JNK inhibitor SP600125 nor the p38 MAPK inhibitor SB203580, blunted the ability of butyrate to upregulate GADD153 mRNA expression.	Butyrates	73-81	DNA damage inducible transcript 3	Homo sapiens	85-92
18785111-2	2008	In the present study, we found that the beta-lapachone-induced apoptosis of DU145 human prostate carcinoma cells was associated with endoplasmic reticulum (ER) stress, as shown by increased intracellular calcium levels and induction of GRP-78 and GADD-153 proteins, suggesting that the endoplasmic reticulum is a target of beta-lapachone.	beta-lapachone	40-54	DNA damage inducible transcript 3	Homo sapiens	247-255
18664592-7	2008	Growth arrest and DNA damage inducible (GADD) 153, an ER stress-response gene, is up-regulated after treatment with BG plus cisplatin compared with cisplatin alone in SQ20b and SKOV-3x cells, but not in A549 cells.	Cisplatin	124-133	DNA damage inducible transcript 3	Homo sapiens	0-49
18664592-7	2008	Growth arrest and DNA damage inducible (GADD) 153, an ER stress-response gene, is up-regulated after treatment with BG plus cisplatin compared with cisplatin alone in SQ20b and SKOV-3x cells, but not in A549 cells.	Cisplatin	148-157	DNA damage inducible transcript 3	Homo sapiens	0-49
18664592-9	2008	Inhibition of ER stress in the SQ20b cell line by salubrinal, an inhibitor of eIF2alpha dephosphorylation, or GADD153 small interfering RNA, abrogated BG-enhancement of cisplatin cytotoxicity and apoptosis through caspase 3 and 12 cleavage.	Cisplatin	169-178	DNA damage inducible transcript 3	Homo sapiens	110-117
18664592-10	2008	These data indicate GADD153 up-regulation plays an important role in BG-enhanced cisplatin cytotoxicity and apoptosis.	Cisplatin	81-90	DNA damage inducible transcript 3	Homo sapiens	20-27
18852146-0	2008	15-deoxy-Delta12,14-prostaglandin J2 up-regulates death receptor 5 gene expression in HCT116 cells: involvement of reactive oxygen species and C/EBP homologous transcription factor gene transcription.	14-prostaglandin j2	17-36	DNA damage inducible transcript 3	Homo sapiens	143-180
18772138-2	2008	We have previously shown that in human T lymphocytes the CHOP phosphorylation induced by prostaglandin E(2) (PGE(2))-increased interleukin-8 (IL-8) gene expression.	Dinoprostone	89-107	DNA damage inducible transcript 3	Homo sapiens	57-61
18772138-2	2008	We have previously shown that in human T lymphocytes the CHOP phosphorylation induced by prostaglandin E(2) (PGE(2))-increased interleukin-8 (IL-8) gene expression.	Prostaglandins E	109-112	DNA damage inducible transcript 3	Homo sapiens	57-61
18772138-3	2008	Given the CHOP positive role in the regulation of transcription, here we have investigated the molecular mechanism(s) by which CHOP increases IL-8 gene activity under PGE(2) stimulus.	Prostaglandins E	167-170	DNA damage inducible transcript 3	Homo sapiens	127-131
18772138-6	2008	Moreover, PGE(2) induced CHOP-DNA complexes only when the entire IL-8/AP-1 promoter or the wild type sequences encompassing the AP-1 upstream region were employed.	Prostaglandins E	10-13	DNA damage inducible transcript 3	Homo sapiens	25-29
18772138-9	2008	Finally, chromatin immunoprecipitation data confirmed in vivo that PGE(2) induces CHOP binding to the IL-8 promoter.	Dinoprostone	67-73	DNA damage inducible transcript 3	Homo sapiens	82-86
18772138-10	2008	Taken together, our results suggest that the increased expression of CHOP in response to PGE(2) exerts a positive transcriptional regulation of the IL-8 promoter mediated by direct binding to a novel consensus site.	Prostaglandins E	89-92	DNA damage inducible transcript 3	Homo sapiens	69-73
18544678-0	2008	Gene expression predicts overall survival in paraffin-embedded tissues of diffuse large B-cell lymphoma treated with R-CHOP.	Paraffin	45-53	DNA damage inducible transcript 3	Homo sapiens	119-123
18840722-0	2008	Blocks to paraffin get the CHOP, +R.	Paraffin	10-18	DNA damage inducible transcript 3	Homo sapiens	27-31
18700142-4	2008	We found that vanadate inhibited the endoplasmic reticulum stress-induced increase in GRP78 and CHOP expressions at both mRNA and protein levels.	Vanadates	14-22	DNA damage inducible transcript 3	Homo sapiens	96-100
18852146-6	2008	A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation.	Reactive Oxygen Species	48-71	DNA damage inducible transcript 3	Homo sapiens	107-111
18852146-6	2008	A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation.	Reactive Oxygen Species	73-76	DNA damage inducible transcript 3	Homo sapiens	107-111
18852146-6	2008	A mechanistic study showed the contributions of reactive oxygen species (ROS) and intracellular calcium in CHOP and DR5 gene up-regulation.	Calcium	96-103	DNA damage inducible transcript 3	Homo sapiens	107-111
18852146-11	2008	In summary, the effect of up-regulation of DR5 by 15dPGJ(2) in colon cancer cells is independent of PPAR-gamma and p53 but relies on CHOP induction through gene transcription involving ROS and calcium.	Reactive Oxygen Species	185-188	DNA damage inducible transcript 3	Homo sapiens	133-137
18852146-11	2008	In summary, the effect of up-regulation of DR5 by 15dPGJ(2) in colon cancer cells is independent of PPAR-gamma and p53 but relies on CHOP induction through gene transcription involving ROS and calcium.	Calcium	193-200	DNA damage inducible transcript 3	Homo sapiens	133-137
18544642-8	2008	In vitro, palmitate, thapsigargin, and tunicamycin but not oleate induced endoplasmic reticulum stress in HepG2 cells, including increased transcripts CHOP, ERN1, GADD34, and PERK, and increased XBP1 splicing along with phosphorylation of eukaryotic initiation factor eIF2alpha, JNK1, and c-jun.	Palmitates	10-19	DNA damage inducible transcript 3	Homo sapiens	151-155
18794136-0	2008	Coupling of endoplasmic reticulum stress to CDDO-Me-induced up-regulation of death receptor 5 via a CHOP-dependent mechanism involving JNK activation.	bardoxolone methyl	44-51	DNA damage inducible transcript 3	Homo sapiens	100-104
18794136-4	2008	Analysis of DR5 promoter regions defines that the CCAAT/enhancer binding protein homologous protein (CHOP) binding site is responsible for CDDO-Me-induced transactivation of the DR5 gene.	bardoxolone methyl	139-146	DNA damage inducible transcript 3	Homo sapiens	50-99
18794136-4	2008	Analysis of DR5 promoter regions defines that the CCAAT/enhancer binding protein homologous protein (CHOP) binding site is responsible for CDDO-Me-induced transactivation of the DR5 gene.	bardoxolone methyl	139-146	DNA damage inducible transcript 3	Homo sapiens	101-105
18794136-5	2008	Consistently, CDDO-Me induced DR5 expression and parallel CHOP up-regulation.	bardoxolone methyl	14-21	DNA damage inducible transcript 3	Homo sapiens	58-62
18794136-6	2008	Blockade of CHOP up-regulation also abrogated CDDO-Me-induced DR5 expression.	bardoxolone methyl	46-53	DNA damage inducible transcript 3	Homo sapiens	12-16
18794136-7	2008	These results indicate that CDDO-Me induces CHOP-dependent DR5 up-regulation.	bardoxolone methyl	28-35	DNA damage inducible transcript 3	Homo sapiens	44-48
18631371-6	2008	Additionally, H(2)O(2) treatment induced upregulation of CHOP, GRP78 and several representative endoplasmic reticulum (ER) stress-responsive proteins, including heme oxygenase-1.	Hydrogen Peroxide	14-22	DNA damage inducible transcript 3	Homo sapiens	57-61
18502831-1	2008	Chemotherapy with alemtuzumab and the combination of cyclophosphamide, adriamycin, oncovin, and prednisone (CHOP) has become experimental trial therapy for aggressive T-cell lymphoma.	Cyclophosphamide	53-69	DNA damage inducible transcript 3	Homo sapiens	108-112
18502831-1	2008	Chemotherapy with alemtuzumab and the combination of cyclophosphamide, adriamycin, oncovin, and prednisone (CHOP) has become experimental trial therapy for aggressive T-cell lymphoma.	Doxorubicin	71-81	DNA damage inducible transcript 3	Homo sapiens	108-112
18502831-1	2008	Chemotherapy with alemtuzumab and the combination of cyclophosphamide, adriamycin, oncovin, and prednisone (CHOP) has become experimental trial therapy for aggressive T-cell lymphoma.	Prednisone	96-106	DNA damage inducible transcript 3	Homo sapiens	108-112
18533110-0	2008	Induction of the endoplasmic reticulum stress protein GADD153/CHOP by capsaicin in prostate PC-3 cells: a microarray study.	Capsaicin	70-79	DNA damage inducible transcript 3	Homo sapiens	54-61
18533110-0	2008	Induction of the endoplasmic reticulum stress protein GADD153/CHOP by capsaicin in prostate PC-3 cells: a microarray study.	Capsaicin	70-79	DNA damage inducible transcript 3	Homo sapiens	62-66
18533110-6	2008	We then tested the contribution of GADD153/CHOP to protection against capsaicin-induced cell death using RNA interference.	Capsaicin	70-79	DNA damage inducible transcript 3	Homo sapiens	35-42
18533110-7	2008	Blockage of GADD153/CHOP expression by small interfering RNA, significantly reduced capsaicin-induced cell death in PC-3 cells.	Capsaicin	84-93	DNA damage inducible transcript 3	Homo sapiens	12-19
18533110-7	2008	Blockage of GADD153/CHOP expression by small interfering RNA, significantly reduced capsaicin-induced cell death in PC-3 cells.	Capsaicin	84-93	DNA damage inducible transcript 3	Homo sapiens	20-24
18794136-8	2008	Moreover, the JNK inhibitor SP600125 abrogated CHOP induction by CDDO-Me, suggesting a JNK-dependent CHOP up-regulation by CDDO-Me as well.	pyrazolanthrone	28-36	DNA damage inducible transcript 3	Homo sapiens	47-51
18794136-8	2008	Moreover, the JNK inhibitor SP600125 abrogated CHOP induction by CDDO-Me, suggesting a JNK-dependent CHOP up-regulation by CDDO-Me as well.	pyrazolanthrone	28-36	DNA damage inducible transcript 3	Homo sapiens	101-105
18794136-8	2008	Moreover, the JNK inhibitor SP600125 abrogated CHOP induction by CDDO-Me, suggesting a JNK-dependent CHOP up-regulation by CDDO-Me as well.	bardoxolone methyl	65-72	DNA damage inducible transcript 3	Homo sapiens	47-51
18794136-8	2008	Moreover, the JNK inhibitor SP600125 abrogated CHOP induction by CDDO-Me, suggesting a JNK-dependent CHOP up-regulation by CDDO-Me as well.	bardoxolone methyl	65-72	DNA damage inducible transcript 3	Homo sapiens	101-105
18794136-8	2008	Moreover, the JNK inhibitor SP600125 abrogated CHOP induction by CDDO-Me, suggesting a JNK-dependent CHOP up-regulation by CDDO-Me as well.	bardoxolone methyl	123-130	DNA damage inducible transcript 3	Homo sapiens	47-51
18794136-8	2008	Moreover, the JNK inhibitor SP600125 abrogated CHOP induction by CDDO-Me, suggesting a JNK-dependent CHOP up-regulation by CDDO-Me as well.	bardoxolone methyl	123-130	DNA damage inducible transcript 3	Homo sapiens	101-105
18794136-9	2008	Importantly, knockdown of CHOP attenuated CDDO-Me-induced apoptosis, showing that CHOP induction is involved in CDDO-Me-induced apoptosis.	bardoxolone methyl	42-49	DNA damage inducible transcript 3	Homo sapiens	26-30
18794136-9	2008	Importantly, knockdown of CHOP attenuated CDDO-Me-induced apoptosis, showing that CHOP induction is involved in CDDO-Me-induced apoptosis.	bardoxolone methyl	42-49	DNA damage inducible transcript 3	Homo sapiens	82-86
18794136-9	2008	Importantly, knockdown of CHOP attenuated CDDO-Me-induced apoptosis, showing that CHOP induction is involved in CDDO-Me-induced apoptosis.	bardoxolone methyl	112-119	DNA damage inducible transcript 3	Homo sapiens	26-30
18794136-9	2008	Importantly, knockdown of CHOP attenuated CDDO-Me-induced apoptosis, showing that CHOP induction is involved in CDDO-Me-induced apoptosis.	bardoxolone methyl	112-119	DNA damage inducible transcript 3	Homo sapiens	82-86
18794136-11	2008	Furthermore, salubrinal, an inhibitor of ER stress-induced apoptosis, inhibited JNK activation and up-regulation of CHOP and DR5 by CDDO-Me and protected cells from CDDO-Me-induced apoptosis.	salubrinal	13-23	DNA damage inducible transcript 3	Homo sapiens	116-120
18794136-11	2008	Furthermore, salubrinal, an inhibitor of ER stress-induced apoptosis, inhibited JNK activation and up-regulation of CHOP and DR5 by CDDO-Me and protected cells from CDDO-Me-induced apoptosis.	bardoxolone methyl	132-139	DNA damage inducible transcript 3	Homo sapiens	116-120
18794136-12	2008	Thus, ER stress seems to be important for CDDO-Me-induced JNK activation, CHOP and DR5 up-regulation, and apoptosis.	bardoxolone methyl	42-49	DNA damage inducible transcript 3	Homo sapiens	74-78
18794136-13	2008	Collectively, we conclude that CDDO-Me triggers ER stress, leading to JNK-dependent, CHOP-mediated DR5 up-regulation and apoptosis.	bardoxolone methyl	31-38	DNA damage inducible transcript 3	Homo sapiens	85-89
19106649-7	2008	SUMMARY: Dose-intensified approaches, either cyclophosphamide, hydroxydaunorubicin (adriamycin), oncovin (vincristine), and prednisone (CHOP) +/- high-dose Ara-C followed by autologous stem cell transplantation or HyperCVAD with the addition of rituximab remain the current standard approach in younger patients up to 65 years.	Prednisone	124-134	DNA damage inducible transcript 3	Homo sapiens	136-140
18188576-4	2008	The patient was treated with CHOP (cyclophosfamide, doxorubicin, vincristin and prednisone) chemotherapy and involved-field radiotherapy.	cyclophosfamide	35-50	DNA damage inducible transcript 3	Homo sapiens	29-33
18603558-14	2008	An anthracycline-based chemotherapy with CHOP, MACOP-B or VACOP-B is recommended (grade B).	Anthracyclines	3-16	DNA damage inducible transcript 3	Homo sapiens	41-45
18544642-8	2008	In vitro, palmitate, thapsigargin, and tunicamycin but not oleate induced endoplasmic reticulum stress in HepG2 cells, including increased transcripts CHOP, ERN1, GADD34, and PERK, and increased XBP1 splicing along with phosphorylation of eukaryotic initiation factor eIF2alpha, JNK1, and c-jun.	Thapsigargin	21-33	DNA damage inducible transcript 3	Homo sapiens	151-155
18544642-8	2008	In vitro, palmitate, thapsigargin, and tunicamycin but not oleate induced endoplasmic reticulum stress in HepG2 cells, including increased transcripts CHOP, ERN1, GADD34, and PERK, and increased XBP1 splicing along with phosphorylation of eukaryotic initiation factor eIF2alpha, JNK1, and c-jun.	Tunicamycin	39-50	DNA damage inducible transcript 3	Homo sapiens	151-155
18701864-12	2008	The patient was treated with 6 cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone(CHOP)chemotherapy followed by the involved field irradiation.	Prednisone	89-99	DNA damage inducible transcript 3	Homo sapiens	100-104
18937075-3	2008	We describe the clinical course of hypopituitarism as a complication of IVL, successfully treated with immunochemotherapy (cyclophosphamide/doxorubicin/vincristine/prednisone-CHOP) plus Rituximab anti-CD20 humanized antibody).	Cyclophosphamide	123-139	DNA damage inducible transcript 3	Homo sapiens	175-179
18394432-8	2008	Our results revealed that: (1) CS induces ER stress in vitro and in vivo, (2) ER stress mediates CS-triggered apoptosis downstream of oxidative stress, (3) CS-initiated apoptosis is caused through oxidative stress-dependent induction of CHOP, (4) O(2)(*-) may play a dominant role in this process, and (5) oxidative stress-independent induction of GRP78 counterbalances the proapoptotic action of CHOP.	Cesium	31-33	DNA damage inducible transcript 3	Homo sapiens	397-401
18723477-3	2008	Here, we, using immunoblotting analysis, observed that the expression of BiP, CHOP, and XBP-1 is up-regulated in bortezomib-induced apoptosis in human multiple myeloma cell lines NCI-H929 and RPMI-8226/S, strongly suggesting that endoplasmic reticulum (ER) stress response or the unfolded protein response (UPR), a signaling pathway activated by the accumulation of unfolded proteins within ER, is initiated.	Bortezomib	113-123	DNA damage inducible transcript 3	Homo sapiens	78-82
18559892-9	2008	Blocking the transcription factor CHOP delayed palmitate-induced beta-cell apoptosis.	Palmitates	47-56	DNA damage inducible transcript 3	Homo sapiens	34-38
18508033-8	2008	Rotenone had a modest effect on the expression of CHOP.	Rotenone	0-8	DNA damage inducible transcript 3	Homo sapiens	50-54
18718094-5	2008	The results showed that the CR rate in R-CHOP group was higher than that in CHOP group (69.7% vs 47.2%, p = 0.049); especially in patients of male, Ann Arbor III - IV and IPI 3 - 5 (p = 0.017, p = 0.005 and p = 0.000).	Chromium	28-30	DNA damage inducible transcript 3	Homo sapiens	41-45
18718094-5	2008	The results showed that the CR rate in R-CHOP group was higher than that in CHOP group (69.7% vs 47.2%, p = 0.049); especially in patients of male, Ann Arbor III - IV and IPI 3 - 5 (p = 0.017, p = 0.005 and p = 0.000).	Chromium	28-30	DNA damage inducible transcript 3	Homo sapiens	76-80
18534616-0	2008	Intrinsically disordered human C/EBP homologous protein regulates biological activity of colon cancer cells during calcium stress.	Calcium	115-122	DNA damage inducible transcript 3	Homo sapiens	31-55
18394432-2	2008	Exposure of hBEC to CS or CS extract (CSE) caused expression of endogenous ER stress markers GRP78 and CHOP and induction of apoptosis evidenced by nuclear condensation, membrane blebbing, and activation of caspase-3 and caspase-4.	Cesium	20-22	DNA damage inducible transcript 3	Homo sapiens	103-107
18394432-2	2008	Exposure of hBEC to CS or CS extract (CSE) caused expression of endogenous ER stress markers GRP78 and CHOP and induction of apoptosis evidenced by nuclear condensation, membrane blebbing, and activation of caspase-3 and caspase-4.	Cesium	26-28	DNA damage inducible transcript 3	Homo sapiens	103-107
18394432-6	2008	Interestingly, antioxidants including a scavenger of O(2)(*-) blunted induction of CHOP by CSE without affecting the level of GRP78, and dominant-negative inhibition of CHOP abolished CSE-induced apoptosis.	o(2)	53-57	DNA damage inducible transcript 3	Homo sapiens	83-87
18394432-7	2008	Furthermore, a generator of O(2)(*-) selectively induced CHOP and apoptosis in hBEC.	o(2)(*-)	28-36	DNA damage inducible transcript 3	Homo sapiens	57-61
18394432-8	2008	Our results revealed that: (1) CS induces ER stress in vitro and in vivo, (2) ER stress mediates CS-triggered apoptosis downstream of oxidative stress, (3) CS-initiated apoptosis is caused through oxidative stress-dependent induction of CHOP, (4) O(2)(*-) may play a dominant role in this process, and (5) oxidative stress-independent induction of GRP78 counterbalances the proapoptotic action of CHOP.	Cesium	97-99	DNA damage inducible transcript 3	Homo sapiens	237-241
18394432-8	2008	Our results revealed that: (1) CS induces ER stress in vitro and in vivo, (2) ER stress mediates CS-triggered apoptosis downstream of oxidative stress, (3) CS-initiated apoptosis is caused through oxidative stress-dependent induction of CHOP, (4) O(2)(*-) may play a dominant role in this process, and (5) oxidative stress-independent induction of GRP78 counterbalances the proapoptotic action of CHOP.	Cesium	31-33	DNA damage inducible transcript 3	Homo sapiens	237-241
18394432-8	2008	Our results revealed that: (1) CS induces ER stress in vitro and in vivo, (2) ER stress mediates CS-triggered apoptosis downstream of oxidative stress, (3) CS-initiated apoptosis is caused through oxidative stress-dependent induction of CHOP, (4) O(2)(*-) may play a dominant role in this process, and (5) oxidative stress-independent induction of GRP78 counterbalances the proapoptotic action of CHOP.	Cesium	97-99	DNA damage inducible transcript 3	Homo sapiens	397-401
18394432-8	2008	Our results revealed that: (1) CS induces ER stress in vitro and in vivo, (2) ER stress mediates CS-triggered apoptosis downstream of oxidative stress, (3) CS-initiated apoptosis is caused through oxidative stress-dependent induction of CHOP, (4) O(2)(*-) may play a dominant role in this process, and (5) oxidative stress-independent induction of GRP78 counterbalances the proapoptotic action of CHOP.	Cesium	97-99	DNA damage inducible transcript 3	Homo sapiens	237-241
18394432-8	2008	Our results revealed that: (1) CS induces ER stress in vitro and in vivo, (2) ER stress mediates CS-triggered apoptosis downstream of oxidative stress, (3) CS-initiated apoptosis is caused through oxidative stress-dependent induction of CHOP, (4) O(2)(*-) may play a dominant role in this process, and (5) oxidative stress-independent induction of GRP78 counterbalances the proapoptotic action of CHOP.	Cesium	97-99	DNA damage inducible transcript 3	Homo sapiens	397-401
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphf	16-26	DNA damage inducible transcript 3	Homo sapiens	44-48
18445689-0	2008	Paraffin-based 6-gene model predicts outcome in diffuse large B-cell lymphoma patients treated with R-CHOP.	Paraffin	0-8	DNA damage inducible transcript 3	Homo sapiens	102-106
18445689-4	2008	However, the standard therapy has evolved into rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP).	Prednisone	105-115	DNA damage inducible transcript 3	Homo sapiens	119-123
18445689-5	2008	Herein, we evaluated the predictive power of a paraffin-based 6-gene model in R-CHOP-treated DLBCL patients.	Paraffin	47-55	DNA damage inducible transcript 3	Homo sapiens	80-84
18760704-1	2008	The concurrent use of rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has established the utility of chemoimmunotherapy for the treatment of aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	99-103
18760704-1	2008	The concurrent use of rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has established the utility of chemoimmunotherapy for the treatment of aggressive non-Hodgkin"s lymphoma (NHL).	Prednisone	85-95	DNA damage inducible transcript 3	Homo sapiens	99-103
18702436-7	2008	Treatment included a combination of the chemotherapy regimen of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) with the monoclonal anti-CD20 antibody rituximab.	Prednisone	111-121	DNA damage inducible transcript 3	Homo sapiens	123-127
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	Phosphorus	41-42	DNA damage inducible transcript 3	Homo sapiens	176-225
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	Phosphorus	41-42	DNA damage inducible transcript 3	Homo sapiens	227-231
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphf	16-26	DNA damage inducible transcript 3	Homo sapiens	86-90
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	Phosphorus	41-42	DNA damage inducible transcript 3	Homo sapiens	232-239
32038787-6	2008	Palmitate led to increased expressions of the spliced form of X-box-protein (Xbp)-1 mRNA and C/EBP homologous transcription factor (CHOP) protein, suggesting activation of the unfolded-protein response.	Palmitates	0-9	DNA damage inducible transcript 3	Homo sapiens	93-130
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	dim-c-pphbr	50-61	DNA damage inducible transcript 3	Homo sapiens	176-225
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	dim-c-pphbr	50-61	DNA damage inducible transcript 3	Homo sapiens	227-231
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	dim-c-pphbr	50-61	DNA damage inducible transcript 3	Homo sapiens	232-239
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	dim-c-pphf	77-87	DNA damage inducible transcript 3	Homo sapiens	176-225
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	dim-c-pphf	77-87	DNA damage inducible transcript 3	Homo sapiens	227-231
18460448-2	2008	Structure-activity studies show that the p-bromo (DIM-C-pPhBr) and p-fluoro (DIM-C-pPhF) analogs, which exhibit minimal activation of Nur77 and PPARgamma, induce expression of CCAAT/enhancer-binding protein homologous protein (CHOP/GADD153) in colon cancer cells.	dim-c-pphf	77-87	DNA damage inducible transcript 3	Homo sapiens	232-239
18460448-3	2008	Moreover, among a series of bromo and fluoro C-DIM analogs, their induction of CHOP was dependent on the position of the phenyl substituents (para &gt;/= meta &gt;/= ortho) and required a free indole group.	indole	193-199	DNA damage inducible transcript 3	Homo sapiens	79-83
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphbr	0-11	DNA damage inducible transcript 3	Homo sapiens	44-48
18460448-4	2008	DIM-C-pPhBr and DIM-C-pPhF not only induced CHOP but also activated death receptor 5 (CHOP dependent), cleavage of caspase 8 and poly (ADP ribose) polymerase (PARP) that is consistent with activation of the extrinsic pathway of apoptosis.	dim-c-pphbr	0-11	DNA damage inducible transcript 3	Homo sapiens	86-90
18583880-1	2008	The objective of the current study was to investigate the treatment outcomes for the use of cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP) chemotherapy in adult patients with hemophagocytic lymphohistiocytosis (HLH).	Cyclophosphamide	92-108	DNA damage inducible transcript 3	Homo sapiens	153-157
18583880-1	2008	The objective of the current study was to investigate the treatment outcomes for the use of cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP) chemotherapy in adult patients with hemophagocytic lymphohistiocytosis (HLH).	Prednisolone	139-151	DNA damage inducible transcript 3	Homo sapiens	153-157
17997372-10	2008	Subsequently, he underwent five cycles of CHOP (cyclofosfamide, doxorubicin, vincristin, prednison) chemotherapy with further partial regression of the abdominal tumour.	cyclofosfamide	48-62	DNA damage inducible transcript 3	Homo sapiens	42-46
17997372-10	2008	Subsequently, he underwent five cycles of CHOP (cyclofosfamide, doxorubicin, vincristin, prednison) chemotherapy with further partial regression of the abdominal tumour.	Doxorubicin	64-75	DNA damage inducible transcript 3	Homo sapiens	42-46
18463134-5	2008	In contrast to the inhibition of transcription by JDP2, JDP2-CHOP complex strongly enhances transcription from promoters containing TPA response elements (TRE), but not from those containing cyclic AMP response elements (CRE).	Tetradecanoylphorbol Acetate	132-135	DNA damage inducible transcript 3	Homo sapiens	61-65
32038787-6	2008	Palmitate led to increased expressions of the spliced form of X-box-protein (Xbp)-1 mRNA and C/EBP homologous transcription factor (CHOP) protein, suggesting activation of the unfolded-protein response.	Palmitates	0-9	DNA damage inducible transcript 3	Homo sapiens	132-136
18193086-7	2008	In addition, a transcriptional mechanism powered by CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) induction was responsible for DR5 upregulation by dipyridamole.	Dipyridamole	167-179	DNA damage inducible transcript 3	Homo sapiens	111-115
18465033-8	2008	Histology confirmed necrotic diffuse large B-cell lymphoma and the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy regime was subsequently commenced.	Prednisone	114-124	DNA damage inducible transcript 3	Homo sapiens	126-130
18292286-2	2008	One hundred forty-seven patients received a cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP)-like regimen with intensified courses in half of them.	Prednisone	92-102	DNA damage inducible transcript 3	Homo sapiens	104-108
18278507-8	2008	GRP-78 and GADD153 mRNA and protein expression in cultured RPE cells were significantly upregulated by treatment with tBH.	tert-Butylhydroperoxide	118-121	DNA damage inducible transcript 3	Homo sapiens	11-18
18278507-9	2008	CONCLUSION: tBH increases oxidative stress, increases accumulation of ROS in the ER, and upregulates expression of GRP-78 and GADD153.	tert-Butylhydroperoxide	12-15	DNA damage inducible transcript 3	Homo sapiens	126-133
18384088-0	2008	6-Shogaol induces apoptosis in human colorectal carcinoma cells via ROS production, caspase activation, and GADD 153 expression.	shogaol	0-9	DNA damage inducible transcript 3	Homo sapiens	108-116
18630529-4	2008	The ROS caused endoplasmic reticulum (ER) stress, confirmed by the increase of GADD153 and GRP78 in the examined cells.	Reactive Oxygen Species	4-7	DNA damage inducible transcript 3	Homo sapiens	79-86
18409079-1	2008	Several authors have reported interstitial pneumonia (IP) during rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy, while others have encountered Pneumocystis jirovecii pneumonia during rituximab-combined bi-weekly CHOP.	Prednisone	128-138	DNA damage inducible transcript 3	Homo sapiens	142-146
18409079-4	2008	Among R-CHOP-treated patients, serum beta-D-glucan was increased in 8 of 12 (75%) IP patients compared with none of 30 non-IP patients examined.	maltotriose	37-50	DNA damage inducible transcript 3	Homo sapiens	8-12
18384088-7	2008	The growth arrest and DNA damage (GADD)-inducible transcription factor 153 (GADD153) mRNA and protein is markedly induced in a time- and concentration-dependent manner in response to 6-shogaol.	gadd	34-38	DNA damage inducible transcript 3	Homo sapiens	76-83
18384088-7	2008	The growth arrest and DNA damage (GADD)-inducible transcription factor 153 (GADD153) mRNA and protein is markedly induced in a time- and concentration-dependent manner in response to 6-shogaol.	shogaol	183-192	DNA damage inducible transcript 3	Homo sapiens	76-83
17968315-0	2008	Celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 expression via GADD153/CHOP.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	89-96
17968315-0	2008	Celecoxib and a novel COX-2 inhibitor ON09310 upregulate death receptor 5 expression via GADD153/CHOP.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	97-101
18294352-4	2008	She was successfully treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) and maintained subsequently on sirolimus and prednisone.	Prednisone	92-102	DNA damage inducible transcript 3	Homo sapiens	106-110
18413750-6	2008	Furthermore, the OSU-03012/EGFR inhibitor combination induced GADD153-mediated up-regulation of death receptor 5 expression and subsequent activation of the extrinsic apoptosis pathway.	OSU 03012	17-26	DNA damage inducible transcript 3	Homo sapiens	62-69
17579865-1	2008	BACKGROUND: The addition of etoposide to the CHOP protocol (CHOEP) has been shown to improve outcome in patients with aggressive non-Hodgkin"s lymphoma.	Etoposide	28-37	DNA damage inducible transcript 3	Homo sapiens	45-49
18420078-5	2008	Following combined chemotherapy with rituximab and mini-CHOP (cyclophosphamide, adriamycin, oncovin and prednisone), complete remission was obtained rapidly, with no relapse at two years.	Cyclophosphamide	62-78	DNA damage inducible transcript 3	Homo sapiens	56-60
18420078-5	2008	Following combined chemotherapy with rituximab and mini-CHOP (cyclophosphamide, adriamycin, oncovin and prednisone), complete remission was obtained rapidly, with no relapse at two years.	Doxorubicin	80-90	DNA damage inducible transcript 3	Homo sapiens	56-60
18420078-5	2008	Following combined chemotherapy with rituximab and mini-CHOP (cyclophosphamide, adriamycin, oncovin and prednisone), complete remission was obtained rapidly, with no relapse at two years.	Vincristine	92-99	DNA damage inducible transcript 3	Homo sapiens	56-60
18420078-5	2008	Following combined chemotherapy with rituximab and mini-CHOP (cyclophosphamide, adriamycin, oncovin and prednisone), complete remission was obtained rapidly, with no relapse at two years.	Prednisone	104-114	DNA damage inducible transcript 3	Homo sapiens	56-60
18712992-4	2008	The patient was treated with 6 courses of CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	42-46
18712992-4	2008	The patient was treated with 6 courses of CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Doxorubicin	79-90	DNA damage inducible transcript 3	Homo sapiens	42-46
18712992-4	2008	The patient was treated with 6 courses of CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Vincristine	92-103	DNA damage inducible transcript 3	Homo sapiens	42-46
18712992-4	2008	The patient was treated with 6 courses of CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	42-46
18228003-7	2008	Tunicamycin induced a rapid decline of cyclin D1 and cyclin A expression and an early increase of glucose-related protein (GRP) 78 and growth arrest and DNA damage-inducible transcription factor (GADD) 153 levels.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	135-205
18408447-4	2008	The patient was treated with rituximab and cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP).	Prednisolone	90-102	DNA damage inducible transcript 3	Homo sapiens	104-108
18303033-1	2008	BACKGROUND: A prospective, single-arm, open-label, nonrandomized phase II combination chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus radioimmunotherapy trial was conducted to evaluate the efficacy and safety in untreated elderly diffuse large B-cell lymphoma (DLBCL) patients.	Cyclophosphamide	104-120	DNA damage inducible transcript 3	Homo sapiens	164-168
17957723-6	2008	DIM-C-pPhOCH(3) also activated the extrinsic apoptosis pathway through increased phosphorylation of c-jun N-terminal kinase which, in turn, activated C/EBP homologous transcription factor (CHOP) and death receptor 5 (DR5).	dim-c-pphoch(3)	0-15	DNA damage inducible transcript 3	Homo sapiens	150-187
17957723-6	2008	DIM-C-pPhOCH(3) also activated the extrinsic apoptosis pathway through increased phosphorylation of c-jun N-terminal kinase which, in turn, activated C/EBP homologous transcription factor (CHOP) and death receptor 5 (DR5).	dim-c-pphoch(3)	0-15	DNA damage inducible transcript 3	Homo sapiens	189-193
17278123-3	2008	We present a case of advanced stage Burkitt lymphoma in an 8-year-old female with acquired immunodeficiency syndrome (AIDS), who was successfully treated with a 3 month course of modified CHOP-R (cyclophosphamide, daunorubicin, vincristine, prednisone, and rituximab) and HAART therapy.	Daunorubicin	214-226	DNA damage inducible transcript 3	Homo sapiens	188-192
17278123-3	2008	We present a case of advanced stage Burkitt lymphoma in an 8-year-old female with acquired immunodeficiency syndrome (AIDS), who was successfully treated with a 3 month course of modified CHOP-R (cyclophosphamide, daunorubicin, vincristine, prednisone, and rituximab) and HAART therapy.	Vincristine	228-239	DNA damage inducible transcript 3	Homo sapiens	188-192
17278123-3	2008	We present a case of advanced stage Burkitt lymphoma in an 8-year-old female with acquired immunodeficiency syndrome (AIDS), who was successfully treated with a 3 month course of modified CHOP-R (cyclophosphamide, daunorubicin, vincristine, prednisone, and rituximab) and HAART therapy.	Prednisone	241-251	DNA damage inducible transcript 3	Homo sapiens	188-192
18388378-7	2008	The patient received five cycles of a cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen which resulted in the regression in her skin lesions and constitutional symptoms.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	97-101
18381103-3	2008	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP regimen) improves the response rate, progression-free survival (PFS), and overall survival (OS) in diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
18381103-3	2008	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy (R-CHOP regimen) improves the response rate, progression-free survival (PFS), and overall survival (OS) in diffuse large B-cell lymphoma (DLBCL).	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	89-93
18388378-7	2008	The patient received five cycles of a cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen which resulted in the regression in her skin lesions and constitutional symptoms.	Doxorubicin	56-67	DNA damage inducible transcript 3	Homo sapiens	97-101
18388378-7	2008	The patient received five cycles of a cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen which resulted in the regression in her skin lesions and constitutional symptoms.	Prednisone	85-95	DNA damage inducible transcript 3	Homo sapiens	97-101
18082618-2	2008	We herein demonstrate that CD437 induces endoplasmic reticulum (ER) stress, including the up-regulation of CHOP, BIP and GADD34 mRNA through ER stress transducer (PERK and IRE1alpha) activation in an ovarian adenocarcinoma cell line, SKOV3.	CD 437	27-32	DNA damage inducible transcript 3	Homo sapiens	107-111
17941056-7	2008	Using SH-SY5Y neuroblastoma cells and primary cerebellar granule neurons as in vitro models, we demonstrated that exposure to ethanol alone had little effect on the expression of markers for ER stress; however, ethanol drastically enhanced the expression of GRP78, CHOP, ATF4, ATF6, and phosphorylated PERK and eIF2 alpha when induced by tunicamycin and thapsigargin.	Ethanol	211-218	DNA damage inducible transcript 3	Homo sapiens	265-269
17941056-11	2008	We further demonstrated that CHOP played an important role in ethanol-promoted cell death.	Ethanol	62-69	DNA damage inducible transcript 3	Homo sapiens	29-33
18306483-2	2008	Shortness of breath developed following the 5th course of Rituximab-CHOP chemotherapy (cyclophosphamide, Vincristine, Doxorubicin, Prednisolone).	Cyclophosphamide	87-103	DNA damage inducible transcript 3	Homo sapiens	68-72
18306483-2	2008	Shortness of breath developed following the 5th course of Rituximab-CHOP chemotherapy (cyclophosphamide, Vincristine, Doxorubicin, Prednisolone).	Vincristine	105-116	DNA damage inducible transcript 3	Homo sapiens	68-72
18306483-2	2008	Shortness of breath developed following the 5th course of Rituximab-CHOP chemotherapy (cyclophosphamide, Vincristine, Doxorubicin, Prednisolone).	Doxorubicin	118-129	DNA damage inducible transcript 3	Homo sapiens	68-72
18306483-2	2008	Shortness of breath developed following the 5th course of Rituximab-CHOP chemotherapy (cyclophosphamide, Vincristine, Doxorubicin, Prednisolone).	Prednisolone	131-143	DNA damage inducible transcript 3	Homo sapiens	68-72
18082618-3	2008	It was also shown that CD437 induced the CHOP and GADD34 expressions in another four ovarian adenocarcinoma cell lines, indicating that CD437 functions as an ER stress inducer in these cell lines.	CD 437	23-28	DNA damage inducible transcript 3	Homo sapiens	41-45
18082618-4	2008	Moreover, the siRNA-mediated knockdown of inducible CHOP expression prevented the cytotoxic effect of CD437.	CD 437	102-107	DNA damage inducible transcript 3	Homo sapiens	52-56
18226581-1	2008	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is used to treat patients with non-Hodgkin lymphoma.	Cyclophosphamide	12-28	DNA damage inducible transcript 3	Homo sapiens	74-78
17709599-9	2008	We conclude that PGE-2 stimulates IL-8 production through the CHOP transcription factor in CF cells.	Dinoprostone	17-22	DNA damage inducible transcript 3	Homo sapiens	62-66
18245486-6	2008	When combined, bortezomib and celecoxib triggered elevated expression of the ER stress markers GRP78/BiP and CHOP/GADD153, caused activation of c-Jun NH(2)-terminal kinase and ER stress-associated caspase-4, and greatly increased apoptotic cell death.	Bortezomib	15-25	DNA damage inducible transcript 3	Homo sapiens	109-113
18245486-6	2008	When combined, bortezomib and celecoxib triggered elevated expression of the ER stress markers GRP78/BiP and CHOP/GADD153, caused activation of c-Jun NH(2)-terminal kinase and ER stress-associated caspase-4, and greatly increased apoptotic cell death.	Bortezomib	15-25	DNA damage inducible transcript 3	Homo sapiens	114-121
18245486-6	2008	When combined, bortezomib and celecoxib triggered elevated expression of the ER stress markers GRP78/BiP and CHOP/GADD153, caused activation of c-Jun NH(2)-terminal kinase and ER stress-associated caspase-4, and greatly increased apoptotic cell death.	Celecoxib	30-39	DNA damage inducible transcript 3	Homo sapiens	109-113
18245486-6	2008	When combined, bortezomib and celecoxib triggered elevated expression of the ER stress markers GRP78/BiP and CHOP/GADD153, caused activation of c-Jun NH(2)-terminal kinase and ER stress-associated caspase-4, and greatly increased apoptotic cell death.	Celecoxib	30-39	DNA damage inducible transcript 3	Homo sapiens	114-121
18162120-1	2008	Immunochemotherapy with cyclophosphamide, adriamycin, vincristine, prednisone and rituximab (R-CHOP) is the standard treatment in non-immunosuppressed patients with diffuse large B-cell lymphoma (DLBCL), but its adequacy has not been definitively established in patients with human immunodeficiency virus (HIV)-related lymphoma.	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	95-99
18162120-1	2008	Immunochemotherapy with cyclophosphamide, adriamycin, vincristine, prednisone and rituximab (R-CHOP) is the standard treatment in non-immunosuppressed patients with diffuse large B-cell lymphoma (DLBCL), but its adequacy has not been definitively established in patients with human immunodeficiency virus (HIV)-related lymphoma.	Doxorubicin	42-52	DNA damage inducible transcript 3	Homo sapiens	95-99
18269578-7	2008	MDM2 amplification and cyclophosphamide doxorubicin hydrochloride (adriamycin), vincristine and prednisolone (CHOP) translocation was studied in seven cases by fluorescence in situ hybridization.	Prednisolone	96-108	DNA damage inducible transcript 3	Homo sapiens	110-114
18226581-1	2008	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is used to treat patients with non-Hodgkin lymphoma.	Doxorubicin	30-41	DNA damage inducible transcript 3	Homo sapiens	74-78
18226581-1	2008	BACKGROUND: Cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) is used to treat patients with non-Hodgkin lymphoma.	Prednisolone	60-72	DNA damage inducible transcript 3	Homo sapiens	74-78
18172319-6	2008	The involvement of CHOP in this process was confirmed by siRNA-mediated CHOP suppression, which not only attenuated As(2)O(3)-induced DR5 up-regulation but also inhibited the As(2)O(3)-stimulated TRAIL-induced apoptosis.	(2)o(3)	118-125	DNA damage inducible transcript 3	Homo sapiens	19-23
18172319-6	2008	The involvement of CHOP in this process was confirmed by siRNA-mediated CHOP suppression, which not only attenuated As(2)O(3)-induced DR5 up-regulation but also inhibited the As(2)O(3)-stimulated TRAIL-induced apoptosis.	(2)o(3)	118-125	DNA damage inducible transcript 3	Homo sapiens	72-76
18172319-6	2008	The involvement of CHOP in this process was confirmed by siRNA-mediated CHOP suppression, which not only attenuated As(2)O(3)-induced DR5 up-regulation but also inhibited the As(2)O(3)-stimulated TRAIL-induced apoptosis.	(2)o(3)	177-184	DNA damage inducible transcript 3	Homo sapiens	19-23
18172319-6	2008	The involvement of CHOP in this process was confirmed by siRNA-mediated CHOP suppression, which not only attenuated As(2)O(3)-induced DR5 up-regulation but also inhibited the As(2)O(3)-stimulated TRAIL-induced apoptosis.	(2)o(3)	177-184	DNA damage inducible transcript 3	Homo sapiens	72-76
18172319-10	2008	In addition, As(2)O(3)-mediated up-regulation of CHOP and DR5, as well as partial proteolytic processing of procaspase-3 by TRAIL, was not induced in astrocytes.	(2)o(3)	15-22	DNA damage inducible transcript 3	Homo sapiens	49-53
18190241-6	2008	OPG levels were found to increase after treatment with CHOP (Vincristini, Cyklofosfamid, Adriamycin and Prednisol) and they decreased after administration of Leukeran (Chlorambucyl) and CMC (2CdA/Cladrybin, Mitoxanton and Cyklofosfamid).	vincristini	61-72	DNA damage inducible transcript 3	Homo sapiens	55-59
18081361-3	2008	Before the development of monoclonal antibodies, the standard treatment of newly diagnosed DLBCL was based on combination therapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Prednisone	182-192	DNA damage inducible transcript 3	Homo sapiens	194-198
18415035-7	2008	Cumulative doxorubicin doses were 280 and 286 mg/m(2) on CHOP and R-CHOP (P = 0.65), respectively.	Doxorubicin	11-22	DNA damage inducible transcript 3	Homo sapiens	57-61
18415035-7	2008	Cumulative doxorubicin doses were 280 and 286 mg/m(2) on CHOP and R-CHOP (P = 0.65), respectively.	Doxorubicin	11-22	DNA damage inducible transcript 3	Homo sapiens	68-72
18670848-8	2008	The patient received three courses of combination chemotherapy [cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP)], and there was no evidence of recurrence 45 months after the surgery.	Prednisolone	111-123	DNA damage inducible transcript 3	Homo sapiens	125-129
21423838-13	2008	The CAT-Tox data on the other hand indicate that copper overload induces proteotoxic effects (HMTIIA, HSP70, GRP78), inflammatory reactions/oxidative stress (c-fos), and growth arrest and DNA damage (p53, GADD153).	Copper	49-55	DNA damage inducible transcript 3	Homo sapiens	205-212
17912235-3	2008	By achieving selective, targeted, and early inhibition of NF-kappaB activity, we demonstrate that NF-kappaB plays a critical role in Dox-induced chemoresistance by regulating genes involved in proliferation (Ki-67), response to DNA damage (GADD153), antiapoptosis (Bcl-XL), and pH regulation (CA9).	Doxorubicin	133-136	DNA damage inducible transcript 3	Homo sapiens	240-247
17927985-6	2007	We observed that IP3-mediated calcium release from ER, stimulated by Abeta exposure, mediated both CHOP expression and NF-kappaB DNA binding activity.	Calcium	30-37	DNA damage inducible transcript 3	Homo sapiens	99-103
17872950-5	2007	In addition, trichostatin A, a histone deacetylase inhibitor, repressed the degradation of CHOP protein via the N-terminal domain.	trichostatin A	13-27	DNA damage inducible transcript 3	Homo sapiens	91-95
18284716-1	2007	Among the strategies developed to improve results in patients with diffuse large B-cell lymphoma, increasing the dose of CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen (dose-intense regimen) and decreasing the duration of cycles (dose-dense regimen) or doing both had been proposed before the rituximab era.	Cyclophosphamide	127-143	DNA damage inducible transcript 3	Homo sapiens	121-125
18284716-1	2007	Among the strategies developed to improve results in patients with diffuse large B-cell lymphoma, increasing the dose of CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen (dose-intense regimen) and decreasing the duration of cycles (dose-dense regimen) or doing both had been proposed before the rituximab era.	Doxorubicin	144-155	DNA damage inducible transcript 3	Homo sapiens	121-125
18284716-1	2007	Among the strategies developed to improve results in patients with diffuse large B-cell lymphoma, increasing the dose of CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen (dose-intense regimen) and decreasing the duration of cycles (dose-dense regimen) or doing both had been proposed before the rituximab era.	Vincristine	156-167	DNA damage inducible transcript 3	Homo sapiens	121-125
18284716-1	2007	Among the strategies developed to improve results in patients with diffuse large B-cell lymphoma, increasing the dose of CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen (dose-intense regimen) and decreasing the duration of cycles (dose-dense regimen) or doing both had been proposed before the rituximab era.	Prednisone	168-178	DNA damage inducible transcript 3	Homo sapiens	121-125
17927985-0	2007	NF-kappaB activated by ER calcium release inhibits Abeta-mediated expression of CHOP protein: enhancement by AD-linked mutant presenilin 1.	Calcium	26-33	DNA damage inducible transcript 3	Homo sapiens	80-84
17927985-4	2007	One of the primary death effectors of ER stress is CHOP, also termed GADD153, which acts to transcriptionally inhibit protective cellular molecules such as Bcl-2 and glutathione.	Glutathione	166-177	DNA damage inducible transcript 3	Homo sapiens	51-55
17927985-4	2007	One of the primary death effectors of ER stress is CHOP, also termed GADD153, which acts to transcriptionally inhibit protective cellular molecules such as Bcl-2 and glutathione.	Glutathione	166-177	DNA damage inducible transcript 3	Homo sapiens	69-76
17927985-8	2007	The enhanced release of calcium from IP3-mediated ER stores in mPS1 neurons stimulated increased NF-kappaB compared to normal neurons, which inhibited CHOP expression.	Calcium	24-31	DNA damage inducible transcript 3	Homo sapiens	151-155
17927985-5	2007	Because both CHOP and NF-kappaB are activated by increased intracellular calcium and stress, yet have diametrically opposite effects on neuronal vulnerability, we sought to examine this interaction in greater detail.	Calcium	73-80	DNA damage inducible transcript 3	Homo sapiens	13-17
17927985-6	2007	We observed that IP3-mediated calcium release from ER, stimulated by Abeta exposure, mediated both CHOP expression and NF-kappaB DNA binding activity.	Inositol 1,4,5-Trisphosphate	17-20	DNA damage inducible transcript 3	Homo sapiens	99-103
17968021-11	2007	CONCLUSION: The longer OS at 3 years and higher CR rate with VCAP-AMP-VECP compared with biweekly CHOP suggest that VCAP-AMP-VECP might be a more effective regimen at the expense of higher toxicities, providing the basis for future investigations in the treatment of ATLL.	vcap-amp	116-124	DNA damage inducible transcript 3	Homo sapiens	98-102
17927985-8	2007	The enhanced release of calcium from IP3-mediated ER stores in mPS1 neurons stimulated increased NF-kappaB compared to normal neurons, which inhibited CHOP expression.	Inositol 1,4,5-Trisphosphate	37-40	DNA damage inducible transcript 3	Homo sapiens	151-155
17868644-3	2007	In addition, triglyceride induces the expression of endogenous endoplasmic reticulum (ER) stress markers, including GRP 78, IRE-1alpha, XBP-1, p-eIF2alpha, CHOP, and p-JNK.	Triglycerides	13-25	DNA damage inducible transcript 3	Homo sapiens	156-160
17869220-4	2007	Subsequent experiments revealed that K-7174 had the potential to induce endoplasmic reticulum (ER) stress evidenced by induction of GRP78 and CHOP.	K 7174	37-43	DNA damage inducible transcript 3	Homo sapiens	142-146
18025288-6	2007	Additionally, 2-DG induces an unfolded protein response, including up-regulation of GADD153 (C/EBP-homologous protein), an unfolded protein response-specific mediator of apoptosis, more effectively in 2-DG-sensitive cells.	Deoxyglucose	14-18	DNA damage inducible transcript 3	Homo sapiens	84-91
17620318-7	2007	CHOP may play a role in altered beta-cell glucose metabolism, in beta-cell apoptosis, and in lack of beta-cell replication.	Glucose	42-49	DNA damage inducible transcript 3	Homo sapiens	0-4
17705221-7	2007	BHMT expression inhibited homocysteine-induced glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP) and homocysteine-induced cell death.	Homocysteine	26-38	DNA damage inducible transcript 3	Homo sapiens	88-112
17705221-7	2007	BHMT expression inhibited homocysteine-induced glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP) and homocysteine-induced cell death.	Homocysteine	26-38	DNA damage inducible transcript 3	Homo sapiens	114-118
18040146-4	2007	The patient was treated with R-CHOP (rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone) and achieved complete remission for more than 2 years.	Prednisone	95-105	DNA damage inducible transcript 3	Homo sapiens	31-35
18025288-6	2007	Additionally, 2-DG induces an unfolded protein response, including up-regulation of GADD153 (C/EBP-homologous protein), an unfolded protein response-specific mediator of apoptosis, more effectively in 2-DG-sensitive cells.	Deoxyglucose	201-205	DNA damage inducible transcript 3	Homo sapiens	84-91
17525289-4	2007	Treatment with thapsigargin and tunicamycin led to the activation of all 3 branches of the UPR, with early splicing of XBP1 indicative of IRE1 activation, upregulation of CHOP consistent with ER resident kinase (PERK) activation, and activating transcription factor 6 (ATF6) splicing.	Thapsigargin	15-27	DNA damage inducible transcript 3	Homo sapiens	171-175
17914584-3	2007	Treatment of HT29 human colon carcinoma cells with resveratrol was found to induce a number of signature ER stress markers; phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), ER stress-specific XBP1 splicing and CCAAT/enhancer-binding protein-homologous protein (CHOP).	Resveratrol	51-62	DNA damage inducible transcript 3	Homo sapiens	230-279
17914584-3	2007	Treatment of HT29 human colon carcinoma cells with resveratrol was found to induce a number of signature ER stress markers; phosphorylation of eukaryotic initiation factor-2alpha (eIF-2alpha), ER stress-specific XBP1 splicing and CCAAT/enhancer-binding protein-homologous protein (CHOP).	Resveratrol	51-62	DNA damage inducible transcript 3	Homo sapiens	281-285
17652152-9	2007	These results suggest that asoprisnil elicits ER stress-induced apoptosis in cultured leiomyoma cells and that GADD153 plays a role in asoprisnil-induced apoptosis by modulating the Bcl-2 family of proteins, GADD34, and TRB3.	asoprisnil	135-145	DNA damage inducible transcript 3	Homo sapiens	111-118
17525289-4	2007	Treatment with thapsigargin and tunicamycin led to the activation of all 3 branches of the UPR, with early splicing of XBP1 indicative of IRE1 activation, upregulation of CHOP consistent with ER resident kinase (PERK) activation, and activating transcription factor 6 (ATF6) splicing.	Tunicamycin	32-43	DNA damage inducible transcript 3	Homo sapiens	171-175
17525289-5	2007	17-AAG and radicicol also induced splicing of XBP1, with the induction of CHOP and activation of ATF6, whereas bortezomib resulted in the induction of CHOP and activation of ATF6 with minimal effects on XBP1.	tanespimycin	0-6	DNA damage inducible transcript 3	Homo sapiens	74-78
17525289-5	2007	17-AAG and radicicol also induced splicing of XBP1, with the induction of CHOP and activation of ATF6, whereas bortezomib resulted in the induction of CHOP and activation of ATF6 with minimal effects on XBP1.	monorden	11-20	DNA damage inducible transcript 3	Homo sapiens	74-78
17700714-8	2007	KEY RESULTS: Macrophages and SMCs treated with spermine NONOate or SNAP showed several signs of ER stress, including upregulation of CHOP expression, hyperphosphorylation of eIF2 alpha, inhibition of de novo protein synthesis and splicing of XBP1 mRNA.	spermine nitric oxide complex	47-63	DNA damage inducible transcript 3	Homo sapiens	133-137
17700714-10	2007	Plaques from molsidomine-treated atherosclerotic rabbits showed a 2.7-fold increase in CHOP expression as compared to placebo.	Molsidomine	13-24	DNA damage inducible transcript 3	Homo sapiens	87-91
17525289-5	2007	17-AAG and radicicol also induced splicing of XBP1, with the induction of CHOP and activation of ATF6, whereas bortezomib resulted in the induction of CHOP and activation of ATF6 with minimal effects on XBP1.	Bortezomib	111-121	DNA damage inducible transcript 3	Homo sapiens	151-155
17970084-0	2007	GADD153 mediates berberine-induced apoptosis in human cervical cancer Ca ski cells.	Berberine	17-26	DNA damage inducible transcript 3	Homo sapiens	0-7
17572895-1	2007	The objective of this study is to evaluate the long-term efficacy and safety of rituximab combined with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in Chinese patients with newly diagnosed diffuse large B cell lymphoma (DLBCL).	Prednisone	152-162	DNA damage inducible transcript 3	Homo sapiens	164-168
17686866-8	2007	We further observed a transient phosphorylation of eIF2alpha and induction of the proapoptotic cyclic AMP response element-binding transcription factor homologous protein (CHOP).	Cyclic AMP	95-105	DNA damage inducible transcript 3	Homo sapiens	172-176
17696482-8	2007	Pterostilbene markedly enhanced the expression of growth arrest DNA damage-inducible gene 45 and 153 (GADD45 and GADD153) in a time-dependent manner.	pterostilbene	0-13	DNA damage inducible transcript 3	Homo sapiens	113-120
17970084-5	2007	Western blot also showed that berberine induced the expression of GADD153, a transcription factor involved in apoptosis.	Berberine	30-39	DNA damage inducible transcript 3	Homo sapiens	66-73
17970084-6	2007	Thus berberine increased ROS levels leading to endoplasmic reticulum (ER) stress based on the increase of GADD153 and shown by Ca2+ release from the ER.	Berberine	5-14	DNA damage inducible transcript 3	Homo sapiens	106-113
17957940-9	2007	At this time, he was treated with cyclophosphamide, adriamycin, vincristine, and prednisolone (CHOP) with whole brain irradiation.	Prednisolone	81-93	DNA damage inducible transcript 3	Homo sapiens	95-99
17804742-4	2007	Silibinin treatment up-regulated DR5, a death receptor of TRAIL, in a transcription factor CHOP-dependent manner.	Silybin	0-9	DNA damage inducible transcript 3	Homo sapiens	91-95
17876158-3	2007	Lamivudine (LAM) was administered orally from the start of R-CHOP.	Lamivudine	0-10	DNA damage inducible transcript 3	Homo sapiens	61-65
17699800-6	2007	This analysis revealed that many genes implicated in endoplasmic reticulum (ER) stress signaling, including ATF3, DDIT3, HERPUD1, HSPA5, XBP1, PDIA4, and PHLDA1, were highly up-regulated within 4 h of FOH treatment, suggesting that FOH-induced apoptosis involves an ER stress response.	foh	201-204	DNA damage inducible transcript 3	Homo sapiens	114-119
17939339-5	2007	A CT scan performed following three cycles of chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) showed that the mass had nearly disappeared.	Cyclophosphamide	64-80	DNA damage inducible transcript 3	Homo sapiens	126-130
17939339-5	2007	A CT scan performed following three cycles of chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) showed that the mass had nearly disappeared.	Doxorubicin	82-93	DNA damage inducible transcript 3	Homo sapiens	126-130
17939339-5	2007	A CT scan performed following three cycles of chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) showed that the mass had nearly disappeared.	Prednisolone	112-124	DNA damage inducible transcript 3	Homo sapiens	126-130
17786711-1	2007	This study was performed to investigate hematotoxicity and occurrence of PPE in patients with high-grade non-Hodgkins lymphoma treated with a modified CHOP regimen (CLAOP), where doxorubicin had been substituted by a noncardiotoxic pegliposomal doxorubicin.	claop	165-170	DNA damage inducible transcript 3	Homo sapiens	151-155
17699800-6	2007	This analysis revealed that many genes implicated in endoplasmic reticulum (ER) stress signaling, including ATF3, DDIT3, HERPUD1, HSPA5, XBP1, PDIA4, and PHLDA1, were highly up-regulated within 4 h of FOH treatment, suggesting that FOH-induced apoptosis involves an ER stress response.	foh	232-235	DNA damage inducible transcript 3	Homo sapiens	114-119
17094093-5	2007	She received two cycles of cyclophosphamide, vincristine, doxorubicin, and prednisolone (CHOP) that started 10 weeks after the initiation of antiretroviral therapy.	Prednisolone	75-87	DNA damage inducible transcript 3	Homo sapiens	89-93
17464326-3	2007	Cadmium chloride (CdCl(2)) induced expression of endogenous ER stress markers, GRP78, GRP94 and CHOP in vitro and in vivo, and subsequently caused cytological changes typical of apoptosis.	Cadmium Chloride	0-16	DNA damage inducible transcript 3	Homo sapiens	96-100
17464326-3	2007	Cadmium chloride (CdCl(2)) induced expression of endogenous ER stress markers, GRP78, GRP94 and CHOP in vitro and in vivo, and subsequently caused cytological changes typical of apoptosis.	cdcl	18-22	DNA damage inducible transcript 3	Homo sapiens	96-100
17464326-8	2007	CdCl(2) also triggered activation of the inositol-requiring ER-to-nucleus signal kinase 1 (IRE1)-X-box-binding protein 1 (XBP1) pathway and inhibition of XBP1 attenuated apoptosis independent of GRP78 and CHOP.	cdcl	0-4	DNA damage inducible transcript 3	Homo sapiens	205-209
17464326-8	2007	CdCl(2) also triggered activation of the inositol-requiring ER-to-nucleus signal kinase 1 (IRE1)-X-box-binding protein 1 (XBP1) pathway and inhibition of XBP1 attenuated apoptosis independent of GRP78 and CHOP.	Inositol	41-49	DNA damage inducible transcript 3	Homo sapiens	205-209
17683387-2	2007	We report an elderly patient with C-ALCL which recurred after cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy, but was effectively treated with the third-generation etoposide, mitoxantrone, cyclophosphamide, vincristine, prednisolone and bleomycin (VNCOP-B) regimen.	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	121-125
17683387-2	2007	We report an elderly patient with C-ALCL which recurred after cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy, but was effectively treated with the third-generation etoposide, mitoxantrone, cyclophosphamide, vincristine, prednisolone and bleomycin (VNCOP-B) regimen.	Etoposide	190-199	DNA damage inducible transcript 3	Homo sapiens	121-125
17440927-2	2007	Japanese drink green tea throughout the day, so we studied whether multiple treatments of cells with EGCG would enhance the expression of apoptosis-related genes, such as growth arrest and DNA damage-inducible gene (GADD153) and cyclin-dependent kinase inhibitor gene (p21(waf1)): The results suggest that the synergistic enhancement of both GADD153 and p21(waf1) gene expressions by multiple treatments plays a significant role in human cancer prevention with green tea beverage.	epigallocatechin gallate	101-105	DNA damage inducible transcript 3	Homo sapiens	216-223
17440927-2	2007	Japanese drink green tea throughout the day, so we studied whether multiple treatments of cells with EGCG would enhance the expression of apoptosis-related genes, such as growth arrest and DNA damage-inducible gene (GADD153) and cyclin-dependent kinase inhibitor gene (p21(waf1)): The results suggest that the synergistic enhancement of both GADD153 and p21(waf1) gene expressions by multiple treatments plays a significant role in human cancer prevention with green tea beverage.	epigallocatechin gallate	101-105	DNA damage inducible transcript 3	Homo sapiens	342-349
17429839-5	2007	Six RCTs compared rituximab in conjunction with the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) versus CHOP alone for the treatment of B-cell non-Hodgkin lymphoma (NHL).	Prednisone	115-125	DNA damage inducible transcript 3	Homo sapiens	127-131
17548474-4	2007	Notably, treatment with sorafenib induced endoplasmic reticulum (ER) stress in human leukemia cells (U937) manifested by immediate cytosolic-calcium mobilization, GADD153 and GADD34 protein induction, PKR-like ER kinase (PERK) and eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation, XBP1 splicing, and a general reduction in protein synthesis as assessed by [35S]methionine incorporation.	Sorafenib	24-33	DNA damage inducible transcript 3	Homo sapiens	163-170
17615236-3	2007	Here we show that CHOP expression is induced in cultured pancreatic beta-cells maintained in a basal glucose concentration of 5.5 mM and repressed by stimulatory glucose (&gt;or=11 mM).	Glucose	101-108	DNA damage inducible transcript 3	Homo sapiens	18-22
17615236-3	2007	Here we show that CHOP expression is induced in cultured pancreatic beta-cells maintained in a basal glucose concentration of 5.5 mM and repressed by stimulatory glucose (&gt;or=11 mM).	Glucose	162-169	DNA damage inducible transcript 3	Homo sapiens	18-22
17536822-8	2007	5-OH-HxMF markedly enhanced growth arrest DNA damage-inducible gene 153 (GADD153) protein in a time-dependent manner.	5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone	0-9	DNA damage inducible transcript 3	Homo sapiens	28-71
17536822-8	2007	5-OH-HxMF markedly enhanced growth arrest DNA damage-inducible gene 153 (GADD153) protein in a time-dependent manner.	5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone	0-9	DNA damage inducible transcript 3	Homo sapiens	73-80
17536822-9	2007	N-acetylcysteine (NAC) and catalase prevented up-regulation of GADD153 expression caused by 5-OH-HxMF.	Acetylcysteine	0-16	DNA damage inducible transcript 3	Homo sapiens	63-70
17536822-9	2007	N-acetylcysteine (NAC) and catalase prevented up-regulation of GADD153 expression caused by 5-OH-HxMF.	Acetylcysteine	18-21	DNA damage inducible transcript 3	Homo sapiens	63-70
17536822-9	2007	N-acetylcysteine (NAC) and catalase prevented up-regulation of GADD153 expression caused by 5-OH-HxMF.	5-oh	92-96	DNA damage inducible transcript 3	Homo sapiens	63-70
17536822-10	2007	These findings suggest that 5-OH-HxMF creates an oxidative cellular environment that induces DNA damage and GADD153 gene activation, which in turn helps trigger apoptosis in HL-60 cells.	5-hydroxy-3,6,7,8,3',4'-hexamethoxyflavone	28-37	DNA damage inducible transcript 3	Homo sapiens	108-115
17217928-5	2007	RESULTS: Compared with control subjects, thapsigargin- and tunicamycin-induced increases in XBP1 and CHOP but not GRP78 messenger RNA levels were significantly lower in BD-I patients.	Thapsigargin	41-53	DNA damage inducible transcript 3	Homo sapiens	101-105
17217928-5	2007	RESULTS: Compared with control subjects, thapsigargin- and tunicamycin-induced increases in XBP1 and CHOP but not GRP78 messenger RNA levels were significantly lower in BD-I patients.	Tunicamycin	59-70	DNA damage inducible transcript 3	Homo sapiens	101-105
17591563-3	2007	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy has been the standard systemic therapy for this disease with a cure rate of 40% to 50%, although, more recently, the addition of rituximab has been shown in phase III trials to confer a significant survival benefit in both older and younger patients.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
17591563-3	2007	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy has been the standard systemic therapy for this disease with a cure rate of 40% to 50%, although, more recently, the addition of rituximab has been shown in phase III trials to confer a significant survival benefit in both older and younger patients.	Doxorubicin	18-29	DNA damage inducible transcript 3	Homo sapiens	60-64
17591563-3	2007	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy has been the standard systemic therapy for this disease with a cure rate of 40% to 50%, although, more recently, the addition of rituximab has been shown in phase III trials to confer a significant survival benefit in both older and younger patients.	Prednisone	48-58	DNA damage inducible transcript 3	Homo sapiens	60-64
17493934-0	2007	The farnesyltransferase inhibitor lonafarnib induces CCAAT/enhancer-binding protein homologous protein-dependent expression of death receptor 5, leading to induction of apoptosis in human cancer cells.	lonafarnib	34-44	DNA damage inducible transcript 3	Homo sapiens	53-102
17493934-10	2007	By analyzing the DR5 promoter, we found that lonafarnib induced a CCAAT/enhancer-binding protein homologous protein (CHOP)-dependent transactivation of the DR5 promoter.	lonafarnib	45-55	DNA damage inducible transcript 3	Homo sapiens	66-115
17493934-10	2007	By analyzing the DR5 promoter, we found that lonafarnib induced a CCAAT/enhancer-binding protein homologous protein (CHOP)-dependent transactivation of the DR5 promoter.	lonafarnib	45-55	DNA damage inducible transcript 3	Homo sapiens	117-121
17493934-11	2007	Lonafarnib increased CHOP expression, whereas silencing of CHOP expression abrogated lonafarnib-induced DR5 expression.	lonafarnib	0-10	DNA damage inducible transcript 3	Homo sapiens	21-25
17493934-11	2007	Lonafarnib increased CHOP expression, whereas silencing of CHOP expression abrogated lonafarnib-induced DR5 expression.	lonafarnib	85-95	DNA damage inducible transcript 3	Homo sapiens	59-63
17493934-12	2007	These results thus indicate that lonafarnib induces CHOP-dependent DR5 up-regulation.	lonafarnib	33-43	DNA damage inducible transcript 3	Homo sapiens	52-56
17493934-13	2007	We conclude that CHOP-dependent DR5 up-regulation contributes to lonafarnib-induced apoptosis.	lonafarnib	65-75	DNA damage inducible transcript 3	Homo sapiens	17-21
17575218-1	2007	PURPOSE: To evaluate 3"-deoxy-3"-[(18)F]fluorothymidine-positron emission tomography (FLT-PET) for early monitoring response of high-grade non-Hodgkin"s lymphoma to treatment with cyclophosphamide-adriamycin-vincristine-prednisone chemotherapy with or without rituximab immunotherapy (R-CHOP/CHOP).	3"-deoxy-3"-[(	21-35	DNA damage inducible transcript 3	Homo sapiens	287-291
17575218-1	2007	PURPOSE: To evaluate 3"-deoxy-3"-[(18)F]fluorothymidine-positron emission tomography (FLT-PET) for early monitoring response of high-grade non-Hodgkin"s lymphoma to treatment with cyclophosphamide-adriamycin-vincristine-prednisone chemotherapy with or without rituximab immunotherapy (R-CHOP/CHOP).	3"-deoxy-3"-[(	21-35	DNA damage inducible transcript 3	Homo sapiens	292-296
17455323-0	2007	Brain-derived neurotrophic factor suppresses tunicamycin-induced upregulation of CHOP in neurons.	Tunicamycin	45-56	DNA damage inducible transcript 3	Homo sapiens	81-85
17341418-7	2007	Indomethacin treatment was associated with increased expression of glucose-regulated protein 78 (GRP78) and C/EBP homologus protein (CHOP) and activation of ATF-6, characteristics of endoplasmic reticulum stress.	Indomethacin	0-12	DNA damage inducible transcript 3	Homo sapiens	108-131
17341418-7	2007	Indomethacin treatment was associated with increased expression of glucose-regulated protein 78 (GRP78) and C/EBP homologus protein (CHOP) and activation of ATF-6, characteristics of endoplasmic reticulum stress.	Indomethacin	0-12	DNA damage inducible transcript 3	Homo sapiens	133-137
17341418-10	2007	Selective inhibitors of ERK, p38 MAPK, and JNK suppressed the induction of GRP78, CHOP, and PPAR-beta, attenuated indomethacin-induced cytotoxicity and reduced increased caspase activity.	Indomethacin	114-126	DNA damage inducible transcript 3	Homo sapiens	82-86
17562513-5	2007	We present multidetector CT (MDCT) findings in a case of Hodgkin disease status one month post-chemotherapy (CHOP protocol; cyclophosphamide, doxorubicin, vincristine, prednisone) that presented with acute lower GIS bleeding.	Cyclophosphamide	124-140	DNA damage inducible transcript 3	Homo sapiens	109-113
17562513-5	2007	We present multidetector CT (MDCT) findings in a case of Hodgkin disease status one month post-chemotherapy (CHOP protocol; cyclophosphamide, doxorubicin, vincristine, prednisone) that presented with acute lower GIS bleeding.	Prednisone	168-178	DNA damage inducible transcript 3	Homo sapiens	109-113
17513780-6	2007	Such treated nuclei contain only C/EBPzeta (also known as CHOP10 and GADD153) because the C/EBP-binding consensus oligonucleotide binds to all C/EBP family proteins except C/EBPzeta.	Oligonucleotides	114-129	DNA damage inducible transcript 3	Homo sapiens	33-42
17513780-6	2007	Such treated nuclei contain only C/EBPzeta (also known as CHOP10 and GADD153) because the C/EBP-binding consensus oligonucleotide binds to all C/EBP family proteins except C/EBPzeta.	Oligonucleotides	114-129	DNA damage inducible transcript 3	Homo sapiens	58-64
17513780-6	2007	Such treated nuclei contain only C/EBPzeta (also known as CHOP10 and GADD153) because the C/EBP-binding consensus oligonucleotide binds to all C/EBP family proteins except C/EBPzeta.	Oligonucleotides	114-129	DNA damage inducible transcript 3	Homo sapiens	69-76
17621460-8	2007	With HAART, OS was 33% for CT and 86% for CHOP-R; HR for CHOP-R was 0.4 (95% CI 0.1-1.2).	Osmium	12-14	DNA damage inducible transcript 3	Homo sapiens	42-46
17368854-6	2007	Importantly, we showed that, following H2O2 treatment, gadd153 gene reached higher levels of expression in replicon cells.	Hydrogen Peroxide	39-43	DNA damage inducible transcript 3	Homo sapiens	55-62
17368854-8	2007	Treatment of replicon cells with a specific small interfering RNA, targeted to gadd153 gene, reduced basal expression of gadd153 and decreased cell death following H2O2.	Hydrogen Peroxide	164-168	DNA damage inducible transcript 3	Homo sapiens	79-86
17488991-5	2007	However, response rate is usually lower in elderly patients compared with young patients, even if the patients are treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Cyclophosphamide	132-148	DNA damage inducible transcript 3	Homo sapiens	192-196
17488991-5	2007	However, response rate is usually lower in elderly patients compared with young patients, even if the patients are treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Doxorubicin	150-161	DNA damage inducible transcript 3	Homo sapiens	192-196
17530014-5	2007	A combination of rituximab plus chemotherapy, rituximab+cyclophosphamide+doxorubicin+vincristine+prednisolone (R-CHOP), has the highest efficacy ever described with any chemotherapy in DLBCL and FL.	Cyclophosphamide	56-72	DNA damage inducible transcript 3	Homo sapiens	113-117
17530014-5	2007	A combination of rituximab plus chemotherapy, rituximab+cyclophosphamide+doxorubicin+vincristine+prednisolone (R-CHOP), has the highest efficacy ever described with any chemotherapy in DLBCL and FL.	Doxorubicin	73-84	DNA damage inducible transcript 3	Homo sapiens	113-117
17530014-5	2007	A combination of rituximab plus chemotherapy, rituximab+cyclophosphamide+doxorubicin+vincristine+prednisolone (R-CHOP), has the highest efficacy ever described with any chemotherapy in DLBCL and FL.	Vincristine	85-96	DNA damage inducible transcript 3	Homo sapiens	113-117
17530014-5	2007	A combination of rituximab plus chemotherapy, rituximab+cyclophosphamide+doxorubicin+vincristine+prednisolone (R-CHOP), has the highest efficacy ever described with any chemotherapy in DLBCL and FL.	Prednisolone	97-109	DNA damage inducible transcript 3	Homo sapiens	113-117
17171638-0	2007	Curcumin-induced GADD153 upregulation: modulation by glutathione.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-0	2007	Curcumin-induced GADD153 upregulation: modulation by glutathione.	Glutathione	53-64	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-1	2007	As we reported previously, GADD153 is upregulated in colon cancer cells exposed to curcumin.	Curcumin	83-91	DNA damage inducible transcript 3	Homo sapiens	27-34
17171638-2	2007	In the present study, we ascertained the involvement of glutathione and certain sulfhydryl enzymes associated with signal transduction in mediating the effect of curcumin on GADD153.	Glutathione	56-67	DNA damage inducible transcript 3	Homo sapiens	174-181
17171638-2	2007	In the present study, we ascertained the involvement of glutathione and certain sulfhydryl enzymes associated with signal transduction in mediating the effect of curcumin on GADD153.	Curcumin	162-170	DNA damage inducible transcript 3	Homo sapiens	174-181
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Glutathione	69-80	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Glutathione	82-85	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	90-106	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Acetylcysteine	108-111	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Glutathione	136-147	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	l-buthionine sulfoximine	169-199	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-3	2007	Curcumin-induced GADD153 gene upregulation was attenuated by reduced glutathione (GSH) or N-acetylcysteine (NAC) and potentiated by the glutathione synthesis inhibitor, L-buthionine-(S,R)-sulfoximine (BSO).	Buthionine Sulfoximine	201-204	DNA damage inducible transcript 3	Homo sapiens	17-24
17171638-6	2007	In affecting the thiol redox status, curcumin caused activation of certain sulfhydryl enzymes involved in signal transduction linked to GADD153 expression.	Sulfhydryl Compounds	17-22	DNA damage inducible transcript 3	Homo sapiens	136-143
17171638-6	2007	In affecting the thiol redox status, curcumin caused activation of certain sulfhydryl enzymes involved in signal transduction linked to GADD153 expression.	Curcumin	37-45	DNA damage inducible transcript 3	Homo sapiens	136-143
17171638-8	2007	Furthermore, selective inhibitors of PI3K and PKC-delta attenuated curcumin-induced GADD153 upregulation.	Curcumin	67-75	DNA damage inducible transcript 3	Homo sapiens	84-91
17171638-9	2007	Collectively, these findings suggest that a regulatory thiol redox-sensitive signaling cascade exists in the molecular pathway leading to induction of GADD153 expression as caused by curcumin.	Sulfhydryl Compounds	55-60	DNA damage inducible transcript 3	Homo sapiens	151-158
17171638-9	2007	Collectively, these findings suggest that a regulatory thiol redox-sensitive signaling cascade exists in the molecular pathway leading to induction of GADD153 expression as caused by curcumin.	Curcumin	183-191	DNA damage inducible transcript 3	Homo sapiens	151-158
17488991-5	2007	However, response rate is usually lower in elderly patients compared with young patients, even if the patients are treated with the cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen.	Prednisone	180-190	DNA damage inducible transcript 3	Homo sapiens	192-196
17284450-6	2007	Although salicylate treatment did not trigger activation of inositol-requiring enzyme 1, there was an increased expression of the pro-apoptotic transcription factor CHOP-(gadd153), a downstream event to eIF2alpha phosphorylation known to mediate endoplasmic reticulum stress-mediated responses.	Salicylates	9-19	DNA damage inducible transcript 3	Homo sapiens	165-178
17353921-4	2007	The retinoid analogue fenretinide [N-(4-hydroxyphenyl) retinamide] is a new cancer preventive and chemotherapeutic drug, that induces apoptosis of some cancer cell types via oxidative stress, accompanied by induction of an ER stress-related transcription factor, GADD153.	Retinoids	4-12	DNA damage inducible transcript 3	Homo sapiens	263-270
17353921-4	2007	The retinoid analogue fenretinide [N-(4-hydroxyphenyl) retinamide] is a new cancer preventive and chemotherapeutic drug, that induces apoptosis of some cancer cell types via oxidative stress, accompanied by induction of an ER stress-related transcription factor, GADD153.	Fenretinide	22-33	DNA damage inducible transcript 3	Homo sapiens	263-270
17353921-4	2007	The retinoid analogue fenretinide [N-(4-hydroxyphenyl) retinamide] is a new cancer preventive and chemotherapeutic drug, that induces apoptosis of some cancer cell types via oxidative stress, accompanied by induction of an ER stress-related transcription factor, GADD153.	Fenretinide	35-65	DNA damage inducible transcript 3	Homo sapiens	263-270
16997373-10	2007	The patient was treated with six cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	102-106
16997373-10	2007	The patient was treated with six cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	102-106
17361405-2	2007	Six cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone-21 (CHOP-21) with rituximab (R-CHOP-21) achieved an event free survival after 3 years of &gt; 90% in patients with a very good prognosis (IPI 0, without bulk).	Cyclophosphamide	14-30	DNA damage inducible transcript 3	Homo sapiens	77-81
17218490-1	2007	BACKGROUND: As patients with B-cell lymphomas suffering from an underlying autoimmune condition undergoing therapy with the CD20 antibody rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) offer the unique possibility of monitoring effects of therapy on various rheumatologic parameters, we have evaluated serologic autoimmune markers and the clinical outcome of patients with autoimmune diseases (ADs) who received lymphoma treatment with R-CHOP during the course of their disease.	Vincristine	180-191	DNA damage inducible transcript 3	Homo sapiens	210-214
17218490-1	2007	BACKGROUND: As patients with B-cell lymphomas suffering from an underlying autoimmune condition undergoing therapy with the CD20 antibody rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) offer the unique possibility of monitoring effects of therapy on various rheumatologic parameters, we have evaluated serologic autoimmune markers and the clinical outcome of patients with autoimmune diseases (ADs) who received lymphoma treatment with R-CHOP during the course of their disease.	Vincristine	180-191	DNA damage inducible transcript 3	Homo sapiens	469-473
17361405-2	2007	Six cycles of cyclophosphamide, doxorubicin, vincristine, and prednisone-21 (CHOP-21) with rituximab (R-CHOP-21) achieved an event free survival after 3 years of &gt; 90% in patients with a very good prognosis (IPI 0, without bulk).	Prednisone	62-72	DNA damage inducible transcript 3	Homo sapiens	77-81
17273769-4	2007	In this study, we report that fenretinide induces death receptor 5 (DR5)/TRAIL-R2 up-regulation via the induction of the transcription factor CHOP in colon cancer cell lines.	Fenretinide	30-41	DNA damage inducible transcript 3	Homo sapiens	142-146
17431104-4	2007	We show that DMC increases intracellular free calcium levels and potently triggers the ESR in various tumor cell lines, as indicated by transient inhibition of protein synthesis, activation of ER stress-associated proteins GRP78/BiP, CHOP/GADD153, and caspase-4, and subsequent tumor cell death.	2,5-dimethylcelecoxib	13-16	DNA damage inducible transcript 3	Homo sapiens	239-246
17143626-2	2007	Clinical manifestations and laboratory parameters were improved after treatment with CHOP chemotherapy and enalapril.	Enalapril	107-116	DNA damage inducible transcript 3	Homo sapiens	85-89
16917513-6	2007	However, we found that Fas/CD95 was significantly induced in response to hypoxia in a p53-dependent manner, along with several novel p53 target genes including ANXA1, DDIT3/GADD153 (CHOP), SEL1L and SMURF1.	ammonium ferrous sulfate	23-26	DNA damage inducible transcript 3	Homo sapiens	173-180
16917513-6	2007	However, we found that Fas/CD95 was significantly induced in response to hypoxia in a p53-dependent manner, along with several novel p53 target genes including ANXA1, DDIT3/GADD153 (CHOP), SEL1L and SMURF1.	ammonium ferrous sulfate	23-26	DNA damage inducible transcript 3	Homo sapiens	182-186
17454628-7	2007	Zosuquidar.3HCL can be safely administered with CHOP therapy using a 24-h schedule.	Zosuquidar	0-10	DNA damage inducible transcript 3	Homo sapiens	48-52
17454628-7	2007	Zosuquidar.3HCL can be safely administered with CHOP therapy using a 24-h schedule.	3hcl	11-15	DNA damage inducible transcript 3	Homo sapiens	48-52
17188247-6	2007	Genistein induced the activation of several ER stress-relevant regulators, including m-calpain, GADD153, GRP78 and caspase-12.	Genistein	0-9	DNA damage inducible transcript 3	Homo sapiens	96-103
17188247-7	2007	Furthermore, genistein-induced effect was inhibited in cells transfected with antisense GADD153 cDNA, indicating a functional role of GADD153.	Genistein	13-22	DNA damage inducible transcript 3	Homo sapiens	88-95
17188247-7	2007	Furthermore, genistein-induced effect was inhibited in cells transfected with antisense GADD153 cDNA, indicating a functional role of GADD153.	Genistein	13-22	DNA damage inducible transcript 3	Homo sapiens	134-141
17105812-9	2007	In the era of R-CHOP treatment, the R-IPI is a clinically useful prognostic index that may help guide treatment planning and interpretation of clinical trials.	r-ipi	36-41	DNA damage inducible transcript 3	Homo sapiens	16-20
17273769-0	2007	Fenretinide up-regulates DR5/TRAIL-R2 expression via the induction of the transcription factor CHOP and combined treatment with fenretinide and TRAIL induces synergistic apoptosis in colon cancer cell lines.	Fenretinide	0-11	DNA damage inducible transcript 3	Homo sapiens	95-99
17273769-3	2007	Oxidative stress induced by fenretinide has been shown to mediate apoptosis through a mitochondrial pathway by the induction of a transcription factor CCAAT/enhancer binding protein homologous protein (CHOP) and Bak.	Fenretinide	28-39	DNA damage inducible transcript 3	Homo sapiens	151-200
17273769-3	2007	Oxidative stress induced by fenretinide has been shown to mediate apoptosis through a mitochondrial pathway by the induction of a transcription factor CCAAT/enhancer binding protein homologous protein (CHOP) and Bak.	Fenretinide	28-39	DNA damage inducible transcript 3	Homo sapiens	202-206
17273769-6	2007	Furthermore, fenretinide increased DR5 promoter activity and the enhanced activity decreased by mutation of the CHOP binding site.	Fenretinide	13-24	DNA damage inducible transcript 3	Homo sapiens	112-116
17273769-7	2007	CHOP was also up-regulated by fenretinide at the promoter level.	Fenretinide	30-41	DNA damage inducible transcript 3	Homo sapiens	0-4
17167033-9	2007	In contrast, siRNA for ORP150 stimulated apoptosis and expression of CHOP in the presence of celecoxib but not staurosporine.	Celecoxib	93-102	DNA damage inducible transcript 3	Homo sapiens	69-73
17198682-3	2007	In HL-60 cells, curcumin induced apoptosis and endoplasmic reticulum (ER) stress as evidenced by the survival molecules such as phosphorylated protein kinase-like ER-resident kinase, phosphorylated eukaryotic initiation factor-2alpha, glucose-regulated protein-78, and the apoptotic molecules such as caspase-4 and CAAT/enhancer binding protein homologous protein (CHOP).	Curcumin	16-24	DNA damage inducible transcript 3	Homo sapiens	365-369
17198682-4	2007	Inhibition of caspase-4 activity by z-LEVD-FMK, blockage of CHOP expression by small interfering RNA, and treatment with salubrinal, an ER inhibitor, significantly reduced curcumin-induced apoptosis.	Curcumin	172-180	DNA damage inducible transcript 3	Homo sapiens	60-64
17031849-3	2007	We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1.	Tretinoin	78-82	DNA damage inducible transcript 3	Homo sapiens	152-179
17308121-7	2007	Preferentially in immunoglobulin-high myeloma cells, bortezomib triggered activation of caspases and induction of proapoptotic CHOP, a component of the terminal unfolded protein response induced by endoplasmic reticulum (ER) stress.	Bortezomib	53-63	DNA damage inducible transcript 3	Homo sapiens	127-131
17031849-3	2007	We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1.	Tretinoin	78-82	DNA damage inducible transcript 3	Homo sapiens	181-185
17031849-3	2007	We show here that ER stress is enhanced in GnT-V-AS/7721 cells with 80 microM ATRA treatment for 24 h, which is evidenced by the increase of GRP78/Bip, C/EBP-homologous protein-10 (CHOP, also known as GADD153) and spliced XBP1.	Tretinoin	78-82	DNA damage inducible transcript 3	Homo sapiens	201-208
17031689-1	2007	Although adding rituximab to standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy is an efficacious and well-tolerated regimen in elderly patients with diffuse large B cell lymphoma (DLBCL), it may increase susceptibility to opportunistic infections, and such cases have been reported.	Doxorubicin	56-67	DNA damage inducible transcript 3	Homo sapiens	98-102
17140562-0	2007	Ilimaquinone, a marine sponge metabolite, displays anticancer activity via GADD153-mediated pathway.	ilimaquinone	0-12	DNA damage inducible transcript 3	Homo sapiens	75-82
17140562-9	2007	The data demonstrated that ilimaquinone did not activate extracellular signal-regulated kinase and phosphatidylinositol 3-kinase but induce the up-regulation and nuclear translocation of growth arrest and DNA damage inducible gene 153 (CHOP/GADD153).	ilimaquinone	27-39	DNA damage inducible transcript 3	Homo sapiens	236-240
17140562-9	2007	The data demonstrated that ilimaquinone did not activate extracellular signal-regulated kinase and phosphatidylinositol 3-kinase but induce the up-regulation and nuclear translocation of growth arrest and DNA damage inducible gene 153 (CHOP/GADD153).	ilimaquinone	27-39	DNA damage inducible transcript 3	Homo sapiens	241-248
17140562-10	2007	Furthermore, ilimaquinone-mediated anti-proliferative effect is significantly reduced in the antisense CHOP/GADD153-overexpressing cells.	ilimaquinone	13-25	DNA damage inducible transcript 3	Homo sapiens	103-107
17140562-10	2007	Furthermore, ilimaquinone-mediated anti-proliferative effect is significantly reduced in the antisense CHOP/GADD153-overexpressing cells.	ilimaquinone	13-25	DNA damage inducible transcript 3	Homo sapiens	108-115
17140562-12	2007	In summary, it is suggested that ilimaquinone induces the anti-proliferative effect through the G(1) arrest of the cell cycle and the up-regulation and nuclear translocation of CHOP/GADD153.	ilimaquinone	33-45	DNA damage inducible transcript 3	Homo sapiens	177-181
17140562-12	2007	In summary, it is suggested that ilimaquinone induces the anti-proliferative effect through the G(1) arrest of the cell cycle and the up-regulation and nuclear translocation of CHOP/GADD153.	ilimaquinone	33-45	DNA damage inducible transcript 3	Homo sapiens	182-189
17031689-1	2007	Although adding rituximab to standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy is an efficacious and well-tolerated regimen in elderly patients with diffuse large B cell lymphoma (DLBCL), it may increase susceptibility to opportunistic infections, and such cases have been reported.	Prednisone	86-96	DNA damage inducible transcript 3	Homo sapiens	98-102
17018705-10	2007	The 3-year progression-free survival in patients who received rituximab plus combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOPR) chemotherapy was 88% compared with 52% in those who received CHOP-like chemotherapy without rituximab (P=0.005).	Prednisone	154-164	DNA damage inducible transcript 3	Homo sapiens	166-170
17242689-0	2007	Geldanamycin induces CHOP expression through a 4-(2-aminoethyl)-benzenesulfonyl fluoride-responsive serine protease.	geldanamycin	0-12	DNA damage inducible transcript 3	Homo sapiens	21-25
17242689-0	2007	Geldanamycin induces CHOP expression through a 4-(2-aminoethyl)-benzenesulfonyl fluoride-responsive serine protease.	4-(2-aminoethyl)-benzenesulfonyl	47-79	DNA damage inducible transcript 3	Homo sapiens	21-25
17113167-6	2007	Chelation of intracellular Ca(2+) with BAPTA-AM revealed that enhanced CHOP expression after store depletion occurred in a Ca(2+)-dependent manner in APP-overexpressing cells.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	39-47	DNA damage inducible transcript 3	Homo sapiens	71-75
17113167-7	2007	Prevention of CHOP induction by BAPTA-AM and by RNA interference was also able to abrogate the potentiating effect of APP on thapsigargin-induced apoptosis.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	32-40	DNA damage inducible transcript 3	Homo sapiens	14-18
17113167-7	2007	Prevention of CHOP induction by BAPTA-AM and by RNA interference was also able to abrogate the potentiating effect of APP on thapsigargin-induced apoptosis.	Thapsigargin	125-137	DNA damage inducible transcript 3	Homo sapiens	14-18
17370641-13	2007	Rituximab with CHOP (CVP) therapy is a possible treatment for primary follicular lymphoma in the duodenum.	COP protocol 2	21-24	DNA damage inducible transcript 3	Homo sapiens	15-19
17109853-0	2007	Inhibitory effect of 4-(2-aminoethyl)-benzenesulfonyl fluoride, a serine protease inhibitor, on PI3K inhibitor-induced CHOP expression.	4-(2-aminoethyl)benzenesulfonylfluoride	21-62	DNA damage inducible transcript 3	Homo sapiens	119-123
17109853-3	2007	In the present study, we investigated the effect of 4-(2-aminoethyl)-benzenesulfonyl fluoride (AEBSF), a serine protease inhibitor, on PI3K inhibitor-induced CHOP expression.	4-(2-aminoethyl)benzenesulfonylfluoride	52-93	DNA damage inducible transcript 3	Homo sapiens	158-162
17109853-3	2007	In the present study, we investigated the effect of 4-(2-aminoethyl)-benzenesulfonyl fluoride (AEBSF), a serine protease inhibitor, on PI3K inhibitor-induced CHOP expression.	4-(2-aminoethyl)benzenesulfonylfluoride	95-100	DNA damage inducible transcript 3	Homo sapiens	158-162
17049495-0	2007	Elevated gadd153/chop expression during resveratrol-induced apoptosis in human colon cancer cells.	Resveratrol	40-51	DNA damage inducible transcript 3	Homo sapiens	9-16
17352223-0	2007	ROS mediates baicalin-induced apoptosis in human promyelocytic leukemia HL-60 cells through the expression of the Gadd153 and mitochondrial-dependent pathway.	ros	0-3	DNA damage inducible transcript 3	Homo sapiens	114-121
17352223-0	2007	ROS mediates baicalin-induced apoptosis in human promyelocytic leukemia HL-60 cells through the expression of the Gadd153 and mitochondrial-dependent pathway.	baicalin	13-21	DNA damage inducible transcript 3	Homo sapiens	114-121
17352223-6	2007	Western blot demonstrated that baicalin promoted the levels of Gadd153, Bax, cytochrome c and caspase-3 and -12, but decreased the levels of Grp78 and Bcl-2 in HL-60 cells.	baicalin	31-39	DNA damage inducible transcript 3	Homo sapiens	63-70
17049495-0	2007	Elevated gadd153/chop expression during resveratrol-induced apoptosis in human colon cancer cells.	Resveratrol	40-51	DNA damage inducible transcript 3	Homo sapiens	17-21
17049495-3	2007	We demonstrate for the first time that resveratrol induce CCAAT/enhancer-binding protein-homologous protein (CHOP).	Resveratrol	39-50	DNA damage inducible transcript 3	Homo sapiens	58-107
17049495-3	2007	We demonstrate for the first time that resveratrol induce CCAAT/enhancer-binding protein-homologous protein (CHOP).	Resveratrol	39-50	DNA damage inducible transcript 3	Homo sapiens	109-113
17049495-4	2007	Resveratrol-induced CHOP mRNA (and also protein) expression was inhibited by JNK specific inhibitor, but not ERK, p38 MAPK, PI3K and NF-kappaB inhibitors.	Resveratrol	0-11	DNA damage inducible transcript 3	Homo sapiens	20-24
17049495-5	2007	Resveratrol-induced expression of CHOP involves the putative Sp1 site within the CHOP promoter region.	Resveratrol	0-11	DNA damage inducible transcript 3	Homo sapiens	34-38
17049495-5	2007	Resveratrol-induced expression of CHOP involves the putative Sp1 site within the CHOP promoter region.	Resveratrol	0-11	DNA damage inducible transcript 3	Homo sapiens	81-85
17049495-6	2007	Using a combination of the Sp1 cDNA transfection, the luciferase reporter assay and Sp1 inhibitor assay, we found that Sp1 site is required for resveratrol-mediated activation of the CHOP promoter.	Resveratrol	144-155	DNA damage inducible transcript 3	Homo sapiens	183-187
17049495-7	2007	Suppression of CHOP expression by CHOP siRNA and treatment with mithramycin A attenuated resveratrol-induced apoptosis.	Resveratrol	89-100	DNA damage inducible transcript 3	Homo sapiens	15-19
17049495-8	2007	Taken together, the present studies suggest that induction of CHOP protein may be involved, at least in part, in resveratrol-induced apoptosis.	Resveratrol	113-124	DNA damage inducible transcript 3	Homo sapiens	62-66
17166886-0	2007	GADD153 mediates celecoxib-induced apoptosis in cervical cancer cells.	Celecoxib	17-26	DNA damage inducible transcript 3	Homo sapiens	0-7
17166886-3	2007	Screening of a microarray cDNA-chip containing 225 different genes revealed that growth arrest and DNA damage inducible gene (GADD153), a transcription factor involved in apoptosis, showed the strongest differential expression following celecoxib treatment in all three cervical cancer cell lines.	Celecoxib	237-246	DNA damage inducible transcript 3	Homo sapiens	126-133
17166886-4	2007	Notably, siRNA-induced silencing of GADD153 suppressed celecoxib-induced apoptosis in all the three cell lines, and exogenous expression of GADD153 triggered apoptosis in cervical cancer cells in the absence of other apoptotic stimuli.	Celecoxib	55-64	DNA damage inducible transcript 3	Homo sapiens	36-43
17166886-5	2007	A luciferase reporter gene assay and mRNA stability tests revealed that expression of GADD153 was regulated at both the transcriptional and post-transcriptional levels following celecoxib treatment.	Celecoxib	178-187	DNA damage inducible transcript 3	Homo sapiens	86-93
17166886-6	2007	The region between -649 and -249, containing an intact C/EBP-ATF binding site, was required for the basal activity and celecoxib-induced stimulation of GADD153 promoter activity.	Celecoxib	119-128	DNA damage inducible transcript 3	Homo sapiens	152-159
17166886-7	2007	Also, mRNA stability test showed that celecoxib prolonged the half-life of GADD153 mRNA.	Celecoxib	38-47	DNA damage inducible transcript 3	Homo sapiens	75-82
17166886-10	2007	These novel findings collectively suggest that GADD153 may play a key role in celecoxib-induced apoptosis in cervical cancer cells by regulating the expression of proapoptotic proteins such as Bak.	Celecoxib	78-87	DNA damage inducible transcript 3	Homo sapiens	47-54
17220687-3	2007	Lymphoma enlarged even after the fourth courses of chemotherapy consisting of cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP).	Prednisolone	126-138	DNA damage inducible transcript 3	Homo sapiens	140-144
16996026-0	2006	Lactacystin inhibits 3T3-L1 adipocyte differentiation through induction of CHOP-10 expression.	lactacystin	0-11	DNA damage inducible transcript 3	Homo sapiens	75-82
16972258-0	2006	N-(4-hydroxyphenyl)retinamide induces apoptosis in human retinal pigment epithelial cells: retinoic acid receptors regulate apoptosis, reactive oxygen species generation, and the expression of heme oxygenase-1 and Gadd153.	Fenretinide	0-29	DNA damage inducible transcript 3	Homo sapiens	214-221
16972258-7	2006	In addition, the increase in the expression of heme oxygenase-1 (HO-1), a stress response protein, and the growth arrest and DNA damage-inducible transcription factor 153 (Gadd153) in response to the ROS generation were also blocked by these receptor antagonists.	Reactive Oxygen Species	200-203	DNA damage inducible transcript 3	Homo sapiens	172-179
16972258-8	2006	Pyrrolidine dithiocarbamate (PDTC), a free-radical scavenger, inhibited 4HPR-induced ROS generation, the expression of its downstream mediator, Gadd153, and apoptosis in the pretreated cells.	pyrrolidine dithiocarbamic acid	0-27	DNA damage inducible transcript 3	Homo sapiens	144-151
16972258-8	2006	Pyrrolidine dithiocarbamate (PDTC), a free-radical scavenger, inhibited 4HPR-induced ROS generation, the expression of its downstream mediator, Gadd153, and apoptosis in the pretreated cells.	pyrrolidine dithiocarbamic acid	29-33	DNA damage inducible transcript 3	Homo sapiens	144-151
16972258-8	2006	Pyrrolidine dithiocarbamate (PDTC), a free-radical scavenger, inhibited 4HPR-induced ROS generation, the expression of its downstream mediator, Gadd153, and apoptosis in the pretreated cells.	Fenretinide	72-76	DNA damage inducible transcript 3	Homo sapiens	144-151
17940628-13	2006	The patient was treated with rituximab, plus cyclophosphamide, Adriamycin, vincristine, and prednisone (CHOP-R), with intrathecal methotrexate prophylaxis.	Prednisone	92-102	DNA damage inducible transcript 3	Homo sapiens	104-108
16624596-1	2007	INTRODUCTION: Resistance to an anthracycline-based regimen, such as CHOP, constitutes a problem for curing non-Hodgkin"s lymphoma (NHL) patients.	Anthracyclines	31-44	DNA damage inducible transcript 3	Homo sapiens	68-72
17085516-4	2006	The management of patients with AIDS-related NHL with either infusional chemotherapy or CHOP-like regimens (cyclophosphamide, doxorubicin, vincristine and prednisolone) achieves response and survival rates approaching those observed in the general population.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	88-92
17085516-4	2006	The management of patients with AIDS-related NHL with either infusional chemotherapy or CHOP-like regimens (cyclophosphamide, doxorubicin, vincristine and prednisolone) achieves response and survival rates approaching those observed in the general population.	Doxorubicin	126-137	DNA damage inducible transcript 3	Homo sapiens	88-92
17085516-4	2006	The management of patients with AIDS-related NHL with either infusional chemotherapy or CHOP-like regimens (cyclophosphamide, doxorubicin, vincristine and prednisolone) achieves response and survival rates approaching those observed in the general population.	Vincristine	139-150	DNA damage inducible transcript 3	Homo sapiens	88-92
17085516-4	2006	The management of patients with AIDS-related NHL with either infusional chemotherapy or CHOP-like regimens (cyclophosphamide, doxorubicin, vincristine and prednisolone) achieves response and survival rates approaching those observed in the general population.	Prednisolone	155-167	DNA damage inducible transcript 3	Homo sapiens	88-92
16996026-4	2006	Evidences are presented in this report that lactacystin, a proteasome inhibitor, up-regulated the CHOP-10 expression, blocked the DNA-binding activity of C/EBPbeta, and subsequently inhibited MCE as well as adipocyte differentiation.	lactacystin	44-55	DNA damage inducible transcript 3	Homo sapiens	98-105
16609067-1	2006	The precise mechanism of rituximab plus cyclophosphamide/doxorubicin/vincristine/prednisone (R-CHOP) therapy in diffuse large B-cell lymphoma (DLBCL) is not fully elucidated.	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	95-99
16945918-3	2006	Cephalostatin 1 initiates a rapid endoplasmic reticulum stress response characterized by phosphorylation of eukaryotic initiation factor-2 alpha-subunit and increased expression of the chaperone immunoglobulin heavy chain-binding protein GRP78 as well as the transcription factor C/EBP homologous protein (CHOP)/GADD153.	cephalostatin I	0-15	DNA damage inducible transcript 3	Homo sapiens	280-304
16945918-3	2006	Cephalostatin 1 initiates a rapid endoplasmic reticulum stress response characterized by phosphorylation of eukaryotic initiation factor-2 alpha-subunit and increased expression of the chaperone immunoglobulin heavy chain-binding protein GRP78 as well as the transcription factor C/EBP homologous protein (CHOP)/GADD153.	cephalostatin I	0-15	DNA damage inducible transcript 3	Homo sapiens	306-310
16945918-3	2006	Cephalostatin 1 initiates a rapid endoplasmic reticulum stress response characterized by phosphorylation of eukaryotic initiation factor-2 alpha-subunit and increased expression of the chaperone immunoglobulin heavy chain-binding protein GRP78 as well as the transcription factor C/EBP homologous protein (CHOP)/GADD153.	cephalostatin I	0-15	DNA damage inducible transcript 3	Homo sapiens	312-319
17277854-2	2006	The standard treatment for advanced NHL is 8 cycles of combined chemotherapy, cyclophosphamide, adriamycin, vincristine and prednisone (CHOP).	Prednisone	124-134	DNA damage inducible transcript 3	Homo sapiens	136-140
16609067-1	2006	The precise mechanism of rituximab plus cyclophosphamide/doxorubicin/vincristine/prednisone (R-CHOP) therapy in diffuse large B-cell lymphoma (DLBCL) is not fully elucidated.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	95-99
16609067-5	2006	The FCGR3A valine (V) allele was significantly correlated with a higher complete response rate to R-CHOP compared with the phenylalanine (F) allele (88% in V/V vs 79% in V/F vs 50% in F/F; P = .002), while no difference was found between FCGR2A polymorphisms.	Valine	11-17	DNA damage inducible transcript 3	Homo sapiens	100-104
16613838-0	2006	Curcumin sensitizes tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis through CHOP-independent DR5 upregulation.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	111-115
16597647-0	2006	GADD153 mediates celecoxib-induced apoptosis in cervical cancer cells.	Celecoxib	17-26	DNA damage inducible transcript 3	Homo sapiens	0-7
16597647-3	2006	Screening of a cDNA microarray chip containing 225 different genes revealed that GADD153 (growth arrest and DNA damage inducible gene), a transcription factor involved in apoptosis, showed the strongest differential expression following celecoxib treatment in all three cervical cancer cell lines.	Celecoxib	237-246	DNA damage inducible transcript 3	Homo sapiens	81-88
16613838-4	2006	Curcumin also induced the expression of a potential pro-apoptotic gene, C/EBP homologous protein (CHOP), both at its mRNA and protein levels.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	72-96
16597647-4	2006	Notably, siRNA-induced silencing of GADD153 suppressed celecoxib-induced apoptosis in all three cell lines, and exogenous expression of GADD153 triggered apoptosis in cervical cancer cells in the absence of other apoptotic stimuli.	Celecoxib	55-64	DNA damage inducible transcript 3	Homo sapiens	36-43
16597647-5	2006	A luciferase reporter gene assay and mRNA stability tests revealed that the expression of GADD153 was regulated at both the transcriptional and post-transcriptional levels following celecoxib treatment.	Celecoxib	182-191	DNA damage inducible transcript 3	Homo sapiens	90-97
16613838-4	2006	Curcumin also induced the expression of a potential pro-apoptotic gene, C/EBP homologous protein (CHOP), both at its mRNA and protein levels.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	98-102
16597647-6	2006	The region between -649 and -249, containing an intact C/EBP-ATF binding site, is required for celecoxib-induced stimulation of GADD153 promoter activity.	Celecoxib	95-104	DNA damage inducible transcript 3	Homo sapiens	128-135
16613838-6	2006	Taken together, the present study demonstrates that curcumin enhances TRAIL-induced apoptosis by CHOP-independent upregulation of DR5.	Curcumin	52-60	DNA damage inducible transcript 3	Homo sapiens	97-101
16896003-2	2006	This study was performed to determine the efficacy of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy followed by tositumomab/iodine I-131 tositumomab.	Prednisone	102-112	DNA damage inducible transcript 3	Homo sapiens	114-118
16597647-9	2006	These novel findings collectively suggest that GADD153 may play a key role in celecoxib-induced apoptosis in cervical cancer cells by regulating the expression of proapoptotic proteins such as Bak.	Celecoxib	78-87	DNA damage inducible transcript 3	Homo sapiens	47-54
16597647-9	2006	These novel findings collectively suggest that GADD153 may play a key role in celecoxib-induced apoptosis in cervical cancer cells by regulating the expression of proapoptotic proteins such as Bak.	bakuchiol	193-196	DNA damage inducible transcript 3	Homo sapiens	47-54
17027654-4	2006	Second, the discovery of a potential curative combination of drugs, including cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), for use in advanced disease could eradicate micro-metastatic disease in patients with LD.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	138-142
17027654-4	2006	Second, the discovery of a potential curative combination of drugs, including cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), for use in advanced disease could eradicate micro-metastatic disease in patients with LD.	Doxorubicin	96-107	DNA damage inducible transcript 3	Homo sapiens	138-142
17027654-4	2006	Second, the discovery of a potential curative combination of drugs, including cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), for use in advanced disease could eradicate micro-metastatic disease in patients with LD.	Prednisone	126-136	DNA damage inducible transcript 3	Homo sapiens	138-142
16985248-1	2006	BACKGROUND: Follicular lymphoma is considered incurable, although cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy can induce sequential remissions.	Cyclophosphamide	66-82	DNA damage inducible transcript 3	Homo sapiens	126-130
16985248-1	2006	BACKGROUND: Follicular lymphoma is considered incurable, although cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy can induce sequential remissions.	Doxorubicin	84-95	DNA damage inducible transcript 3	Homo sapiens	126-130
16985248-1	2006	BACKGROUND: Follicular lymphoma is considered incurable, although cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy can induce sequential remissions.	Prednisone	114-124	DNA damage inducible transcript 3	Homo sapiens	126-130
16943530-2	2006	This conclusion is mainly derived from patients with mixed international prognostic index (IPI) risk profiles treated with CHOP-like therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Cyclophosphamide	142-158	DNA damage inducible transcript 3	Homo sapiens	123-127
16943530-2	2006	This conclusion is mainly derived from patients with mixed international prognostic index (IPI) risk profiles treated with CHOP-like therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Doxorubicin	160-171	DNA damage inducible transcript 3	Homo sapiens	123-127
16943530-2	2006	This conclusion is mainly derived from patients with mixed international prognostic index (IPI) risk profiles treated with CHOP-like therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Vincristine	173-184	DNA damage inducible transcript 3	Homo sapiens	123-127
16788784-5	2006	The standard chemotherapy for aggressive non-Hodgkin"s lymphomas is the CHOP regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone.	Cyclophosphamide	99-115	DNA damage inducible transcript 3	Homo sapiens	72-76
16788784-5	2006	The standard chemotherapy for aggressive non-Hodgkin"s lymphomas is the CHOP regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone.	Doxorubicin	117-128	DNA damage inducible transcript 3	Homo sapiens	72-76
16788784-5	2006	The standard chemotherapy for aggressive non-Hodgkin"s lymphomas is the CHOP regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone.	Vincristine	130-141	DNA damage inducible transcript 3	Homo sapiens	72-76
16788784-5	2006	The standard chemotherapy for aggressive non-Hodgkin"s lymphomas is the CHOP regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone.	Prednisone	147-157	DNA damage inducible transcript 3	Homo sapiens	72-76
16943530-2	2006	This conclusion is mainly derived from patients with mixed international prognostic index (IPI) risk profiles treated with CHOP-like therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone).	Prednisone	190-200	DNA damage inducible transcript 3	Homo sapiens	123-127
16518603-1	2006	Our aim was to study the efficacy of the addition of etoposide and bleomycin to a [cyclophosphamide (CPA), doxorubicin (DXR), vincristine (VCR), and prednisone (PDN)] CHOP-like regimen for the treatment of aggressive lymphoma.	Etoposide	53-62	DNA damage inducible transcript 3	Homo sapiens	167-171
16925484-1	2006	For more than 25 years, the combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was considered the gold standard for the treatment of aggressive lymphomas, 90% of which are diffuse, large B-cell lymphomas (DLBCLs).	Cyclophosphamide	43-59	DNA damage inducible transcript 3	Homo sapiens	102-106
16925484-1	2006	For more than 25 years, the combination of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was considered the gold standard for the treatment of aggressive lymphomas, 90% of which are diffuse, large B-cell lymphomas (DLBCLs).	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	102-106
16631627-0	2006	Doxazosin induces activation of GADD153 and cleavage of focal adhesion kinase in cardiomyocytes en route to apoptosis.	Doxazosin	0-9	DNA damage inducible transcript 3	Homo sapiens	32-39
16631627-5	2006	Doxazosin considerably increased transcription and translation of gadd153, C/epb beta, and DOC-1 in cardiomyocytes as well as translocation of GADD153 to the nucleus, phosphorylation of p38 MAPK (a GADD153 activator), and the initial phosphorylation and subsequent cleavage of focal adhesion kinase (FAK).	Doxazosin	0-9	DNA damage inducible transcript 3	Homo sapiens	66-73
16631627-5	2006	Doxazosin considerably increased transcription and translation of gadd153, C/epb beta, and DOC-1 in cardiomyocytes as well as translocation of GADD153 to the nucleus, phosphorylation of p38 MAPK (a GADD153 activator), and the initial phosphorylation and subsequent cleavage of focal adhesion kinase (FAK).	Doxazosin	0-9	DNA damage inducible transcript 3	Homo sapiens	143-150
16631627-5	2006	Doxazosin considerably increased transcription and translation of gadd153, C/epb beta, and DOC-1 in cardiomyocytes as well as translocation of GADD153 to the nucleus, phosphorylation of p38 MAPK (a GADD153 activator), and the initial phosphorylation and subsequent cleavage of focal adhesion kinase (FAK).	Doxazosin	0-9	DNA damage inducible transcript 3	Homo sapiens	198-205
16463383-0	2006	Green tea polyphenol stimulates cancer preventive effects of celecoxib in human lung cancer cells by upregulation of GADD153 gene.	Polyphenols	10-20	DNA damage inducible transcript 3	Homo sapiens	117-124
16463383-0	2006	Green tea polyphenol stimulates cancer preventive effects of celecoxib in human lung cancer cells by upregulation of GADD153 gene.	Celecoxib	61-70	DNA damage inducible transcript 3	Homo sapiens	117-124
16463383-2	2006	We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did.	epigallocatechin gallate	223-227	DNA damage inducible transcript 3	Homo sapiens	110-152
16463383-2	2006	We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did.	epigallocatechin gallate	223-227	DNA damage inducible transcript 3	Homo sapiens	154-161
16463383-2	2006	We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did.	epigallocatechin gallate	223-227	DNA damage inducible transcript 3	Homo sapiens	283-290
16463383-2	2006	We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did.	Celecoxib	233-242	DNA damage inducible transcript 3	Homo sapiens	110-152
16463383-2	2006	We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did.	Celecoxib	233-242	DNA damage inducible transcript 3	Homo sapiens	154-161
16463383-2	2006	We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did.	epigallocatechin gallate	343-347	DNA damage inducible transcript 3	Homo sapiens	154-161
16507771-6	2006	However, bortezomib rapidly induced components of the proapoptotic/terminal UPR, including PERK, the ER stress-specific eIF-2alpha kinase; ATF4, an ER stress-induced transcription factor; and its proapoptotic target, CHOP/GADD153.	Bortezomib	9-19	DNA damage inducible transcript 3	Homo sapiens	222-229
16631627-7	2006	CONCLUSION: Doxazosin induces the apoptosis of cardiomyocytes via the ER pathway, with increased production of C/EBP beta, GADD153 and DOC-1.	Doxazosin	12-21	DNA damage inducible transcript 3	Homo sapiens	123-130
16463383-2	2006	We specifically looked for induction of apoptosis and expression of apoptosis related genes, with emphasis on growth arrest and DNA damage-inducible 153 (GADD153) gene, in human lung cancer cell line PC-9: Cotreatment with EGCG plus celecoxib strongly induced the expression of both GADD153 mRNA level and protein in PC-9 cells, while neither EGCG nor celecoxib alone did.	Celecoxib	352-361	DNA damage inducible transcript 3	Homo sapiens	154-161
16463383-4	2006	Judging by upregulation of GADD153, only cotreatment with EGCG plus celecoxib synergistically induced apoptosis of PC-9 cells.	epigallocatechin gallate	58-62	DNA damage inducible transcript 3	Homo sapiens	27-34
16463383-7	2006	Thus, upregulation of GADD153 is closely correlated with synergistic enhancement of apoptosis with EGCG.	epigallocatechin gallate	99-103	DNA damage inducible transcript 3	Homo sapiens	22-29
16463383-8	2006	Cotreatment also activated the mitogen-activated protein kinases (MAPKs), such as ERK1/2 and p38 MAPK: Preteatment with PD98059 (ERK1/2 inhibitor) and UO126 (selective MEK inhibitor) abrogated both upregulation of GADD153 and synergistic induction of apoptosis of PC-9 cells, while SB203580 (p38 MAPK inhibitor) did not do so, indicating that GADD153 expression was mediated through the ERK signaling pathway.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	120-127	DNA damage inducible transcript 3	Homo sapiens	214-221
16463383-8	2006	Cotreatment also activated the mitogen-activated protein kinases (MAPKs), such as ERK1/2 and p38 MAPK: Preteatment with PD98059 (ERK1/2 inhibitor) and UO126 (selective MEK inhibitor) abrogated both upregulation of GADD153 and synergistic induction of apoptosis of PC-9 cells, while SB203580 (p38 MAPK inhibitor) did not do so, indicating that GADD153 expression was mediated through the ERK signaling pathway.	2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one	120-127	DNA damage inducible transcript 3	Homo sapiens	343-350
16463383-8	2006	Cotreatment also activated the mitogen-activated protein kinases (MAPKs), such as ERK1/2 and p38 MAPK: Preteatment with PD98059 (ERK1/2 inhibitor) and UO126 (selective MEK inhibitor) abrogated both upregulation of GADD153 and synergistic induction of apoptosis of PC-9 cells, while SB203580 (p38 MAPK inhibitor) did not do so, indicating that GADD153 expression was mediated through the ERK signaling pathway.	U 0126	151-156	DNA damage inducible transcript 3	Homo sapiens	214-221
16463383-8	2006	Cotreatment also activated the mitogen-activated protein kinases (MAPKs), such as ERK1/2 and p38 MAPK: Preteatment with PD98059 (ERK1/2 inhibitor) and UO126 (selective MEK inhibitor) abrogated both upregulation of GADD153 and synergistic induction of apoptosis of PC-9 cells, while SB203580 (p38 MAPK inhibitor) did not do so, indicating that GADD153 expression was mediated through the ERK signaling pathway.	U 0126	151-156	DNA damage inducible transcript 3	Homo sapiens	343-350
16463383-9	2006	These findings indicate that high upregulation of GADD153 is a key requirement for cancer prevention in combination with EGCG.	epigallocatechin gallate	121-125	DNA damage inducible transcript 3	Homo sapiens	50-57
16621797-8	2006	The inhibition of the major stress-inducible transcription factor CHOP (CCAAT/enhancer-binding protein homologous protein)/GADD153 together with bortezomib was most effective in repressing NFkappaB-mediated IL8 activation compared with interference of VCP, MLN-273 (proteasome inhibitor), or 4-phenylbutyrate (histone deacetylase inhibitor).	gadd153	123-130	DNA damage inducible transcript 3	Homo sapiens	66-70
16621797-8	2006	The inhibition of the major stress-inducible transcription factor CHOP (CCAAT/enhancer-binding protein homologous protein)/GADD153 together with bortezomib was most effective in repressing NFkappaB-mediated IL8 activation compared with interference of VCP, MLN-273 (proteasome inhibitor), or 4-phenylbutyrate (histone deacetylase inhibitor).	Bortezomib	145-155	DNA damage inducible transcript 3	Homo sapiens	66-70
16621797-8	2006	The inhibition of the major stress-inducible transcription factor CHOP (CCAAT/enhancer-binding protein homologous protein)/GADD153 together with bortezomib was most effective in repressing NFkappaB-mediated IL8 activation compared with interference of VCP, MLN-273 (proteasome inhibitor), or 4-phenylbutyrate (histone deacetylase inhibitor).	N-(4-morpholine)carbonyl-beta-(1-naphthyl)-alanyl-leucine boronic acid	257-264	DNA damage inducible transcript 3	Homo sapiens	66-70
16621797-8	2006	The inhibition of the major stress-inducible transcription factor CHOP (CCAAT/enhancer-binding protein homologous protein)/GADD153 together with bortezomib was most effective in repressing NFkappaB-mediated IL8 activation compared with interference of VCP, MLN-273 (proteasome inhibitor), or 4-phenylbutyrate (histone deacetylase inhibitor).	4-phenylbutyric acid	292-308	DNA damage inducible transcript 3	Homo sapiens	66-70
16518603-13	2006	The addition of etoposide and bleomycin to CHOP therapy may enhance the effect of CHOP therapy for aggressive lymphoma.	Etoposide	16-25	DNA damage inducible transcript 3	Homo sapiens	43-47
16518603-13	2006	The addition of etoposide and bleomycin to CHOP therapy may enhance the effect of CHOP therapy for aggressive lymphoma.	Etoposide	16-25	DNA damage inducible transcript 3	Homo sapiens	82-86
16518603-13	2006	The addition of etoposide and bleomycin to CHOP therapy may enhance the effect of CHOP therapy for aggressive lymphoma.	Bleomycin	30-39	DNA damage inducible transcript 3	Homo sapiens	82-86
16770736-2	2006	In this study, we examined the expression of CHOP/Gadd153 and Bip/Grp78 in human neuroblastoma SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA), which is used to prepare animal models of Parkinson"s disease.	Oxidopamine	122-139	DNA damage inducible transcript 3	Homo sapiens	45-49
16841665-6	2006	CONCLUSION: Shenqi Fuzheng injection combined with CT-CHOP on malignant non-Hodgkin"s lymphoma can reduce the adverse reaction of chemotherapy, ameliorate the compliance of patients to chemotherapy, and improve the immune function and QOL of patients.	Carbon Tetrachloride	51-53	DNA damage inducible transcript 3	Homo sapiens	54-58
16702186-1	2006	Rituximab has greatly improved standard cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, but prospects remain poor in patients with adverse risk factors.	Prednisone	87-97	DNA damage inducible transcript 3	Homo sapiens	99-103
16840195-1	2006	Recently, the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen plus rituximab (R-CHOP) have been used widely to treat patients with follicular lymphoma.	Cyclophosphamide	14-30	DNA damage inducible transcript 3	Homo sapiens	73-77
16840195-1	2006	Recently, the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen plus rituximab (R-CHOP) have been used widely to treat patients with follicular lymphoma.	Prednisone	61-71	DNA damage inducible transcript 3	Homo sapiens	73-77
16753869-3	2006	We used clinical information obtained during pretreatment evaluation to develop a predictive model for severe neutropenia in the first cycle of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy.	Cyclophosphamide	144-160	DNA damage inducible transcript 3	Homo sapiens	203-207
16753869-3	2006	We used clinical information obtained during pretreatment evaluation to develop a predictive model for severe neutropenia in the first cycle of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy.	Prednisone	191-201	DNA damage inducible transcript 3	Homo sapiens	203-207
16770736-1	2006	Endoplasmic reticulum (ER) dysfunction is known to activate the unfolded protein response, which is characterized by the activation of two divergent processes, i.e., suppression of the initiation process in global protein synthesis and expression of glucose-regulated protein 78 (Bip/Grp78) and the C/EBP homologous transcription factor CHOP/Gadd153.	Glucose	250-257	DNA damage inducible transcript 3	Homo sapiens	337-341
16770736-1	2006	Endoplasmic reticulum (ER) dysfunction is known to activate the unfolded protein response, which is characterized by the activation of two divergent processes, i.e., suppression of the initiation process in global protein synthesis and expression of glucose-regulated protein 78 (Bip/Grp78) and the C/EBP homologous transcription factor CHOP/Gadd153.	Glucose	250-257	DNA damage inducible transcript 3	Homo sapiens	342-349
16770736-2	2006	In this study, we examined the expression of CHOP/Gadd153 and Bip/Grp78 in human neuroblastoma SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA), which is used to prepare animal models of Parkinson"s disease.	Oxidopamine	122-139	DNA damage inducible transcript 3	Homo sapiens	50-57
16770736-2	2006	In this study, we examined the expression of CHOP/Gadd153 and Bip/Grp78 in human neuroblastoma SH-SY5Y cells treated with 6-hydroxydopamine (6-OHDA), which is used to prepare animal models of Parkinson"s disease.	Oxidopamine	141-147	DNA damage inducible transcript 3	Homo sapiens	50-57
16770736-5	2006	Furthermore, 6-OHDA induced a marked increase in the expression of both CHOP/Gadd153 and Bip/Grp78.	Oxidopamine	13-19	DNA damage inducible transcript 3	Homo sapiens	72-76
16770736-5	2006	Furthermore, 6-OHDA induced a marked increase in the expression of both CHOP/Gadd153 and Bip/Grp78.	Oxidopamine	13-19	DNA damage inducible transcript 3	Homo sapiens	77-84
16205636-4	2006	Celecoxib, an NSAID, upregulated ER chaperones (GRP78 and its cochaperones ERdj3 and ERdj4) but also C/EBP homologous transcription factor (CHOP), a transcription factor involved in apoptosis.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	101-138
16416337-1	2006	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been shown to improve the outcome in all age groups with newly diagnosed diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
16416337-1	2006	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been shown to improve the outcome in all age groups with newly diagnosed diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	47-58	DNA damage inducible transcript 3	Homo sapiens	89-93
16416337-1	2006	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been shown to improve the outcome in all age groups with newly diagnosed diffuse large B-cell lymphoma (DLBCL).	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	89-93
16502436-2	2006	The German ARL Study Group investigated whether HAART administered concomitantly with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy compromised the course of immune parameters during and after chemotherapy and exerted a positive effect on remission and survival.	Prednisone	134-144	DNA damage inducible transcript 3	Homo sapiens	146-150
16505371-8	2006	Furthermore, arylating quinones induced endoplasmic reticulum (ER) stress by activating the pancreatic ER kinase (PERK) signaling pathway including elF2alpha, ATF4, and C/EBP homologous protein (CHOP).	Quinones	23-31	DNA damage inducible transcript 3	Homo sapiens	169-193
16505371-8	2006	Furthermore, arylating quinones induced endoplasmic reticulum (ER) stress by activating the pancreatic ER kinase (PERK) signaling pathway including elF2alpha, ATF4, and C/EBP homologous protein (CHOP).	Quinones	23-31	DNA damage inducible transcript 3	Homo sapiens	195-199
16505371-9	2006	Detoxification by NAC greatly attenuates CHOP induction in arylating quinone-treated cells, suggesting that ER stress is a cellular mechanism for arylating quinone cytotoxicity.	Acetylcysteine	18-21	DNA damage inducible transcript 3	Homo sapiens	41-45
16505371-9	2006	Detoxification by NAC greatly attenuates CHOP induction in arylating quinone-treated cells, suggesting that ER stress is a cellular mechanism for arylating quinone cytotoxicity.	quinone	69-76	DNA damage inducible transcript 3	Homo sapiens	41-45
16505371-9	2006	Detoxification by NAC greatly attenuates CHOP induction in arylating quinone-treated cells, suggesting that ER stress is a cellular mechanism for arylating quinone cytotoxicity.	quinone	156-163	DNA damage inducible transcript 3	Homo sapiens	41-45
16550755-9	2006	Despite treatment with rituximab and CHOP (prednisolone, doxorubicin, vincristine, cyclophosphamide) for 3 cycles at 1-month intervals, the renal dysfunction did not change.	Prednisolone	43-55	DNA damage inducible transcript 3	Homo sapiens	37-41
16332727-5	2006	The subsequent downstream effects of DIM/DIM-C-pPhtBu- and Tg-induced ER stress included CHOP-dependent induction of death receptor DR5 and subsequent cleavage of caspase 8, caspase 3, Bid and PARP.	Thapsigargin	59-61	DNA damage inducible transcript 3	Homo sapiens	89-93
16640819-3	2006	In this regard, we report an 80-year-old patient with follicular grade 3 non-Hodgkin"s lymphoma who developed a fatal interstitial pneumonitis related to treatment with a rituximab/CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen.	Cyclophosphamide	187-203	DNA damage inducible transcript 3	Homo sapiens	181-185
16640819-3	2006	In this regard, we report an 80-year-old patient with follicular grade 3 non-Hodgkin"s lymphoma who developed a fatal interstitial pneumonitis related to treatment with a rituximab/CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen.	Doxorubicin	204-215	DNA damage inducible transcript 3	Homo sapiens	181-185
16640819-3	2006	In this regard, we report an 80-year-old patient with follicular grade 3 non-Hodgkin"s lymphoma who developed a fatal interstitial pneumonitis related to treatment with a rituximab/CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen.	Vincristine	216-227	DNA damage inducible transcript 3	Homo sapiens	181-185
16640819-3	2006	In this regard, we report an 80-year-old patient with follicular grade 3 non-Hodgkin"s lymphoma who developed a fatal interstitial pneumonitis related to treatment with a rituximab/CHOP (cyclophosphamide/doxorubicin/vincristine/prednisone) regimen.	Prednisone	228-238	DNA damage inducible transcript 3	Homo sapiens	181-185
16503553-0	2006	The effect of pre-irradiation dose intense CHOP on anthracyline resistance in localized nasal NK/T-cell lymphoma.	Daunorubicin	51-63	DNA damage inducible transcript 3	Homo sapiens	43-47
16205636-4	2006	Celecoxib, an NSAID, upregulated ER chaperones (GRP78 and its cochaperones ERdj3 and ERdj4) but also C/EBP homologous transcription factor (CHOP), a transcription factor involved in apoptosis.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	140-144
16205636-10	2006	Overexpression of GRP78 partially suppressed the apoptosis and induction of CHOP in the presence of celecoxib and this suppression was stimulated by coexpression of either ERdj3 or ERdj4.	Celecoxib	100-109	DNA damage inducible transcript 3	Homo sapiens	76-80
16430465-2	2006	The lymphoma responded to rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) chemotherapy.	Prednisolone	84-96	DNA damage inducible transcript 3	Homo sapiens	100-104
16575475-1	2006	Authors conducted a one-year prospective study to determine whether CHOP regimen (cyclophosphamide, doxorubicin, vincristin, and prednisone), used in the treatment of aggressive non-Hodgkin s lymphoma, is associated with the presence of an early impairment of cardiac function.	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	68-72
16414987-10	2006	Introduction of CHOP10 significantly impaired induction of the ZTA, RTA, and BMRF1 proteins in chemically treated AGS/BX1 cells.	zta	63-66	DNA damage inducible transcript 3	Homo sapiens	16-22
16400006-4	2006	Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein).	Superoxides	0-17	DNA damage inducible transcript 3	Homo sapiens	116-120
16400006-4	2006	Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein).	Superoxides	0-17	DNA damage inducible transcript 3	Homo sapiens	122-144
16400006-4	2006	Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein).	Hydrogen Peroxide	22-30	DNA damage inducible transcript 3	Homo sapiens	116-120
16400006-4	2006	Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein).	Hydrogen Peroxide	22-30	DNA damage inducible transcript 3	Homo sapiens	122-144
16400006-5	2006	Cultured podocytes overexpressing CHOP showed increased generation of superoxide anions compared to controls.	Superoxides	70-87	DNA damage inducible transcript 3	Homo sapiens	34-38
16400006-9	2006	CHOP was weakly expressed in podocytes of control kidneys but up-regulated in most proteinuric human kidneys and in rat puromycin nephrosis.	Puromycin	120-129	DNA damage inducible transcript 3	Homo sapiens	0-4
16400006-10	2006	Our data suggest that CHOP-via increased ROS generation-regulates cell-matrix adhesion of podocytes in glomerular disease.	Reactive Oxygen Species	41-44	DNA damage inducible transcript 3	Homo sapiens	22-26
16831024-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
16831024-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Vincristine	65-76	DNA damage inducible transcript 3	Homo sapiens	198-202
16831024-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
16831024-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	198-202
16706552-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Cyclophosphamide	34-50	DNA damage inducible transcript 3	Homo sapiens	93-97
16706552-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Vincristine	65-76	DNA damage inducible transcript 3	Homo sapiens	198-202
16706552-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
16706552-5	2006	The combination of rituximab with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) was cost effective as first-line therapy for advanced-stage diffuse large B-cell NHL compared with CHOP alone.	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	198-202
16205645-7	2006	In the presence of selenium, CHOP/GADD153 expression was raised even higher by BiP/GRP78 knockdown.	Selenium	19-27	DNA damage inducible transcript 3	Homo sapiens	29-33
16205645-7	2006	In the presence of selenium, CHOP/GADD153 expression was raised even higher by BiP/GRP78 knockdown.	Selenium	19-27	DNA damage inducible transcript 3	Homo sapiens	34-41
16331635-2	2006	Attempts to improve the results achieved with the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) using second-generation or third-generation chemotherapy have failed.	Cyclophosphamide	65-81	DNA damage inducible transcript 3	Homo sapiens	125-129
16331635-2	2006	Attempts to improve the results achieved with the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) using second-generation or third-generation chemotherapy have failed.	Prednisone	113-123	DNA damage inducible transcript 3	Homo sapiens	125-129
16386220-10	2006	Indeed, we demonstrated that mitochondrial ROS act as key elements in the control of white adipose tissue development by specific up-regulation of the anti-adipogenic transcription factor CHOP-10/GADD153.	Reactive Oxygen Species	43-46	DNA damage inducible transcript 3	Homo sapiens	188-195
16386220-10	2006	Indeed, we demonstrated that mitochondrial ROS act as key elements in the control of white adipose tissue development by specific up-regulation of the anti-adipogenic transcription factor CHOP-10/GADD153.	Reactive Oxygen Species	43-46	DNA damage inducible transcript 3	Homo sapiens	196-203
16575475-1	2006	Authors conducted a one-year prospective study to determine whether CHOP regimen (cyclophosphamide, doxorubicin, vincristin, and prednisone), used in the treatment of aggressive non-Hodgkin s lymphoma, is associated with the presence of an early impairment of cardiac function.	Doxorubicin	100-111	DNA damage inducible transcript 3	Homo sapiens	68-72
16575475-1	2006	Authors conducted a one-year prospective study to determine whether CHOP regimen (cyclophosphamide, doxorubicin, vincristin, and prednisone), used in the treatment of aggressive non-Hodgkin s lymphoma, is associated with the presence of an early impairment of cardiac function.	Prednisone	129-139	DNA damage inducible transcript 3	Homo sapiens	68-72
16575475-14	2006	The results show that subclinical cardiac impairment was frequent in patients receiving the CHOP regimen with safe cumulative doses of doxorubicin.	Doxorubicin	135-146	DNA damage inducible transcript 3	Homo sapiens	92-96
16351800-1	2005	BACKGROUND &amp; OBJECTIVE: CHOP regimen is the standard treatment for patients with diffuse large B-cell lymphoma.	Adenosine Monophosphate	12-15	DNA damage inducible transcript 3	Homo sapiens	28-32
16464750-4	2006	Like other proteasome inhibitors, curcumin exposure induces neurite outgrowth and the stress response, as evident from the induction of various cytosolic and endoplasmic reticulum chaperones as well as induction of transcription factor CHOP/GADD153.	Curcumin	34-42	DNA damage inducible transcript 3	Homo sapiens	236-240
16464750-4	2006	Like other proteasome inhibitors, curcumin exposure induces neurite outgrowth and the stress response, as evident from the induction of various cytosolic and endoplasmic reticulum chaperones as well as induction of transcription factor CHOP/GADD153.	Curcumin	34-42	DNA damage inducible transcript 3	Homo sapiens	241-248
16123223-0	2005	Frontline therapy with rituximab added to the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly improves the outcome for patients with advanced-stage follicular lymphoma compared with therapy with CHOP alone: results of a prospective randomized study of the German Low-Grade Lymphoma Study Group.	Cyclophosphamide	61-77	DNA damage inducible transcript 3	Homo sapiens	121-125
16351785-1	2005	BACKGROUND &amp; OBJECTIVE: CHOP regimen is a standard treatment for patients with diffuse large B-cell non-Hodgkin"s lymphoma (NHL), and its 5-year overall survival (OS) rate is 30%-40%.	Adenosine Monophosphate	12-15	DNA damage inducible transcript 3	Homo sapiens	28-32
16123223-0	2005	Frontline therapy with rituximab added to the combination of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) significantly improves the outcome for patients with advanced-stage follicular lymphoma compared with therapy with CHOP alone: results of a prospective randomized study of the German Low-Grade Lymphoma Study Group.	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	121-125
16247790-6	2005	RESULTS: CHOP induced transient increases in the left ventricular end-diastolic diameter in an echocardiogram, the QTc interval and QTc dispersion in an electrocardiogram, and in the plasma brain and atrial natriuretic peptides.	qtc	115-118	DNA damage inducible transcript 3	Homo sapiens	9-13
16247790-6	2005	RESULTS: CHOP induced transient increases in the left ventricular end-diastolic diameter in an echocardiogram, the QTc interval and QTc dispersion in an electrocardiogram, and in the plasma brain and atrial natriuretic peptides.	qtc	132-135	DNA damage inducible transcript 3	Homo sapiens	9-13
16307545-3	2005	Complete remission of CLL with resolution of the osteolytic lesion was achieved with rituximab and cyclophosphamide, adriamycin, oncovin and prednisolone [CHOP (R-CHOP)] combination chemotherapy.	Prednisolone	141-153	DNA damage inducible transcript 3	Homo sapiens	155-159
16001425-0	2005	CHOP plays a pivotal role in the astrocyte death induced by oxygen and glucose deprivation.	Oxygen	60-66	DNA damage inducible transcript 3	Homo sapiens	0-4
16001425-5	2005	Our study revealed that the expression of the CEBP homologous protein (CHOP)-coding gene is promptly an intensely upregulated following astrocyte oxygen and glucose deprivation.	Oxygen	146-152	DNA damage inducible transcript 3	Homo sapiens	46-69
16001425-5	2005	Our study revealed that the expression of the CEBP homologous protein (CHOP)-coding gene is promptly an intensely upregulated following astrocyte oxygen and glucose deprivation.	Oxygen	146-152	DNA damage inducible transcript 3	Homo sapiens	71-75
16001425-9	2005	Not only the levels of CHOP mRNA and protein correlate perfectly with the degree of OGD-triggered cell injury, but also astrocyte death induced by OGD is significantly overcome by CHOP antisense oligonucleotide treatment.	Oligonucleotides	195-210	DNA damage inducible transcript 3	Homo sapiens	23-27
16001425-9	2005	Not only the levels of CHOP mRNA and protein correlate perfectly with the degree of OGD-triggered cell injury, but also astrocyte death induced by OGD is significantly overcome by CHOP antisense oligonucleotide treatment.	Oligonucleotides	195-210	DNA damage inducible transcript 3	Homo sapiens	180-184
16135078-0	2005	CHOP/GADD153 is a mediator of apoptotic death in substantia nigra dopamine neurons in an in vivo neurotoxin model of parkinsonism.	Dopamine	66-74	DNA damage inducible transcript 3	Homo sapiens	0-4
16277400-0	2005	Induction of apoptosis by 1-(2-hydroxy-5-methylphenyl)-3-phenyl-1,3-propanedione through reactive oxygen species production, GADD153 expression, and caspases activation in human epidermoid carcinoma cells.	1-(2-hydroxy-5-methylphenyl)-3-phenyl-1,3-propanedione	26-80	DNA damage inducible transcript 3	Homo sapiens	125-132
16277400-8	2005	NAC prevented up-regulation of GADD153 mRNA expression caused by HMDB.	Acetylcysteine	0-3	DNA damage inducible transcript 3	Homo sapiens	31-38
16135078-0	2005	CHOP/GADD153 is a mediator of apoptotic death in substantia nigra dopamine neurons in an in vivo neurotoxin model of parkinsonism.	Dopamine	66-74	DNA damage inducible transcript 3	Homo sapiens	5-12
16135078-6	2005	Nuclear expression of CHOP protein is observed in developmental and adult models of dopamine neuron death induced by intrastriatal injection of 6-hydroxydopamine (6OHDA) and in models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	Dopamine	84-92	DNA damage inducible transcript 3	Homo sapiens	22-26
16135078-6	2005	Nuclear expression of CHOP protein is observed in developmental and adult models of dopamine neuron death induced by intrastriatal injection of 6-hydroxydopamine (6OHDA) and in models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	Oxidopamine	144-161	DNA damage inducible transcript 3	Homo sapiens	22-26
16135078-6	2005	Nuclear expression of CHOP protein is observed in developmental and adult models of dopamine neuron death induced by intrastriatal injection of 6-hydroxydopamine (6OHDA) and in models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	Oxidopamine	163-168	DNA damage inducible transcript 3	Homo sapiens	22-26
16135078-6	2005	Nuclear expression of CHOP protein is observed in developmental and adult models of dopamine neuron death induced by intrastriatal injection of 6-hydroxydopamine (6OHDA) and in models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	195-239	DNA damage inducible transcript 3	Homo sapiens	22-26
16135078-6	2005	Nuclear expression of CHOP protein is observed in developmental and adult models of dopamine neuron death induced by intrastriatal injection of 6-hydroxydopamine (6OHDA) and in models induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP).	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	241-245	DNA damage inducible transcript 3	Homo sapiens	22-26
16135078-8	2005	In the chronic MPTP model, however, while CHOP is robustly expressed, the null mutation does not protect from the loss of neurons.	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine	15-19	DNA damage inducible transcript 3	Homo sapiens	42-46
16203857-2	2005	A likely cause of macrophage death is accumulation of free cholesterol (FC) in the ER, leading to activation of the unfolded protein response (UPR) and C/EBP homologous protein (CHOP)-induced apoptosis.	Cholesterol	59-70	DNA damage inducible transcript 3	Homo sapiens	152-176
16023761-11	2005	CONCLUSIONS: It is suggested that bromovulone III induces apoptosis in Hep3B cells through a mechanism that induces ER stress and leads to activation of CHOP/GADD153 and caspase-12.	bromovulone III	34-49	DNA damage inducible transcript 3	Homo sapiens	153-157
16203857-2	2005	A likely cause of macrophage death is accumulation of free cholesterol (FC) in the ER, leading to activation of the unfolded protein response (UPR) and C/EBP homologous protein (CHOP)-induced apoptosis.	Cholesterol	59-70	DNA damage inducible transcript 3	Homo sapiens	178-182
16203857-8	2005	Thus, FC-induced apoptosis requires cholesterol trafficking to the ER, which triggers p38-CHOP and JNK2, and engagement of the SRA.	Cholesterol	36-47	DNA damage inducible transcript 3	Homo sapiens	90-94
16023761-11	2005	CONCLUSIONS: It is suggested that bromovulone III induces apoptosis in Hep3B cells through a mechanism that induces ER stress and leads to activation of CHOP/GADD153 and caspase-12.	bromovulone III	34-49	DNA damage inducible transcript 3	Homo sapiens	158-165
16081421-5	2005	Here, we showed that the transcription factor CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) directly interacts with GABA(B) receptors in a subtype-selective manner to regulate cell surface expression of GABA(B1a)/GABA(B2) receptors upon co-expression in HEK 293 cells.	gamma-Aminobutyric Acid	135-139	DNA damage inducible transcript 3	Homo sapiens	105-109
16440771-7	2005	The patient received a regimen of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Prednisone	81-91	DNA damage inducible transcript 3	Homo sapiens	93-97
16081421-7	2005	This regulation required the interaction of CHOP via two distinct domains with the heterodimeric receptor; its C-terminal leucine zipper associates with the leucine zipper present in the C-terminal domain of GABA(B2), and its N-terminal domain associates with an as yet unidentified site on GABA(B1a).	gamma-Aminobutyric Acid	208-212	DNA damage inducible transcript 3	Homo sapiens	44-48
16081421-7	2005	This regulation required the interaction of CHOP via two distinct domains with the heterodimeric receptor; its C-terminal leucine zipper associates with the leucine zipper present in the C-terminal domain of GABA(B2), and its N-terminal domain associates with an as yet unidentified site on GABA(B1a).	gamma-Aminobutyric Acid	291-295	DNA damage inducible transcript 3	Homo sapiens	44-48
15987693-10	2005	Celecoxib-dependent CHOP-induction was partially inhibited by the intracellular Ca2+ chelator but not by the calpain inhibitor.	Celecoxib	0-9	DNA damage inducible transcript 3	Homo sapiens	20-24
15987693-11	2005	These results suggest that Ca2+-stimulated calpain activity and CHOP expression play important roles in celecoxib-induced apoptosis in gastric mucosal cells.	Celecoxib	104-113	DNA damage inducible transcript 3	Homo sapiens	64-68
16093796-4	2005	Phase II trials combining rituximab with either standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy or infusional chemotherapy have reported encouraging results, suggesting a similar benefit in HIV-positive individuals.	Prednisone	105-115	DNA damage inducible transcript 3	Homo sapiens	117-121
16000304-4	2005	Here we report that glucose withdrawal, tunicamycin, and thapsigargin induce up-regulation of GADD153 and caspase-12, two markers of endoplasmic reticulum stress, in both primary chondrocytes and a chondrocyte cell line.	Glucose	20-27	DNA damage inducible transcript 3	Homo sapiens	94-101
16000304-4	2005	Here we report that glucose withdrawal, tunicamycin, and thapsigargin induce up-regulation of GADD153 and caspase-12, two markers of endoplasmic reticulum stress, in both primary chondrocytes and a chondrocyte cell line.	Tunicamycin	40-51	DNA damage inducible transcript 3	Homo sapiens	94-101
15914552-1	2005	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy results in significant improvement in clinical outcome for individuals with non-HIV-associated aggressive B-cell lymphoma.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	89-93
15914552-1	2005	The addition of rituximab to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy results in significant improvement in clinical outcome for individuals with non-HIV-associated aggressive B-cell lymphoma.	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	89-93
16000304-4	2005	Here we report that glucose withdrawal, tunicamycin, and thapsigargin induce up-regulation of GADD153 and caspase-12, two markers of endoplasmic reticulum stress, in both primary chondrocytes and a chondrocyte cell line.	Thapsigargin	57-69	DNA damage inducible transcript 3	Homo sapiens	94-101
16093797-5	2005	Liposomal encapsulation of doxorubicin when substituted for doxorubicin in the CHOP regimen (cyclophosphamide, doxorubicin, vincristine, prednisone) seems to overcome P-glycoprotein-mediated drug resistance in AIDS-related lymphoma.	Doxorubicin	27-38	DNA damage inducible transcript 3	Homo sapiens	79-83
16024639-8	2005	Tunicamycin increased DR5 promoter activity and this enhanced activity was diminished by mutation of a CHOP-binding site.	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	103-107
15955905-1	2005	PURPOSE: For more than two decades, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the standard therapy for diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	96-100
15955905-1	2005	PURPOSE: For more than two decades, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the standard therapy for diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	54-65	DNA damage inducible transcript 3	Homo sapiens	96-100
15955905-1	2005	PURPOSE: For more than two decades, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the standard therapy for diffuse large B-cell lymphoma (DLBCL).	Prednisone	84-94	DNA damage inducible transcript 3	Homo sapiens	96-100
16024639-9	2005	In addition, suppression of CHOP expression by small interfering RNA reduced the tunicamycin-mediated induction of DR5.	Tunicamycin	81-92	DNA damage inducible transcript 3	Homo sapiens	28-32
16024639-10	2005	Of note, tunicamycin-mediated induction of CHOP and DR5 protein expression was not observed in normal human peripheral blood mononuclear cells.	Tunicamycin	9-20	DNA damage inducible transcript 3	Homo sapiens	43-47
15994939-11	2005	Furthermore, CHOP small interfering RNA attenuated the DR5 up-regulation due to MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	80-85	DNA damage inducible transcript 3	Homo sapiens	13-17
15994939-0	2005	Proteasome inhibitor MG132 induces death receptor 5 through CCAAT/enhancer-binding protein homologous protein.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	21-26	DNA damage inducible transcript 3	Homo sapiens	60-109
15994939-3	2005	In this study, we report that CCAAT/enhancer-binding protein homologous protein (CHOP) is a regulator of DR5 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	DNA damage inducible transcript 3	Homo sapiens	30-79
15994939-3	2005	In this study, we report that CCAAT/enhancer-binding protein homologous protein (CHOP) is a regulator of DR5 induction by proteasome inhibitor MG132.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	143-148	DNA damage inducible transcript 3	Homo sapiens	81-85
15994939-9	2005	An electrophoretic mobility shift assay showed that CHOP directly bound to the MG132-responsive site on the DR5 promoter.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	79-84	DNA damage inducible transcript 3	Homo sapiens	52-56
15994939-10	2005	Expression of the CHOP protein was increased with MG132 along with DR5 up-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	50-55	DNA damage inducible transcript 3	Homo sapiens	18-22
15994939-12	2005	These results indicate that the proteasome inhibitor MG132 induces DR5 expression through CHOP up-regulation.	benzyloxycarbonylleucyl-leucyl-leucine aldehyde	53-58	DNA damage inducible transcript 3	Homo sapiens	90-94
15605392-5	2005	Increasing intracellular nitric oxide levels by SNAP treatment or inhibiting protein folding in the ER lumen by tunicamycin induced the ER stress response as evidenced by increased protein and gene expression of GADD153 as well as PERK and eIF2-alpha phosphorylation, and resulted in apoptosis.	Nitric Oxide	25-37	DNA damage inducible transcript 3	Homo sapiens	212-219
15605392-5	2005	Increasing intracellular nitric oxide levels by SNAP treatment or inhibiting protein folding in the ER lumen by tunicamycin induced the ER stress response as evidenced by increased protein and gene expression of GADD153 as well as PERK and eIF2-alpha phosphorylation, and resulted in apoptosis.	Tunicamycin	112-123	DNA damage inducible transcript 3	Homo sapiens	212-219
16006279-1	2005	Treatment of non-Hodgkin"s lymphoma with the CHOP regimen consists of intravenous cyclophosphamide 750 mg/m2 (day 1), intravenous doxorubicin 50 mg/m2 (day 1), intravenous vincristine 1.4 mg/m2 (day 1), and oral prednisone 100 mg (days 1-5).	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	45-49
16006279-1	2005	Treatment of non-Hodgkin"s lymphoma with the CHOP regimen consists of intravenous cyclophosphamide 750 mg/m2 (day 1), intravenous doxorubicin 50 mg/m2 (day 1), intravenous vincristine 1.4 mg/m2 (day 1), and oral prednisone 100 mg (days 1-5).	Doxorubicin	130-141	DNA damage inducible transcript 3	Homo sapiens	45-49
16006279-1	2005	Treatment of non-Hodgkin"s lymphoma with the CHOP regimen consists of intravenous cyclophosphamide 750 mg/m2 (day 1), intravenous doxorubicin 50 mg/m2 (day 1), intravenous vincristine 1.4 mg/m2 (day 1), and oral prednisone 100 mg (days 1-5).	Vincristine	172-183	DNA damage inducible transcript 3	Homo sapiens	45-49
16006279-1	2005	Treatment of non-Hodgkin"s lymphoma with the CHOP regimen consists of intravenous cyclophosphamide 750 mg/m2 (day 1), intravenous doxorubicin 50 mg/m2 (day 1), intravenous vincristine 1.4 mg/m2 (day 1), and oral prednisone 100 mg (days 1-5).	Prednisone	212-222	DNA damage inducible transcript 3	Homo sapiens	45-49
16440745-0	2005	[Effective treatment for a methotrexate-associated lymphoproliferative disorder with R-CHOP following administration of rituximab].	Methotrexate	27-39	DNA damage inducible transcript 3	Homo sapiens	87-91
15909111-1	2005	Fenretinide induces apoptosis in SH-SY5Y neuroblastoma cells via a signaling pathway involving the production of reactive oxygen species (ROS), 12-lipoxygenase activity and the induction of the GADD153 transcription factor.	Fenretinide	0-11	DNA damage inducible transcript 3	Homo sapiens	194-201
15917187-0	2005	ROS mediates 4HPR-induced posttranscriptional expression of the Gadd153 gene.	ros	0-3	DNA damage inducible transcript 3	Homo sapiens	64-71
15917187-0	2005	ROS mediates 4HPR-induced posttranscriptional expression of the Gadd153 gene.	Fenretinide	13-17	DNA damage inducible transcript 3	Homo sapiens	64-71
15917187-3	2005	We have investigated the role of 4HPR-induced production of ROS in mediating the expression of the recently identified 4HPR-responsive gene Gadd153.	ros	60-63	DNA damage inducible transcript 3	Homo sapiens	140-147
15917187-4	2005	In 4HPR-treated cells, the elevation of Gadd153 protein level was prevented by vitamin C, which had no effect on the activation of the Gadd153 gene promoter.	Fenretinide	3-7	DNA damage inducible transcript 3	Homo sapiens	40-47
15917187-4	2005	In 4HPR-treated cells, the elevation of Gadd153 protein level was prevented by vitamin C, which had no effect on the activation of the Gadd153 gene promoter.	Ascorbic Acid	79-88	DNA damage inducible transcript 3	Homo sapiens	40-47
15917187-5	2005	The 4HPR-induced elevation of Gadd153 mRNA level persisted even after transcription was blocked with actinomycin D, but declined rapidly upon the addition of antioxidants to the transcription-arrested cells.	Dactinomycin	101-114	DNA damage inducible transcript 3	Homo sapiens	30-37
15917187-8	2005	The inhibition of 4HPR-induced expression of Gadd153 protein by vitamin C was independent of intracellular proteasome activity and vitamin C had no effect on the intracellular decay of Gadd153 protein.	Fenretinide	18-22	DNA damage inducible transcript 3	Homo sapiens	45-52
15917187-8	2005	The inhibition of 4HPR-induced expression of Gadd153 protein by vitamin C was independent of intracellular proteasome activity and vitamin C had no effect on the intracellular decay of Gadd153 protein.	Ascorbic Acid	64-73	DNA damage inducible transcript 3	Homo sapiens	45-52
15918208-2	2005	The patient was successfully treated with a first generation therapy, CHOP modified regimen (cyclophosphamide 600 mg/m2 intravenously on d 1, epirubicin 55 mg/m2 intravenously on d 1, vincristine 1.2 mg/m2 intravenously on d 1, prednisone 60 mg/m2 on d 1-5), and a complete response was achieved.	Cyclophosphamide	93-109	DNA damage inducible transcript 3	Homo sapiens	70-74
15917187-9	2005	Our data provide the first evidence that the posttranscriptional expression of the Gadd153 gene can be regulated by ROS produced by 4HPR.	ros	116-119	DNA damage inducible transcript 3	Homo sapiens	83-90
15865936-3	2005	This ganglioside triggers the activation of 12-Lox (12-lipoxygenase) leading to oxidative stress and apoptosis via the induction of the transcription factor Gadd153 and the Bcl-2-family member protein Bak.	Gangliosides	5-16	DNA damage inducible transcript 3	Homo sapiens	157-164
16158823-8	2005	We first treated the patient with fludarabine and then with the CHOP regimen (cyclophosphamide, hydroxydaunomycin, vincristine [Oncovin], and prednisone), but the disease was so refractory that the patient died of the disease 13 months after the splenectomy.	Cyclophosphamide	78-94	DNA damage inducible transcript 3	Homo sapiens	64-68
16158823-8	2005	We first treated the patient with fludarabine and then with the CHOP regimen (cyclophosphamide, hydroxydaunomycin, vincristine [Oncovin], and prednisone), but the disease was so refractory that the patient died of the disease 13 months after the splenectomy.	Doxorubicin	96-113	DNA damage inducible transcript 3	Homo sapiens	64-68
15756658-1	2005	BACKGROUND: Findings from the Groupe d"Etude des Lymphomes Adultes LNH 98-5 study showed that rituximab added to combined cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) prolonged progression-free survival and overall survival in adults age &gt;/= 60 years with diffuse large B-cell non-Hodgkin lymphoma (DLBCL).	Vincristine	153-164	DNA damage inducible transcript 3	Homo sapiens	182-186
15921395-2	2005	In this study we found that HIV-infected patients with diffuse large B-cell lymphoma treated with cyclophosphamide, hydroxydoxorubicin, vincristine and prednisone (CHOP) and HAART showed a similar response rate to chemotherapy, disease-free survival and overall survival as those of HIV-negative patients receiving CHOP.	Cyclophosphamide	98-114	DNA damage inducible transcript 3	Homo sapiens	164-168
15791475-3	2005	The patient was treated for diffuse large B-cell non-Hodgkin"s lymphoma with CHOP therapy (doxorubicin, cyclophosphamide, vincristine, and prednisone).	Doxorubicin	91-102	DNA damage inducible transcript 3	Homo sapiens	77-81
15791475-3	2005	The patient was treated for diffuse large B-cell non-Hodgkin"s lymphoma with CHOP therapy (doxorubicin, cyclophosphamide, vincristine, and prednisone).	Cyclophosphamide	104-120	DNA damage inducible transcript 3	Homo sapiens	77-81
15791475-3	2005	The patient was treated for diffuse large B-cell non-Hodgkin"s lymphoma with CHOP therapy (doxorubicin, cyclophosphamide, vincristine, and prednisone).	Vincristine	122-133	DNA damage inducible transcript 3	Homo sapiens	77-81
15791475-3	2005	The patient was treated for diffuse large B-cell non-Hodgkin"s lymphoma with CHOP therapy (doxorubicin, cyclophosphamide, vincristine, and prednisone).	Prednisone	139-149	DNA damage inducible transcript 3	Homo sapiens	77-81
15659384-0	2005	Prostaglandin E2 induces interleukin-8 gene transcription by activating C/EBP homologous protein in human T lymphocytes.	Dinoprostone	0-16	DNA damage inducible transcript 3	Homo sapiens	72-96
15659384-2	2005	Here, we demonstrate that, in human T cells, PGE(2) induced IL-8 mRNA transcription through prostaglandin E(2) receptors 1- and 4-dependent signal transduction pathways leading to the activation of the transcription factor C/EBP homologous protein (CHOP), never before implicated in IL-8 transcription.	Prostaglandins E	45-48	DNA damage inducible transcript 3	Homo sapiens	223-247
15659384-2	2005	Here, we demonstrate that, in human T cells, PGE(2) induced IL-8 mRNA transcription through prostaglandin E(2) receptors 1- and 4-dependent signal transduction pathways leading to the activation of the transcription factor C/EBP homologous protein (CHOP), never before implicated in IL-8 transcription.	Prostaglandins E	45-48	DNA damage inducible transcript 3	Homo sapiens	249-253
15659384-3	2005	Several kinases, including protein kinase C, Src family tyrosine kinases, phosphatidylinositol 3-kinase, and p38 MAPK, were involved in PGE(2)-induced CHOP activation and IL-8 production.	Dinoprostone	136-142	DNA damage inducible transcript 3	Homo sapiens	151-155
15921395-2	2005	In this study we found that HIV-infected patients with diffuse large B-cell lymphoma treated with cyclophosphamide, hydroxydoxorubicin, vincristine and prednisone (CHOP) and HAART showed a similar response rate to chemotherapy, disease-free survival and overall survival as those of HIV-negative patients receiving CHOP.	3'-deamino-3'-hydroxydoxorubicin	116-134	DNA damage inducible transcript 3	Homo sapiens	315-319
15921395-2	2005	In this study we found that HIV-infected patients with diffuse large B-cell lymphoma treated with cyclophosphamide, hydroxydoxorubicin, vincristine and prednisone (CHOP) and HAART showed a similar response rate to chemotherapy, disease-free survival and overall survival as those of HIV-negative patients receiving CHOP.	Vincristine	136-147	DNA damage inducible transcript 3	Homo sapiens	315-319
15921395-2	2005	In this study we found that HIV-infected patients with diffuse large B-cell lymphoma treated with cyclophosphamide, hydroxydoxorubicin, vincristine and prednisone (CHOP) and HAART showed a similar response rate to chemotherapy, disease-free survival and overall survival as those of HIV-negative patients receiving CHOP.	Prednisone	152-162	DNA damage inducible transcript 3	Homo sapiens	315-319
15781252-4	2005	The induction of hNIPK gene in response to thapsigargin and arsenite treatments is mediated by a promoter segment consisting of tandemly arranged 33-bp repeats that contain a regulatory element similar to C/EBP-ATF composite site of the Chop gene promoter.	Thapsigargin	43-55	DNA damage inducible transcript 3	Homo sapiens	237-241
15781252-4	2005	The induction of hNIPK gene in response to thapsigargin and arsenite treatments is mediated by a promoter segment consisting of tandemly arranged 33-bp repeats that contain a regulatory element similar to C/EBP-ATF composite site of the Chop gene promoter.	arsenite	60-68	DNA damage inducible transcript 3	Homo sapiens	237-241
15659384-5	2005	Our data suggest that PGE(2) acts as a potent pro-inflammatory mediator by inducing IL-8 gene transcription in activated T cells through different signal transduction pathways leading to CHOP activation.	Prostaglandins E	22-25	DNA damage inducible transcript 3	Homo sapiens	187-191
15728147-4	2005	Chemotherapy consisted of adriamycin, cyclophosphamide, vincristine and prednisolone (CHOP).	Prednisolone	72-84	DNA damage inducible transcript 3	Homo sapiens	86-90
15820070-1	2005	BACKGROUND &amp; OBJECTIVE: CHOP regimen is the routine modality for moderately or highly malignant non-Hodgkin"s lymphoma (NHL).	Adenosine Monophosphate	12-15	DNA damage inducible transcript 3	Homo sapiens	28-32
15728147-6	2005	RESULTS: When indinavir was given concomitantly with CHOP, the AUC(0-8) increased by 38% (20.5 +/- 9.0 versus 14.9 +/- 9.5 mg.h/L; P=0.03), and was comparable to historical controls.	Indinavir	14-23	DNA damage inducible transcript 3	Homo sapiens	53-57
15728147-7	2005	By contrast, the AUC(0-8) of indinavir administered without CHOP was lower than expected.	Indinavir	29-38	DNA damage inducible transcript 3	Homo sapiens	60-64
15775988-5	2005	Tunicamycin treatment enhanced the TRB3 promoter activity, while dominant-negative forms of CHOP suppressed the tunicamycin-induced activation.	Tunicamycin	112-123	DNA damage inducible transcript 3	Homo sapiens	92-96
15775988-6	2005	In addition, the tunicamycin response region in the TRB3 promoter contains amino-acid response elements overlapping the CHOP-binding site, and CHOP and ATF4 cooperated to activate this promoter activity.	Tunicamycin	17-28	DNA damage inducible transcript 3	Homo sapiens	120-124
15775988-7	2005	Knockdown of endogenous ATF4 or CHOP expression dramatically repressed tunicamycin-induced TRB3 induction.	Tunicamycin	71-82	DNA damage inducible transcript 3	Homo sapiens	32-36
15666323-1	2005	BACKGROUND: The standard treatment for patients with aggressive non-Hodgkin lymphoma (NHL) is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	94-110	DNA damage inducible transcript 3	Homo sapiens	154-158
15666323-1	2005	BACKGROUND: The standard treatment for patients with aggressive non-Hodgkin lymphoma (NHL) is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Doxorubicin	112-123	DNA damage inducible transcript 3	Homo sapiens	154-158
15666323-1	2005	BACKGROUND: The standard treatment for patients with aggressive non-Hodgkin lymphoma (NHL) is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Prednisone	142-152	DNA damage inducible transcript 3	Homo sapiens	154-158
15621841-5	2005	The patient responded to chemotherapy with CHOP (doxorubicin, cyclophosphamide, vincristine and prednisone) therapy, with disappearance of the abnormal clone from the bone marrow.	Doxorubicin	49-60	DNA damage inducible transcript 3	Homo sapiens	43-47
15693788-1	2005	OBJECTIVE: To determine the incremental cost-effectiveness ratio (ICER) of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) vs. CHOP plus rituximab (R-CHOP) in diffuse large B-cell lymphoma (DLBCL) patients in the Netherlands.	Prednisone	122-132	DNA damage inducible transcript 3	Homo sapiens	134-138
15794864-2	2005	Cyclophosphamide/doxorubicin/vincristine/prednisone/rituximab (CHOP-R) is a stem cellsparing regimen that has been extensively evaluated in patients without WM or non-Hodgkin"s lymphoma.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	63-67
15794864-2	2005	Cyclophosphamide/doxorubicin/vincristine/prednisone/rituximab (CHOP-R) is a stem cellsparing regimen that has been extensively evaluated in patients without WM or non-Hodgkin"s lymphoma.	Doxorubicin	17-28	DNA damage inducible transcript 3	Homo sapiens	63-67
15794864-2	2005	Cyclophosphamide/doxorubicin/vincristine/prednisone/rituximab (CHOP-R) is a stem cellsparing regimen that has been extensively evaluated in patients without WM or non-Hodgkin"s lymphoma.	Vincristine	29-40	DNA damage inducible transcript 3	Homo sapiens	63-67
15794864-2	2005	Cyclophosphamide/doxorubicin/vincristine/prednisone/rituximab (CHOP-R) is a stem cellsparing regimen that has been extensively evaluated in patients without WM or non-Hodgkin"s lymphoma.	Prednisone	41-51	DNA damage inducible transcript 3	Homo sapiens	63-67
15621841-5	2005	The patient responded to chemotherapy with CHOP (doxorubicin, cyclophosphamide, vincristine and prednisone) therapy, with disappearance of the abnormal clone from the bone marrow.	Cyclophosphamide	62-78	DNA damage inducible transcript 3	Homo sapiens	43-47
15621841-5	2005	The patient responded to chemotherapy with CHOP (doxorubicin, cyclophosphamide, vincristine and prednisone) therapy, with disappearance of the abnormal clone from the bone marrow.	Vincristine	80-91	DNA damage inducible transcript 3	Homo sapiens	43-47
15621841-5	2005	The patient responded to chemotherapy with CHOP (doxorubicin, cyclophosphamide, vincristine and prednisone) therapy, with disappearance of the abnormal clone from the bone marrow.	Prednisone	96-106	DNA damage inducible transcript 3	Homo sapiens	43-47
15603752-11	2005	Nevertheless, other regular participants in the DNA damage response, such as Gadd45a, Gadd153, p53, Hsp70, and ATM are still upregulated by high NaCl.	Sodium Chloride	145-149	DNA damage inducible transcript 3	Homo sapiens	86-93
15680548-0	2005	Induction of C/EBP beta and GADD153 expression by dopamine in human neuroblastoma cells.	Dopamine	50-58	DNA damage inducible transcript 3	Homo sapiens	28-35
15680548-2	2005	Expression of CCAAT/enhancer-binding protein beta (C/EBP beta) and growth-arrest DNA damage-inducible 153/C/EBP beta homology protein (GADD153/CHOP) increased after incubation of human neuroblastoma SH-SY5Y cells with a range of dopamine concentrations.	Dopamine	229-237	DNA damage inducible transcript 3	Homo sapiens	135-142
15680548-2	2005	Expression of CCAAT/enhancer-binding protein beta (C/EBP beta) and growth-arrest DNA damage-inducible 153/C/EBP beta homology protein (GADD153/CHOP) increased after incubation of human neuroblastoma SH-SY5Y cells with a range of dopamine concentrations.	Dopamine	229-237	DNA damage inducible transcript 3	Homo sapiens	143-147
15680548-4	2005	Dopamine (500 microM) led to the appearance of autophagic-like vacuoles and a marked increase in GADD153/CHOP between 6 and 24 h of treatment.	Dopamine	0-8	DNA damage inducible transcript 3	Homo sapiens	97-104
15680548-4	2005	Dopamine (500 microM) led to the appearance of autophagic-like vacuoles and a marked increase in GADD153/CHOP between 6 and 24 h of treatment.	Dopamine	0-8	DNA damage inducible transcript 3	Homo sapiens	105-109
15680548-8	2005	Inhibition of JNK by SP600125 reduced increases in C/EBP beta and alpha-synuclein expression, whereas inhibition of both JNK and p38MAPK (with SB203580) blocked the increase in GADD153 expression.	SB 203580	143-151	DNA damage inducible transcript 3	Homo sapiens	177-184
15680548-9	2005	We conclude that dopamine, through a mechanism driven by stress-activated MAPKs, triggers C/EBP beta and GADD153 expression in a dose-dependent way.	Dopamine	17-25	DNA damage inducible transcript 3	Homo sapiens	105-112
15680548-11	2005	GADD153 increase seems to be related with the endoplasmic reticulum stress, autophagy and cell death observed at high dopamine concentrations.	Dopamine	118-126	DNA damage inducible transcript 3	Homo sapiens	0-7
16110296-6	2005	We instituted initial therapy, with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) plus intrathecal chemotherapy without performing a chromosome analysis, because the clinical course was very aggressive.	Prednisone	84-94	DNA damage inducible transcript 3	Homo sapiens	96-100
15858449-7	2005	Four courses of adjuvant chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) were subsequently performed.	Prednisone	90-100	DNA damage inducible transcript 3	Homo sapiens	102-106
17532718-4	2005	METHODS: A decision-analysis model described clinical events and economic consequences for theoretical patients who were to receive eight consecutive cycles of a CHOP regimen containing 50 mg/m(2) of doxorubicin as first-line chemotherapy.	Doxorubicin	200-211	DNA damage inducible transcript 3	Homo sapiens	162-166
15316935-7	2005	In further studying GADD153 in particular, the effect of DOC on GADD153 mRNA was prevented by actinomycin-D (Act-D), but not by antioxidants or MAPK inhibitors.	Deoxycholic Acid	57-60	DNA damage inducible transcript 3	Homo sapiens	20-27
15316935-7	2005	In further studying GADD153 in particular, the effect of DOC on GADD153 mRNA was prevented by actinomycin-D (Act-D), but not by antioxidants or MAPK inhibitors.	Deoxycholic Acid	57-60	DNA damage inducible transcript 3	Homo sapiens	64-71
15316935-7	2005	In further studying GADD153 in particular, the effect of DOC on GADD153 mRNA was prevented by actinomycin-D (Act-D), but not by antioxidants or MAPK inhibitors.	Dactinomycin	94-107	DNA damage inducible transcript 3	Homo sapiens	20-27
15316935-7	2005	In further studying GADD153 in particular, the effect of DOC on GADD153 mRNA was prevented by actinomycin-D (Act-D), but not by antioxidants or MAPK inhibitors.	Dactinomycin	94-107	DNA damage inducible transcript 3	Homo sapiens	64-71
15316935-9	2005	Induction of GADD153 protein by DOC was prevented by either anisomycin or cycloheximide.	Deoxycholic Acid	32-35	DNA damage inducible transcript 3	Homo sapiens	13-20
15316935-9	2005	Induction of GADD153 protein by DOC was prevented by either anisomycin or cycloheximide.	Anisomycin	60-70	DNA damage inducible transcript 3	Homo sapiens	13-20
15316935-9	2005	Induction of GADD153 protein by DOC was prevented by either anisomycin or cycloheximide.	Cycloheximide	74-87	DNA damage inducible transcript 3	Homo sapiens	13-20
15316935-10	2005	These findings suggest that DOC-induced upregulation of GADD153 mRNA expression occurred at the level of transcription without involving reactive oxygen species and MAPK signaling, and that the expression of GADD153 protein was due also to translation of pre-existing, and not just newly synthesized, mRNA.	Deoxycholic Acid	28-31	DNA damage inducible transcript 3	Homo sapiens	56-63
15316935-10	2005	These findings suggest that DOC-induced upregulation of GADD153 mRNA expression occurred at the level of transcription without involving reactive oxygen species and MAPK signaling, and that the expression of GADD153 protein was due also to translation of pre-existing, and not just newly synthesized, mRNA.	Deoxycholic Acid	28-31	DNA damage inducible transcript 3	Homo sapiens	208-215
15338194-14	2004	Delayed HBV reactivation can occur in lymphoma patients receiving R+CHOP after withdrawal of preemptive lamivudine.	Lamivudine	104-114	DNA damage inducible transcript 3	Homo sapiens	68-72
16116910-15	2005	CHOP therapy cannot be recommended for patients with ABLL because of poor efficacy (all the CHOP patients died).	abll	53-57	DNA damage inducible transcript 3	Homo sapiens	0-4
15650234-3	2004	This is mediated by a signaling pathway characterized by the generation of reactive oxygen species (ROS) via 12-lipoxygenase (12-LOX), and an oxidative-stress-dependent induction of the transcription factor, GADD153 and the BCL2-related protein BAK.	bakuchiol	245-248	DNA damage inducible transcript 3	Homo sapiens	208-215
15308577-2	2004	In this study, we have identified the C/EBP homologous protein (CHOP) as a novel retinoid-responsive gene using a polymerase chain reaction (PCR)-based cDNA subtraction method.	Retinoids	81-89	DNA damage inducible transcript 3	Homo sapiens	38-62
15308577-2	2004	In this study, we have identified the C/EBP homologous protein (CHOP) as a novel retinoid-responsive gene using a polymerase chain reaction (PCR)-based cDNA subtraction method.	Retinoids	81-89	DNA damage inducible transcript 3	Homo sapiens	64-68
15308577-3	2004	All-trans retinoic acid (ATRA) induced a biphasic expression of CHOP mRNA in the NB4 and HL60 AML cell lines.	Tretinoin	0-23	DNA damage inducible transcript 3	Homo sapiens	64-68
15308577-3	2004	All-trans retinoic acid (ATRA) induced a biphasic expression of CHOP mRNA in the NB4 and HL60 AML cell lines.	Tretinoin	25-29	DNA damage inducible transcript 3	Homo sapiens	64-68
15308577-4	2004	Levels of CHOP expression increased within 1 hour of exposure to ATRA.	Tretinoin	65-69	DNA damage inducible transcript 3	Homo sapiens	10-14
15308577-6	2004	Retinoid-dependent regulation of CHOP expression was also observed in normal human neutrophils but not in peripheral blood mononuclear cells.	Retinoids	0-8	DNA damage inducible transcript 3	Homo sapiens	33-37
15308577-7	2004	In addition, retinoid-dependent regulation of CHOP expression was not observed in retinoid-nonresponsive cell lines HL60R and NB4-R2.	Retinoids	13-21	DNA damage inducible transcript 3	Homo sapiens	46-50
15308577-11	2004	RA signaling in granulocytic differentiation involves regulated expression of CHOP and C/EBPepsilon in a coordinated fashion.	Tretinoin	0-2	DNA damage inducible transcript 3	Homo sapiens	78-82
15550586-1	2004	BACKGROUND: We demonstrated that highly active antiretroviral therapy (HAART) increases the toxic effect of cyclophosphamide, vincristine, doxorubicin (DOX) and prednisone (CHOP) in HIV-patients with non-Hodgkin"s lymphoma (NHL).	Doxorubicin	152-155	DNA damage inducible transcript 3	Homo sapiens	173-177
15550586-1	2004	BACKGROUND: We demonstrated that highly active antiretroviral therapy (HAART) increases the toxic effect of cyclophosphamide, vincristine, doxorubicin (DOX) and prednisone (CHOP) in HIV-patients with non-Hodgkin"s lymphoma (NHL).	Prednisone	161-171	DNA damage inducible transcript 3	Homo sapiens	173-177
15550586-7	2004	Significant associations (P=0.012) were observed between DOX AUC0-infinity (area under the concentration curve) and G3-G4 WHO haematologic toxicity, in patients treated with CHOP alone, but not in those treated with CHOP + HAART (P = not significant).	Doxorubicin	57-60	DNA damage inducible transcript 3	Homo sapiens	174-178
15550586-7	2004	Significant associations (P=0.012) were observed between DOX AUC0-infinity (area under the concentration curve) and G3-G4 WHO haematologic toxicity, in patients treated with CHOP alone, but not in those treated with CHOP + HAART (P = not significant).	Doxorubicin	57-60	DNA damage inducible transcript 3	Homo sapiens	216-220
15550586-9	2004	DOX AUC appears to be a predictor of toxicity only in patients treated with CHOP alone.	Doxorubicin	0-3	DNA damage inducible transcript 3	Homo sapiens	76-80
15550586-10	2004	Other factors beside DOX plasma levels are detrimental for toxicity after CHOP + HAART.	Doxorubicin	21-24	DNA damage inducible transcript 3	Homo sapiens	74-78
15650234-5	2004	These gangliosides may be involved in the regulation of 12-LOX leading to oxidative stress and apoptosis via the induction of GADD153 and BAK.	Gangliosides	6-18	DNA damage inducible transcript 3	Homo sapiens	126-133
15550586-1	2004	BACKGROUND: We demonstrated that highly active antiretroviral therapy (HAART) increases the toxic effect of cyclophosphamide, vincristine, doxorubicin (DOX) and prednisone (CHOP) in HIV-patients with non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	173-177
15322075-3	2004	Here, we provide evidence that CHOP is involved in THG up-regulation of DR5, which is a critical step for ER stress-induced apoptosis in human cancer cells.	Thapsigargin	51-54	DNA damage inducible transcript 3	Homo sapiens	31-35
15271854-0	2004	Curcumin-induced GADD153 gene up-regulation in human colon cancer cells.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	17-24
15271854-5	2004	To identify a potential pro-apoptotic gene that could be responsive to the DNA damage in curcumin-treated cells, growth arrest and DNA damage-inducible gene 153 (GADD153) was considered.	Curcumin	89-97	DNA damage inducible transcript 3	Homo sapiens	113-160
15271854-5	2004	To identify a potential pro-apoptotic gene that could be responsive to the DNA damage in curcumin-treated cells, growth arrest and DNA damage-inducible gene 153 (GADD153) was considered.	Curcumin	89-97	DNA damage inducible transcript 3	Homo sapiens	162-169
15271854-6	2004	Curcumin increased GADD153 mRNA (and also protein) expression, which was prevented by actinomycin D and also by a broad protein kinase C inhibitor, but not by selective MAPK inhibitors.	Curcumin	0-8	DNA damage inducible transcript 3	Homo sapiens	19-26
15271854-6	2004	Curcumin increased GADD153 mRNA (and also protein) expression, which was prevented by actinomycin D and also by a broad protein kinase C inhibitor, but not by selective MAPK inhibitors.	Dactinomycin	86-99	DNA damage inducible transcript 3	Homo sapiens	19-26
15271854-7	2004	These findings suggest that curcumin-induced up-regulation of GADD153 mRNA expression was at the level of transcription, but apparently without depending on upstream MAPK.	Curcumin	28-36	DNA damage inducible transcript 3	Homo sapiens	62-69
15271854-8	2004	In determining the involvement of reactive oxygen species in mediating the effect of curcumin on GADD153, the antioxidants pyrrolidine dithiocarbamate and N-acetylcysteine (NAC), but neither alpha-tocopherol nor catalase, also blunted or prevented up-regulation of GADD153 mRNA expression caused by curcumin.	Curcumin	85-93	DNA damage inducible transcript 3	Homo sapiens	97-104
15271854-10	2004	Because expression of GADD153 protein was detected before the appearance of apoptotic features, this observation raises the possibility that GADD153 protein might be important for curcumin-induced apoptosis.	Curcumin	180-188	DNA damage inducible transcript 3	Homo sapiens	22-29
15271854-10	2004	Because expression of GADD153 protein was detected before the appearance of apoptotic features, this observation raises the possibility that GADD153 protein might be important for curcumin-induced apoptosis.	Curcumin	180-188	DNA damage inducible transcript 3	Homo sapiens	141-148
15585627-7	2004	Of the 54 patients with CS III or IV treated with CHOP, 28 (52%) had elevated plasma GSTP1-1 levels.	Cesium	24-26	DNA damage inducible transcript 3	Homo sapiens	50-54
15585627-9	2004	The CR rates in patients at CS III and CS IV treated by CHOP, 55.2% (14 of 26) and 16.0% (5 of 28) for the low and high plasma GSTP1-1 groups, respectively, were significantly different (P &lt; 0.01).	Chromium	4-6	DNA damage inducible transcript 3	Homo sapiens	56-60
15585627-9	2004	The CR rates in patients at CS III and CS IV treated by CHOP, 55.2% (14 of 26) and 16.0% (5 of 28) for the low and high plasma GSTP1-1 groups, respectively, were significantly different (P &lt; 0.01).	Cesium	39-41	DNA damage inducible transcript 3	Homo sapiens	56-60
15322075-5	2004	Moreover, inhibition of CHOP expression attenuated DR5 up-regulation and apoptosis induced by THG, whereas ectopic expression of DR5 restored the sensitivity of CHOP siRNA-transfected cells to THG-induced apoptosis.	Thapsigargin	94-97	DNA damage inducible transcript 3	Homo sapiens	24-28
15322075-5	2004	Moreover, inhibition of CHOP expression attenuated DR5 up-regulation and apoptosis induced by THG, whereas ectopic expression of DR5 restored the sensitivity of CHOP siRNA-transfected cells to THG-induced apoptosis.	Thapsigargin	193-196	DNA damage inducible transcript 3	Homo sapiens	161-165
15322075-6	2004	In addition to HCT116 cells, inhibition of CHOP or DR5 induction also attenuated THG-induced cell death in other cancer cell lines including LNCaP, A2780S, and DU145, indicating that CHOP and DR5 are critical for ER stress-mediated apoptosis in human carcinoma cells.	Thapsigargin	81-84	DNA damage inducible transcript 3	Homo sapiens	43-47
15322075-6	2004	In addition to HCT116 cells, inhibition of CHOP or DR5 induction also attenuated THG-induced cell death in other cancer cell lines including LNCaP, A2780S, and DU145, indicating that CHOP and DR5 are critical for ER stress-mediated apoptosis in human carcinoma cells.	Thapsigargin	81-84	DNA damage inducible transcript 3	Homo sapiens	183-187
21289975-8	2004	The patient received chemotherapy with 2 courses of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP).	Prednisolone	99-111	DNA damage inducible transcript 3	Homo sapiens	113-117
15346335-1	2004	Phosphorylcholine (ChoP) is an antigenic component on the cell surface of many commensal and pathogenic bacteria that reside in the upper airway.	Phosphorylcholine	0-17	DNA damage inducible transcript 3	Homo sapiens	19-23
15132987-3	2004	We demonstrate here that 6-OHDA evoked endoplasmic reticulum (ER) stress, which was characterized by an up-regulation in the expression of GRP78 and GADD153 (Chop), cleavage of procaspase-12, and phosphorylation of eukaryotic initiation factor-2 alpha in a human dopaminergic neuronal cell line (SH-SY5Y) and cultured rat cerebellar granule neurons (CGNs).	Oxidopamine	25-31	DNA damage inducible transcript 3	Homo sapiens	149-156
15626054-10	2004	Cyclophosphamide, doxorubicin, vincristine and prednisone, (CHOP) chemotherapy was given to 68.7% of the patients with complete remission rates of 55.6% for those who got a minimum of six courses of chemotherapy.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
15016643-1	2004	Cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21), is standard chemotherapy for aggressive lymphomas.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	81-85
15016643-1	2004	Cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21), is standard chemotherapy for aggressive lymphomas.	Prednisone	48-58	DNA damage inducible transcript 3	Homo sapiens	81-85
15034757-7	2004	Treatment with high-dose corticosteroids was initiated, with clinical improvement, and was immediately followed by therapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP), which induced complete remission with a follow-up of 1 year.	Cyclophosphamide	128-144	DNA damage inducible transcript 3	Homo sapiens	194-198
15301718-11	2004	In CHOP+HD-MTX group, CR rate was 83%, PR rate was 16%.	Chromium	22-24	DNA damage inducible transcript 3	Homo sapiens	3-7
14982884-1	2004	The combination of cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21) is standard chemotherapy for aggressive lymphomas.	Cyclophosphamide	19-35	DNA damage inducible transcript 3	Homo sapiens	100-104
14982884-1	2004	The combination of cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21) is standard chemotherapy for aggressive lymphomas.	Doxorubicin	37-48	DNA damage inducible transcript 3	Homo sapiens	100-104
14982884-1	2004	The combination of cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21) is standard chemotherapy for aggressive lymphomas.	Vincristine	50-61	DNA damage inducible transcript 3	Homo sapiens	100-104
14982884-1	2004	The combination of cyclophosphamide, doxorubicin, vincristine, and prednisone, given every 3 weeks (CHOP-21) is standard chemotherapy for aggressive lymphomas.	Prednisone	67-77	DNA damage inducible transcript 3	Homo sapiens	100-104
15205201-10	2004	CONCLUSIONS: BL/BLL in adolescents and adults can successfully be treated with 5-day blocks of intensified chemotherapy such as the BFM regimen or CHOP/methotrexate-based chemotherapy consolidated with high-dose therapy.	Methotrexate	152-164	DNA damage inducible transcript 3	Homo sapiens	147-151
15205203-0	2004	Rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) for treatment of early-stage gastric diffuse large B-cell lymphoma.	Prednisone	58-68	DNA damage inducible transcript 3	Homo sapiens	72-76
15205203-2	2004	Recently, chemotherapy consisting of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) has been reported as effective treatment for early-stage gastric DLBCL.	Doxorubicin	37-48	DNA damage inducible transcript 3	Homo sapiens	96-100
15205203-2	2004	Recently, chemotherapy consisting of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) has been reported as effective treatment for early-stage gastric DLBCL.	Cyclophosphamide	50-66	DNA damage inducible transcript 3	Homo sapiens	96-100
15205203-2	2004	Recently, chemotherapy consisting of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) has been reported as effective treatment for early-stage gastric DLBCL.	Prednisone	84-94	DNA damage inducible transcript 3	Homo sapiens	96-100
15132987-3	2004	We demonstrate here that 6-OHDA evoked endoplasmic reticulum (ER) stress, which was characterized by an up-regulation in the expression of GRP78 and GADD153 (Chop), cleavage of procaspase-12, and phosphorylation of eukaryotic initiation factor-2 alpha in a human dopaminergic neuronal cell line (SH-SY5Y) and cultured rat cerebellar granule neurons (CGNs).	Oxidopamine	25-31	DNA damage inducible transcript 3	Homo sapiens	158-162
15159414-2	2004	We performed a randomized comparative trial of FM with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) front-line chemotherapy with and without sequential rituximab.	Prednisone	103-113	DNA damage inducible transcript 3	Homo sapiens	115-119
15359915-9	2004	The bilateral adrenal masses dramatically reduced in size after CHOP chemotherapy with hydrocortisone supplementation.	Hydrocortisone	87-101	DNA damage inducible transcript 3	Homo sapiens	64-68
15181605-5	2004	In patients with aggressive lymphoma who receive cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, 40% to 70% of patients attain a complete remission, depending on risk factors such as age and extranodal involvement.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	109-113
15181605-5	2004	In patients with aggressive lymphoma who receive cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, 40% to 70% of patients attain a complete remission, depending on risk factors such as age and extranodal involvement.	Doxorubicin	67-78	DNA damage inducible transcript 3	Homo sapiens	109-113
15181605-5	2004	In patients with aggressive lymphoma who receive cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, 40% to 70% of patients attain a complete remission, depending on risk factors such as age and extranodal involvement.	Prednisone	97-107	DNA damage inducible transcript 3	Homo sapiens	109-113
28140109-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	13-17
15021909-4	2004	We show that c-Myc represses the expression of GADD45a and GADD153 in response to thapsigargin, a nongenotoxic stress, as well as other endoplasmic reticulum (ER) stress agents.	Thapsigargin	82-94	DNA damage inducible transcript 3	Homo sapiens	59-66
15053923-0	2004	Increased GADD153 gene expression during iron chelation-induced apoptosis in Jurkat T-lymphocytes.	Iron	41-45	DNA damage inducible transcript 3	Homo sapiens	10-17
15053923-9	2004	DFO also caused GADD153 protein to be expressed.	Deferoxamine	0-3	DNA damage inducible transcript 3	Homo sapiens	16-23
15053923-10	2004	Because GADD153 is recognized as a pro-apoptotic gene, these findings generate the notion that GADD153 might help mediate apoptosis in iron-deficient cells.	Iron	135-139	DNA damage inducible transcript 3	Homo sapiens	8-15
15053923-10	2004	Because GADD153 is recognized as a pro-apoptotic gene, these findings generate the notion that GADD153 might help mediate apoptosis in iron-deficient cells.	Iron	135-139	DNA damage inducible transcript 3	Homo sapiens	95-102
15005254-8	2004	The patient was treated with chemotherapy by cyclophosphamide, hydroxydoxorubicin, vincristine and prednisolone (CHOP), however, it was ineffective, and the patient died of hemorrhage from the lymphoma involvement of the intestine 5 months after the onset of disease.	Prednisolone	99-111	DNA damage inducible transcript 3	Homo sapiens	113-117
15060745-2	2004	The risk is significantly evident in patients with aggressive lymphoma, which is highly responsive to standard chemotherapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP) achieving a complete response rate of 60-80% and 5-year survival rate of 30-50% with only 1% of treatment-related mortality.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	195-199
15060745-2	2004	The risk is significantly evident in patients with aggressive lymphoma, which is highly responsive to standard chemotherapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP) achieving a complete response rate of 60-80% and 5-year survival rate of 30-50% with only 1% of treatment-related mortality.	Doxorubicin	147-164	DNA damage inducible transcript 3	Homo sapiens	195-199
15060745-2	2004	The risk is significantly evident in patients with aggressive lymphoma, which is highly responsive to standard chemotherapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP) achieving a complete response rate of 60-80% and 5-year survival rate of 30-50% with only 1% of treatment-related mortality.	Prednisone	183-193	DNA damage inducible transcript 3	Homo sapiens	195-199
16696176-12	2004	These results indicate that the metabolism of iprodione involves Phase II biotransformation in the liver (XRE, GSTYa), and that this chemical has the potential to cause cell proliferation and/or inflammatory reactions (c-fos, NF-kB), proteotoxic effects (HSP70, GRP78), metabolic disruption (CRE), and DNA damage (GADD45, GADD153).	iprodione	46-55	DNA damage inducible transcript 3	Homo sapiens	322-329
15042528-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	13-17
15042528-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Doxorubicin	50-61	DNA damage inducible transcript 3	Homo sapiens	13-17
15042528-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Vincristine	63-74	DNA damage inducible transcript 3	Homo sapiens	13-17
15042528-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Prednisone	76-86	DNA damage inducible transcript 3	Homo sapiens	13-17
28140109-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Doxorubicin	50-61	DNA damage inducible transcript 3	Homo sapiens	13-17
28140109-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Vincristine	63-74	DNA damage inducible transcript 3	Homo sapiens	13-17
28140109-1	2004	In the past, CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisone) was considered the gold standard treatment for aggressive non-Hodgkin"s lymphoma (NHL).	Prednisone	76-86	DNA damage inducible transcript 3	Homo sapiens	13-17
14971657-8	2004	At 50 microg/mL of lead nitrate, the average fold inductions were: 2.1 +/- 1.0, 5.4 +/- 0.4, 12.1 +/- 6.2, 5.0 +/- 1.7, 2.5 +/- 1.3, and 4.8 +/- 4.5 for XRE, HSP70, CRE, GADD153, and GRP78, respectively.	lead nitrate	19-31	DNA damage inducible transcript 3	Homo sapiens	170-177
15360053-4	2004	LTBI started 4-6 weeks following the last CHOP course and was given in two courses, each with 4 daily fractions of 0.2 Gy, separated by 2 weeks of rest.	ltbi	0-4	DNA damage inducible transcript 3	Homo sapiens	42-46
12955471-12	2004	CONCLUSIONS: The pharmacokinetics of IDA and its main metabolite idarubicinol in CHOP-derived protocols were not different from data obtained with other combinations or monotherapy.	idarubicinol	65-77	DNA damage inducible transcript 3	Homo sapiens	81-85
14971665-9	2004	DU, (5-50 microg/ml) produced a complex profile of activity demonstrating significant dose-dependent induction of the hMTIIA FOS, p53RE, Gadd153, Gadd45, NFkappaBRE, CRE, HSP70, RARE, and GRP78 promoters.	du	0-2	DNA damage inducible transcript 3	Homo sapiens	137-144
15153709-1	2004	BACKGROUND: Patients with chronic lymphocytic leukemia (CLL) are sometimes resistant to treatment or relapse soon after the administration of the currently available frontline therapy including chlorambucil-prednisolone CHOP and fludarabine.	Chlorambucil	194-206	DNA damage inducible transcript 3	Homo sapiens	220-224
15493360-10	2004	In contrast, arsenic trioxide markedly enhanced the expression of the p21 protein, GADD45 and GADD153, in a time-dependent manner.	Arsenic Trioxide	13-29	DNA damage inducible transcript 3	Homo sapiens	94-101
14752912-4	2004	Current chemotherapy of choice is CHOP [Cyclophosphamide, Hydroxydaunomycin (doxorubicin), Oncovin (vincristine sulfate) and Prednisone].	Cyclophosphamide	40-56	DNA damage inducible transcript 3	Homo sapiens	34-38
14752912-4	2004	Current chemotherapy of choice is CHOP [Cyclophosphamide, Hydroxydaunomycin (doxorubicin), Oncovin (vincristine sulfate) and Prednisone].	Doxorubicin	58-75	DNA damage inducible transcript 3	Homo sapiens	34-38
14752912-4	2004	Current chemotherapy of choice is CHOP [Cyclophosphamide, Hydroxydaunomycin (doxorubicin), Oncovin (vincristine sulfate) and Prednisone].	Doxorubicin	77-88	DNA damage inducible transcript 3	Homo sapiens	34-38
14752912-4	2004	Current chemotherapy of choice is CHOP [Cyclophosphamide, Hydroxydaunomycin (doxorubicin), Oncovin (vincristine sulfate) and Prednisone].	Vincristine	91-98	DNA damage inducible transcript 3	Homo sapiens	34-38
14752912-4	2004	Current chemotherapy of choice is CHOP [Cyclophosphamide, Hydroxydaunomycin (doxorubicin), Oncovin (vincristine sulfate) and Prednisone].	Vincristine	100-119	DNA damage inducible transcript 3	Homo sapiens	34-38
14752912-4	2004	Current chemotherapy of choice is CHOP [Cyclophosphamide, Hydroxydaunomycin (doxorubicin), Oncovin (vincristine sulfate) and Prednisone].	Prednisone	125-135	DNA damage inducible transcript 3	Homo sapiens	34-38
14667815-12	2004	Mutation of the CHOP-binding site in the human promoter abolishes CHOP binding and significantly reduces ethoxyquin induction, suggesting that CHOP mediates stimulated expression in response to antioxidants in the human.	Ethoxyquin	105-115	DNA damage inducible transcript 3	Homo sapiens	16-20
14971657-9	2004	These results indicate the potential for lead nitrate to undergo biotransformation in the liver (XRE), to cause cell proliferation (c-fos), protein damage (HSP70, GRP78), metabolic perturbation (CRE), and growth arrest and DNA damage (GADD153).	lead nitrate	41-53	DNA damage inducible transcript 3	Homo sapiens	235-242
15031599-8	2004	cDNA microarray revealed that PTX treatment upregulated expression of caspase 1, 2, 3, 4, 6, 9, 10, their activator apaf-1, and stress reaction-related genes, gadd34, gadd153 in KF, although most of them were unchanged or downregulated in KFTX.	Paclitaxel	30-33	DNA damage inducible transcript 3	Homo sapiens	167-174
15755073-1	2004	Since it exerts a stronger antitumor action than predinisolone, dexamethasone was used for therapy of patients with non-Hodgkin"s lymphoma refractory to CHOP.	Dexamethasone	64-77	DNA damage inducible transcript 3	Homo sapiens	153-157
15327748-0	2004	Hydrogen peroxide induces GADD153 in Jurkat cells through the protein kinase C-dependent pathway.	Hydrogen Peroxide	0-17	DNA damage inducible transcript 3	Homo sapiens	26-33
15327748-3	2004	GADD153 mRNA expression was immediately enhanced following hydrogen peroxide exposure and was significantly inhibited by treatment with H-7, staurosporin, and Ro-31-8220.	Hydrogen Peroxide	59-76	DNA damage inducible transcript 3	Homo sapiens	0-7
15327748-3	2004	GADD153 mRNA expression was immediately enhanced following hydrogen peroxide exposure and was significantly inhibited by treatment with H-7, staurosporin, and Ro-31-8220.	1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine	136-139	DNA damage inducible transcript 3	Homo sapiens	0-7
15327748-3	2004	GADD153 mRNA expression was immediately enhanced following hydrogen peroxide exposure and was significantly inhibited by treatment with H-7, staurosporin, and Ro-31-8220.	Staurosporine	141-153	DNA damage inducible transcript 3	Homo sapiens	0-7
15327748-4	2004	In particular, rottlerin, a PKCdelta specific inhibitor, markedly attenuated hydrogen peroxide-induced GADD153 mRNA expression even at 1 microM.	rottlerin	15-24	DNA damage inducible transcript 3	Homo sapiens	103-110
15327748-4	2004	In particular, rottlerin, a PKCdelta specific inhibitor, markedly attenuated hydrogen peroxide-induced GADD153 mRNA expression even at 1 microM.	Hydrogen Peroxide	77-94	DNA damage inducible transcript 3	Homo sapiens	103-110
15327748-5	2004	Treatment with a potent PKC activator, phorbol-12-myristate-13-acetate (PMA), augmented GADD153 mRNA in Jurkat cells in the presence of hydrogen peroxide, although PMA alone induced GADD153 mRNA marginally.	Tetradecanoylphorbol Acetate	39-70	DNA damage inducible transcript 3	Homo sapiens	88-95
15327748-5	2004	Treatment with a potent PKC activator, phorbol-12-myristate-13-acetate (PMA), augmented GADD153 mRNA in Jurkat cells in the presence of hydrogen peroxide, although PMA alone induced GADD153 mRNA marginally.	Tetradecanoylphorbol Acetate	39-70	DNA damage inducible transcript 3	Homo sapiens	182-189
15327748-5	2004	Treatment with a potent PKC activator, phorbol-12-myristate-13-acetate (PMA), augmented GADD153 mRNA in Jurkat cells in the presence of hydrogen peroxide, although PMA alone induced GADD153 mRNA marginally.	Tetradecanoylphorbol Acetate	72-75	DNA damage inducible transcript 3	Homo sapiens	88-95
15327748-5	2004	Treatment with a potent PKC activator, phorbol-12-myristate-13-acetate (PMA), augmented GADD153 mRNA in Jurkat cells in the presence of hydrogen peroxide, although PMA alone induced GADD153 mRNA marginally.	Tetradecanoylphorbol Acetate	72-75	DNA damage inducible transcript 3	Homo sapiens	182-189
15327748-5	2004	Treatment with a potent PKC activator, phorbol-12-myristate-13-acetate (PMA), augmented GADD153 mRNA in Jurkat cells in the presence of hydrogen peroxide, although PMA alone induced GADD153 mRNA marginally.	Hydrogen Peroxide	136-153	DNA damage inducible transcript 3	Homo sapiens	88-95
15327748-6	2004	Hydrogen peroxide significantly enhanced the AP-1 binding activity of the nuclear extract from Jurkat cells to the GADD153 AP-1 binding site.	Hydrogen Peroxide	0-17	DNA damage inducible transcript 3	Homo sapiens	115-122
14649730-3	2003	Exposure of retinoic acid (RA)-differentiated SH-SY5Y cells to MPP+ (1 mM, 72 h) also resulted in a decrease in RMB3 expression and an increase in GADD153 expression.	Tretinoin	27-29	DNA damage inducible transcript 3	Homo sapiens	147-154
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	phenethyl isothiocyanate	14-19	DNA damage inducible transcript 3	Homo sapiens	23-30
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	phenethyl isothiocyanate	14-19	DNA damage inducible transcript 3	Homo sapiens	137-144
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Dactinomycin	56-69	DNA damage inducible transcript 3	Homo sapiens	23-30
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Dactinomycin	56-69	DNA damage inducible transcript 3	Homo sapiens	137-144
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Acetylcysteine	73-89	DNA damage inducible transcript 3	Homo sapiens	23-30
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Acetylcysteine	73-89	DNA damage inducible transcript 3	Homo sapiens	137-144
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	phenethyl isothiocyanate	107-112	DNA damage inducible transcript 3	Homo sapiens	23-30
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	phenethyl isothiocyanate	107-112	DNA damage inducible transcript 3	Homo sapiens	137-144
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Reactive Oxygen Species	225-248	DNA damage inducible transcript 3	Homo sapiens	23-30
14635187-8	2003	The effect of PEITC on GADD153 was attenuated by either actinomycin D or N-acetylcysteine, suggesting that PEITC-induced upregulation of GADD153 mRNA expression was partly at the level of transcriptional activation involving reactive oxygen species.	Reactive Oxygen Species	225-248	DNA damage inducible transcript 3	Homo sapiens	137-144
14635187-9	2003	Additionally, PEITC-induced upregulation of GADD153 mRNA expression did not appear to require p53, based on the observation that PEITC also increased GADD153 mRNA expression in HCT-15 colonocytes, which are known to express mutant p53.	phenethyl isothiocyanate	14-19	DNA damage inducible transcript 3	Homo sapiens	44-51
14635187-9	2003	Additionally, PEITC-induced upregulation of GADD153 mRNA expression did not appear to require p53, based on the observation that PEITC also increased GADD153 mRNA expression in HCT-15 colonocytes, which are known to express mutant p53.	phenethyl isothiocyanate	14-19	DNA damage inducible transcript 3	Homo sapiens	150-157
14635187-9	2003	Additionally, PEITC-induced upregulation of GADD153 mRNA expression did not appear to require p53, based on the observation that PEITC also increased GADD153 mRNA expression in HCT-15 colonocytes, which are known to express mutant p53.	phenethyl isothiocyanate	129-134	DNA damage inducible transcript 3	Homo sapiens	150-157
14635075-2	2003	METHODS: Medical records of 1355 patients with intermediate-grade non-Hodgkin lymphoma receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) or similar chemotherapy were reviewed.	Prednisone	145-155	DNA damage inducible transcript 3	Homo sapiens	157-161
14649730-3	2003	Exposure of retinoic acid (RA)-differentiated SH-SY5Y cells to MPP+ (1 mM, 72 h) also resulted in a decrease in RMB3 expression and an increase in GADD153 expression.	Tretinoin	12-25	DNA damage inducible transcript 3	Homo sapiens	147-154
14645667-3	2003	Because BCL2-family proteins are important in apoptosis induced by chemotherapeutic drugs, GADD153 may be a key mediator of synergy between fenretinide and chemotherapeutic drugs.	Fenretinide	140-151	DNA damage inducible transcript 3	Homo sapiens	91-98
14645667-5	2003	Increased expression of GADD153 raised the background level of apoptosis and increased apoptosis induced by fenretinide or the chemotherapeutic drugs cisplatin and etoposide.	Fenretinide	108-119	DNA damage inducible transcript 3	Homo sapiens	24-31
14645667-5	2003	Increased expression of GADD153 raised the background level of apoptosis and increased apoptosis induced by fenretinide or the chemotherapeutic drugs cisplatin and etoposide.	Cisplatin	150-159	DNA damage inducible transcript 3	Homo sapiens	24-31
14645667-5	2003	Increased expression of GADD153 raised the background level of apoptosis and increased apoptosis induced by fenretinide or the chemotherapeutic drugs cisplatin and etoposide.	Etoposide	164-173	DNA damage inducible transcript 3	Homo sapiens	24-31
14645667-7	2003	Conversely, expression of antisense-GADD153 virtually abolished the induction of apoptosis in response to fenretinide but overall had no significant effect on apoptosis induced by chemotherapeutic drugs.	Fenretinide	106-117	DNA damage inducible transcript 3	Homo sapiens	36-43
14645667-8	2003	The effect of antisense-GADD153 on synergy between chemotherapeutic drugs and fenretinide varied with the drug used: there was no effect on synergy between fenretinide and cisplatin, but the combination of fenretinide with etoposide became antagonistic.	Fenretinide	78-89	DNA damage inducible transcript 3	Homo sapiens	24-31
14645667-9	2003	These results suggest that mechanisms mediating synergy between fenretinide and chemotherapeutic drugs lie upstream of GADD153.	Fenretinide	64-75	DNA damage inducible transcript 3	Homo sapiens	119-126
14617177-1	2003	Haemophilus influenzae obtains choline from either its growth medium or host cell membrane lipids and expresses it on its lipopolysaccharide (LPS) in the form of phosphorylcholine (ChoP), which contributes to its pathogenesis by mimicry of host cell molecules.	Phosphorylcholine	162-179	DNA damage inducible transcript 3	Homo sapiens	181-185
14612528-7	2003	Bak expression was also induced in cells overexpressing the stress-induced transcription factor GADD153, but Bak expression was inhibited in cells expressing an antisense GADD153 construct.	bakuchiol	0-3	DNA damage inducible transcript 3	Homo sapiens	96-103
14612528-7	2003	Bak expression was also induced in cells overexpressing the stress-induced transcription factor GADD153, but Bak expression was inhibited in cells expressing an antisense GADD153 construct.	bakuchiol	109-112	DNA damage inducible transcript 3	Homo sapiens	171-178
14581418-5	2003	Eight of 11 patients were treated with a cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP)-like regimen.	Prednisone	89-99	DNA damage inducible transcript 3	Homo sapiens	101-105
12876286-4	2003	Phosphorylation of CHOP at serine 79 and serine 81 by p38-MAP kinase enhances its transcriptional activity.	Serine	27-33	DNA damage inducible transcript 3	Homo sapiens	19-23
14511657-0	2003	Gadd153 restores resistance to radiation-induced apoptosis after thiol depletion.	Sulfhydryl Compounds	65-70	DNA damage inducible transcript 3	Homo sapiens	0-7
14511657-3	2003	Among other genes we found the transcription factor Gadd153 to be upregulated after exposing the cells to cystine/methionine free culture medium.	Cystine	106-113	DNA damage inducible transcript 3	Homo sapiens	52-59
14511657-3	2003	Among other genes we found the transcription factor Gadd153 to be upregulated after exposing the cells to cystine/methionine free culture medium.	Methionine	114-124	DNA damage inducible transcript 3	Homo sapiens	52-59
14511657-5	2003	We found that overexpression of Gadd153 slightly reduced the amount of radiation-induced apoptosis in cells kept in normal medium but very significantly reduced apoptosis (from 55% to 18%) in cells which were treated with cystine/methionine free culture medium.	Cystine	222-229	DNA damage inducible transcript 3	Homo sapiens	32-39
14511657-5	2003	We found that overexpression of Gadd153 slightly reduced the amount of radiation-induced apoptosis in cells kept in normal medium but very significantly reduced apoptosis (from 55% to 18%) in cells which were treated with cystine/methionine free culture medium.	Methionine	230-240	DNA damage inducible transcript 3	Homo sapiens	32-39
14511657-6	2003	The observed protective effect of Gadd153 against radiation-induced apoptosis in thiol depleted lymphoma cells argues for an anti-apoptotic function of Gadd153 after perturbation of the cellular redox state.	Sulfhydryl Compounds	81-86	DNA damage inducible transcript 3	Homo sapiens	34-41
14575689-0	2003	15-Deoxy-Delta(12,14)-prostaglandin J2 induces apoptosis through activation of the CHOP gene in HeLa cells.	15-deoxy-delta(12,14)-prostaglandin J2	0-38	DNA damage inducible transcript 3	Homo sapiens	83-87
14575689-3	2003	We recently reported that cyclopentenone PGs accumulate in the endoplasmic reticulum (ER) and it has been shown that the transcription factor CHOP is induced by ER-stresses and elicits apoptosis.	cyclopentenone	26-40	DNA damage inducible transcript 3	Homo sapiens	142-146
12907753-6	2003	The use of pharmacological inhibitors indicated that cAMP-induced CHOP expression was dependent on protein kinase A (PKA), mammalian target of rapamycin pathway, and reactive oxygen species.	Cyclic AMP	53-57	DNA damage inducible transcript 3	Homo sapiens	66-70
12907753-6	2003	The use of pharmacological inhibitors indicated that cAMP-induced CHOP expression was dependent on protein kinase A (PKA), mammalian target of rapamycin pathway, and reactive oxygen species.	Reactive Oxygen Species	166-189	DNA damage inducible transcript 3	Homo sapiens	66-70
14739562-8	2003	Treatment with salsolinol and 1BnTIQ induced several genes involved in ER stress and unfolded protein response (UPR), such as ER chaperones and GADD153 (CHOP).	salsolinol	15-25	DNA damage inducible transcript 3	Homo sapiens	144-151
14739562-8	2003	Treatment with salsolinol and 1BnTIQ induced several genes involved in ER stress and unfolded protein response (UPR), such as ER chaperones and GADD153 (CHOP).	salsolinol	15-25	DNA damage inducible transcript 3	Homo sapiens	153-157
14739562-8	2003	Treatment with salsolinol and 1BnTIQ induced several genes involved in ER stress and unfolded protein response (UPR), such as ER chaperones and GADD153 (CHOP).	1,2,3,4-tetrahydro-1-(phenylmethyl)isoquinoline	30-36	DNA damage inducible transcript 3	Homo sapiens	144-151
14739562-8	2003	Treatment with salsolinol and 1BnTIQ induced several genes involved in ER stress and unfolded protein response (UPR), such as ER chaperones and GADD153 (CHOP).	1,2,3,4-tetrahydro-1-(phenylmethyl)isoquinoline	30-36	DNA damage inducible transcript 3	Homo sapiens	153-157
14604284-5	2003	Because of an allergic reaction to L-asparaginase, 6 courses of CHOP (adriamycin, cyclophosphamide, vincristine and prednisolone) therapy were administered as consolidation after 4 courses of L-asparaginase.	Doxorubicin	70-80	DNA damage inducible transcript 3	Homo sapiens	64-68
14513044-1	2003	For the last decade, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the best available standard of care for aggressive non-Hodgkin"s lymphoma (NHL), based on equivalent therapeutic results with other multiagent chemotherapy accompanied by lower costs and lesser toxicity.	Cyclophosphamide	21-37	DNA damage inducible transcript 3	Homo sapiens	81-85
14513044-1	2003	For the last decade, cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) has been the best available standard of care for aggressive non-Hodgkin"s lymphoma (NHL), based on equivalent therapeutic results with other multiagent chemotherapy accompanied by lower costs and lesser toxicity.	Prednisone	69-79	DNA damage inducible transcript 3	Homo sapiens	81-85
14617177-4	2003	The licB gene has homology to bacterial permeases including betT and is encoded in the lic1 locus, which is essential for the expression of LPS-ChoP.	bett	60-64	DNA damage inducible transcript 3	Homo sapiens	144-148
14617177-9	2003	We conclude that H. influenzae may have multiple mechanisms for choline uptake and distinct pathways for choline utilization in LPS-ChoP biosynthesis and osmoregulation.	Choline	105-112	DNA damage inducible transcript 3	Homo sapiens	132-136
12963864-7	2003	RESULTS: Eight genes (GAS1, CDH4, MT1L, CST3, ATF4, ASNS/TS11, CHOP, HSPA5) were identified that are at least a thousand times more likely to be differentially expressed due to DEX treatment and six genes (TSC22, LDHA, IGFBP2, TAGLN, SCG2, WARS) were identified that are at least a hundred times more likely to be differentially expressed due to DEX treatment.	Dexamethasone	177-180	DNA damage inducible transcript 3	Homo sapiens	63-67
12963864-7	2003	RESULTS: Eight genes (GAS1, CDH4, MT1L, CST3, ATF4, ASNS/TS11, CHOP, HSPA5) were identified that are at least a thousand times more likely to be differentially expressed due to DEX treatment and six genes (TSC22, LDHA, IGFBP2, TAGLN, SCG2, WARS) were identified that are at least a hundred times more likely to be differentially expressed due to DEX treatment.	Dexamethasone	346-349	DNA damage inducible transcript 3	Homo sapiens	63-67
12939601-3	2003	Previously, we observed that a synthetic retinoid N-(4-hydroxyphenyl)retinamide (4HPR) effectively impaired cell growth and survival (induction of growth arrest and apoptosis) in human hepatoma cells, which was accompanied by over expression of GADD153.	Fenretinide	50-79	DNA damage inducible transcript 3	Homo sapiens	245-252
14581895-1	2003	BACKGROUND: Six to eight cycles of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard for intermediate-grade non-Hodgkin"s lymphoma (NHL) but is associated with toxicity that may cause premature termination of therapy.	Cyclophosphamide	49-65	DNA damage inducible transcript 3	Homo sapiens	35-39
14581895-1	2003	BACKGROUND: Six to eight cycles of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard for intermediate-grade non-Hodgkin"s lymphoma (NHL) but is associated with toxicity that may cause premature termination of therapy.	Doxorubicin	67-78	DNA damage inducible transcript 3	Homo sapiens	35-39
14581895-1	2003	BACKGROUND: Six to eight cycles of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard for intermediate-grade non-Hodgkin"s lymphoma (NHL) but is associated with toxicity that may cause premature termination of therapy.	Vincristine	80-91	DNA damage inducible transcript 3	Homo sapiens	35-39
14581895-1	2003	BACKGROUND: Six to eight cycles of CHOP therapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) is standard for intermediate-grade non-Hodgkin"s lymphoma (NHL) but is associated with toxicity that may cause premature termination of therapy.	Prednisone	97-107	DNA damage inducible transcript 3	Homo sapiens	35-39
12939601-3	2003	Previously, we observed that a synthetic retinoid N-(4-hydroxyphenyl)retinamide (4HPR) effectively impaired cell growth and survival (induction of growth arrest and apoptosis) in human hepatoma cells, which was accompanied by over expression of GADD153.	Fenretinide	81-85	DNA damage inducible transcript 3	Homo sapiens	245-252
12915593-1	2003	PURPOSE: To investigate whether the relative dose-intensity of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy could be improved by prophylactic administration of granulocyte colony-stimulating factor (G-CSF) in elderly patients with aggressive non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	63-79	DNA damage inducible transcript 3	Homo sapiens	123-127
12907943-3	2003	Here we report that the unfolded protein response (UPR) in the endoplasmic reticulum is activated in cholesterol-loaded macrophages, resulting in expression of the cell death effector CHOP.	Cholesterol	101-112	DNA damage inducible transcript 3	Homo sapiens	184-188
12907943-5	2003	Furthermore, endoplasmic reticulum calcium depletion, the UPR, caspase-3 activation and apoptosis are markedly inhibited by selective inhibition of cholesterol trafficking to the endoplasmic reticulum, and Chop-/- macrophages are protected from cholesterol-induced apoptosis.	Cholesterol	245-256	DNA damage inducible transcript 3	Homo sapiens	206-210
12907943-6	2003	We propose that cholesterol trafficking to endoplasmic reticulum membranes, resulting in activation of the CHOP arm of the UPR, is the key signalling step in cholesterol-induced apoptosis in macrophages.	Cholesterol	16-27	DNA damage inducible transcript 3	Homo sapiens	107-111
12907943-6	2003	We propose that cholesterol trafficking to endoplasmic reticulum membranes, resulting in activation of the CHOP arm of the UPR, is the key signalling step in cholesterol-induced apoptosis in macrophages.	Cholesterol	158-169	DNA damage inducible transcript 3	Homo sapiens	107-111
12915593-1	2003	PURPOSE: To investigate whether the relative dose-intensity of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy could be improved by prophylactic administration of granulocyte colony-stimulating factor (G-CSF) in elderly patients with aggressive non-Hodgkin"s lymphoma (NHL).	Prednisone	111-121	DNA damage inducible transcript 3	Homo sapiens	123-127
12815281-8	2003	Based on the up-regulations observed at the mRNA level, it is speculated that etoposide-induced apoptosis in the HL-60 cells proceeds via pathways involving factors such as TNFalpha, IGFBP3, SAPK1, AP-1 and GADD153/CHOP10.	Etoposide	78-87	DNA damage inducible transcript 3	Homo sapiens	207-214
12917038-1	2003	BACKGROUND &amp; OBJECTIVE: For newly diagnosed non-Hodgkin"s lymphoma (NHL), CHOP regimen shows good response, but quite a few patients belong to intrinsic drug resistance, or relapse after complete remission (CR).	Adenosine Monophosphate	12-15	DNA damage inducible transcript 3	Homo sapiens	78-82
12815281-8	2003	Based on the up-regulations observed at the mRNA level, it is speculated that etoposide-induced apoptosis in the HL-60 cells proceeds via pathways involving factors such as TNFalpha, IGFBP3, SAPK1, AP-1 and GADD153/CHOP10.	Etoposide	78-87	DNA damage inducible transcript 3	Homo sapiens	215-221
12906019-2	2003	The first-line treatment for diffuse large-B-cell non Hodgkin"s lymphoma, a highly malignant lymphoma, is CHOP chemotherapy (cyclophosphamide + doxorubicin + vincristine + prednisone).	Cyclophosphamide	125-141	DNA damage inducible transcript 3	Homo sapiens	106-110
12955576-4	2003	A recent European phase III study in elderly patients with untreated diffuse large B-cell lymphoma suggested that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy is superior to CHOP chemotherapy alone in terms of complete response rate and event-free and overall survivals.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	191-195
12955576-4	2003	A recent European phase III study in elderly patients with untreated diffuse large B-cell lymphoma suggested that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy is superior to CHOP chemotherapy alone in terms of complete response rate and event-free and overall survivals.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	225-229
12955576-4	2003	A recent European phase III study in elderly patients with untreated diffuse large B-cell lymphoma suggested that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy is superior to CHOP chemotherapy alone in terms of complete response rate and event-free and overall survivals.	Prednisolone	177-189	DNA damage inducible transcript 3	Homo sapiens	191-195
12955576-4	2003	A recent European phase III study in elderly patients with untreated diffuse large B-cell lymphoma suggested that rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) chemotherapy is superior to CHOP chemotherapy alone in terms of complete response rate and event-free and overall survivals.	Prednisolone	177-189	DNA damage inducible transcript 3	Homo sapiens	225-229
12883267-9	2003	Arsenic trioxide markedly enhanced the expression of GADD45 and GADD153 in a time-dependent manner.	Arsenic Trioxide	0-16	DNA damage inducible transcript 3	Homo sapiens	64-71
12956443-10	2003	In this study, the t(11;16) was seen in 2 patients with previous lymphomas treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	88-104	DNA damage inducible transcript 3	Homo sapiens	148-152
12764549-9	2003	Cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP)-like chemotherapy with or without local irradiation led to 17% relapses in patients with localized aggressive lymphoma.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	66-70
12764549-9	2003	Cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP)-like chemotherapy with or without local irradiation led to 17% relapses in patients with localized aggressive lymphoma.	Doxorubicin	18-35	DNA damage inducible transcript 3	Homo sapiens	66-70
12880976-0	2003	Induction of GADD153 and Bak: novel molecular targets of fenretinide-induced apoptosis of neuroblastoma.	Fenretinide	57-68	DNA damage inducible transcript 3	Homo sapiens	13-20
12880976-2	2003	The stress-induced transcription factor GADD153 and the Bcl2-related protein Bak are upregulated in response to fenretinide.	Fenretinide	112-123	DNA damage inducible transcript 3	Homo sapiens	40-47
12880976-5	2003	Neither GADD153 or Bak were induced by chemotherapeutic agents but over expression of GADD153 results in increased sensitivity to fenretinide-induced apoptosis.	Fenretinide	130-141	DNA damage inducible transcript 3	Homo sapiens	86-93
12880976-6	2003	Therefore, fenretinide induces apoptosis via RAR-dependent and -independent pathways in which the RAR-independent pathway is characterised by the reactive oxygen species-dependent induction of GADD153 and Bak.	Fenretinide	11-22	DNA damage inducible transcript 3	Homo sapiens	193-200
12880976-6	2003	Therefore, fenretinide induces apoptosis via RAR-dependent and -independent pathways in which the RAR-independent pathway is characterised by the reactive oxygen species-dependent induction of GADD153 and Bak.	Reactive Oxygen Species	146-169	DNA damage inducible transcript 3	Homo sapiens	193-200
12764549-9	2003	Cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP)-like chemotherapy with or without local irradiation led to 17% relapses in patients with localized aggressive lymphoma.	Prednisone	54-64	DNA damage inducible transcript 3	Homo sapiens	66-70
12956443-10	2003	In this study, the t(11;16) was seen in 2 patients with previous lymphomas treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Doxorubicin	106-117	DNA damage inducible transcript 3	Homo sapiens	148-152
12956443-10	2003	In this study, the t(11;16) was seen in 2 patients with previous lymphomas treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Prednisone	136-146	DNA damage inducible transcript 3	Homo sapiens	148-152
12706007-5	2003	Further, we investigated the effects of isoliquiritigenin on the GADD153 mRNA and protein expression, and promoter activity.	isoliquiritigenin	40-57	DNA damage inducible transcript 3	Homo sapiens	65-72
12829664-1	2003	PURPOSE: To test the hypothesis that therapy of intermediate- and high-grade (excluding Burkitt lymphoblastic) lymphoma with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) could be safely dose-intensified with routine filgrastim support.	Prednisone	173-183	DNA damage inducible transcript 3	Homo sapiens	185-189
12931670-4	2003	Prior to pathological diagnosis, CHOP therapy with cyclophosphamide, adriamycin, vincristine and prednisolone was performed under mechanical ventilation for the purpose of resuscitation.	Cyclophosphamide	51-67	DNA damage inducible transcript 3	Homo sapiens	33-37
12931670-11	2003	Thus, the present case is rare because an RSCC relapse after a long free period went into remission as a result of CHOP therapy.	rscc	42-46	DNA damage inducible transcript 3	Homo sapiens	115-119
12598533-3	2003	Microarray analysis of RNA isolated from toxin treated samples revealed that the stress-induced transcription factor CHOP/Gadd153 was dramatically up-regulated by both 6-OHDA and MPP+.	Oxidopamine	168-174	DNA damage inducible transcript 3	Homo sapiens	117-121
12598533-3	2003	Microarray analysis of RNA isolated from toxin treated samples revealed that the stress-induced transcription factor CHOP/Gadd153 was dramatically up-regulated by both 6-OHDA and MPP+.	Oxidopamine	168-174	DNA damage inducible transcript 3	Homo sapiens	122-129
12598533-3	2003	Microarray analysis of RNA isolated from toxin treated samples revealed that the stress-induced transcription factor CHOP/Gadd153 was dramatically up-regulated by both 6-OHDA and MPP+.	mangion-purified polysaccharide (Candida albicans)	179-183	DNA damage inducible transcript 3	Homo sapiens	117-121
12598533-3	2003	Microarray analysis of RNA isolated from toxin treated samples revealed that the stress-induced transcription factor CHOP/Gadd153 was dramatically up-regulated by both 6-OHDA and MPP+.	mangion-purified polysaccharide (Candida albicans)	179-183	DNA damage inducible transcript 3	Homo sapiens	122-129
12707721-2	2003	During pregnancy chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) stabilized the disease for 4 months before new manifestations appeared.	Cyclophosphamide	35-51	DNA damage inducible transcript 3	Homo sapiens	95-99
12707721-2	2003	During pregnancy chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) stabilized the disease for 4 months before new manifestations appeared.	Doxorubicin	53-64	DNA damage inducible transcript 3	Homo sapiens	95-99
12707721-2	2003	During pregnancy chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) stabilized the disease for 4 months before new manifestations appeared.	Prednisone	83-93	DNA damage inducible transcript 3	Homo sapiens	95-99
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P &lt; 0.05).	Doxorubicin	83-94	DNA damage inducible transcript 3	Homo sapiens	142-146
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P &lt; 0.05).	Cyclophosphamide	96-112	DNA damage inducible transcript 3	Homo sapiens	142-146
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P &lt; 0.05).	Prednisone	130-140	DNA damage inducible transcript 3	Homo sapiens	142-146
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P &lt; 0.05).	Vincristine	214-225	DNA damage inducible transcript 3	Homo sapiens	142-146
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P &lt; 0.05).	Prednisone	227-237	DNA damage inducible transcript 3	Homo sapiens	142-146
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P &lt; 0.05).	Etoposide	242-251	DNA damage inducible transcript 3	Homo sapiens	142-146
14653077-5	2003	The CR rate and 5-year survival rate of patients who were treated by the scheme of doxorubicin, cyclophosphamide, vincristine and prednisone (CHOP) were higher than those treated by the scheme of cyclophosphamide, vincristine, prednisone and etoposide (COP + VP16) (P &lt; 0.05).	Etoposide	259-263	DNA damage inducible transcript 3	Homo sapiens	142-146
12706007-8	2003	Isoliquiritigenin enhanced the expression of GADD153 mRNA and protein associated with cell cycle arrest.	isoliquiritigenin	0-17	DNA damage inducible transcript 3	Homo sapiens	45-52
12706007-9	2003	Further, isoliquiritigenin stimulated transcriptional activity of GADD153 promoter dose-dependently.	isoliquiritigenin	9-26	DNA damage inducible transcript 3	Homo sapiens	66-73
12706007-10	2003	CONCLUSION: These findings suggest that isoliquiritigenin is a candidate agent for the treatment of prostate cancer and GADD153 may play an important role in isoliquiritigenin-induced cell cycle arrest and cell growth inhibition.	isoliquiritigenin	158-175	DNA damage inducible transcript 3	Homo sapiens	120-127
12601496-4	2003	Immunosuppression was discontinued and chemotherapy with cyclophosphamide, hydroxydaunomycin, vincristine, and prednisone (CHOP) was started.	Prednisone	111-121	DNA damage inducible transcript 3	Homo sapiens	123-127
12769354-3	2003	This case report concern a patient with stage IV follicular lymphoma who, relapsing after autologous transplant and having failed multiply systemic therapies, including retuximab and CHOP, achieved a prolonged remission with denileukin diftitox.	diftitox	236-244	DNA damage inducible transcript 3	Homo sapiens	183-187
12531903-1	2003	Cholesterol efflux from CHOP cells transfected with sterol 27-hydroxylase (CYP27A1) was compared with non-transfected and mock-transfected cells.	Cholesterol	0-11	DNA damage inducible transcript 3	Homo sapiens	24-28
12531903-5	2003	Time course and dose dependence studies showed that expression of CYP27A1 in CHOP cells mostly affected the efflux of the "fast" cholesterol pool, and relatively more cholesterol was released with low concentrations of an acceptor.	Cholesterol	129-140	DNA damage inducible transcript 3	Homo sapiens	77-81
12531903-5	2003	Time course and dose dependence studies showed that expression of CYP27A1 in CHOP cells mostly affected the efflux of the "fast" cholesterol pool, and relatively more cholesterol was released with low concentrations of an acceptor.	Cholesterol	167-178	DNA damage inducible transcript 3	Homo sapiens	77-81
12760267-6	2003	The lesions of the bladder and left urinary tract were nearly completely regressed after two cycles of systemic cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy with simultaneous restoration of urinary function.	Prednisone	159-169	DNA damage inducible transcript 3	Homo sapiens	171-175
12769340-3	2003	This study was designed to compare the effectiveness of an escalated dose of mitoxantrone with that of standard doxorubicin, used in the CHOP regimen in patients with ANHL.	Mitoxantrone	77-89	DNA damage inducible transcript 3	Homo sapiens	137-141
12612910-10	2003	The acetaldehyde-stimulated mitochondrial cholesterol content was preceded by increased levels of endoplasmic reticulum (ER)-responsive gene GADD153 and transcription factor sterol regulatory element-binding protein 1 and mimicked by the ER stress-inducing agents tunicamycin and homocysteine.	Acetaldehyde	4-16	DNA damage inducible transcript 3	Homo sapiens	141-148
12612910-10	2003	The acetaldehyde-stimulated mitochondrial cholesterol content was preceded by increased levels of endoplasmic reticulum (ER)-responsive gene GADD153 and transcription factor sterol regulatory element-binding protein 1 and mimicked by the ER stress-inducing agents tunicamycin and homocysteine.	Cholesterol	42-53	DNA damage inducible transcript 3	Homo sapiens	141-148
12490805-7	2002	Eventually the patient responded to CHOP (cyclophosphamide, Oncovin [vincristine, Eli Lilly, Indianapolis, IN], prednisone, and doxorubicin) therapy.	Cyclophosphamide	42-58	DNA damage inducible transcript 3	Homo sapiens	36-40
14988743-10	2003	Impressive results have been seen in combination with CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone) in follicular and high-grade lymphomas.	Cyclophosphamide	73-89	DNA damage inducible transcript 3	Homo sapiens	54-58
14988743-10	2003	Impressive results have been seen in combination with CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone) in follicular and high-grade lymphomas.	Doxorubicin	91-102	DNA damage inducible transcript 3	Homo sapiens	54-58
14988743-10	2003	Impressive results have been seen in combination with CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone) in follicular and high-grade lymphomas.	Vincristine	104-115	DNA damage inducible transcript 3	Homo sapiens	54-58
14988743-10	2003	Impressive results have been seen in combination with CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone) in follicular and high-grade lymphomas.	Prednisone	120-130	DNA damage inducible transcript 3	Homo sapiens	54-58
12521569-9	2003	For diffuse large B-cell lymphoma, the most frequently diagnosed subtype of non-Hodgkin"s lymphoma (NHL), the CHOP regimen (cyclophosphamide, doxorubicin, vincristine, and prednisone) is still the gold standard.	Cyclophosphamide	124-140	DNA damage inducible transcript 3	Homo sapiens	110-114
14569947-2	2003	Distinct prophylactic antiemetic effect, delayed effect (94%) included, was reported in the CHOP group: full control--64% and partial control in gemzar + cisplatin treatment (27%).	gemcitabine	145-151	DNA damage inducible transcript 3	Homo sapiens	92-96
14569947-2	2003	Distinct prophylactic antiemetic effect, delayed effect (94%) included, was reported in the CHOP group: full control--64% and partial control in gemzar + cisplatin treatment (27%).	Cisplatin	154-163	DNA damage inducible transcript 3	Homo sapiens	92-96
12490805-7	2002	Eventually the patient responded to CHOP (cyclophosphamide, Oncovin [vincristine, Eli Lilly, Indianapolis, IN], prednisone, and doxorubicin) therapy.	Vincristine	60-67	DNA damage inducible transcript 3	Homo sapiens	36-40
12490805-7	2002	Eventually the patient responded to CHOP (cyclophosphamide, Oncovin [vincristine, Eli Lilly, Indianapolis, IN], prednisone, and doxorubicin) therapy.	Vincristine	69-80	DNA damage inducible transcript 3	Homo sapiens	36-40
12490805-7	2002	Eventually the patient responded to CHOP (cyclophosphamide, Oncovin [vincristine, Eli Lilly, Indianapolis, IN], prednisone, and doxorubicin) therapy.	Doxorubicin	128-139	DNA damage inducible transcript 3	Homo sapiens	36-40
12478738-0	2002	Insights into the Schrock "chop-chop" reaction gained from density functional theory and preparation and structure of W2(mu-PhCCPh)(SC6H4-2-Me)6.	w2	118-120	DNA damage inducible transcript 3	Homo sapiens	27-31
12478738-0	2002	Insights into the Schrock "chop-chop" reaction gained from density functional theory and preparation and structure of W2(mu-PhCCPh)(SC6H4-2-Me)6.	w2	118-120	DNA damage inducible transcript 3	Homo sapiens	32-36
12478738-0	2002	Insights into the Schrock "chop-chop" reaction gained from density functional theory and preparation and structure of W2(mu-PhCCPh)(SC6H4-2-Me)6.	mu-phccph	121-130	DNA damage inducible transcript 3	Homo sapiens	27-31
12478738-0	2002	Insights into the Schrock "chop-chop" reaction gained from density functional theory and preparation and structure of W2(mu-PhCCPh)(SC6H4-2-Me)6.	mu-phccph	121-130	DNA damage inducible transcript 3	Homo sapiens	32-36
12478738-0	2002	Insights into the Schrock "chop-chop" reaction gained from density functional theory and preparation and structure of W2(mu-PhCCPh)(SC6H4-2-Me)6.	sc6h4-2-me	132-142	DNA damage inducible transcript 3	Homo sapiens	27-31
12478738-0	2002	Insights into the Schrock "chop-chop" reaction gained from density functional theory and preparation and structure of W2(mu-PhCCPh)(SC6H4-2-Me)6.	sc6h4-2-me	132-142	DNA damage inducible transcript 3	Homo sapiens	32-36
12520757-0	2002	Induction of GADD45 and GADD153 in neuroblastoma cells by dopamine-induced toxicity.	Dopamine	58-66	DNA damage inducible transcript 3	Homo sapiens	24-31
12613518-0	2002	Alternation of epirubicin and mitoxantrone in CHOP-like regimens retains efficacy and reduces overall toxicity in elderly patients with high and intermediate grade non-Hodgkin lymphomas.	Epirubicin	15-25	DNA damage inducible transcript 3	Homo sapiens	46-50
12613518-0	2002	Alternation of epirubicin and mitoxantrone in CHOP-like regimens retains efficacy and reduces overall toxicity in elderly patients with high and intermediate grade non-Hodgkin lymphomas.	Mitoxantrone	30-42	DNA damage inducible transcript 3	Homo sapiens	46-50
12520757-4	2002	cDNA hybridization array (microarray) technology demonstrated that GADD45 and GADD153 (growth arrest and DNA-damage inducible) gene expression was increased in dopamine-treated cells (333 microM for 18 h).	Dopamine	160-168	DNA damage inducible transcript 3	Homo sapiens	78-85
12353227-0	2002	Upregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR).	Fenretinide	65-94	DNA damage inducible transcript 3	Homo sapiens	16-23
12710585-5	2002	The most significant of these strategies is the combination of rituximab and CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone), which is proving a highly effective combination in the treatment of NHL.	Cyclophosphamide	96-112	DNA damage inducible transcript 3	Homo sapiens	77-81
12710585-5	2002	The most significant of these strategies is the combination of rituximab and CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone), which is proving a highly effective combination in the treatment of NHL.	Doxorubicin	114-125	DNA damage inducible transcript 3	Homo sapiens	77-81
12710585-5	2002	The most significant of these strategies is the combination of rituximab and CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone), which is proving a highly effective combination in the treatment of NHL.	Vincristine	127-138	DNA damage inducible transcript 3	Homo sapiens	77-81
12710585-5	2002	The most significant of these strategies is the combination of rituximab and CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine and prednisone), which is proving a highly effective combination in the treatment of NHL.	Prednisone	143-153	DNA damage inducible transcript 3	Homo sapiens	77-81
12710590-1	2002	The standard therapy for patients with aggressive lymphoma is cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which achieves a complete response in more than 60% of patients but is curative in only about 40-50%.	Cyclophosphamide	62-78	DNA damage inducible transcript 3	Homo sapiens	121-125
12710590-1	2002	The standard therapy for patients with aggressive lymphoma is cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy, which achieves a complete response in more than 60% of patients but is curative in only about 40-50%.	Prednisone	109-119	DNA damage inducible transcript 3	Homo sapiens	121-125
12353227-9	2002	In the HeLa cells, both 4HPR and ATRA caused a 2- to 4-fold stimulation of the promoter activity of gadd153, but similar to the CNE3 cells, ATRA was incapable of upregulating the protein level of gadd153.	Fenretinide	24-28	DNA damage inducible transcript 3	Homo sapiens	100-107
12353227-9	2002	In the HeLa cells, both 4HPR and ATRA caused a 2- to 4-fold stimulation of the promoter activity of gadd153, but similar to the CNE3 cells, ATRA was incapable of upregulating the protein level of gadd153.	Tretinoin	33-37	DNA damage inducible transcript 3	Homo sapiens	100-107
12151389-8	2002	Furthermore, stable overexpression of GADD153 sensitized the cells to apoptosis induced by parthenolide, and this susceptibility could be reversed by transfection with an antisense to GADD153.	parthenolide	91-103	DNA damage inducible transcript 3	Homo sapiens	38-45
12546311-7	2002	In conclusion, low-dose oral granisetron combined with intravenous dexamethasone had significantly higher protective effects against both acute and delayed nausea and vomiting induced by CHOP-therapy.	Granisetron	29-40	DNA damage inducible transcript 3	Homo sapiens	187-191
12546311-7	2002	In conclusion, low-dose oral granisetron combined with intravenous dexamethasone had significantly higher protective effects against both acute and delayed nausea and vomiting induced by CHOP-therapy.	Dexamethasone	67-80	DNA damage inducible transcript 3	Homo sapiens	187-191
12138118-0	2002	GADD153-mediated anticancer effects of N-(4-hydroxyphenyl)retinamide on human hepatoma cells.	Fenretinide	39-68	DNA damage inducible transcript 3	Homo sapiens	0-7
12138118-9	2002	N-Acetyl-l-cysteine or GADD153 antisense significantly protected the cells from 4HPR-induced apoptosis, accompanying by the inhibition of GADD153 overexpression.	Acetylcysteine	0-19	DNA damage inducible transcript 3	Homo sapiens	138-145
12138118-9	2002	N-Acetyl-l-cysteine or GADD153 antisense significantly protected the cells from 4HPR-induced apoptosis, accompanying by the inhibition of GADD153 overexpression.	Fenretinide	80-84	DNA damage inducible transcript 3	Homo sapiens	23-30
12138118-9	2002	N-Acetyl-l-cysteine or GADD153 antisense significantly protected the cells from 4HPR-induced apoptosis, accompanying by the inhibition of GADD153 overexpression.	Fenretinide	80-84	DNA damage inducible transcript 3	Homo sapiens	138-145
12546311-0	2002	Comparative study of low-dose oral granisetron plus dexamethasone and high-dose metoclopramide plus dexamethasone in prevention of nausea and vomiting induced by CHOP-therapy in young patients with non-Hodgkin"s lymphoma.	Granisetron	35-46	DNA damage inducible transcript 3	Homo sapiens	162-166
12546311-0	2002	Comparative study of low-dose oral granisetron plus dexamethasone and high-dose metoclopramide plus dexamethasone in prevention of nausea and vomiting induced by CHOP-therapy in young patients with non-Hodgkin"s lymphoma.	Metoclopramide	80-94	DNA damage inducible transcript 3	Homo sapiens	162-166
12546311-0	2002	Comparative study of low-dose oral granisetron plus dexamethasone and high-dose metoclopramide plus dexamethasone in prevention of nausea and vomiting induced by CHOP-therapy in young patients with non-Hodgkin"s lymphoma.	Dexamethasone	100-113	DNA damage inducible transcript 3	Homo sapiens	162-166
12533055-2	2002	A 43-year-old female with DLCL, who relapsed after first line chemotherapy (CHOP--cyclophosphamide, doxorubicin, vincristine, and prednisone) and progressed despite salvage chemotherapy (EPOCH-etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin), was treated effectively with 8 cycles of Rituximab.	Cyclophosphamide	82-98	DNA damage inducible transcript 3	Homo sapiens	76-80
12138118-10	2002	Parthenolide-mediated overexpression of GADD153 resulted in enhanced 4HPR-induced apoptosis.	parthenolide	0-12	DNA damage inducible transcript 3	Homo sapiens	40-47
12151389-8	2002	Furthermore, stable overexpression of GADD153 sensitized the cells to apoptosis induced by parthenolide, and this susceptibility could be reversed by transfection with an antisense to GADD153.	parthenolide	91-103	DNA damage inducible transcript 3	Homo sapiens	184-191
12151389-10	2002	Oxidative stress may contribute to parthenolide-induced apoptosis and to GADD153 overexpression in a glutathione-sensitive manner.	Glutathione	101-112	DNA damage inducible transcript 3	Homo sapiens	73-80
12176789-1	2002	BACKGROUND: Recent data suggest that chemotherapy with the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen is a highly effective treatment for localised primary gastric lymphoma of diffuse large B-cell histology (DLBCL).	Cyclophosphamide	59-75	DNA damage inducible transcript 3	Homo sapiens	118-122
12234979-10	2002	These results suggest that fenretinide induces apoptosis via RAR-dependent and -independent pathways in which the RAR-independent pathway is characterized by a fenretinide-dependent increase in 12-LOX activity, leading to the induction of GADD153.	Fenretinide	160-171	DNA damage inducible transcript 3	Homo sapiens	239-246
12222701-3	2002	If this disease could be diagnosed earlier, therapy with chlorpropamide, doxorubicin, vincristine and prednisone (CHOP) could bring about a remission (2,3,4).	Chlorpropamide	57-71	DNA damage inducible transcript 3	Homo sapiens	114-118
12222701-3	2002	If this disease could be diagnosed earlier, therapy with chlorpropamide, doxorubicin, vincristine and prednisone (CHOP) could bring about a remission (2,3,4).	Doxorubicin	73-84	DNA damage inducible transcript 3	Homo sapiens	114-118
12222701-3	2002	If this disease could be diagnosed earlier, therapy with chlorpropamide, doxorubicin, vincristine and prednisone (CHOP) could bring about a remission (2,3,4).	Prednisone	102-112	DNA damage inducible transcript 3	Homo sapiens	114-118
12114539-6	2002	Among the members of the GADD family of genes, GADD153, GADD45 alpha, and GADD34 displayed marked, and GADD45 gamma showed minimal induction.	gadd	25-29	DNA damage inducible transcript 3	Homo sapiens	47-54
12234979-0	2002	GADD153 and 12-lipoxygenase mediate fenretinide-induced apoptosis of neuroblastoma.	Fenretinide	36-47	DNA damage inducible transcript 3	Homo sapiens	0-7
12234979-4	2002	Expression of the stress-induced transcription factor, GADD153, was up-regulated at both the protein and mRNA levels in response to fenretinide.	Fenretinide	132-143	DNA damage inducible transcript 3	Homo sapiens	55-62
12234979-5	2002	Overexpression of GADD153 increased apoptosis in the presence and absence of fenretinide, whereas reduced expression of GADD153 by expression of antisense DNA abrogated the response to fenretinide.	Fenretinide	77-88	DNA damage inducible transcript 3	Homo sapiens	18-25
12234979-5	2002	Overexpression of GADD153 increased apoptosis in the presence and absence of fenretinide, whereas reduced expression of GADD153 by expression of antisense DNA abrogated the response to fenretinide.	Fenretinide	185-196	DNA damage inducible transcript 3	Homo sapiens	120-127
12234979-10	2002	These results suggest that fenretinide induces apoptosis via RAR-dependent and -independent pathways in which the RAR-independent pathway is characterized by a fenretinide-dependent increase in 12-LOX activity, leading to the induction of GADD153.	Fenretinide	27-38	DNA damage inducible transcript 3	Homo sapiens	239-246
12532739-2	2002	When the authors used their own methods of "extracapsular half-nuclei" fragmentation, endothelial losses are rather greater than those with the similar method "stop &amp; "chop", which is associated with closer disposition of the US tip to the posterior corneal surface.	stop &amp	160-169	DNA damage inducible transcript 3	Homo sapiens	172-177
12225878-6	2002	Arsenite induced a transient inhibition of energy metabolism after 1 h of exposure, but energy state recovered completely after 3 h. Arsenite exposure affected the expression and translation of genes coding for HSP70 and GRP78, GRP94, GADD153 to different extents.	arsenite	0-8	DNA damage inducible transcript 3	Homo sapiens	235-242
12225878-6	2002	Arsenite induced a transient inhibition of energy metabolism after 1 h of exposure, but energy state recovered completely after 3 h. Arsenite exposure affected the expression and translation of genes coding for HSP70 and GRP78, GRP94, GADD153 to different extents.	arsenite	133-141	DNA damage inducible transcript 3	Homo sapiens	235-242
12176789-1	2002	BACKGROUND: Recent data suggest that chemotherapy with the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen is a highly effective treatment for localised primary gastric lymphoma of diffuse large B-cell histology (DLBCL).	Doxorubicin	77-88	DNA damage inducible transcript 3	Homo sapiens	118-122
12176789-1	2002	BACKGROUND: Recent data suggest that chemotherapy with the cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) regimen is a highly effective treatment for localised primary gastric lymphoma of diffuse large B-cell histology (DLBCL).	Prednisone	106-116	DNA damage inducible transcript 3	Homo sapiens	118-122
12097658-9	2002	Chalcone was the only phytochemical that activated all three transcription factors [Elk-1, 2.7-fold (P &lt; 0.001); c-Jun, 2.7-fold (P = 0.025); CHOP, 3.0-fold (P = 0.002)], whereas apigenin stimulated CHOP (3.9-fold; P &lt; 0.001), but inhibited phorbol myristoyl acetate-induced c-Jun activity (71%;P = 0.006).	Chalcone	0-8	DNA damage inducible transcript 3	Homo sapiens	145-149
12270058-9	2002	Rituximab thus led to CR in 10/14 patients [71% (95% CI: 42-92%)] who had merely achieved partial remission (PR) with CHOP.	Chromium	22-24	DNA damage inducible transcript 3	Homo sapiens	118-122
12097658-9	2002	Chalcone was the only phytochemical that activated all three transcription factors [Elk-1, 2.7-fold (P &lt; 0.001); c-Jun, 2.7-fold (P = 0.025); CHOP, 3.0-fold (P = 0.002)], whereas apigenin stimulated CHOP (3.9-fold; P &lt; 0.001), but inhibited phorbol myristoyl acetate-induced c-Jun activity (71%;P = 0.006).	Chalcone	0-8	DNA damage inducible transcript 3	Homo sapiens	202-206
12069855-0	2002	Activator protein-1 and CCAAT/enhancer-binding protein mediated GADD153 expression is involved in deoxycholic acid-induced apoptosis.	Deoxycholic Acid	98-114	DNA damage inducible transcript 3	Homo sapiens	64-71
12162217-6	2002	FUTURE PROSPECTS AND PROJECTS: For elderly patients with good performance status and without severe co morbidity, curative strategy with anthracyclin-containing regimen like CHOP is still the standard chemotherapy.	anthracyclin	137-149	DNA damage inducible transcript 3	Homo sapiens	174-178
12082616-6	2002	GADD153 expression was upregulated by the lactogenic hormones insulin and progesterone and associated with differentiation of normal mammary epithelial cells.	Progesterone	74-86	DNA damage inducible transcript 3	Homo sapiens	0-7
12082616-9	2002	Because cyclic AMP responsive element and ATF binding sites are present in a variety of growth-regulating cellular genes, these findings suggest that stimulation of GADD153 expression and its transactivating functions may constitute an important mechanism of regulation of putative genes having diverse functions during cell growth and differentiation.	Cyclic AMP	8-18	DNA damage inducible transcript 3	Homo sapiens	165-172
12069855-10	2002	These results suggest that GADD153 expression is critical for DCA-induced apoptosis and that multiple signaling pathways that include AP-1 and C/EBP transcription factors are involved in DCA-induced GADD153 expression.	Deoxycholic Acid	62-65	DNA damage inducible transcript 3	Homo sapiens	27-34
12408775-4	2002	RESULTS: The complete remission rate and overall response rate were 57.5% (23/40) and 87.5% (35/40) in CHOP-PVP group and they were 33.3% (13/39) and 69.2% (27/39) in CHOP group.	Povidone	108-111	DNA damage inducible transcript 3	Homo sapiens	103-107
12408775-4	2002	RESULTS: The complete remission rate and overall response rate were 57.5% (23/40) and 87.5% (35/40) in CHOP-PVP group and they were 33.3% (13/39) and 69.2% (27/39) in CHOP group.	Povidone	108-111	DNA damage inducible transcript 3	Homo sapiens	167-171
12111836-0	2002	Specific up-regulation of GADD153/CHOP in 1-methyl-4-phenyl-pyridinium-treated SH-SY5Y cells.	1-Methyl-4-phenylpyridinium	42-70	DNA damage inducible transcript 3	Homo sapiens	26-33
12111836-0	2002	Specific up-regulation of GADD153/CHOP in 1-methyl-4-phenyl-pyridinium-treated SH-SY5Y cells.	1-Methyl-4-phenylpyridinium	42-70	DNA damage inducible transcript 3	Homo sapiens	34-38
12111836-1	2002	Growth arrest DNA damage-inducible 153 (GADD153) expression was increased in 1-methyl-4-phenyl-pyridinium (MPP(+))-treated human SH-SY5Y neuroblastoma cells as determined by gene microarray analysis.	1-Methyl-4-phenylpyridinium	77-105	DNA damage inducible transcript 3	Homo sapiens	40-47
12111836-1	2002	Growth arrest DNA damage-inducible 153 (GADD153) expression was increased in 1-methyl-4-phenyl-pyridinium (MPP(+))-treated human SH-SY5Y neuroblastoma cells as determined by gene microarray analysis.	mangion-purified polysaccharide (Candida albicans)	107-110	DNA damage inducible transcript 3	Homo sapiens	40-47
12111836-3	2002	Comparison of GADD153 expression among cultures treated with other toxins whose primary mode of action is either via mitochondrial impairment (rotenone) or via oxidative stress (6-hydroxydopamine or hydrogen peroxide) showed that GADD153 was uniquely up-regulated by MPP(+).	Oxidopamine	178-195	DNA damage inducible transcript 3	Homo sapiens	230-237
12069855-10	2002	These results suggest that GADD153 expression is critical for DCA-induced apoptosis and that multiple signaling pathways that include AP-1 and C/EBP transcription factors are involved in DCA-induced GADD153 expression.	Deoxycholic Acid	187-190	DNA damage inducible transcript 3	Homo sapiens	27-34
12069855-10	2002	These results suggest that GADD153 expression is critical for DCA-induced apoptosis and that multiple signaling pathways that include AP-1 and C/EBP transcription factors are involved in DCA-induced GADD153 expression.	Deoxycholic Acid	187-190	DNA damage inducible transcript 3	Homo sapiens	199-206
12069855-4	2002	In this study, we examined the effect of DCA on the GADD153 (growth arrest- and DNA damage-inducible gene 153) proapoptotic gene and its role in DCA-induced apoptosis in a human colon cancer cell line, HCT116.	Deoxycholic Acid	41-44	DNA damage inducible transcript 3	Homo sapiens	52-59
12069855-4	2002	In this study, we examined the effect of DCA on the GADD153 (growth arrest- and DNA damage-inducible gene 153) proapoptotic gene and its role in DCA-induced apoptosis in a human colon cancer cell line, HCT116.	Deoxycholic Acid	41-44	DNA damage inducible transcript 3	Homo sapiens	61-109
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	70-73	DNA damage inducible transcript 3	Homo sapiens	24-31
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	70-73	DNA damage inducible transcript 3	Homo sapiens	115-122
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	70-73	DNA damage inducible transcript 3	Homo sapiens	115-122
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	163-166	DNA damage inducible transcript 3	Homo sapiens	24-31
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	163-166	DNA damage inducible transcript 3	Homo sapiens	115-122
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	163-166	DNA damage inducible transcript 3	Homo sapiens	115-122
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	163-166	DNA damage inducible transcript 3	Homo sapiens	24-31
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	163-166	DNA damage inducible transcript 3	Homo sapiens	115-122
12069855-5	2002	Our results showed that GADD153 expression was strongly stimulated by DCA and disruption of this with an antisense GADD153 transcript could significantly suppress DCA-induced apoptosis, suggesting GADD153 is essential for DCA induction of apoptosis.	Deoxycholic Acid	163-166	DNA damage inducible transcript 3	Homo sapiens	115-122
12069855-6	2002	Further studies were conducted to investigate the upstream regulatory factors that participated in DCA mediated GADD153 expression.	Deoxycholic Acid	99-102	DNA damage inducible transcript 3	Homo sapiens	112-119
12069855-7	2002	Activator protein-1 (AP-1) was activated by DCA and an AP-1 regulatory element was identified in the human GADD153 promoter in our previous studies.	Deoxycholic Acid	44-47	DNA damage inducible transcript 3	Homo sapiens	107-114
12069855-8	2002	However, inhibition of the AP-1 activation by the dominant negative mutant c-Jun, Tam67, caused only a partial suppression of both DCA-induced GADD153 expression and apoptosis, indicating AP-1 plays an important but not exclusive role in DCA mediated GADD153 pathway.	tam67	82-87	DNA damage inducible transcript 3	Homo sapiens	143-150
12069855-8	2002	However, inhibition of the AP-1 activation by the dominant negative mutant c-Jun, Tam67, caused only a partial suppression of both DCA-induced GADD153 expression and apoptosis, indicating AP-1 plays an important but not exclusive role in DCA mediated GADD153 pathway.	tam67	82-87	DNA damage inducible transcript 3	Homo sapiens	251-258
12069855-8	2002	However, inhibition of the AP-1 activation by the dominant negative mutant c-Jun, Tam67, caused only a partial suppression of both DCA-induced GADD153 expression and apoptosis, indicating AP-1 plays an important but not exclusive role in DCA mediated GADD153 pathway.	Deoxycholic Acid	131-134	DNA damage inducible transcript 3	Homo sapiens	143-150
12069855-8	2002	However, inhibition of the AP-1 activation by the dominant negative mutant c-Jun, Tam67, caused only a partial suppression of both DCA-induced GADD153 expression and apoptosis, indicating AP-1 plays an important but not exclusive role in DCA mediated GADD153 pathway.	Deoxycholic Acid	131-134	DNA damage inducible transcript 3	Homo sapiens	251-258
12069855-8	2002	However, inhibition of the AP-1 activation by the dominant negative mutant c-Jun, Tam67, caused only a partial suppression of both DCA-induced GADD153 expression and apoptosis, indicating AP-1 plays an important but not exclusive role in DCA mediated GADD153 pathway.	Deoxycholic Acid	238-241	DNA damage inducible transcript 3	Homo sapiens	251-258
12069855-9	2002	By further promoter analyses, a novel DCA response element, which is located downstream of the AP-1 binding site in the human GADD153 promoter, was determined and identified as C/EBP regulatory element.	Deoxycholic Acid	38-41	DNA damage inducible transcript 3	Homo sapiens	126-133
12168880-0	2002	Pegylated liposomal doxorubicin in the CHOP regimen for older patients with aggressive (stages III/IV) non-Hodgkin"s lymphoma.	Doxorubicin	20-31	DNA damage inducible transcript 3	Homo sapiens	39-43
12090052-2	2002	A 39-year-old woman with non-resectable mesenteric malignant lymphoma obtained a better QOL and outcome from prolonged oral administration of low-dose etoposide as a maintenance therapy after CHOP therapy.	Etoposide	151-160	DNA damage inducible transcript 3	Homo sapiens	192-196
12173380-2	2002	METHODS: All patients were treated with radical surgery followed by six cycles of combined chemotherapy: CHOP-Bleo (cyclophosphamide, doxorubicine, vincristine, prednisone, and bleomycin) or variants (epirubicin instead of doxorubicin).	Bleomycin	110-114	DNA damage inducible transcript 3	Homo sapiens	105-109
12225393-0	2002	A prospective study of P-IMVP-16/CBDCA: a novel salvage chemotherapy for patients with aggressive non-Hodgkin"s lymphoma who had previously received CHOP therapy as first-line chemotherapy.	p-imvp-16	23-32	DNA damage inducible transcript 3	Homo sapiens	149-153
12225393-0	2002	A prospective study of P-IMVP-16/CBDCA: a novel salvage chemotherapy for patients with aggressive non-Hodgkin"s lymphoma who had previously received CHOP therapy as first-line chemotherapy.	Carboplatin	33-38	DNA damage inducible transcript 3	Homo sapiens	149-153
11865634-1	2002	We evaluated the efficacy and safety of ondansetron hydrochloride (OND) on nausea and vomiting during repeated courses of CHOP or ACOMP-B therapy in patients with malignant lymphoma.	Ondansetron	40-65	DNA damage inducible transcript 3	Homo sapiens	122-126
12042984-9	2002	Results of a gallium scan with SPECT imaging may be an important method of confirming complete response, and should be incorporated into treatment programs, whether the treatment is standard CHOP or an investigational program.	Gallium	13-20	DNA damage inducible transcript 3	Homo sapiens	191-195
11948400-5	2002	Western blot analysis revealed that troglitazone also increased GADD153 protein levels in a time-dependent manner.	Troglitazone	36-48	DNA damage inducible transcript 3	Homo sapiens	64-71
11948400-7	2002	Activity of the GADD153 promoter occurred in a NSCLC cell line in transient transcription assays and was significantly stimulated by troglitazone, although binding of PPAR/retinoid X receptor heterodimer was not detected in the promoter region in gel retardation assays.	Troglitazone	133-145	DNA damage inducible transcript 3	Homo sapiens	16-23
11948400-8	2002	Inhibition of GADD153 gene expression by an antisense phosphorothionate oligonucleotide attenuated the troglitazone-induced growth inhibition.	phosphorothionate oligonucleotide	54-87	DNA damage inducible transcript 3	Homo sapiens	14-21
11948400-8	2002	Inhibition of GADD153 gene expression by an antisense phosphorothionate oligonucleotide attenuated the troglitazone-induced growth inhibition.	Troglitazone	103-115	DNA damage inducible transcript 3	Homo sapiens	14-21
11870171-1	2002	PURPOSE: To evaluate the efficacy of rituximab and cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) induction therapy in patients with newly diagnosed mantle-cell lymphoma (MCL).	Prednisone	99-109	DNA damage inducible transcript 3	Homo sapiens	111-115
11984085-11	2002	The patients received a total of 207 cycles of amifostine-CHOP.	Amifostine	47-57	DNA damage inducible transcript 3	Homo sapiens	58-62
11984085-17	2002	One patient died after the first CHOP administration because of anthracycline-related acute cardiomyopathy (corresponding to a toxic death rate of 2.4%).	Anthracyclines	64-77	DNA damage inducible transcript 3	Homo sapiens	33-37
11792410-0	2002	Efficacy of carboplatin with an MEP (mitoxantrone, etoposide and prednisone) regimen for relapsed and CHOP-resistant diffuse large B-cell lymphomas.	Carboplatin	12-23	DNA damage inducible transcript 3	Homo sapiens	102-106
11792410-1	2002	Mitoxantrone, etoposide and prednisone (MEP)-based regimens using granulocyte colony-stimulating factor (G-CSF) were designed for relapsed and CHOP-resistant diffuse large B-cell lymphomas in a single institution, and the therapeutic effects and adverse reactions were studied.	Mitoxantrone	0-12	DNA damage inducible transcript 3	Homo sapiens	143-147
11792410-1	2002	Mitoxantrone, etoposide and prednisone (MEP)-based regimens using granulocyte colony-stimulating factor (G-CSF) were designed for relapsed and CHOP-resistant diffuse large B-cell lymphomas in a single institution, and the therapeutic effects and adverse reactions were studied.	Prednisone	28-38	DNA damage inducible transcript 3	Homo sapiens	143-147
11792410-1	2002	Mitoxantrone, etoposide and prednisone (MEP)-based regimens using granulocyte colony-stimulating factor (G-CSF) were designed for relapsed and CHOP-resistant diffuse large B-cell lymphomas in a single institution, and the therapeutic effects and adverse reactions were studied.	mep	40-43	DNA damage inducible transcript 3	Homo sapiens	143-147
11792410-3	2002	Among 38 CHOP-resistant patients, however, the overall response rate to C-MEP [42% (10/24)] was significantly superior compared with MEP [7% (1/14)] (P=0.023), and the overall survival to C-MEP was superior compared with MEP (P=0.088).	c-mep	72-77	DNA damage inducible transcript 3	Homo sapiens	9-13
11792410-4	2002	Taken together, our results, although non-randomized, suggest that a combination of MEP with carboplatin is better than MEP alone in CHOP-resistant diffuse large B-cell lymphomas.	Carboplatin	93-104	DNA damage inducible transcript 3	Homo sapiens	133-137
12168790-6	2002	We therefore decided to establish a PCR assay for detection of GADD153 in paraffin-embedded tissue.	Paraffin	74-82	DNA damage inducible transcript 3	Homo sapiens	63-70
11802205-6	2002	The TLS-CHOP-green fluorescent protein nuclear structures are resistant to high salt concentration and nuclease treatment.	Salts	80-84	DNA damage inducible transcript 3	Homo sapiens	8-12
11807147-1	2002	BACKGROUND: The standard treatment for patients with diffuse large-B-cell lymphoma is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Cyclophosphamide	86-102	DNA damage inducible transcript 3	Homo sapiens	146-150
11807147-1	2002	BACKGROUND: The standard treatment for patients with diffuse large-B-cell lymphoma is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Doxorubicin	104-115	DNA damage inducible transcript 3	Homo sapiens	146-150
11807147-1	2002	BACKGROUND: The standard treatment for patients with diffuse large-B-cell lymphoma is cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Prednisone	134-144	DNA damage inducible transcript 3	Homo sapiens	146-150
12479593-3	2002	The gold standard for primary treatment of aggressive NHL is combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	150-154
12479593-3	2002	The gold standard for primary treatment of aggressive NHL is combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Doxorubicin	109-120	DNA damage inducible transcript 3	Homo sapiens	150-154
12479593-3	2002	The gold standard for primary treatment of aggressive NHL is combination chemotherapy with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP).	Prednisone	138-148	DNA damage inducible transcript 3	Homo sapiens	150-154
12091638-20	2002	The CHOP regimen is cyclophosphamide, doxorubicine, vincristine and prednisone.	Cyclophosphamide	20-36	DNA damage inducible transcript 3	Homo sapiens	4-8
12091638-20	2002	The CHOP regimen is cyclophosphamide, doxorubicine, vincristine and prednisone.	Doxorubicin	38-50	DNA damage inducible transcript 3	Homo sapiens	4-8
12091638-20	2002	The CHOP regimen is cyclophosphamide, doxorubicine, vincristine and prednisone.	Vincristine	52-63	DNA damage inducible transcript 3	Homo sapiens	4-8
12091638-20	2002	The CHOP regimen is cyclophosphamide, doxorubicine, vincristine and prednisone.	Prednisone	68-78	DNA damage inducible transcript 3	Homo sapiens	4-8
11518796-5	2001	Both GH and BAPTA-AM caused a rapid induction of the transcription factor C/EBP homology protein (CHOP) and an additive effect was observed with combined treatment, which suggests a regulatory role of GH on endoplasmic reticulum stress.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	12-20	DNA damage inducible transcript 3	Homo sapiens	74-96
11526215-5	2001	CHOP, a C/EBP homologous protein that is induced by endoplasmic reticulum (ER) stress and plays a role in growth arrest and cell death, was induced by a NO donor, S-nitroso-N-acetyl-D,L-penicillamine (SNAP).	snap	163-199	DNA damage inducible transcript 3	Homo sapiens	0-4
11526215-5	2001	CHOP, a C/EBP homologous protein that is induced by endoplasmic reticulum (ER) stress and plays a role in growth arrest and cell death, was induced by a NO donor, S-nitroso-N-acetyl-D,L-penicillamine (SNAP).	snap	201-205	DNA damage inducible transcript 3	Homo sapiens	0-4
11762410-5	2001	High intensity chemotherapy consisting of the anthracycline, doxorubicin along with cyclophosphamide, vincristine and prednisone (CHOP) is offered as standard treatment for intermediate-grade NHL.	Anthracyclines	46-59	DNA damage inducible transcript 3	Homo sapiens	130-134
11762410-5	2001	High intensity chemotherapy consisting of the anthracycline, doxorubicin along with cyclophosphamide, vincristine and prednisone (CHOP) is offered as standard treatment for intermediate-grade NHL.	Prednisone	118-128	DNA damage inducible transcript 3	Homo sapiens	130-134
11729479-2	2001	In this multi-center collaborative study, doxorubicin hydrochloride was replaced by amrubicin hydrochloride in CHOP therapy, a standard regimen for non-Hodgkin"s lymphoma consisting of cyclophosphamide, doxorubicin hydrochloride, vincristine sulfate and prednisolone.	amrubicin	84-107	DNA damage inducible transcript 3	Homo sapiens	111-115
11878581-1	2001	PURPOSE: The authors report the use of a cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP)-based chemotherapy regimen in treating six children with posttransplantation lymphoproliferative disorder (PTLD) that developed after solid organ transplantation.	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	109-113
11878581-1	2001	PURPOSE: The authors report the use of a cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP)-based chemotherapy regimen in treating six children with posttransplantation lymphoproliferative disorder (PTLD) that developed after solid organ transplantation.	Doxorubicin	59-78	DNA damage inducible transcript 3	Homo sapiens	109-113
11878581-1	2001	PURPOSE: The authors report the use of a cyclophosphamide, hydroxydaunorubicin, vincristine, and prednisone (CHOP)-based chemotherapy regimen in treating six children with posttransplantation lymphoproliferative disorder (PTLD) that developed after solid organ transplantation.	Prednisone	97-107	DNA damage inducible transcript 3	Homo sapiens	109-113
11518796-5	2001	Both GH and BAPTA-AM caused a rapid induction of the transcription factor C/EBP homology protein (CHOP) and an additive effect was observed with combined treatment, which suggests a regulatory role of GH on endoplasmic reticulum stress.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	12-20	DNA damage inducible transcript 3	Homo sapiens	98-102
11508932-3	2001	A study of rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemoimmunotherapy has been carried out in 40 patients with low-grade NHL.	Prednisone	73-83	DNA damage inducible transcript 3	Homo sapiens	85-89
11584710-9	2001	Standard treatment of advanced aggressive NHL is polychemotherapy with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP).	Cyclophosphamide	71-87	DNA damage inducible transcript 3	Homo sapiens	129-133
11584710-9	2001	Standard treatment of advanced aggressive NHL is polychemotherapy with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP).	Doxorubicin	89-99	DNA damage inducible transcript 3	Homo sapiens	129-133
11584710-9	2001	Standard treatment of advanced aggressive NHL is polychemotherapy with cyclophosphamide, adriamycin, vincristine and prednisone (CHOP).	Prednisone	117-127	DNA damage inducible transcript 3	Homo sapiens	129-133
11433756-8	2001	After improvement of his performance status, he received combination chemotherapy consisting of cyclophosphamide, adriamycin, vincristine and predonisone (CHOP regimen).	predonisone	142-153	DNA damage inducible transcript 3	Homo sapiens	155-159
11699226-16	2001	We conclude that the substitution of DaunoXome for doxorubicin in the CHOP regimen to form COP-X provides excellent efficacy against non-Hodgkin"s lymphoma.	Daunorubicin	37-46	DNA damage inducible transcript 3	Homo sapiens	70-74
11699226-16	2001	We conclude that the substitution of DaunoXome for doxorubicin in the CHOP regimen to form COP-X provides excellent efficacy against non-Hodgkin"s lymphoma.	Doxorubicin	51-62	DNA damage inducible transcript 3	Homo sapiens	70-74
11381086-1	2001	Phosphorylation of the alpha subunit of eukaryotic translation initiation factor 2 (eIF2alpha) on serine 51 integrates general translation repression with activation of stress-inducible genes such as ATF4, CHOP, and BiP in the unfolded protein response.	Serine	98-104	DNA damage inducible transcript 3	Homo sapiens	206-210
11409192-7	2001	These results show the potential for TNT and 2,4-DNT to cause protein damage and/or perturbations of protein biosynthesis (HSP70 and GRP78), alterations in DNA sequence or its helical structure (c-fos, GADD153, GADD45), and the potential involvement of TNT in the biotransformation process (CYP 1A1, GST Ya, XRE), and in the toxicokinetics of metal ions (HMTIIA).	Trinitrotoluene	37-40	DNA damage inducible transcript 3	Homo sapiens	202-209
11269797-6	2001	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy was given, and the patient became asymptomatic with normal blood tests and was thought to be in remission.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
11360202-3	2001	In this report, we demonstrate that NF-kappaB inhibits GADD153 activation in breast cancer cells exposed to nutrient deprived media, tunicamycin (which blocks protein folding in ER) or calcium ionopore (which depletes calcium stores in ER).	Tunicamycin	133-144	DNA damage inducible transcript 3	Homo sapiens	55-62
11360202-3	2001	In this report, we demonstrate that NF-kappaB inhibits GADD153 activation in breast cancer cells exposed to nutrient deprived media, tunicamycin (which blocks protein folding in ER) or calcium ionopore (which depletes calcium stores in ER).	Calcium	185-192	DNA damage inducible transcript 3	Homo sapiens	55-62
11360202-3	2001	In this report, we demonstrate that NF-kappaB inhibits GADD153 activation in breast cancer cells exposed to nutrient deprived media, tunicamycin (which blocks protein folding in ER) or calcium ionopore (which depletes calcium stores in ER).	Calcium	218-225	DNA damage inducible transcript 3	Homo sapiens	55-62
11269797-6	2001	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy was given, and the patient became asymptomatic with normal blood tests and was thought to be in remission.	Prednisone	48-58	DNA damage inducible transcript 3	Homo sapiens	60-64
11276342-6	2001	The patient was treated with combination chemotherapy, including cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP), which resulted in complete clinical remission after two courses.	Cyclophosphamide	65-81	DNA damage inducible transcript 3	Homo sapiens	126-130
11276342-6	2001	The patient was treated with combination chemotherapy, including cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP), which resulted in complete clinical remission after two courses.	Prednisolone	112-124	DNA damage inducible transcript 3	Homo sapiens	126-130
11284065-3	2001	The currently accepted therapy of pCBCL (excision and/or radiotherapy, systemic interleukin 2 and interferon alpha 2a, local injection of cisplatin or multiagent chemotherapy, i.e. CHOP) is insufficient for treatment of multifocal pCBCL and secondary extracutaneous involvement.	pcbcl	34-39	DNA damage inducible transcript 3	Homo sapiens	181-185
11284065-3	2001	The currently accepted therapy of pCBCL (excision and/or radiotherapy, systemic interleukin 2 and interferon alpha 2a, local injection of cisplatin or multiagent chemotherapy, i.e. CHOP) is insufficient for treatment of multifocal pCBCL and secondary extracutaneous involvement.	pcbcl	231-236	DNA damage inducible transcript 3	Homo sapiens	181-185
11230885-1	2001	BACKGROUND: A limited number cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy followed by involved field radiotherapy is the treatment of choice for Ann Arbor stage I intermediate or high grade non-Hodgkin"s lymphomas (NHL).	Cyclophosphamide	39-55	DNA damage inducible transcript 3	Homo sapiens	98-102
11179352-3	2001	CRP binds to phosphorylcholine (ChoP), a constituent of eukaryotic membranes that is also found on the cell surface of major bacterial pathogens of the human respiratory tract, including Streptococcus pneumoniae and Haemophilus influenzae.	Phosphorylcholine	13-30	DNA damage inducible transcript 3	Homo sapiens	32-36
11259510-5	2001	Peroxide treatment of cells triggered an almost 12-fold increase in hsp70 mRNA levels, but a significant decrease in grp78, grp94 and gadd153 mRNA levels.	Peroxides	0-8	DNA damage inducible transcript 3	Homo sapiens	134-141
11259510-7	2001	Tg exposure induced 7.2-fold, 3.6-fold and 8.8-fold increase in grp78, grp94 and gadd153 mRNA levels, respectively.	Thapsigargin	0-2	DNA damage inducible transcript 3	Homo sapiens	81-88
11259510-8	2001	However, after peroxide pre-exposure, the Tg-induced effect on grp78, grp94 and gadd153 mRNA levels was completely blocked.	Peroxides	15-23	DNA damage inducible transcript 3	Homo sapiens	80-87
11259510-8	2001	However, after peroxide pre-exposure, the Tg-induced effect on grp78, grp94 and gadd153 mRNA levels was completely blocked.	Thapsigargin	42-44	DNA damage inducible transcript 3	Homo sapiens	80-87
11230885-1	2001	BACKGROUND: A limited number cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy followed by involved field radiotherapy is the treatment of choice for Ann Arbor stage I intermediate or high grade non-Hodgkin"s lymphomas (NHL).	Doxorubicin	57-68	DNA damage inducible transcript 3	Homo sapiens	98-102
11230885-1	2001	BACKGROUND: A limited number cycles of cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy followed by involved field radiotherapy is the treatment of choice for Ann Arbor stage I intermediate or high grade non-Hodgkin"s lymphomas (NHL).	Prednisone	86-96	DNA damage inducible transcript 3	Homo sapiens	98-102
11002232-2	2000	The Medical Research Council therefore conducted the current randomized trial to assess the impact on survival of postradiotherapy chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in nonimmunocompromised adult patients with pathologically proven PCL.	Cyclophosphamide	149-165	DNA damage inducible transcript 3	Homo sapiens	209-213
11226373-5	2001	Carbaryl and to a lesser extent thiabendazole also activated other stress genes such as c-fos and NF-kappaBRE, HSP70 and GRP78, and GADD153 at a transcriptional level.	Carbaryl	0-8	DNA damage inducible transcript 3	Homo sapiens	132-139
11226373-5	2001	Carbaryl and to a lesser extent thiabendazole also activated other stress genes such as c-fos and NF-kappaBRE, HSP70 and GRP78, and GADD153 at a transcriptional level.	Thiabendazole	32-45	DNA damage inducible transcript 3	Homo sapiens	132-139
11163539-2	2001	A peroxynitrite generator, 3-morpholinosydonimine (SIN-1), was found to induce the expression of three different growth arrest and DNA damage-inducible (GADD) mRNA, GADD34, GADD45, and GADD153, at the early phase during cell death in human neuroblastoma SH-SY5Y cells.	Peroxynitrous Acid	2-15	DNA damage inducible transcript 3	Homo sapiens	185-192
11163539-2	2001	A peroxynitrite generator, 3-morpholinosydonimine (SIN-1), was found to induce the expression of three different growth arrest and DNA damage-inducible (GADD) mRNA, GADD34, GADD45, and GADD153, at the early phase during cell death in human neuroblastoma SH-SY5Y cells.	linsidomine	27-49	DNA damage inducible transcript 3	Homo sapiens	185-192
11441934-21	2001	At progression on single alkylating agents, the purine analogues or various combinations, mostly CHOP, frequently induce tumour remissions.	purine	48-54	DNA damage inducible transcript 3	Homo sapiens	97-101
11121490-5	2000	The CHOP ERSE is a novel variant of the ERSE as it contains two different functional domains, and a GA- instead of GC-rich intervening sequence.	Gallium	100-102	DNA damage inducible transcript 3	Homo sapiens	4-8
11156256-0	2000	The addition of bryostatin 1 to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy improves response in a CHOP-resistant human diffuse large cell lymphoma xenograft model.	bryostatin 1	16-28	DNA damage inducible transcript 3	Homo sapiens	92-96
11156256-0	2000	The addition of bryostatin 1 to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy improves response in a CHOP-resistant human diffuse large cell lymphoma xenograft model.	bryostatin 1	16-28	DNA damage inducible transcript 3	Homo sapiens	134-138
11156256-0	2000	The addition of bryostatin 1 to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy improves response in a CHOP-resistant human diffuse large cell lymphoma xenograft model.	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	92-96
11345781-3	2001	CHOP + etoposide (CHOP-E) was used as an initial chemotherapy and as a chemotherapy agent for the purpose of cell harvesting.	Etoposide	7-16	DNA damage inducible transcript 3	Homo sapiens	18-22
11251981-4	2001	The exogenous GADD153 promoter in this clone was activated by N-methl-N"-nitro-N-nitrosoguanidine (MNNG) in a concentration-dependent manner with kinetics that closely paralleled perturbation of cell cycle phase distribution.	n-methl-n"-nitro-n-nitrosoguanidine	62-97	DNA damage inducible transcript 3	Homo sapiens	14-21
11251981-4	2001	The exogenous GADD153 promoter in this clone was activated by N-methl-N"-nitro-N-nitrosoguanidine (MNNG) in a concentration-dependent manner with kinetics that closely paralleled perturbation of cell cycle phase distribution.	1-Methyl-3-nitro-1-nitrosoguanidine	99-103	DNA damage inducible transcript 3	Homo sapiens	14-21
11158311-6	2001	Investigation of the mechanisms contributing to this effect revealed that elevated Gadd153 expression results in the down-regulation of Bcl2 expression, depletion of cellular glutathione, and exaggerated production of reactive oxygen species.	Glutathione	175-186	DNA damage inducible transcript 3	Homo sapiens	83-90
11158311-6	2001	Investigation of the mechanisms contributing to this effect revealed that elevated Gadd153 expression results in the down-regulation of Bcl2 expression, depletion of cellular glutathione, and exaggerated production of reactive oxygen species.	Reactive Oxygen Species	218-241	DNA damage inducible transcript 3	Homo sapiens	83-90
11158311-7	2001	Restoration of Bcl2 expression in Gadd153-overexpressing cells led to replenishment of glutathione and a reduction in levels of reactive oxygen species, and it protected cells from ER stress-induced cell death.	Glutathione	87-98	DNA damage inducible transcript 3	Homo sapiens	34-41
11158311-7	2001	Restoration of Bcl2 expression in Gadd153-overexpressing cells led to replenishment of glutathione and a reduction in levels of reactive oxygen species, and it protected cells from ER stress-induced cell death.	Reactive Oxygen Species	128-151	DNA damage inducible transcript 3	Homo sapiens	34-41
11145585-8	2001	This is the first evidence that the insulin-like growth factor I/phosphatidylinositol 3-kinase/mammalian target of rapamycin pathway is required for gene regulation by amino acid deprivation and that this pathway is involved in the induction of CHOP by both amino acid deficiency and oxidative stress by hydrogen peroxide.	Hydrogen Peroxide	304-321	DNA damage inducible transcript 3	Homo sapiens	245-249
11113529-6	2000	After 6 h treatment, gadd153, grp78 and grp94 mRNA levels increased markedly, but only when cells were exposed to levels of homocysteine high enough to induce cell injury.	Homocysteine	124-136	DNA damage inducible transcript 3	Homo sapiens	21-28
19002820-1	2000	The use of the gadd153promoter to induce expression of a reporter geneunder heat stress conditions was investigated,since the results of previous studies have suggestedthat the gadd153promoter is likely to be activated by the indirecteffects of hyperthermia, that is, by DNA damage thatoccurs when reactive oxygen species are produced byheat stress.	Reactive Oxygen Species	298-321	DNA damage inducible transcript 3	Homo sapiens	177-184
10955857-13	2000	We recommend treating patients with aggressive NHL of the breast with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, followed by involved field radiation and treating those patients with indolent lymphoma with involved field radiation alone.	Prednisone	118-128	DNA damage inducible transcript 3	Homo sapiens	130-134
11758972-3	2000	Gadd153 mRNA content was increased in PASMCs cultured for 24 hours in 1% oxygen.	pasmcs	38-44	DNA damage inducible transcript 3	Homo sapiens	0-7
10931302-5	2000	Competitive inhibition studies with a panel of compounds containing structures found within NTHi LOS suggested that a phosphorylcholine (ChoP) moiety was involved in adherence.	Phosphorylcholine	118-135	DNA damage inducible transcript 3	Homo sapiens	137-141
11758972-3	2000	Gadd153 mRNA content was increased in PASMCs cultured for 24 hours in 1% oxygen.	Oxygen	73-79	DNA damage inducible transcript 3	Homo sapiens	0-7
10942057-1	2000	BACKGROUND: Standard therapy for lymphoma consists of a cyclophosphamide (C), doxorubicin, vincristine (V), and prednisone (P) (CHOP) combination regimen.	Prednisone	112-122	DNA damage inducible transcript 3	Homo sapiens	128-132
10688535-2	2000	PGA(2), a metabolite of PGE(2), induces the expression of stress response genes, including gadd153 and hsp70, in HeLa cells and human diploid fibroblasts.	Prostaglandins A	0-3	DNA damage inducible transcript 3	Homo sapiens	91-98
10748108-2	2000	In this study, we examined the molecular mechanisms underlying bile acid-mediated gene regulation using GADD153 as our model gene.	Bile Acids and Salts	63-72	DNA damage inducible transcript 3	Homo sapiens	104-111
10748108-3	2000	Promoter deletion analyses revealed that the activator protein-1 (AP-1) transcription factor was crucial for deoxycholic acid (DCA)-mediated GADD153 gene transcription.	Deoxycholic Acid	109-125	DNA damage inducible transcript 3	Homo sapiens	141-148
10748108-3	2000	Promoter deletion analyses revealed that the activator protein-1 (AP-1) transcription factor was crucial for deoxycholic acid (DCA)-mediated GADD153 gene transcription.	Deoxycholic Acid	127-130	DNA damage inducible transcript 3	Homo sapiens	141-148
10942065-2	2000	CASE REPORT: A 52-year-old female painter suffering from high-grade non-Hodgkin"s lymphoma (stage IVB) was treated with a total of 4 mg of vincristine during two courses of CHOP chemotherapy (cyclophosphamide, vincristine, adriamycin, prednisone).	Vincristine	139-150	DNA damage inducible transcript 3	Homo sapiens	173-177
10688535-2	2000	PGA(2), a metabolite of PGE(2), induces the expression of stress response genes, including gadd153 and hsp70, in HeLa cells and human diploid fibroblasts.	Prostaglandins E	24-27	DNA damage inducible transcript 3	Homo sapiens	91-98
10688535-11	2000	TGHQ induces the early (60 min) expression of gadd153 and hsp70.	2,3,5-(triglutathion-S-yl)hydroquinone	0-4	DNA damage inducible transcript 3	Homo sapiens	46-53
10688535-13	2000	In contrast, a stable PGE(2) analogue, 11-deoxy-16, 16-dimethyl-PGE(2) (DDM-PGE(2)), which protects LLC-PK(1) cells against TGHQ-mediated cytotoxicity, modestly elevates the levels of gadd153 and hsp70 expression.	Prostaglandins E	22-25	DNA damage inducible transcript 3	Homo sapiens	184-191
10688535-13	2000	In contrast, a stable PGE(2) analogue, 11-deoxy-16, 16-dimethyl-PGE(2) (DDM-PGE(2)), which protects LLC-PK(1) cells against TGHQ-mediated cytotoxicity, modestly elevates the levels of gadd153 and hsp70 expression.	11-deoxy-16, 16-dimethyl-pge	39-67	DNA damage inducible transcript 3	Homo sapiens	184-191
10688535-13	2000	In contrast, a stable PGE(2) analogue, 11-deoxy-16, 16-dimethyl-PGE(2) (DDM-PGE(2)), which protects LLC-PK(1) cells against TGHQ-mediated cytotoxicity, modestly elevates the levels of gadd153 and hsp70 expression.	Prostaglandins E	64-67	DNA damage inducible transcript 3	Homo sapiens	184-191
10688535-13	2000	In contrast, a stable PGE(2) analogue, 11-deoxy-16, 16-dimethyl-PGE(2) (DDM-PGE(2)), which protects LLC-PK(1) cells against TGHQ-mediated cytotoxicity, modestly elevates the levels of gadd153 and hsp70 expression.	2,3,5-(triglutathion-S-yl)hydroquinone	124-128	DNA damage inducible transcript 3	Homo sapiens	184-191
10674903-1	2000	A regimen which incorporates cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) is the standard treatment for patients with non-Hodgkin"s lymphoma (NHL), but it has not been effective in patients with aggressive NHL who are at high risk.	Cyclophosphamide	29-45	DNA damage inducible transcript 3	Homo sapiens	90-94
10713659-3	2000	We hypothesized that adding high-dose tamoxifen, which is known to have multiple drug resistance-modulatory effects, to the CHOP regimen could increase the response rate, and consequently enhance the survival of patients with NHL.	Tamoxifen	38-47	DNA damage inducible transcript 3	Homo sapiens	124-128
10803921-0	2000	Increase in tumor GADD153 mRNA level following treatment correlates with response to paclitaxel.	Paclitaxel	85-95	DNA damage inducible transcript 3	Homo sapiens	18-25
10674903-1	2000	A regimen which incorporates cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) is the standard treatment for patients with non-Hodgkin"s lymphoma (NHL), but it has not been effective in patients with aggressive NHL who are at high risk.	Prednisolone	76-88	DNA damage inducible transcript 3	Homo sapiens	90-94
10884502-0	2000	The prednisone dosage in the CHOP chemotherapy regimen for non-Hodgkin"s lymphomas (NHL): is there a standard?	Prednisone	4-14	DNA damage inducible transcript 3	Homo sapiens	29-33
10884502-10	2000	CONCLUSIONS: Discrepancies in steroid dosages used as part of the reported standard CHOP regimens are common and not well recognized in the medical literature nor by practicing U.S. hematologists/oncologists.	Steroids	30-37	DNA damage inducible transcript 3	Homo sapiens	84-88
10661763-4	1999	In this model, TAM resistance resulted in an increase in the detectable basal levels of cyclin E, GADD 153, p16, BAX, Bcl-XL, and wild-type and mutant p53, an increase in TAM induction of p16, and a decrease in the detectable basal levels of cyclin D1, p21 and p27.	Tamoxifen	15-18	DNA damage inducible transcript 3	Homo sapiens	98-106
10497233-0	1999	Glutamine deprivation induces the expression of GADD45 and GADD153 primarily by mRNA stabilization.	Glutamine	0-9	DNA damage inducible transcript 3	Homo sapiens	59-66
10697568-8	1999	These results indicate that the activation of AP-1 binding by taxotere seems to be an important factor in determining its sensitivity in association with internucleosomal DNA ladders, and suggest that the induction of gadd153 gene could be a downstream target of AP-1-regulated genes involved in signal transduction pathways leading to apoptosis in gastric cancer cells.	Docetaxel	62-70	DNA damage inducible transcript 3	Homo sapiens	218-225
10580566-3	1999	The CR rate was 47.0% for CHOP, 76.3% for COP-BLAM, 67.9% for COP-BLAM III, and 74.4% for THP-COPBLM therapy (p = 0.013).	Chromium	4-6	DNA damage inducible transcript 3	Homo sapiens	26-30
10497233-2	1999	GLN deprivation caused rapid elevation of GADD45 and GADD153/CHOP mRNA levels in cells that were highly dependent upon GLN for growth and viability.	Glutamine	119-122	DNA damage inducible transcript 3	Homo sapiens	61-65
10497233-2	1999	GLN deprivation caused rapid elevation of GADD45 and GADD153/CHOP mRNA levels in cells that were highly dependent upon GLN for growth and viability.	Glutamine	0-3	DNA damage inducible transcript 3	Homo sapiens	53-60
10497233-8	1999	Nuclear run-on assays and mRNA decay studies suggested that the primary mechanism leading to increased GADD mRNA levels was not transcriptional, but rather that GADD45 and GADD153/CHOP expression were up-regulated in response to GLN deprivation via marked stabilization of these mRNAs.	gadd	103-107	DNA damage inducible transcript 3	Homo sapiens	180-184
10497233-8	1999	Nuclear run-on assays and mRNA decay studies suggested that the primary mechanism leading to increased GADD mRNA levels was not transcriptional, but rather that GADD45 and GADD153/CHOP expression were up-regulated in response to GLN deprivation via marked stabilization of these mRNAs.	Glutamine	229-232	DNA damage inducible transcript 3	Homo sapiens	172-179
10497233-2	1999	GLN deprivation caused rapid elevation of GADD45 and GADD153/CHOP mRNA levels in cells that were highly dependent upon GLN for growth and viability.	Glutamine	0-3	DNA damage inducible transcript 3	Homo sapiens	61-65
10497233-8	1999	Nuclear run-on assays and mRNA decay studies suggested that the primary mechanism leading to increased GADD mRNA levels was not transcriptional, but rather that GADD45 and GADD153/CHOP expression were up-regulated in response to GLN deprivation via marked stabilization of these mRNAs.	Glutamine	229-232	DNA damage inducible transcript 3	Homo sapiens	180-184
10497233-2	1999	GLN deprivation caused rapid elevation of GADD45 and GADD153/CHOP mRNA levels in cells that were highly dependent upon GLN for growth and viability.	Glutamine	119-122	DNA damage inducible transcript 3	Homo sapiens	53-60
10510472-3	1999	We report the presence of a single EBS in the human GADD153 promoter, and that the GADD45 gene promoter lacks EBSs.	ethylbenzene	35-38	DNA damage inducible transcript 3	Homo sapiens	52-59
10510472-5	1999	In addition, our data show that both ETS1 and FLI-1 strongly activate transcription of the GADD153 EBS linked to the CAT reporter gene.	ethylbenzene	99-102	DNA damage inducible transcript 3	Homo sapiens	91-98
10472808-4	1999	NaDOC was found to activate transcription factors and induce or activate the promoters of genes that respond to protein malfolding (grp78 and hsp70), DNA damage (gadd153, hsp70 and c-fos), oxidative stress (NF-kappaB, c-fos, hsp70 and gadd153), ER stress (grp78) and Ca++ imbalance (grp78).	nadoc	0-5	DNA damage inducible transcript 3	Homo sapiens	235-242
10419887-5	1999	Consistent with its adverse effects on the ER, homocysteine alters the expression of genes sensitive to ER stress (ie, GADD45, GADD153, ATF-4, YY1).	Homocysteine	47-59	DNA damage inducible transcript 3	Homo sapiens	127-134
10419887-6	1999	Several other genes observed to be differentially expressed by homocysteine are known to mediate cell growth and differentiation (ie, GADD45, GADD153, Id-1, cyclin D1, FRA-2), a finding that supports the observation that homocysteine causes a dose-dependent decrease in DNA synthesis in HUVEC.	Homocysteine	63-75	DNA damage inducible transcript 3	Homo sapiens	142-149
9763034-5	1998	She experienced complete remission after dose-intensified therapy with cyclophosphamide, hydroxydaunomycin, vincristine [Oncovin], and prednisone (CHOP), but the disease relapsed in the central nervous system 6 months later.	Prednisone	135-145	DNA damage inducible transcript 3	Homo sapiens	147-151
10563431-4	1999	Conventional systemic lymphoma drug combinations such as cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) are ineffective.	Prednisone	104-114	DNA damage inducible transcript 3	Homo sapiens	116-120
10037704-8	1999	Transfection experiments using GADD153 to create C/EBP-null conditions confirm that C/EBP factors are absolutely required for promoter activity and TPA responsiveness.	Tetradecanoylphorbol Acetate	148-151	DNA damage inducible transcript 3	Homo sapiens	31-38
10463009-13	1999	CHOP (cyclophosphamide 650 mg/m2 day 1, vincristine 1.4 mg/m2 day 1, doxorubicin--45 mg/m2 day 1 and prednisone 100 mg/m2 day 1-5) was the most common chemotherapy regimen used.	Cyclophosphamide	6-22	DNA damage inducible transcript 3	Homo sapiens	0-4
9850025-9	1998	When compared with a historic control group who received a CY, DOX, VCR, and prednisone (CHOP)-like regimen, untreated patients in the study had a 3-year EFS rate of 72% versus 28% (P = .0001) and a better OS rate (92% v 56%; P = .05).	Prednisone	77-87	DNA damage inducible transcript 3	Homo sapiens	89-93
10472808-4	1999	NaDOC was found to activate transcription factors and induce or activate the promoters of genes that respond to protein malfolding (grp78 and hsp70), DNA damage (gadd153, hsp70 and c-fos), oxidative stress (NF-kappaB, c-fos, hsp70 and gadd153), ER stress (grp78) and Ca++ imbalance (grp78).	nadoc	0-5	DNA damage inducible transcript 3	Homo sapiens	162-169
10430059-2	1999	We sought to determine whether the increase of the message of the "growth arrest and DNA damage-inducible" gene, GADD153, could be used to assess the extent of the cellular injury response in model systems and in patients with head and neck cancer after treatment with cDDP.	Cisplatin	269-273	DNA damage inducible transcript 3	Homo sapiens	113-120
10430059-3	1999	The mRNA levels of GADD153, a gene highly transcriptionally activated by cDDP damage, were increased in a transient, concentration-dependent manner by cDDP when human UMSCC10b head and neck carcinoma cells were treated with cDDP both in vitro and when grown as tumor xenografts in nude mice.	Cisplatin	73-77	DNA damage inducible transcript 3	Homo sapiens	19-26
10430059-6	1999	GADD153 mRNA levels were measured in biopsies obtained before and 24 h after treatment with cDDP from 32 patients with stage III/IV head and neck cancer.	Cisplatin	92-96	DNA damage inducible transcript 3	Homo sapiens	0-7
10430059-13	1999	We conclude that the magnitude of the increase in GADD153 mRNA is a promising candidate for service as an intermediate marker of head and neck tumor response to cDDP.	Cisplatin	161-165	DNA damage inducible transcript 3	Homo sapiens	50-57
10407583-2	1999	She received 6 courses of chemotherapy including cyclophosphamide, doxorubicin, vincristine, and prednisolone every two weeks (biweekly CHOP), and was considered to be in partial remission.	Prednisolone	97-109	DNA damage inducible transcript 3	Homo sapiens	136-140
10375088-8	1999	The management of diffuse large B-cell lymphoma is combined-modality therapy with radiation and cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy.	Prednisone	144-154	DNA damage inducible transcript 3	Homo sapiens	156-160
10470115-6	1999	The basal level of gadd153 mRNA was overexpressed in MKN45gadd153 cells, and its induction following the treatment of VP-16 and taxotere was found to a greater extent than that of MKN45neo cells.	Docetaxel	128-136	DNA damage inducible transcript 3	Homo sapiens	19-26
10084428-0	1999	Cutaneous and subcutaneous necrosis following dexrazoxane-CHOP therapy.	Dexrazoxane	46-57	DNA damage inducible transcript 3	Homo sapiens	58-62
10093687-2	1999	Based on the in vitro synergism of fludarabine with anthracyclines and on results showing a higher efficacy of CHOP against COP we attempted to improve treatment results with a combination of fludarabine and an anthracycline.	fludarabine	192-203	DNA damage inducible transcript 3	Homo sapiens	111-115
9755171-7	1998	Over-expression of a dominant-negative form of Ire1 blocks the induction of GRP78/BiP and CHOP in response to the ER stress induced by tunicamycin treatment.	Tunicamycin	135-146	DNA damage inducible transcript 3	Homo sapiens	90-94
9818704-4	1998	She received chemotherapy with the CHOP-etoposide regimen, resulting in partial remission.	Etoposide	40-49	DNA damage inducible transcript 3	Homo sapiens	35-39
9827356-4	1998	CHOP protocol is containing both proved carcinogenic cyclophosphamide and highly mutagenic doxorubicyn.	doxorubicyn	91-102	DNA damage inducible transcript 3	Homo sapiens	0-4
9827356-4	1998	CHOP protocol is containing both proved carcinogenic cyclophosphamide and highly mutagenic doxorubicyn.	Cyclophosphamide	53-69	DNA damage inducible transcript 3	Homo sapiens	0-4
9789293-0	1998	[Primary malignant lymphoma in the central nervous system treated with high dose methotrexate (MTX)-CHOP (M-CHOP)].	Methotrexate	81-93	DNA damage inducible transcript 3	Homo sapiens	100-104
9789293-0	1998	[Primary malignant lymphoma in the central nervous system treated with high dose methotrexate (MTX)-CHOP (M-CHOP)].	Methotrexate	81-93	DNA damage inducible transcript 3	Homo sapiens	108-112
9789293-0	1998	[Primary malignant lymphoma in the central nervous system treated with high dose methotrexate (MTX)-CHOP (M-CHOP)].	Methotrexate	95-98	DNA damage inducible transcript 3	Homo sapiens	100-104
9789293-0	1998	[Primary malignant lymphoma in the central nervous system treated with high dose methotrexate (MTX)-CHOP (M-CHOP)].	Methotrexate	95-98	DNA damage inducible transcript 3	Homo sapiens	108-112
9711921-0	1998	A phase I trial of standard and cyclophosphamide dose-escalated CHOP with granulocyte colony stimulating factor in elderly patients with non-Hodgkin"s lymphoma.	Cyclophosphamide	32-48	DNA damage inducible transcript 3	Homo sapiens	64-68
9712776-1	1998	Phosphorylcholine (ChoP) is a component of the teichoic acids of Streptococcus pneumoniae and has been recently identified on the lipopolysaccharide of Haemophilus influenzae, also a major pathogen of the human respiratory tract.	Phosphorylcholine	0-17	DNA damage inducible transcript 3	Homo sapiens	19-23
9712776-1	1998	Phosphorylcholine (ChoP) is a component of the teichoic acids of Streptococcus pneumoniae and has been recently identified on the lipopolysaccharide of Haemophilus influenzae, also a major pathogen of the human respiratory tract.	Teichoic Acids	47-61	DNA damage inducible transcript 3	Homo sapiens	19-23
9711921-9	1998	Six of 11 patients (55%) given CHOP with cyclophosphamide 900 mg/m2 (CHOP-900) completed treatment.	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	31-35
9711921-9	1998	Six of 11 patients (55%) given CHOP with cyclophosphamide 900 mg/m2 (CHOP-900) completed treatment.	Cyclophosphamide	41-57	DNA damage inducible transcript 3	Homo sapiens	69-73
9711921-1	1998	The purpose of this study was to assess the safety and feasibility of using standard and escalated doses of cyclophosphamide with doxorubicin, vincristine and prednisone (CHOP) plus granulocyte colony stimulating factor (G-CSF) to treat elderly patients who have advanced stage intermediate grade lymphoma.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	171-175
9711921-12	1998	The received dose intensities of cyclophosphamide relative to standard CHOP measured over the actual time on therapy were 96% with standard CHOP and 115% with CHOP-900.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	140-144
9647875-1	1998	BACKGROUND: Patients with clinically localized, intermediate- or high-grade non-Hodgkin"s lymphoma usually receive initial treatment with a doxorubicin-containing regimen such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP).	Doxorubicin	140-151	DNA damage inducible transcript 3	Homo sapiens	239-243
9711921-12	1998	The received dose intensities of cyclophosphamide relative to standard CHOP measured over the actual time on therapy were 96% with standard CHOP and 115% with CHOP-900.	Cyclophosphamide	33-49	DNA damage inducible transcript 3	Homo sapiens	140-144
9576870-3	1998	Here we show that homocysteine increases the expression of GRP78 and GADD153, stress-response genes induced by agents or conditions that adversely affect the function of the endoplasmic reticulum (ER).	Homocysteine	18-30	DNA damage inducible transcript 3	Homo sapiens	69-76
9667250-1	1998	PURPOSE: Standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy repeated at 3-week intervals is difficult to deliver in elderly patients with non-Hodgkin"s lymphoma (NHL).	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	78-82
9667250-1	1998	PURPOSE: Standard cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy repeated at 3-week intervals is difficult to deliver in elderly patients with non-Hodgkin"s lymphoma (NHL).	Prednisone	66-76	DNA damage inducible transcript 3	Homo sapiens	78-82
9649147-3	1998	CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity.	Cyclophosphamide	14-30	DNA damage inducible transcript 3	Homo sapiens	0-4
9649147-3	1998	CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity.	Doxorubicin	32-43	DNA damage inducible transcript 3	Homo sapiens	0-4
9649147-3	1998	CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity.	Vincristine	45-56	DNA damage inducible transcript 3	Homo sapiens	0-4
9649147-3	1998	CHOP therapy (cyclophosphamide, doxorubicin, vincristine and prednisolone) only slightly induces pulmonary toxicity.	Prednisolone	61-73	DNA damage inducible transcript 3	Homo sapiens	0-4
9669685-0	1998	Etoposide and idarubicin in a modified CHOP-like regimen (VICED) for aggressive non-Hodgkin"s lymphomas.	Idarubicin	14-24	DNA damage inducible transcript 3	Homo sapiens	39-43
9669685-2	1998	We have designed a first-line five-drug regimen (vincristine, idarubicin, cyclophosphamide, etoposide and deflazacort), with the aim of potentiating the CHOP protocol without losing tolerability and ease of administration.	Vincristine	49-60	DNA damage inducible transcript 3	Homo sapiens	153-157
9586958-3	1998	The protein kinase inhibitor staurosporine and the temperature sensitive (ts) p34cdc2 mutant reduced induction by the alkylating agent methylmethane sulfonate (MMS) of the rodent gadd45 and gadd153 genes.	Staurosporine	29-42	DNA damage inducible transcript 3	Homo sapiens	190-197
9586958-3	1998	The protein kinase inhibitor staurosporine and the temperature sensitive (ts) p34cdc2 mutant reduced induction by the alkylating agent methylmethane sulfonate (MMS) of the rodent gadd45 and gadd153 genes.	Methyl Methanesulfonate	135-158	DNA damage inducible transcript 3	Homo sapiens	190-197
9586958-6	1998	Suramin, an antitumor drug that interferes with the interaction of growth factors with their receptors, inhibited the UV radiation induction of GADD45 and GADD153 but had no effect on the MMS and IR pathways.	Suramin	0-7	DNA damage inducible transcript 3	Homo sapiens	155-162
9586958-7	1998	Elevated expression of gadd45 by medium depletion (starvation) was partially reduced by the addition of either genistein or tyrphostin, two protein tyrosine kinase inhibitors, while gadd153 was affected by tyrphostin only.	Tyrphostins	206-216	DNA damage inducible transcript 3	Homo sapiens	182-189
9428803-4	1998	In this study, we demonstrate in a variety of cell lines that geldanamycin is a potent inducer of the cellular response to stress in the ER, resulting in the transcriptional up-regulation of ER chaperones and expression of the gadd153/CHOP transcription factor.	geldanamycin	62-74	DNA damage inducible transcript 3	Homo sapiens	227-234
9752311-1	1998	The CHOP regimen (cyclophosphamide vincristine, adriamycin, prednisone) is considered since twenty years as the standard treatment of disseminated aggressive non-Hodgkin"s lymphomas and cures approximately 30% of patients.	Doxorubicin	48-58	DNA damage inducible transcript 3	Homo sapiens	4-8
9752311-1	1998	The CHOP regimen (cyclophosphamide vincristine, adriamycin, prednisone) is considered since twenty years as the standard treatment of disseminated aggressive non-Hodgkin"s lymphomas and cures approximately 30% of patients.	Prednisone	60-70	DNA damage inducible transcript 3	Homo sapiens	4-8
9519935-7	1998	We describe a patient with non-Hodgkin"s lymphoma treated with conventional cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy and high-dose steroids who developed a rapidly progressive fatal leukoencephalopathy.	Cyclophosphamide	76-92	DNA damage inducible transcript 3	Homo sapiens	136-140
9519935-7	1998	We describe a patient with non-Hodgkin"s lymphoma treated with conventional cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy and high-dose steroids who developed a rapidly progressive fatal leukoencephalopathy.	Prednisone	124-134	DNA damage inducible transcript 3	Homo sapiens	136-140
9752311-1	1998	The CHOP regimen (cyclophosphamide vincristine, adriamycin, prednisone) is considered since twenty years as the standard treatment of disseminated aggressive non-Hodgkin"s lymphomas and cures approximately 30% of patients.	Cyclophosphamide	18-34	DNA damage inducible transcript 3	Homo sapiens	4-8
9752311-1	1998	The CHOP regimen (cyclophosphamide vincristine, adriamycin, prednisone) is considered since twenty years as the standard treatment of disseminated aggressive non-Hodgkin"s lymphomas and cures approximately 30% of patients.	Vincristine	35-46	DNA damage inducible transcript 3	Homo sapiens	4-8
9530358-1	1998	A pilot study of high-dose biweekly cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) chemotherapy with granulocyte colony-stimulating factor support was carried out at 11 centers.	Prednisolone	83-95	DNA damage inducible transcript 3	Homo sapiens	97-101
9428803-4	1998	In this study, we demonstrate in a variety of cell lines that geldanamycin is a potent inducer of the cellular response to stress in the ER, resulting in the transcriptional up-regulation of ER chaperones and expression of the gadd153/CHOP transcription factor.	geldanamycin	62-74	DNA damage inducible transcript 3	Homo sapiens	235-239
9491847-0	1997	Results of treatment with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) for non-Hodgkin"s aggressive lymphoma analyzed according to the International Prognostic Index.	Cyclophosphamide	26-42	DNA damage inducible transcript 3	Homo sapiens	85-89
9615833-1	1998	Oral administration of 2 mg kitryl effectively controlled nausea (82.5-96.7%) and vomiting (97.3-99.1%) induced in 127 patients with malignant lymphomas and solid tumors, who received highly emetic cytostatic MOPP, ABVD, CHOP, CHOEP, EVAP, VP and CMP therapy.	kitryl	28-34	DNA damage inducible transcript 3	Homo sapiens	221-225
9384597-6	1997	The glycosylation inhibitor tunicamycin potently induced expression of both ER chaperones and CHOP in ligand-deprived cells, demonstrating that the UPR pathway remains functionally intact in the absence of growth factor-mediated signaling.	Tunicamycin	28-39	DNA damage inducible transcript 3	Homo sapiens	94-98
9409065-1	1997	Cyclophosphamide, doxorubicin, vincristine (Oncovin), and prednisolone (CHOP) has for many years been the standard chemotherapeutic regimen for patients with aggressive non-Hodgkin"s lymphoma.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	72-76
9409065-1	1997	Cyclophosphamide, doxorubicin, vincristine (Oncovin), and prednisolone (CHOP) has for many years been the standard chemotherapeutic regimen for patients with aggressive non-Hodgkin"s lymphoma.	Prednisolone	58-70	DNA damage inducible transcript 3	Homo sapiens	72-76
9491847-0	1997	Results of treatment with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) for non-Hodgkin"s aggressive lymphoma analyzed according to the International Prognostic Index.	Prednisone	73-83	DNA damage inducible transcript 3	Homo sapiens	85-89
9196142-4	1997	All except two patients were treated after first or subsequent relapses after receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy to achieve a good partial (six of 13) or complete (seven of 13) response before stem-cell mobilization with cyclophosphamide 3 g/m2 and filgrastim 300 microg once daily.	Prednisone	136-146	DNA damage inducible transcript 3	Homo sapiens	148-152
9268362-0	1997	Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153.	ammonium ferrous sulfate	0-3	DNA damage inducible transcript 3	Homo sapiens	119-126
9268362-0	1997	Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153.	Ceramides	8-16	DNA damage inducible transcript 3	Homo sapiens	119-126
9268362-1	1997	In the present study, we show that Fas receptor ligation or cellular treatment with synthetic C6-ceramide results in activation or phosphorylation, respectively, of the small G-protein Rac1, Jun N-terminal kinase (JNK)/p38 kinases (p38-K), and the transcription factor GADD153.	N-caproylsphingosine	94-105	DNA damage inducible transcript 3	Homo sapiens	269-276
9268362-2	1997	A signaling cascade from the Fas receptor via ceramide, Ras, Rac1, and JNK/p38-K to GADD153 is demonstrated employing transfection of transdominant inhibitory N17Ras, N17Rac1, c-Jun, or treatment with a specific p38-K inhibitor.	Ceramides	46-54	DNA damage inducible transcript 3	Homo sapiens	84-91
9211906-9	1997	Moreover, CHOP expression is induced at leucine concentrations in the range of those observed in blood of protein-restricted animals suggesting that amino acids can participate, in concert with hormones, in the regulation of gene expression.	Leucine	40-47	DNA damage inducible transcript 3	Homo sapiens	10-14
9413226-8	1997	Our conclusion is that GADD proteins play an important role in the malignant transformation of naevus to melanoma and GADD 45 and GADD 153 proteins can influence patient survival.	gadd	23-27	DNA damage inducible transcript 3	Homo sapiens	130-138
9179527-4	1997	Conventional chemotherapy with CHOP (a chemotherapeutic regimen consisting of a combination of cyclophosphamide, doxorubicin, vincristine and prednisone) or other equivalent third-generation regimens may be considered the standard treatment for the good prognosis group.	Cyclophosphamide	95-111	DNA damage inducible transcript 3	Homo sapiens	31-35
9038301-2	1997	Incorporated choline is in the form of phosphorylcholine (ChoP) based on the reactivity with the monoclonal antibody with specificity for this structure, TEPC-15.	Choline	13-20	DNA damage inducible transcript 3	Homo sapiens	58-62
9115450-3	1997	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy is well tolerated in patients who have a good performance status and who have aggressive histology lymphoma, but briefer 8-week regimens appear to offer similar benefits more quickly.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
9115450-3	1997	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy is well tolerated in patients who have a good performance status and who have aggressive histology lymphoma, but briefer 8-week regimens appear to offer similar benefits more quickly.	Doxorubicin	18-29	DNA damage inducible transcript 3	Homo sapiens	60-64
9115450-3	1997	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy is well tolerated in patients who have a good performance status and who have aggressive histology lymphoma, but briefer 8-week regimens appear to offer similar benefits more quickly.	Prednisone	48-58	DNA damage inducible transcript 3	Homo sapiens	60-64
10173030-3	1997	One such treatment that is considered to have a low potential for inducing fever and neutropenia is the CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone) for non-Hodgkin"s lymphoma.	Cyclophosphamide	118-134	DNA damage inducible transcript 3	Homo sapiens	104-108
10173030-3	1997	One such treatment that is considered to have a low potential for inducing fever and neutropenia is the CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone) for non-Hodgkin"s lymphoma.	Doxorubicin	136-147	DNA damage inducible transcript 3	Homo sapiens	104-108
10173030-3	1997	One such treatment that is considered to have a low potential for inducing fever and neutropenia is the CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone) for non-Hodgkin"s lymphoma.	Vincristine	149-160	DNA damage inducible transcript 3	Homo sapiens	104-108
10173030-3	1997	One such treatment that is considered to have a low potential for inducing fever and neutropenia is the CHOP regimen (cyclophosphamide, doxorubicin, vincristine and prednisone) for non-Hodgkin"s lymphoma.	Prednisone	165-175	DNA damage inducible transcript 3	Homo sapiens	104-108
10920899-5	1997	In 10 untreated patients CR was observed in 7; The CHOP group gave an overall response rate of 65.4%(17/26).	Chromium	25-27	DNA damage inducible transcript 3	Homo sapiens	51-55
9193363-0	1997	Early restaging gallium scans predict outcome in poor-prognosis patients with aggressive non-Hodgkin"s lymphoma treated with high-dose CHOP chemotherapy.	Gallium	16-23	DNA damage inducible transcript 3	Homo sapiens	135-139
9038301-2	1997	Incorporated choline is in the form of phosphorylcholine (ChoP) based on the reactivity with the monoclonal antibody with specificity for this structure, TEPC-15.	Phosphorylcholine	39-56	DNA damage inducible transcript 3	Homo sapiens	58-62
9272145-5	1997	One is a randomized phase II trial of dose-escalated cyclophosphamide, doxorubicin, vincristine, and prednisolone (high CHOP) versus shortened CHOP (biweekly CHOP) with prophylactic use of granulocyte colony-stimulating factor.	Prednisolone	101-113	DNA damage inducible transcript 3	Homo sapiens	120-124
9044846-0	1997	Increased gadd153 messenger RNA level is associated with apoptosis in human leukemic cells treated with etoposide.	Etoposide	104-113	DNA damage inducible transcript 3	Homo sapiens	10-17
9044846-4	1997	We have investigated the relationships between gadd153 gene expression and apoptosis induction in four human leukemic cell lines with different sensitivities to apoptosis induced by etoposide (VP-16), a topoisomerase II inhibitor.	Etoposide	182-191	DNA damage inducible transcript 3	Homo sapiens	47-54
9044846-11	1997	Both gadd153 mRNA level increase and internucleosomal DNA fragmentation were inhibited by N-tosyl-L-phenylalanine chloromethylketone, a serine threonine protease inhibitor, N-acetyl-leucyl-leucyl-norleucinal, an inhibitor of calpain, N-acetylcysteine, an inhibitor of oxidative metabolism, and overexpression of Bcl-2.	Tosylphenylalanyl Chloromethyl Ketone	90-132	DNA damage inducible transcript 3	Homo sapiens	5-12
9044846-11	1997	Both gadd153 mRNA level increase and internucleosomal DNA fragmentation were inhibited by N-tosyl-L-phenylalanine chloromethylketone, a serine threonine protease inhibitor, N-acetyl-leucyl-leucyl-norleucinal, an inhibitor of calpain, N-acetylcysteine, an inhibitor of oxidative metabolism, and overexpression of Bcl-2.	Acetylcysteine	234-250	DNA damage inducible transcript 3	Homo sapiens	5-12
9044846-13	1997	These results indicate that gadd153 gene expression increase occurs downstream of events sensitive to N-tosyl-L-phenylalanine chloromethylketone, calpain inhibitor I, and Bcl-2 and upstream of interleukin 1beta-converting enzyme-related proteases activation in leukemic cells in which treatment with VP-16 induces rapid apoptosis.	Tosylphenylalanyl Chloromethyl Ketone	102-144	DNA damage inducible transcript 3	Homo sapiens	28-35
8996528-1	1997	PURPOSE: DNA damage-inducible genes, such as gadd153, gadd45, p21 and c-jun, have previously been shown to be induced by the chemotherapeutic agent cisplatin.	Cisplatin	148-157	DNA damage inducible transcript 3	Homo sapiens	45-52
8996528-2	1997	One of these genes, gadd153, has previously been reported to be differentially expressed in cisplatin-resistant cell lines and, therefore, to be a potential prognostic indicator for tumor response to cisplatin-based chemotherapy.	Cisplatin	92-101	DNA damage inducible transcript 3	Homo sapiens	20-27
8996528-2	1997	One of these genes, gadd153, has previously been reported to be differentially expressed in cisplatin-resistant cell lines and, therefore, to be a potential prognostic indicator for tumor response to cisplatin-based chemotherapy.	Cisplatin	200-209	DNA damage inducible transcript 3	Homo sapiens	20-27
8996528-9	1997	Induction was maximal between 24 and 48 h following exposure to the drug for all genes except c-jun which was induced by 6 h. At 24 h following cisplatin treatment the overall levels of gadd153 were less in the resistant C13* cell line than in the parental 2008 cell line, while those of gadd45 were greater in C13* than in 2008.	Cisplatin	144-153	DNA damage inducible transcript 3	Homo sapiens	186-193
8996528-12	1997	The more cytotoxic platinum analog, ormaplatin, also induced gadd153 and its induction was also based on cytotoxicity.	Platinum	19-27	DNA damage inducible transcript 3	Homo sapiens	61-68
8996528-12	1997	The more cytotoxic platinum analog, ormaplatin, also induced gadd153 and its induction was also based on cytotoxicity.	ormaplatin	36-46	DNA damage inducible transcript 3	Homo sapiens	61-68
8996528-16	1997	Finally, these results strengthen previous suggestions that the expression of gadd153, and possibly other DNA damage-inducible genes, may be useful indicators of tumor response to cisplatin-based chemotherapy.	Cisplatin	180-189	DNA damage inducible transcript 3	Homo sapiens	78-85
8892739-5	1996	The patient attained complete remission with cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) chemotherapy and remained disease-free for 13 years.	Prednisone	92-102	DNA damage inducible transcript 3	Homo sapiens	104-108
8978792-3	1996	The efficacy of dose intensification of CPA in CHOP regimen for patients with aggressive lymphoma is being investigated in some clinical trials.	Cyclophosphamide	40-43	DNA damage inducible transcript 3	Homo sapiens	47-51
8650547-4	1996	A specific inhibitor of p38 MAP kinase, SB203580, abolished the stress-inducible in vivo phosphorylation of CHOP.	SB 203580	40-48	DNA damage inducible transcript 3	Homo sapiens	108-112
17180111-0	1996	Bile acid activation of the gadd153 promoter and of p53-independent apoptosis: relevance to colon cancer.	Bile Acids and Salts	0-9	DNA damage inducible transcript 3	Homo sapiens	28-35
17180111-4	1996	We present evidence of bile acid activation of the gadd153 promoter (a promoter activated by DNA damaging agents).	Bile Acids and Salts	23-32	DNA damage inducible transcript 3	Homo sapiens	51-58
8892753-3	1996	In contrast, the gadd gene stress response to base-damaging agents, such as methylmethane sulfonate (MMS) or UV radiation, or medium depletion (starvation) occurs in all mammalian cells examined to date regardless of p53 status for both GADD45 and also GADD153, which is not IR-responsive in many lines with functional p53.	gadd	17-21	DNA damage inducible transcript 3	Homo sapiens	253-260
8892753-3	1996	In contrast, the gadd gene stress response to base-damaging agents, such as methylmethane sulfonate (MMS) or UV radiation, or medium depletion (starvation) occurs in all mammalian cells examined to date regardless of p53 status for both GADD45 and also GADD153, which is not IR-responsive in many lines with functional p53.	Methyl Methanesulfonate	101-104	DNA damage inducible transcript 3	Homo sapiens	253-260
8702804-0	1996	Paclitaxel activation of the GADD153 promoter through a cellular injury response element containing an essential Sp1 binding site.	Paclitaxel	0-10	DNA damage inducible transcript 3	Homo sapiens	29-36
8702804-1	1996	The GADD153 promoter is transcriptionally activated by paclitaxel-induced injury.	Paclitaxel	55-65	DNA damage inducible transcript 3	Homo sapiens	4-11
8702804-9	1996	These data indicate that paclitaxel activates the GADD153 promoter through a constitutively occupied Sp1 site at -61 bases.	Paclitaxel	25-35	DNA damage inducible transcript 3	Homo sapiens	50-57
8688344-1	1996	A combination of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been a standard therapy for histologically aggressive non-Hodgkin"s lymphomas for over 20 years, but several newer regimens, referred to as second or third generation, have been reported to give improved results in single-centre studies.	Cyclophosphamide	17-33	DNA damage inducible transcript 3	Homo sapiens	78-82
8688344-1	1996	A combination of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been a standard therapy for histologically aggressive non-Hodgkin"s lymphomas for over 20 years, but several newer regimens, referred to as second or third generation, have been reported to give improved results in single-centre studies.	Doxorubicin	35-46	DNA damage inducible transcript 3	Homo sapiens	78-82
8688344-1	1996	A combination of cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) has been a standard therapy for histologically aggressive non-Hodgkin"s lymphomas for over 20 years, but several newer regimens, referred to as second or third generation, have been reported to give improved results in single-centre studies.	Prednisolone	64-76	DNA damage inducible transcript 3	Homo sapiens	78-82
8754828-5	1996	Surprisingly, attenuated induction of CHOP was also noted in BiP-overexpressing cells treated with methyl methanesulfonate, an agent thought to activate CHOP by causing DNA damage.	Methyl Methanesulfonate	99-122	DNA damage inducible transcript 3	Homo sapiens	38-42
8754828-5	1996	Surprisingly, attenuated induction of CHOP was also noted in BiP-overexpressing cells treated with methyl methanesulfonate, an agent thought to activate CHOP by causing DNA damage.	Methyl Methanesulfonate	99-122	DNA damage inducible transcript 3	Homo sapiens	153-157
8636770-9	1996	Treatment with cyclophosphamide, doxorubicin vincristine, and prednisone (CHOP) or cyclophosphomide, vincristine, and prednisone (COP) resulted in a complete remission in 14 of 15 cases.	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	74-78
8670069-6	1996	Concordantly, GSH peroxidase overexpression in WI38 cells attenuated GADD153 mRNA induction by H2O2.	Hydrogen Peroxide	95-99	DNA damage inducible transcript 3	Homo sapiens	69-76
8670069-7	1996	However, GADD153 induction by arsenite was only modestly reduced in the same cells, suggesting a lesser contribution of peroxides to gene activation by arsenite.	arsenite	30-38	DNA damage inducible transcript 3	Homo sapiens	9-16
8670069-11	1996	Together, these results demonstrate that both free-radical generation and thiol modification can transcriptionally activate GADD153, and that AP-1 is critical to oxidative regulation of this gene.	Free Radicals	46-58	DNA damage inducible transcript 3	Homo sapiens	124-131
8670069-11	1996	Together, these results demonstrate that both free-radical generation and thiol modification can transcriptionally activate GADD153, and that AP-1 is critical to oxidative regulation of this gene.	Sulfhydryl Compounds	74-79	DNA damage inducible transcript 3	Homo sapiens	124-131
8622660-2	1996	We also demonstrate that an ATF3-interacting protein, gadd153/Chop10, forms a nonfunctional heterodimer with ATF3: the heterodimer, in contrast to the ATF3 homodimer, does not bind to the ATF/cyclic AMP response element consensus site and does not repress transcription.	Cyclic AMP	192-202	DNA damage inducible transcript 3	Homo sapiens	54-61
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	119-139	DNA damage inducible transcript 3	Homo sapiens	24-31
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	119-139	DNA damage inducible transcript 3	Homo sapiens	32-38
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	119-139	DNA damage inducible transcript 3	Homo sapiens	161-168
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	119-139	DNA damage inducible transcript 3	Homo sapiens	169-175
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	141-145	DNA damage inducible transcript 3	Homo sapiens	24-31
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	141-145	DNA damage inducible transcript 3	Homo sapiens	32-38
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	141-145	DNA damage inducible transcript 3	Homo sapiens	161-168
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	141-145	DNA damage inducible transcript 3	Homo sapiens	169-175
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	24-31
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	32-38
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	161-168
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	169-175
8670069-3	1996	Both commonalities and distinctions in the induction of GADD153 by H2O2 and the thiol-reactive compound arsenite were demonstrated.	Hydrogen Peroxide	67-71	DNA damage inducible transcript 3	Homo sapiens	56-63
8670069-3	1996	Both commonalities and distinctions in the induction of GADD153 by H2O2 and the thiol-reactive compound arsenite were demonstrated.	Sulfhydryl Compounds	80-85	DNA damage inducible transcript 3	Homo sapiens	56-63
8670069-4	1996	GADD153 mRNA induction by both H2O2 and arsenite was potentiated by GSH depletion, and completely inhibited by N-acetyl-cysteine.	Hydrogen Peroxide	31-35	DNA damage inducible transcript 3	Homo sapiens	0-7
8670069-4	1996	GADD153 mRNA induction by both H2O2 and arsenite was potentiated by GSH depletion, and completely inhibited by N-acetyl-cysteine.	arsenite	40-48	DNA damage inducible transcript 3	Homo sapiens	0-7
8670069-4	1996	GADD153 mRNA induction by both H2O2 and arsenite was potentiated by GSH depletion, and completely inhibited by N-acetyl-cysteine.	Glutathione	68-71	DNA damage inducible transcript 3	Homo sapiens	0-7
8670069-4	1996	GADD153 mRNA induction by both H2O2 and arsenite was potentiated by GSH depletion, and completely inhibited by N-acetyl-cysteine.	Acetylcysteine	111-128	DNA damage inducible transcript 3	Homo sapiens	0-7
8670069-5	1996	o-Phenanthroline and mannitol blocked GADD153 induction by H2O2, indicating that iron-generated hydroxyl radical mediates this induction.	1,10-phenanthroline	0-16	DNA damage inducible transcript 3	Homo sapiens	38-45
8670069-5	1996	o-Phenanthroline and mannitol blocked GADD153 induction by H2O2, indicating that iron-generated hydroxyl radical mediates this induction.	Mannitol	21-29	DNA damage inducible transcript 3	Homo sapiens	38-45
8670069-5	1996	o-Phenanthroline and mannitol blocked GADD153 induction by H2O2, indicating that iron-generated hydroxyl radical mediates this induction.	Hydrogen Peroxide	59-63	DNA damage inducible transcript 3	Homo sapiens	38-45
8670069-5	1996	o-Phenanthroline and mannitol blocked GADD153 induction by H2O2, indicating that iron-generated hydroxyl radical mediates this induction.	Iron	81-85	DNA damage inducible transcript 3	Homo sapiens	38-45
8670069-5	1996	o-Phenanthroline and mannitol blocked GADD153 induction by H2O2, indicating that iron-generated hydroxyl radical mediates this induction.	Hydroxyl Radical	96-112	DNA damage inducible transcript 3	Homo sapiens	38-45
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	24-31
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	32-38
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	161-168
8622660-3	1996	Interestingly, ATF3 and gadd153/Chop10 are expressed in inverse but overlapping manners during the liver"s response to carbon tetrachloride (CCl4): the level of gadd153/Chop10 mRNA is high in the normal liver and greatly decreases upon CCl4 treatment; the level of ATF3 mRNA, on the other hand, is low in the normal liver and greatly increases upon CCl4 treatment.	Carbon Tetrachloride	236-240	DNA damage inducible transcript 3	Homo sapiens	169-175
8622660-4	1996	We hypothesize that in nonstressed liver, gadd153/Chop10 inhibits the limited amount of ATF3 by forming an inactive heterodimer with it, whereas in CCl4-injured liver, the synthesis of gadd153/Chop10 is repressed, allowing the induced ATF3 to function.	Carbon Tetrachloride	148-152	DNA damage inducible transcript 3	Homo sapiens	50-56
8554977-9	1996	We conclude that (1) taxol and cDDP activate GADD153 promoter activity through different mechanisms; (2) the signal transduction pathway mediating induction by cDDP involves a tyrosine kinase inhibitable by tyrphostin B46; and (3) that inhibition of this signal transduction pathway by tyrphostin synergistically enhances cDDP toxicity.	Tyrphostins	207-217	DNA damage inducible transcript 3	Homo sapiens	45-52
8629263-5	1996	The CHOP-regime, consisting of doxorubicin, cyclophosphamide, oncovin and prednisolon, is the standard therapy that should be given outside of clinical trials.	Doxorubicin	31-42	DNA damage inducible transcript 3	Homo sapiens	4-8
8629263-5	1996	The CHOP-regime, consisting of doxorubicin, cyclophosphamide, oncovin and prednisolon, is the standard therapy that should be given outside of clinical trials.	Cyclophosphamide	44-60	DNA damage inducible transcript 3	Homo sapiens	4-8
8629263-5	1996	The CHOP-regime, consisting of doxorubicin, cyclophosphamide, oncovin and prednisolon, is the standard therapy that should be given outside of clinical trials.	Vincristine	62-69	DNA damage inducible transcript 3	Homo sapiens	4-8
8629263-5	1996	The CHOP-regime, consisting of doxorubicin, cyclophosphamide, oncovin and prednisolon, is the standard therapy that should be given outside of clinical trials.	Prednisolone	74-85	DNA damage inducible transcript 3	Homo sapiens	4-8
8554977-0	1996	Cisplatin and taxol activate different signal pathways regulating cellular injury-induced expression of GADD153.	Cisplatin	0-9	DNA damage inducible transcript 3	Homo sapiens	104-111
8554977-0	1996	Cisplatin and taxol activate different signal pathways regulating cellular injury-induced expression of GADD153.	Paclitaxel	14-19	DNA damage inducible transcript 3	Homo sapiens	104-111
8554977-9	1996	We conclude that (1) taxol and cDDP activate GADD153 promoter activity through different mechanisms; (2) the signal transduction pathway mediating induction by cDDP involves a tyrosine kinase inhibitable by tyrphostin B46; and (3) that inhibition of this signal transduction pathway by tyrphostin synergistically enhances cDDP toxicity.	Cisplatin	160-164	DNA damage inducible transcript 3	Homo sapiens	45-52
8554977-4	1996	Activation of the GADD153 promoter coupled to the luciferase gene and transfected into human ovarian carcinoma 2008 cells correlated well with the increase in endogenous GADD153 mRNA after treatment with taxol but not after treatment with cDDP.	Paclitaxel	204-209	DNA damage inducible transcript 3	Homo sapiens	18-25
8554977-4	1996	Activation of the GADD153 promoter coupled to the luciferase gene and transfected into human ovarian carcinoma 2008 cells correlated well with the increase in endogenous GADD153 mRNA after treatment with taxol but not after treatment with cDDP.	Paclitaxel	204-209	DNA damage inducible transcript 3	Homo sapiens	170-177
8523055-3	1995	The study was designed to determine the maximum-tolerated dosages (MTD) of cyclophosphamide and doxorubicin that could be used in a high-dose cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen with granulocyte colony-stimulating factor (G-CSF) support and to assess preliminarily the efficacy of the regimen.	Cyclophosphamide	75-91	DNA damage inducible transcript 3	Homo sapiens	202-206
8554977-5	1996	Following treatment with cDDP, the increase in endogenous GADD153 mRNA was 10-fold greater than the increase in GADD153 promoter activity.	Cisplatin	25-29	DNA damage inducible transcript 3	Homo sapiens	58-65
8554977-5	1996	Following treatment with cDDP, the increase in endogenous GADD153 mRNA was 10-fold greater than the increase in GADD153 promoter activity.	Cisplatin	25-29	DNA damage inducible transcript 3	Homo sapiens	112-119
8554977-6	1996	Likewise, at equitoxic levels of exposure (IC80), cDDP produced a 5-fold greater increase in endogenous GADD153 mRNA than taxol.	Cisplatin	50-54	DNA damage inducible transcript 3	Homo sapiens	104-111
8554977-7	1996	The tyrosine kinase inhibitor tyrophostin B46 had no significant effect on the ability of taxol to activate the GADD153 promoter, but inhibited activation of the GADD153 promoter by cDDP in a concentration-dependent manner.	tyrophostin b46	30-45	DNA damage inducible transcript 3	Homo sapiens	162-169
8554977-7	1996	The tyrosine kinase inhibitor tyrophostin B46 had no significant effect on the ability of taxol to activate the GADD153 promoter, but inhibited activation of the GADD153 promoter by cDDP in a concentration-dependent manner.	Cisplatin	182-186	DNA damage inducible transcript 3	Homo sapiens	162-169
8554977-9	1996	We conclude that (1) taxol and cDDP activate GADD153 promoter activity through different mechanisms; (2) the signal transduction pathway mediating induction by cDDP involves a tyrosine kinase inhibitable by tyrphostin B46; and (3) that inhibition of this signal transduction pathway by tyrphostin synergistically enhances cDDP toxicity.	Paclitaxel	21-26	DNA damage inducible transcript 3	Homo sapiens	45-52
8554977-9	1996	We conclude that (1) taxol and cDDP activate GADD153 promoter activity through different mechanisms; (2) the signal transduction pathway mediating induction by cDDP involves a tyrosine kinase inhibitable by tyrphostin B46; and (3) that inhibition of this signal transduction pathway by tyrphostin synergistically enhances cDDP toxicity.	Cisplatin	31-35	DNA damage inducible transcript 3	Homo sapiens	45-52
8554977-9	1996	We conclude that (1) taxol and cDDP activate GADD153 promoter activity through different mechanisms; (2) the signal transduction pathway mediating induction by cDDP involves a tyrosine kinase inhibitable by tyrphostin B46; and (3) that inhibition of this signal transduction pathway by tyrphostin synergistically enhances cDDP toxicity.	Cisplatin	160-164	DNA damage inducible transcript 3	Homo sapiens	45-52
8554977-9	1996	We conclude that (1) taxol and cDDP activate GADD153 promoter activity through different mechanisms; (2) the signal transduction pathway mediating induction by cDDP involves a tyrosine kinase inhibitable by tyrphostin B46; and (3) that inhibition of this signal transduction pathway by tyrphostin synergistically enhances cDDP toxicity.	alpha-cyano-(3,4-dihydroxy)-N-(3-phenylpropyl)cinnamide	207-221	DNA damage inducible transcript 3	Homo sapiens	45-52
8558202-17	1996	These data are the basis for a randomized trial to compare cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP) with CEOP/IMVP-Dexa.	Prednisolone	107-119	DNA damage inducible transcript 3	Homo sapiens	121-125
8652232-5	1995	In high-grade lymphomas combination chemotherapy with cyclophosphamide, hydroxydaunorubin, vincristine and prednisone (CHOP) represents the treatment of first choice, and may be restricted to 3-4 cycles in patients with limited stages of the disease when followed by involved field radiotherapy.	Cyclophosphamide	54-70	DNA damage inducible transcript 3	Homo sapiens	119-123
8652232-5	1995	In high-grade lymphomas combination chemotherapy with cyclophosphamide, hydroxydaunorubin, vincristine and prednisone (CHOP) represents the treatment of first choice, and may be restricted to 3-4 cycles in patients with limited stages of the disease when followed by involved field radiotherapy.	hydroxydaunorubin	72-89	DNA damage inducible transcript 3	Homo sapiens	119-123
8652232-5	1995	In high-grade lymphomas combination chemotherapy with cyclophosphamide, hydroxydaunorubin, vincristine and prednisone (CHOP) represents the treatment of first choice, and may be restricted to 3-4 cycles in patients with limited stages of the disease when followed by involved field radiotherapy.	Prednisone	107-117	DNA damage inducible transcript 3	Homo sapiens	119-123
8523055-3	1995	The study was designed to determine the maximum-tolerated dosages (MTD) of cyclophosphamide and doxorubicin that could be used in a high-dose cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) regimen with granulocyte colony-stimulating factor (G-CSF) support and to assess preliminarily the efficacy of the regimen.	Doxorubicin	96-107	DNA damage inducible transcript 3	Homo sapiens	202-206
7595704-13	1995	Treatment with CHOP (doxorubicin) results in better CR and survival rates than CNOP (mitoxantrone).	Doxorubicin	21-32	DNA damage inducible transcript 3	Homo sapiens	15-19
7645021-9	1995	A cellular stress response, characterized by an increase in mRNA levels of the two stress response genes, HSP70 and gadd 153, was evident in glutathione-depleted unstimulated cells.	Glutathione	141-152	DNA damage inducible transcript 3	Homo sapiens	116-124
7563607-9	1995	After therapy with plasmapheresis and the CHOP regimen, he was given etoposide.	Etoposide	69-78	DNA damage inducible transcript 3	Homo sapiens	42-46
7813278-1	1995	A 53-year-old granulocytopenic woman with malignant lymphoma treated with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) chemotherapy, including doxorubicin (Adriamycin) and autologues bone marrow transplantation, presented in the clinical state of "refractory septic shock" caused by Escherichia coli.	Prednisone	122-132	DNA damage inducible transcript 3	Homo sapiens	134-138
7590500-1	1995	BACKGROUND: The purpose of our cooperative trial was to investigate whether epirubicin (EPI) at 90 mg/m2 in a CHOP-like combination (called CEOP) could increase complete response (CR) and survival rates in non-Hodgkin lymphoma (NHL) patients while maintaining a tolerable degree of toxicity.	Epirubicin	76-86	DNA damage inducible transcript 3	Homo sapiens	110-114
7898521-5	1995	METHODS: To investigate whether patients with slow responses, defined as only a partial response after three courses of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), would benefit from early transplantation, we conducted a prospective, randomized trial.	Doxorubicin	138-149	DNA damage inducible transcript 3	Homo sapiens	180-184
7898521-5	1995	METHODS: To investigate whether patients with slow responses, defined as only a partial response after three courses of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP), would benefit from early transplantation, we conducted a prospective, randomized trial.	Prednisone	168-178	DNA damage inducible transcript 3	Homo sapiens	180-184
7796361-6	1995	All patients were treated with cyclophosphamide, doxorubicin, vincristine and prednisolone (CHOP) and adjuvant radiotherapy.	Prednisolone	78-90	DNA damage inducible transcript 3	Homo sapiens	92-96
8058339-0	1994	Rare variant (Glu to Lys) in the leucine zipper region of CHOP (GADD153).	Glutamic Acid	14-17	DNA damage inducible transcript 3	Homo sapiens	58-62
7655111-2	1995	Their gene products encode proteins involved in the regulation of cell growth (proto-oncogenes c-myc and c-fos), a gene inducible by growth arrest and DNA damage (GADD153), the cytokine interleukin (IL) 1 alpha and beta and finally a differentiation-associated small proline-rich gene (SPR2).	Proline	267-274	DNA damage inducible transcript 3	Homo sapiens	163-170
7987849-9	1994	As a consequence the normally nontranslated exon 2 is translated and in both types there is in the junction between FUS and CHOP a shift from a FUS glycine codon to a valine codon in the chimeric mRNA.	Glycine	148-155	DNA damage inducible transcript 3	Homo sapiens	124-128
7987849-9	1994	As a consequence the normally nontranslated exon 2 is translated and in both types there is in the junction between FUS and CHOP a shift from a FUS glycine codon to a valine codon in the chimeric mRNA.	Valine	167-173	DNA damage inducible transcript 3	Homo sapiens	124-128
7981060-0	1994	Induction of the growth arrest and DNA damage-inducible gene GADD153 by cisplatin in vitro and in vivo.	Cisplatin	72-81	DNA damage inducible transcript 3	Homo sapiens	61-68
7530823-0	1994	[CHOP-Bleo therapy in high-malignancy non-Hodgkin lymphoma].	Bleomycin	6-10	DNA damage inducible transcript 3	Homo sapiens	1-5
7521788-8	1994	The safety of increasing the dose of cyclophosphamide during biweekly CHOP then was tested.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	70-74
7521788-18	1994	CONCLUSIONS: The dose of cyclophosphamide in biweekly CHOP can be increased up to 1500 mg/m2 with no increase in the incidence of treatment-related early mortalities without any organ damage in younger patients.	Cyclophosphamide	25-41	DNA damage inducible transcript 3	Homo sapiens	54-58
7521788-19	1994	The efficacy of this dose intensification of CHOP currently is being investigated in a multicenter prospective randomized trial using three different dose levels of cyclophosphamide.	Cyclophosphamide	165-181	DNA damage inducible transcript 3	Homo sapiens	45-49
7936304-1	1994	The activity of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) in the treatment of primary central nervous system lymphoma (PCNSL) prior to radiotherapy was studied in six patients.	Prednisone	64-74	DNA damage inducible transcript 3	Homo sapiens	76-80
8058339-0	1994	Rare variant (Glu to Lys) in the leucine zipper region of CHOP (GADD153).	Glutamic Acid	14-17	DNA damage inducible transcript 3	Homo sapiens	64-71
8058339-0	1994	Rare variant (Glu to Lys) in the leucine zipper region of CHOP (GADD153).	Lysine	21-24	DNA damage inducible transcript 3	Homo sapiens	58-62
8058339-0	1994	Rare variant (Glu to Lys) in the leucine zipper region of CHOP (GADD153).	Lysine	21-24	DNA damage inducible transcript 3	Homo sapiens	64-71
8058339-3	1994	This alteration, though not responsible for the Li-Fraumeni phenotype, resulted in a glutamic acid to lysine switch within the leucine zipper domain, at a residue conserved between CHOP and its potential target molecules and between the human and hamster sequences.	Glutamic Acid	85-98	DNA damage inducible transcript 3	Homo sapiens	181-185
8058339-3	1994	This alteration, though not responsible for the Li-Fraumeni phenotype, resulted in a glutamic acid to lysine switch within the leucine zipper domain, at a residue conserved between CHOP and its potential target molecules and between the human and hamster sequences.	Lysine	102-108	DNA damage inducible transcript 3	Homo sapiens	181-185
8168107-2	1994	Unlike GADD45, the response of other DNA damage-inducible genes to IR is not dependent on p53 based on the observation that induction in a panel of cell lines did not correlate with a normal p53 status; this included human GADD153, another member of the gadd (growth arrest and DNA damage inducible) group; MyD118, a gene related to GADD45; and the protooncogenes c-jun and c-fos.	gadd	254-258	DNA damage inducible transcript 3	Homo sapiens	223-230
8076711-3	1994	In this study, the effect of L-arginine supplementation on natural cytotoxicity was determined in patients with breast cancer receiving CHOP chemotherapy.	Arginine	29-39	DNA damage inducible transcript 3	Homo sapiens	136-140
8076711-5	1994	Those patients receiving L-arginine supplementation (30 g/day for 3 days prior to each course of chemotherapy) had a smaller and delayed onset of immunosuppression (day 14), compared with those patients who had CHOP only (day 9).	Arginine	25-35	DNA damage inducible transcript 3	Homo sapiens	211-215
8076711-6	1994	L-Arginine was able to repeatedly stimulate NK and LAK cell cytotoxicity in patients who were receiving CHOP chemotherapy (P &lt; 0.003).	Arginine	0-10	DNA damage inducible transcript 3	Homo sapiens	104-108
7680764-1	1993	BACKGROUND: CHOP is a first-generation, combination-chemotherapy regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone that has cured approximately 30 percent of patients with advanced stages of intermediate-grade or high-grade non-Hodgkin"s lymphoma in national cooperative-group trials.	Cyclophosphamide	87-103	DNA damage inducible transcript 3	Homo sapiens	12-16
8239684-2	1993	CHOP therapy consisted of CPA 650 mg/m2, ADM 45 mg/m2, VCR 1.4 mg/m2 and Pred 40 mg/m2 (po).	prednylidene	73-77	DNA damage inducible transcript 3	Homo sapiens	0-4
8369658-11	1993	Our successful treatment is radiation therapy combined with six courses of CHOP chemotherapy (cyclophosphamide, adriamycin, vincristine, prednisolone).	Cyclophosphamide	94-110	DNA damage inducible transcript 3	Homo sapiens	75-79
8369658-11	1993	Our successful treatment is radiation therapy combined with six courses of CHOP chemotherapy (cyclophosphamide, adriamycin, vincristine, prednisolone).	Doxorubicin	112-122	DNA damage inducible transcript 3	Homo sapiens	75-79
8369658-11	1993	Our successful treatment is radiation therapy combined with six courses of CHOP chemotherapy (cyclophosphamide, adriamycin, vincristine, prednisolone).	Vincristine	124-135	DNA damage inducible transcript 3	Homo sapiens	75-79
8369658-11	1993	Our successful treatment is radiation therapy combined with six courses of CHOP chemotherapy (cyclophosphamide, adriamycin, vincristine, prednisolone).	Prednisolone	137-149	DNA damage inducible transcript 3	Homo sapiens	75-79
8236992-1	1993	In a group of 30 patients with the diagnosis of malignant non-Hodgkin lymphoma of high histological malignancy, a prospective randomized study was carried out concerning the effectiveness and toxicity of the CHOP chemotherapy using adriamycin vs epirubicin.	Doxorubicin	232-242	DNA damage inducible transcript 3	Homo sapiens	208-212
17977418-2	1994	In our series of patients and therapeutical conditions the CHOP protocol proves somewhat superior to the second and third generation protocols: persentige of complete remission (CR) was high (64%), mean duration of CR was among longes (12 months), while neither cases of relapse during the monitoring of patients were noted not toxic effects of therapy.	Chromium	178-180	DNA damage inducible transcript 3	Homo sapiens	59-63
17977418-2	1994	In our series of patients and therapeutical conditions the CHOP protocol proves somewhat superior to the second and third generation protocols: persentige of complete remission (CR) was high (64%), mean duration of CR was among longes (12 months), while neither cases of relapse during the monitoring of patients were noted not toxic effects of therapy.	Chromium	215-217	DNA damage inducible transcript 3	Homo sapiens	59-63
7703552-3	1994	The treatment consisted of a chemotherapy with cyclophosphamide, adriamycine, vincristine and prednisone (CHOP regimen).	Prednisone	94-104	DNA damage inducible transcript 3	Homo sapiens	106-110
8038494-13	1993	In a previous randomized trial, the French Co-operative Group on CLL showed a beneficial role for low-dose adriamycin given with cyclophosphamide, vincristine and prednisone (mini-CHOP) in patients with stage C disease.	Doxorubicin	107-117	DNA damage inducible transcript 3	Homo sapiens	180-184
8038494-13	1993	In a previous randomized trial, the French Co-operative Group on CLL showed a beneficial role for low-dose adriamycin given with cyclophosphamide, vincristine and prednisone (mini-CHOP) in patients with stage C disease.	Cyclophosphamide	129-145	DNA damage inducible transcript 3	Homo sapiens	180-184
8038494-13	1993	In a previous randomized trial, the French Co-operative Group on CLL showed a beneficial role for low-dose adriamycin given with cyclophosphamide, vincristine and prednisone (mini-CHOP) in patients with stage C disease.	Vincristine	147-158	DNA damage inducible transcript 3	Homo sapiens	180-184
8038494-13	1993	In a previous randomized trial, the French Co-operative Group on CLL showed a beneficial role for low-dose adriamycin given with cyclophosphamide, vincristine and prednisone (mini-CHOP) in patients with stage C disease.	Prednisone	163-173	DNA damage inducible transcript 3	Homo sapiens	180-184
8285167-9	1993	After systemic chemotherapy of cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) regimen, renal function improved and the tumor of stomach reduced, but his respiratory condition rapidly worsened, and he died about 1 month after chemotherapy.	Cyclophosphamide	31-47	DNA damage inducible transcript 3	Homo sapiens	86-90
8285167-9	1993	After systemic chemotherapy of cyclophosphamide, adriamycin, vincristine, prednisone (CHOP) regimen, renal function improved and the tumor of stomach reduced, but his respiratory condition rapidly worsened, and he died about 1 month after chemotherapy.	Prednisone	74-84	DNA damage inducible transcript 3	Homo sapiens	86-90
8336711-3	1993	Here we examined the role of glucose in regulating gadd153 expression.	Glucose	29-36	DNA damage inducible transcript 3	Homo sapiens	51-58
8336711-9	1993	Frequent addition of fresh medium to the cells during the differentiation process, as well as supplementation of medium with glucose, reduced gadd153 expression without preventing C/EBP alpha expression or interfering with cellular differentiation.	Glucose	125-132	DNA damage inducible transcript 3	Homo sapiens	142-149
8336711-10	1993	Thus, gadd153 expression is not essential for the process of adipocyte differentiation but is significantly influenced by the availability of glucose to the cell.	Glucose	142-149	DNA damage inducible transcript 3	Homo sapiens	6-13
8469201-6	1993	TREATMENT AND OUTCOME: After initial response to CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisolone), she relapsed and died with central nervous system involvement eight months after the initial diagnosis.	Cyclophosphamide	68-84	DNA damage inducible transcript 3	Homo sapiens	49-53
8469201-6	1993	TREATMENT AND OUTCOME: After initial response to CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisolone), she relapsed and died with central nervous system involvement eight months after the initial diagnosis.	Doxorubicin	86-97	DNA damage inducible transcript 3	Homo sapiens	49-53
8469201-6	1993	TREATMENT AND OUTCOME: After initial response to CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, prednisolone), she relapsed and died with central nervous system involvement eight months after the initial diagnosis.	Prednisolone	112-124	DNA damage inducible transcript 3	Homo sapiens	49-53
7680764-1	1993	BACKGROUND: CHOP is a first-generation, combination-chemotherapy regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone that has cured approximately 30 percent of patients with advanced stages of intermediate-grade or high-grade non-Hodgkin"s lymphoma in national cooperative-group trials.	Doxorubicin	105-116	DNA damage inducible transcript 3	Homo sapiens	12-16
7680764-1	1993	BACKGROUND: CHOP is a first-generation, combination-chemotherapy regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone that has cured approximately 30 percent of patients with advanced stages of intermediate-grade or high-grade non-Hodgkin"s lymphoma in national cooperative-group trials.	Vincristine	118-129	DNA damage inducible transcript 3	Homo sapiens	12-16
7680764-1	1993	BACKGROUND: CHOP is a first-generation, combination-chemotherapy regimen consisting of cyclophosphamide, doxorubicin, vincristine, and prednisone that has cured approximately 30 percent of patients with advanced stages of intermediate-grade or high-grade non-Hodgkin"s lymphoma in national cooperative-group trials.	Prednisone	135-145	DNA damage inducible transcript 3	Homo sapiens	12-16
8431969-9	1993	A partial remission was observed in two of four patients with refractory Non-Hodgkin"s lymphoma who were treated with DFO, ISC, and doxorubicin as part of the CHOP regimen.	Deferoxamine	118-121	DNA damage inducible transcript 3	Homo sapiens	159-163
8426200-8	1993	CONCLUSION: Pelvic XRT and cumulative cyclophosphamide dosages greater than 9.5 g/m2 are associated with a high risk of permanent sterility in lymphoma patients treated with the CHOP-Bleo regimen.	Cyclophosphamide	38-54	DNA damage inducible transcript 3	Homo sapiens	178-182
8426200-8	1993	CONCLUSION: Pelvic XRT and cumulative cyclophosphamide dosages greater than 9.5 g/m2 are associated with a high risk of permanent sterility in lymphoma patients treated with the CHOP-Bleo regimen.	Bleomycin	183-187	DNA damage inducible transcript 3	Homo sapiens	178-182
1383819-8	1992	The median normalized dose intensity for both cyclophosphamide and doxorubicin was found to be greater in the patients treated with CHOP than in those treated with m-BACOD.	Cyclophosphamide	46-62	DNA damage inducible transcript 3	Homo sapiens	132-136
1453209-11	1992	CONCLUSION: ProMACE-MOPP salvage chemotherapy produces a high early-response rate in patients who fail to respond to first-line CHOP, and more than half of the responding patients can be scheduled to receive ABMT, resulting in disease-free survival (DFS) at 3 years in 50% of the transplanted patients and in 25% of the original number of patients intended to receive this treatment.	ProMACE-MOPP protocol	12-24	DNA damage inducible transcript 3	Homo sapiens	128-132
1383819-8	1992	The median normalized dose intensity for both cyclophosphamide and doxorubicin was found to be greater in the patients treated with CHOP than in those treated with m-BACOD.	Doxorubicin	67-78	DNA damage inducible transcript 3	Homo sapiens	132-136
1735464-0	1992	Cell growth inhibition by prostaglandin A2 results in elevated expression of gadd153 mRNA.	prostaglandin A2	26-42	DNA damage inducible transcript 3	Homo sapiens	77-84
1637948-6	1992	The slower [3H]ChoP generation may suggest that PC-specific phospholipase C activation as well as delayed [3H]GPC rise may be due to PC-specific phospholipase A2 and lysophospholipase activation.	Tritium	12-14	DNA damage inducible transcript 3	Homo sapiens	15-19
1637948-6	1992	The slower [3H]ChoP generation may suggest that PC-specific phospholipase C activation as well as delayed [3H]GPC rise may be due to PC-specific phospholipase A2 and lysophospholipase activation.	Tritium	107-109	DNA damage inducible transcript 3	Homo sapiens	15-19
1607914-2	1992	PATIENTS AND METHODS: Twenty-one patients received six monthly courses of cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) and maintenance chemotherapy for 12 months.	Prednisone	122-132	DNA damage inducible transcript 3	Homo sapiens	134-138
1630019-6	1992	The patient was treated with the CHOP regimen (doxorubicin, cyclophosphamide, vincristine and prednisolone), which achieved complete remission.	Doxorubicin	47-58	DNA damage inducible transcript 3	Homo sapiens	33-37
1630019-6	1992	The patient was treated with the CHOP regimen (doxorubicin, cyclophosphamide, vincristine and prednisolone), which achieved complete remission.	Cyclophosphamide	60-76	DNA damage inducible transcript 3	Homo sapiens	33-37
1630019-6	1992	The patient was treated with the CHOP regimen (doxorubicin, cyclophosphamide, vincristine and prednisolone), which achieved complete remission.	Vincristine	78-89	DNA damage inducible transcript 3	Homo sapiens	33-37
1630019-6	1992	The patient was treated with the CHOP regimen (doxorubicin, cyclophosphamide, vincristine and prednisolone), which achieved complete remission.	Prednisolone	94-106	DNA damage inducible transcript 3	Homo sapiens	33-37
1400365-0	1992	Calcium ionophore A23187 induces expression of the growth arrest and DNA damage inducible CCAAT/enhancer-binding protein (C/EBP)-related gene, gadd153.	Calcium	0-7	DNA damage inducible transcript 3	Homo sapiens	143-150
1400365-0	1992	Calcium ionophore A23187 induces expression of the growth arrest and DNA damage inducible CCAAT/enhancer-binding protein (C/EBP)-related gene, gadd153.	Calcimycin	18-24	DNA damage inducible transcript 3	Homo sapiens	143-150
1400365-4	1992	We have demonstrated that treatment of HeLa cells with the calcium ionophores A23187 and ionomycin leads to the induction of gadd153 mRNA.	Calcium	59-66	DNA damage inducible transcript 3	Homo sapiens	125-132
1400365-4	1992	We have demonstrated that treatment of HeLa cells with the calcium ionophores A23187 and ionomycin leads to the induction of gadd153 mRNA.	Calcimycin	78-84	DNA damage inducible transcript 3	Homo sapiens	125-132
1400365-4	1992	We have demonstrated that treatment of HeLa cells with the calcium ionophores A23187 and ionomycin leads to the induction of gadd153 mRNA.	Ionomycin	89-98	DNA damage inducible transcript 3	Homo sapiens	125-132
1400365-8	1992	Buffering intracellular and extracellular Ca2+ by combined treatment with BAPTA-AM (acetoxymethyl ester form of bis(aminophenoxy)ethane N,N"-tetraacetic acid) and EGTA prevented the induction of gadd153 mRNA by A23187.	1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester	74-82	DNA damage inducible transcript 3	Homo sapiens	195-202
1400365-8	1992	Buffering intracellular and extracellular Ca2+ by combined treatment with BAPTA-AM (acetoxymethyl ester form of bis(aminophenoxy)ethane N,N"-tetraacetic acid) and EGTA prevented the induction of gadd153 mRNA by A23187.	acetoxymethyl ester	84-103	DNA damage inducible transcript 3	Homo sapiens	195-202
1400365-8	1992	Buffering intracellular and extracellular Ca2+ by combined treatment with BAPTA-AM (acetoxymethyl ester form of bis(aminophenoxy)ethane N,N"-tetraacetic acid) and EGTA prevented the induction of gadd153 mRNA by A23187.	bis(aminophenoxy)ethane n,n"-tetraacetic acid	112-157	DNA damage inducible transcript 3	Homo sapiens	195-202
1400365-8	1992	Buffering intracellular and extracellular Ca2+ by combined treatment with BAPTA-AM (acetoxymethyl ester form of bis(aminophenoxy)ethane N,N"-tetraacetic acid) and EGTA prevented the induction of gadd153 mRNA by A23187.	Egtazic Acid	163-167	DNA damage inducible transcript 3	Homo sapiens	195-202
1400365-8	1992	Buffering intracellular and extracellular Ca2+ by combined treatment with BAPTA-AM (acetoxymethyl ester form of bis(aminophenoxy)ethane N,N"-tetraacetic acid) and EGTA prevented the induction of gadd153 mRNA by A23187.	Calcimycin	211-217	DNA damage inducible transcript 3	Homo sapiens	195-202
1400365-9	1992	In addition, these treatments prevented the induction of gadd153 mRNA in response to the DNA damaging agent methyl methanesulfonate.	Methyl Methanesulfonate	108-131	DNA damage inducible transcript 3	Homo sapiens	57-64
1434294-9	1992	Chemotherapy (CHOP-Bleo, or PPA) in both cases and additional radiotherapy in case 2 markedly reduced the tumor size.	Bleomycin	19-23	DNA damage inducible transcript 3	Homo sapiens	14-18
1735464-4	1992	PGA2 induction of gadd153 mRNA was completely prevented by the presence of actinomycin D at a concentration sufficient to block transcription and was partially inhibited (50%) by the protein synthesis inhibitor cycloheximide.	Dactinomycin	75-88	DNA damage inducible transcript 3	Homo sapiens	18-25
1735464-4	1992	PGA2 induction of gadd153 mRNA was completely prevented by the presence of actinomycin D at a concentration sufficient to block transcription and was partially inhibited (50%) by the protein synthesis inhibitor cycloheximide.	Cycloheximide	211-224	DNA damage inducible transcript 3	Homo sapiens	18-25
1735464-5	1992	The presence of the protein kinase inhibitor 2-aminopurine decreased the PGA2 induction of gadd153 mRNA by greater than 90%, suggesting that cellular kinases play a role in the induction of gadd153 by PGA2.	2-Aminopurine	45-58	DNA damage inducible transcript 3	Homo sapiens	91-98
1735464-5	1992	The presence of the protein kinase inhibitor 2-aminopurine decreased the PGA2 induction of gadd153 mRNA by greater than 90%, suggesting that cellular kinases play a role in the induction of gadd153 by PGA2.	2-Aminopurine	45-58	DNA damage inducible transcript 3	Homo sapiens	190-197
1735464-5	1992	The presence of the protein kinase inhibitor 2-aminopurine decreased the PGA2 induction of gadd153 mRNA by greater than 90%, suggesting that cellular kinases play a role in the induction of gadd153 by PGA2.	prostaglandin A2	73-77	DNA damage inducible transcript 3	Homo sapiens	91-98
1735464-5	1992	The presence of the protein kinase inhibitor 2-aminopurine decreased the PGA2 induction of gadd153 mRNA by greater than 90%, suggesting that cellular kinases play a role in the induction of gadd153 by PGA2.	prostaglandin A2	73-77	DNA damage inducible transcript 3	Homo sapiens	190-197
1735464-5	1992	The presence of the protein kinase inhibitor 2-aminopurine decreased the PGA2 induction of gadd153 mRNA by greater than 90%, suggesting that cellular kinases play a role in the induction of gadd153 by PGA2.	prostaglandin A2	201-205	DNA damage inducible transcript 3	Homo sapiens	91-98
1735464-5	1992	The presence of the protein kinase inhibitor 2-aminopurine decreased the PGA2 induction of gadd153 mRNA by greater than 90%, suggesting that cellular kinases play a role in the induction of gadd153 by PGA2.	prostaglandin A2	201-205	DNA damage inducible transcript 3	Homo sapiens	190-197
1735464-6	1992	Thus PGA2-mediated growth arrest provides a useful model to further define the role of gadd153 in the negative control of cell growth.	prostaglandin A2	5-9	DNA damage inducible transcript 3	Homo sapiens	87-94
1735464-1	1992	Treatment of Hela cells with prostaglandin A2 (PGA2) resulted in a marked inhibition of cell proliferation which was associated with a significant induction of gadd153 mRNA, a member of a novel class of genes associated with growth arrest and DNA damage.	prostaglandin A2	29-45	DNA damage inducible transcript 3	Homo sapiens	160-167
1735464-1	1992	Treatment of Hela cells with prostaglandin A2 (PGA2) resulted in a marked inhibition of cell proliferation which was associated with a significant induction of gadd153 mRNA, a member of a novel class of genes associated with growth arrest and DNA damage.	prostaglandin A2	47-51	DNA damage inducible transcript 3	Homo sapiens	160-167
1735464-2	1992	Induction of gadd153 mRNA was specific to prostaglandins capable of arresting cell growth and was dose-dependent with the maximum effect seen at 36 microM PGA2.	Prostaglandins	42-56	DNA damage inducible transcript 3	Homo sapiens	13-20
1735464-2	1992	Induction of gadd153 mRNA was specific to prostaglandins capable of arresting cell growth and was dose-dependent with the maximum effect seen at 36 microM PGA2.	prostaglandin A2	155-159	DNA damage inducible transcript 3	Homo sapiens	13-20
1735464-3	1992	Induction was rapid, occurring within 2-4 h and reaching a maximum by 8 h. These effects were reversible as removal of PGA2 resulted in a rapid decline in gadd153 mRNA levels coincident with resumption of cell growth.	prostaglandin A2	119-123	DNA damage inducible transcript 3	Homo sapiens	155-162
1735464-4	1992	PGA2 induction of gadd153 mRNA was completely prevented by the presence of actinomycin D at a concentration sufficient to block transcription and was partially inhibited (50%) by the protein synthesis inhibitor cycloheximide.	prostaglandin A2	0-4	DNA damage inducible transcript 3	Homo sapiens	18-25
2029186-1	1991	We studied retrospectively the influence on the prognosis of patients with localized non-Hodgkin"s lymphoma of extranodal type with regard to the duration of an anthracycline-based combination chemotherapy-modified CHOP regimen.	Anthracyclines	161-174	DNA damage inducible transcript 3	Homo sapiens	215-219
1727386-12	1992	However, the methyl methanesulfonate-induced gadd153 promoter activities were similar in both cell lines.	Methyl Methanesulfonate	13-36	DNA damage inducible transcript 3	Homo sapiens	45-52
1533370-3	1992	Complete remission was achieved by combined cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) chemotherapy and radiotherapy of the heart and mediastinum.	Prednisone	91-101	DNA damage inducible transcript 3	Homo sapiens	103-107
2014946-6	1991	INTERVENTION: Treatment was given according to Ann Arbor stage: Patients in stage IV were treated with CHOP-bleomycin and maintained on interferon therapy; those in stage III received CHOP-bleomycin and radiotherapy; and those in stages I and II received COP-bleomycin and radiotherapy.	Bleomycin	108-117	DNA damage inducible transcript 3	Homo sapiens	103-107
2014946-6	1991	INTERVENTION: Treatment was given according to Ann Arbor stage: Patients in stage IV were treated with CHOP-bleomycin and maintained on interferon therapy; those in stage III received CHOP-bleomycin and radiotherapy; and those in stages I and II received COP-bleomycin and radiotherapy.	Bleomycin	189-198	DNA damage inducible transcript 3	Homo sapiens	184-188
2014946-6	1991	INTERVENTION: Treatment was given according to Ann Arbor stage: Patients in stage IV were treated with CHOP-bleomycin and maintained on interferon therapy; those in stage III received CHOP-bleomycin and radiotherapy; and those in stages I and II received COP-bleomycin and radiotherapy.	Bleomycin	189-198	DNA damage inducible transcript 3	Homo sapiens	184-188
27463485-9	1991	It demonstrated that the polychemotherapy CHOP, i.e. COP + doxorubicin improved these patients (n = 34) as compared with those treated with COP (n = 36), in terms of disease remission as well as survival.	Doxorubicin	59-70	DNA damage inducible transcript 3	Homo sapiens	42-46
2016618-8	1991	These results are comparable to those reported with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy by other investigators.	Prednisone	100-110	DNA damage inducible transcript 3	Homo sapiens	112-116
2246824-6	1990	After chemotherapy using adriamycin, cyclophosphamide, vincristine, and prednisolone (CHOP), lymphadenopathy and splenomegaly reduced and lymphoid blasts disappeared from the blood and bone marrow.	Doxorubicin	25-35	DNA damage inducible transcript 3	Homo sapiens	86-90
1708910-0	1990	[CHOP-bleo versus m-BACOD in the treatment of intermediate and high-grade malignant lymphomas].	Bleomycin	6-10	DNA damage inducible transcript 3	Homo sapiens	1-5
1704933-1	1990	We assessed the response of various tumors, following each of three consecutive courses of CHOP or CHOP-Bleo therapy in 32 untreated patients with intermediate or high-grade non-Hodgkin"s lymphoma (NHL), and also retrospectively compared these results to those for a group in whom complete remission (CR) had been obtained within five courses and a non-CR group.	Bleomycin	104-108	DNA damage inducible transcript 3	Homo sapiens	99-103
2246824-6	1990	After chemotherapy using adriamycin, cyclophosphamide, vincristine, and prednisolone (CHOP), lymphadenopathy and splenomegaly reduced and lymphoid blasts disappeared from the blood and bone marrow.	Cyclophosphamide	37-53	DNA damage inducible transcript 3	Homo sapiens	86-90
2246824-6	1990	After chemotherapy using adriamycin, cyclophosphamide, vincristine, and prednisolone (CHOP), lymphadenopathy and splenomegaly reduced and lymphoid blasts disappeared from the blood and bone marrow.	Prednisolone	72-84	DNA damage inducible transcript 3	Homo sapiens	86-90
2361941-10	1990	A region of homology with the cytochrome P-450s from various organisms was identified in the choP protein and may represent a region associated with a binding site for heme iron.	Heme	168-172	DNA damage inducible transcript 3	Homo sapiens	93-97
1703327-10	1990	It was concluded that the alternate chemotherapy regimen CHOP-Bleo/CMED shows similar effects than the classical CHOP-Bleo treatment, and provides a lesser amount of adriamycin, which makes it feasible to use this or other anthracycline drugs in case of relapse; the use of this regimen must be borne in mind when the patient is carrying a myocardiopathy.	Bleomycin	62-66	DNA damage inducible transcript 3	Homo sapiens	57-61
1703327-10	1990	It was concluded that the alternate chemotherapy regimen CHOP-Bleo/CMED shows similar effects than the classical CHOP-Bleo treatment, and provides a lesser amount of adriamycin, which makes it feasible to use this or other anthracycline drugs in case of relapse; the use of this regimen must be borne in mind when the patient is carrying a myocardiopathy.	Doxorubicin	166-176	DNA damage inducible transcript 3	Homo sapiens	57-61
1703327-10	1990	It was concluded that the alternate chemotherapy regimen CHOP-Bleo/CMED shows similar effects than the classical CHOP-Bleo treatment, and provides a lesser amount of adriamycin, which makes it feasible to use this or other anthracycline drugs in case of relapse; the use of this regimen must be borne in mind when the patient is carrying a myocardiopathy.	Anthracyclines	223-236	DNA damage inducible transcript 3	Homo sapiens	57-61
2361941-10	1990	A region of homology with the cytochrome P-450s from various organisms was identified in the choP protein and may represent a region associated with a binding site for heme iron.	Iron	173-177	DNA damage inducible transcript 3	Homo sapiens	93-97
1699008-5	1990	The four patients with recurrent disease after CHOP therapy exhibited a CR ratio of 50% indicating that therapy is effective in recurrent cases.	Chromium	72-74	DNA damage inducible transcript 3	Homo sapiens	47-51
2190676-0	1990	Vincristine infusion with CHOP-CCNU in diffuse large-cell lymphoma.	Vincristine	0-11	DNA damage inducible transcript 3	Homo sapiens	26-30
2182600-7	1990	In one large randomized study, the response rate as well as survival superiority of CHOP (with low-dose Adriamycin) over COP in previously untreated patients with stage C disease was observed.	Doxorubicin	104-114	DNA damage inducible transcript 3	Homo sapiens	84-88
2182600-8	1990	In another large randomized study, only a response rate advantage of CHOP (with standard dose Adriamycin) over chlorambucil and prednisone (in previously untreated patients with stages B and C) was seen.	Doxorubicin	94-104	DNA damage inducible transcript 3	Homo sapiens	69-73
2317752-4	1990	Continuous CHOP protocol consists of initial 8 weeks of intensive chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone, followed by local/cranial radiotherapy and maintenance therapy.	Cyclophosphamide	84-100	DNA damage inducible transcript 3	Homo sapiens	11-15
2317752-4	1990	Continuous CHOP protocol consists of initial 8 weeks of intensive chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone, followed by local/cranial radiotherapy and maintenance therapy.	Doxorubicin	102-113	DNA damage inducible transcript 3	Homo sapiens	11-15
2317752-4	1990	Continuous CHOP protocol consists of initial 8 weeks of intensive chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone, followed by local/cranial radiotherapy and maintenance therapy.	Vincristine	115-126	DNA damage inducible transcript 3	Homo sapiens	11-15
2317752-4	1990	Continuous CHOP protocol consists of initial 8 weeks of intensive chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisolone, followed by local/cranial radiotherapy and maintenance therapy.	Prednisolone	132-144	DNA damage inducible transcript 3	Homo sapiens	11-15
2190676-3	1990	Repeated 5-day infusions of vincristine 0.25 mg/m2 per day were incorporated into a CHOP-CCNU regimen and administered to 24 patients with advanced diffuse large-cell lymphoma.	Vincristine	28-39	DNA damage inducible transcript 3	Homo sapiens	84-88
2190676-9	1990	Infusion of vincristine may be safely incorporated into multiagent chemotherapy programs of the CHOP type for non-Hodgkin"s lymphoma.	Vincristine	12-23	DNA damage inducible transcript 3	Homo sapiens	96-100
30091025-1	2018	The standard treatment for diffuse large B cell lymphoma (DLBCL) is rituximab with CHOP (cyclophosphamide, doxorubicin, vincristine (VCR), and prednisone).	Cyclophosphamide	89-105	DNA damage inducible transcript 3	Homo sapiens	83-87
33944646-5	2021	The main focus of this study was on newly diagnosed patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) versus other chemotherapy.	Prednisone	119-129	DNA damage inducible transcript 3	Homo sapiens	131-135
33793375-3	2021	In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status.	Mesalamine	129-139	DNA damage inducible transcript 3	Homo sapiens	60-64
33793375-3	2021	In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status.	Mesalamine	129-139	DNA damage inducible transcript 3	Homo sapiens	66-71
33793375-3	2021	In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status.	Mesalamine	141-146	DNA damage inducible transcript 3	Homo sapiens	60-64
33793375-3	2021	In HLA-B27 + or - patients the ER stress-associated markers CHOP (DDIT3) and ATF6 were suppressed.Conclusions: Here we show that mesalazine (5-ASA) inhibits the transcription of proinflammatory and (ER) stress associated cytokines and markers, independently of the HLA-B27 status.	Mesalamine	141-146	DNA damage inducible transcript 3	Homo sapiens	66-71
33591324-1	2021	Rituximab plus cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) is the standard of care for untreated diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	15-31	DNA damage inducible transcript 3	Homo sapiens	70-74
33591324-1	2021	Rituximab plus cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) is the standard of care for untreated diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	32-43	DNA damage inducible transcript 3	Homo sapiens	70-74
33591324-1	2021	Rituximab plus cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) is the standard of care for untreated diffuse large B-cell lymphoma (DLBCL).	vincristine-prednisone	44-66	DNA damage inducible transcript 3	Homo sapiens	70-74
33233444-6	2020	We have previously demonstrated that the induction of hepatic CYP2B6 by CITCO, a selective human CAR (hCAR) agonist, results in CHOP"s enhanced antineoplastic effects in vitro.	6-(4-chlorophenyl)imidazo(2,1-b)(1,3)thiazole-5-carbaldehyde O-(3,4-dichlorobenzyl)oxime	72-77	DNA damage inducible transcript 3	Homo sapiens	128-132
33817185-4	2019	Results: The ER stress caused by thapsigargin strongly up-regulated the expression of GRP78 and CHOP in HT29 cells, which activated the PERK-eIF2a pathway.	Thapsigargin	33-45	DNA damage inducible transcript 3	Homo sapiens	96-100
33817185-7	2019	Importantly, Astragalus polysaccharide significantly inhibited the phosphorylation of PERK and eIF2a, which reduced the mRNA levels of GRP78, CHOP, PERK and eIF2a, and inhibited the ER expansion in HT29 cells after 24 hours of treatment.	2-(chloromethyl)-4-(4-nitrophenyl)-1,3-thiazole	13-38	DNA damage inducible transcript 3	Homo sapiens	142-146
33817185-8	2019	Conclusion: The results indicate that APS reduces the expression of GRP78 and CHOP in HT29 cells, at least in part, by preventing the activation of the PERK-eIF2a signaling pathway.	aps	38-41	DNA damage inducible transcript 3	Homo sapiens	78-82
33944646-5	2021	The main focus of this study was on newly diagnosed patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) versus other chemotherapy.	Cyclophosphamide	71-87	DNA damage inducible transcript 3	Homo sapiens	131-135
33944646-5	2021	The main focus of this study was on newly diagnosed patients receiving cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) versus other chemotherapy.	Doxorubicin	89-100	DNA damage inducible transcript 3	Homo sapiens	131-135
33788639-6	2021	ECs pre-treated with different concentrations RA and co-cultured with thapsigargin-induced ER stressed pancreatic beta-cells showed increased levels of Nrf2 and its downstream targets such as heme oxygenase-1 (HO-1) and NADPH-quinone oxidoreductase-1 (NQO-1), and reduction of ER stress evinced by the decreased levels of glucose-regulated protein (GRP) 78 and C/ERB homologous protein (CHOP).	Thapsigargin	70-82	DNA damage inducible transcript 3	Homo sapiens	361-385
33788639-6	2021	ECs pre-treated with different concentrations RA and co-cultured with thapsigargin-induced ER stressed pancreatic beta-cells showed increased levels of Nrf2 and its downstream targets such as heme oxygenase-1 (HO-1) and NADPH-quinone oxidoreductase-1 (NQO-1), and reduction of ER stress evinced by the decreased levels of glucose-regulated protein (GRP) 78 and C/ERB homologous protein (CHOP).	Thapsigargin	70-82	DNA damage inducible transcript 3	Homo sapiens	387-391
33233444-4	2020	CPA, an integral component of CHOP, is a prodrug that requires CYP2B6-mediated bioactivation to 4-hydroxy-CPA (4-OH-CPA).	Cyclophosphamide	0-3	DNA damage inducible transcript 3	Homo sapiens	30-34
33233444-4	2020	CPA, an integral component of CHOP, is a prodrug that requires CYP2B6-mediated bioactivation to 4-hydroxy-CPA (4-OH-CPA).	4-hydroxycyclophosphamide	96-109	DNA damage inducible transcript 3	Homo sapiens	30-34
33233444-4	2020	CPA, an integral component of CHOP, is a prodrug that requires CYP2B6-mediated bioactivation to 4-hydroxy-CPA (4-OH-CPA).	4-oh-cpa	111-119	DNA damage inducible transcript 3	Homo sapiens	30-34
34851173-3	2022	Results: Fifty-five clinical studies were included, mostly investigating cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) or "CHOP-like" regimens, with combination regimens showing similar effectiveness to CHOP alone.	Prednisone	120-130	DNA damage inducible transcript 3	Homo sapiens	132-136
34977370-5	2022	The results showed that BFA treatment led to enhanced apoptosis and upregulation of proteins involved in ER stress signaling, including inositol-requiring enzyme 1alpha (IRE1alpha), activating transcription factor 6alpha (ATF6alpha), c-Jun N-terminal kinase (JNK), and C/EBP-homologous protein (CHOP).	Brefeldin A	24-27	DNA damage inducible transcript 3	Homo sapiens	269-293
34977370-5	2022	The results showed that BFA treatment led to enhanced apoptosis and upregulation of proteins involved in ER stress signaling, including inositol-requiring enzyme 1alpha (IRE1alpha), activating transcription factor 6alpha (ATF6alpha), c-Jun N-terminal kinase (JNK), and C/EBP-homologous protein (CHOP).	Brefeldin A	24-27	DNA damage inducible transcript 3	Homo sapiens	295-299
34627914-1	2022	Cold heavy oil production with or without sand (CHOPS, or CHOP) are prevalent methods of oil extraction in western Canada.	Oils	89-92	DNA damage inducible transcript 3	Homo sapiens	58-62
34627914-2	2022	CHOP(S) sites account for over 40% of all reported vented methane (CH4) from oil production in Alberta, and high rates of CH4 emissions have been confirmed in independent measurement studies.	Methane	58-65	DNA damage inducible transcript 3	Homo sapiens	0-4
34627914-2	2022	CHOP(S) sites account for over 40% of all reported vented methane (CH4) from oil production in Alberta, and high rates of CH4 emissions have been confirmed in independent measurement studies.	Methane	67-70	DNA damage inducible transcript 3	Homo sapiens	0-4
34627914-2	2022	CHOP(S) sites account for over 40% of all reported vented methane (CH4) from oil production in Alberta, and high rates of CH4 emissions have been confirmed in independent measurement studies.	Oils	77-80	DNA damage inducible transcript 3	Homo sapiens	0-4
34627914-2	2022	CHOP(S) sites account for over 40% of all reported vented methane (CH4) from oil production in Alberta, and high rates of CH4 emissions have been confirmed in independent measurement studies.	Methane	122-125	DNA damage inducible transcript 3	Homo sapiens	0-4
34627914-3	2022	In this study, we used truck-based surveys coupled with qualitative optical gas imaging (OGI) to quantify and characterize methane emission rates and sources at nearly 1350 and 940 well sites in two major CHOP(S) developments respectively in 2016 and 2018.	Methane	123-130	DNA damage inducible transcript 3	Homo sapiens	205-209
34563904-8	2022	The relative abundance of CHO, CHON, CHOS, CHOP and condensed hydrocarbons in PtNM-NOM corona increased with their increase in NOM isolates.	ptnm	78-82	DNA damage inducible transcript 3	Homo sapiens	43-47
34954323-6	2022	Bleomycin and tunicamycin combination models in vivo and in vitro showed that CHOP downregulation rescued alveolar epithelial cell senescence, reduced fibroblast activation mediated by the senescence-associated secretory phenotype, and improved pulmonary fibrosis pathology.	Bleomycin	0-9	DNA damage inducible transcript 3	Homo sapiens	78-82
34954323-6	2022	Bleomycin and tunicamycin combination models in vivo and in vitro showed that CHOP downregulation rescued alveolar epithelial cell senescence, reduced fibroblast activation mediated by the senescence-associated secretory phenotype, and improved pulmonary fibrosis pathology.	Tunicamycin	14-25	DNA damage inducible transcript 3	Homo sapiens	78-82
34954323-7	2022	Mechanistic studies showed that CHOP accelerated alveolar epithelial cell senescence by promoting reactive oxygen species generation, which activated the nuclear factor-kappa B pathway.	Oxygen	107-113	DNA damage inducible transcript 3	Homo sapiens	32-36
34904799-1	2022	BACKGROUND: Diffuse large B-cell lymphoma (DLBCL) is typically treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	135-145	DNA damage inducible transcript 3	Homo sapiens	149-153
34864562-0	2022	Protegrin-1 inhibits porcine ovarian granulosa cell apoptosis from H2O2-induced oxidative stress via the PERK/eIF2alpha/CHOP signaling pathway in vitro.	Hydrogen Peroxide	67-71	DNA damage inducible transcript 3	Homo sapiens	120-124
34864562-8	2022	Using Western blot analysis, it was found that PG-1 decreased the phosphorylation of RNA-like endoplasmic reticulum kinase (PERK) and the alpha-subunit of eukaryotic initiation factor 2 (eIF2alpha) as well as the protein expression level of CCAAT enhancer-binding protein homologous protein (CHOP), all of which were increased by H2O2.	Hydrogen Peroxide	330-334	DNA damage inducible transcript 3	Homo sapiens	241-290
34864562-8	2022	Using Western blot analysis, it was found that PG-1 decreased the phosphorylation of RNA-like endoplasmic reticulum kinase (PERK) and the alpha-subunit of eukaryotic initiation factor 2 (eIF2alpha) as well as the protein expression level of CCAAT enhancer-binding protein homologous protein (CHOP), all of which were increased by H2O2.	Hydrogen Peroxide	330-334	DNA damage inducible transcript 3	Homo sapiens	292-296
34775235-4	2022	Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml).	da-9805	19-26	DNA damage inducible transcript 3	Homo sapiens	103-127
34843406-2	2022	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy is widely used as first-line treatment of PTCL; however, it has limited efficacy.	Cyclophosphamide	0-16	DNA damage inducible transcript 3	Homo sapiens	60-64
34843406-2	2022	Cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) therapy is widely used as first-line treatment of PTCL; however, it has limited efficacy.	Prednisone	48-58	DNA damage inducible transcript 3	Homo sapiens	60-64
34775235-4	2022	Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml).	da-9805	19-26	DNA damage inducible transcript 3	Homo sapiens	129-133
34775235-4	2022	Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml).	Thapsigargin	201-213	DNA damage inducible transcript 3	Homo sapiens	103-127
34775235-4	2022	Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml).	Thapsigargin	201-213	DNA damage inducible transcript 3	Homo sapiens	129-133
34775235-4	2022	Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml).	Tunicamycin	231-242	DNA damage inducible transcript 3	Homo sapiens	103-127
34775235-4	2022	Pre-treatment with DA-9805 (1 mug/ml) attenuated upregulation of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and cleaved caspase-3 in SH-SY5Y neuroblastoma cells treated with thapsigargin (1 microg/ml) or tunicamycin (2 microg/ml).	Tunicamycin	231-242	DNA damage inducible transcript 3	Homo sapiens	129-133
34990525-1	2021	Purpose: Febrile neutropenia (FN) can cause suboptimal treatment and treatment-related mortality (TRM) in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP).	Cyclophosphamide	177-193	DNA damage inducible transcript 3	Homo sapiens	241-245
34414850-0	2022	Ibrutinib- and bortezomib-extended R-CHOP induction in elderly higher-risk patients newly diagnosed with diffuse large B-cell lymphoma - first analysis of toxicity and efficacy signals.	Bortezomib	15-25	DNA damage inducible transcript 3	Homo sapiens	37-41
34808100-19	2022	EVO exposure induced endoplasmic reticulum (ER) stress demonstrated by the activation of PERK/CHOP in cells exposed to EVO, and PERK/CHOP activation was depleted by EUK134 pre-treatment.	evodiamine	0-3	DNA damage inducible transcript 3	Homo sapiens	94-98
34808100-19	2022	EVO exposure induced endoplasmic reticulum (ER) stress demonstrated by the activation of PERK/CHOP in cells exposed to EVO, and PERK/CHOP activation was depleted by EUK134 pre-treatment.	evodiamine	0-3	DNA damage inducible transcript 3	Homo sapiens	133-137
34808100-19	2022	EVO exposure induced endoplasmic reticulum (ER) stress demonstrated by the activation of PERK/CHOP in cells exposed to EVO, and PERK/CHOP activation was depleted by EUK134 pre-treatment.	evodiamine	119-122	DNA damage inducible transcript 3	Homo sapiens	94-98
34990523-2	2021	We investigated the predictive factors affecting CIN and FN incidence in patients with DLBCL receiving rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy with pegfilgrastim and conducted experiments to find reason for the occurrence of CIN even when pegfilgrastim was used.	Prednisone	162-172	DNA damage inducible transcript 3	Homo sapiens	176-180
34969327-7	2021	Our study suggests that targeting cholesterol-using lovastatin could be a therapeutic strategy to enhance responses to R-CHOP in DLBCL patients.	Cholesterol	34-45	DNA damage inducible transcript 3	Homo sapiens	121-125
34969327-7	2021	Our study suggests that targeting cholesterol-using lovastatin could be a therapeutic strategy to enhance responses to R-CHOP in DLBCL patients.	Lovastatin	52-62	DNA damage inducible transcript 3	Homo sapiens	121-125
34990525-1	2021	Purpose: Febrile neutropenia (FN) can cause suboptimal treatment and treatment-related mortality (TRM) in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP).	Doxorubicin	195-206	DNA damage inducible transcript 3	Homo sapiens	241-245
34990525-1	2021	Purpose: Febrile neutropenia (FN) can cause suboptimal treatment and treatment-related mortality (TRM) in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP).	Vincristine	208-219	DNA damage inducible transcript 3	Homo sapiens	241-245
34990525-1	2021	Purpose: Febrile neutropenia (FN) can cause suboptimal treatment and treatment-related mortality (TRM) in diffuse large B-cell lymphoma (DLBCL) patients treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP).	Prednisolone	225-237	DNA damage inducible transcript 3	Homo sapiens	241-245
34921960-2	2022	The ECHELON-2 study demonstrated that brentuximab vedotin plus cyclophosphamide, doxorubicin, and prednisone (A+CHP) exhibited statistically superior progression-free survival (PFS) per independent central review and improvements in overall survival vs cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) for the frontline treatment of patients with systemic anaplastic large cell lymphoma or other CD30-positive PTCL.	SGN-30 monoclonal antibody	38-49	DNA damage inducible transcript 3	Homo sapiens	313-317
34910385-10	2021	Thapsigargin and hydrochloquine induced autophagic response markers of ULK, LC3-II, Beclin1 and Atg5 and severe ER stress marker CHOP.	Thapsigargin	0-12	DNA damage inducible transcript 3	Homo sapiens	129-133
34956386-5	2021	Our results showed that PA-induced oxidative stress, calcium disequilibrium, and subsequent endoplasmic reticulum stress (ERS) mediated cellular injury, with elevated protein levels of GRP78, GRP94, CHOP, and hyperphosphorylation of PERK and IRE1alpha as well as the increased ratio of Bax/Bcl-2, which was restored by PCB2 in a concentration-dependent manner, proving the excellent antiapoptosis effect.	Protactinium	24-26	DNA damage inducible transcript 3	Homo sapiens	199-203
34956386-5	2021	Our results showed that PA-induced oxidative stress, calcium disequilibrium, and subsequent endoplasmic reticulum stress (ERS) mediated cellular injury, with elevated protein levels of GRP78, GRP94, CHOP, and hyperphosphorylation of PERK and IRE1alpha as well as the increased ratio of Bax/Bcl-2, which was restored by PCB2 in a concentration-dependent manner, proving the excellent antiapoptosis effect.	Calcium	53-60	DNA damage inducible transcript 3	Homo sapiens	199-203
34956386-5	2021	Our results showed that PA-induced oxidative stress, calcium disequilibrium, and subsequent endoplasmic reticulum stress (ERS) mediated cellular injury, with elevated protein levels of GRP78, GRP94, CHOP, and hyperphosphorylation of PERK and IRE1alpha as well as the increased ratio of Bax/Bcl-2, which was restored by PCB2 in a concentration-dependent manner, proving the excellent antiapoptosis effect.	procyanidin B2	319-323	DNA damage inducible transcript 3	Homo sapiens	199-203
34956386-6	2021	In addition, 4-phenylbutyric acid (4-PBA), the ER stress inhibitor, increased cell viability and decreased protein levels of GRP78 and CHOP, which is similar to PCB2, and thapsigargin (TG), the ER stress agonist, exhibited conversely meanwhile partly counteracted the hepatic protection of PCB2.	4-phenylbutyric acid	13-33	DNA damage inducible transcript 3	Homo sapiens	135-139
34956386-6	2021	In addition, 4-phenylbutyric acid (4-PBA), the ER stress inhibitor, increased cell viability and decreased protein levels of GRP78 and CHOP, which is similar to PCB2, and thapsigargin (TG), the ER stress agonist, exhibited conversely meanwhile partly counteracted the hepatic protection of PCB2.	4-phenylbutyric acid	35-40	DNA damage inducible transcript 3	Homo sapiens	135-139
34910385-5	2021	Dexamethasone and remdesivir had additive effects on the stress responses in the liver cells, which further increased expression of ATF4 and CHOP and cell death.	Dexamethasone	0-13	DNA damage inducible transcript 3	Homo sapiens	141-145
34910385-5	2021	Dexamethasone and remdesivir had additive effects on the stress responses in the liver cells, which further increased expression of ATF4 and CHOP and cell death.	remdesivir	18-28	DNA damage inducible transcript 3	Homo sapiens	141-145
34910385-10	2021	Thapsigargin and hydrochloquine induced autophagic response markers of ULK, LC3-II, Beclin1 and Atg5 and severe ER stress marker CHOP.	hydrochloquine	17-31	DNA damage inducible transcript 3	Homo sapiens	129-133
34966742-5	2021	The inhibitory effect of 5-HMF on NLRP3 inflammasome was reversed by overexpressing ATF4 or CHOP, indicating the involvement of ER stress in the negative regulation of 5-HMF on NLRP3 inflammasome-mediated inflammation.	5-hydroxymethylfurfural	25-30	DNA damage inducible transcript 3	Homo sapiens	92-96
34739844-4	2021	The 3-year event-free survival of younger patients (age <=60 years) treated with ibrutinib plus R-CHOP was 100% in the MCD and N1 subtypes while the survival of patients with these subtypes treated with R-CHOP alone was significantly inferior (42.9% and 50%, respectively).	ibrutinib	81-90	DNA damage inducible transcript 3	Homo sapiens	205-209
34966742-5	2021	The inhibitory effect of 5-HMF on NLRP3 inflammasome was reversed by overexpressing ATF4 or CHOP, indicating the involvement of ER stress in the negative regulation of 5-HMF on NLRP3 inflammasome-mediated inflammation.	5-hydroxymethylfurfural	168-173	DNA damage inducible transcript 3	Homo sapiens	92-96
34943000-5	2021	In vivo Dox treatment increased mitochondrial iNOS to promote ER stress as there was an increase in Bip (Grp78) response, proapoptotic CHOP (DDIT3) and ER-mediated Caspase 12 activation.	Doxorubicin	8-11	DNA damage inducible transcript 3	Homo sapiens	135-139
34885233-7	2021	The antitumor ether lipid edelfosine colocalized with the endoplasmic reticulum in both PANC-1 cells as well as PANC-1 CSCs by using a fluorescent edelfosine analog, and induced an endoplasmic reticulum stress response in both PANC-1 cells and PANC-1 CSCs, with a potent CHOP/GADD153 upregulation.	Ether	14-19	DNA damage inducible transcript 3	Homo sapiens	271-275
34885233-7	2021	The antitumor ether lipid edelfosine colocalized with the endoplasmic reticulum in both PANC-1 cells as well as PANC-1 CSCs by using a fluorescent edelfosine analog, and induced an endoplasmic reticulum stress response in both PANC-1 cells and PANC-1 CSCs, with a potent CHOP/GADD153 upregulation.	Ether	14-19	DNA damage inducible transcript 3	Homo sapiens	276-283
34885233-7	2021	The antitumor ether lipid edelfosine colocalized with the endoplasmic reticulum in both PANC-1 cells as well as PANC-1 CSCs by using a fluorescent edelfosine analog, and induced an endoplasmic reticulum stress response in both PANC-1 cells and PANC-1 CSCs, with a potent CHOP/GADD153 upregulation.	edelfosine	26-36	DNA damage inducible transcript 3	Homo sapiens	271-275
34885233-7	2021	The antitumor ether lipid edelfosine colocalized with the endoplasmic reticulum in both PANC-1 cells as well as PANC-1 CSCs by using a fluorescent edelfosine analog, and induced an endoplasmic reticulum stress response in both PANC-1 cells and PANC-1 CSCs, with a potent CHOP/GADD153 upregulation.	edelfosine	26-36	DNA damage inducible transcript 3	Homo sapiens	276-283
34710848-5	2021	In vivo, we found that inhibition of GRP78-ATF6-CHOP apoptosis signaling improved ESS symptoms, and the targeted deletion of beta-arrestin2 significantly increased saliva flow, alleviated salivary gland indices, and improved tissue integrity in the ESS model by downregulating GRP78-ATF6-CHOP apoptosis signaling.	ESS	249-252	DNA damage inducible transcript 3	Homo sapiens	288-292
34710848-6	2021	In vitro, we used IFNalpha to stimulate human salivary gland epithelial cells (HSGECs), and the results showed that IFNalpha activated GRP78-ATF6-CHOP apoptosis signaling, decreased cell viability, and induced apoptosis, which were negatively regulated by the ERS inhibitor 4-PBA.	4-phenylbutylamine	274-279	DNA damage inducible transcript 3	Homo sapiens	146-150
34676685-3	2021	METHODS: A total of 267 patients diagnosed with diffuse large B-cell lymphoma who were treated with rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) immunochemotherapy were retrospectively reviewed.	Prednisone	163-173	DNA damage inducible transcript 3	Homo sapiens	177-181
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Cyclophosphamide	103-119	DNA damage inducible transcript 3	Homo sapiens	163-167
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Doxorubicin	121-132	DNA damage inducible transcript 3	Homo sapiens	163-167
34565287-0	2021	Silencing aurora-kinase-A (AURKA) reinforced the sensitivity of diffuse large B-cell lymphoma cells to cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) via suppressing beta-Catenin and RAS-extracellular signal-regulated protein kinase (ERK1/2) pathway.	Prednisone	151-161	DNA damage inducible transcript 3	Homo sapiens	163-167
34565287-1	2021	The therapeutic effects of standard cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy for prevalent lymphoma diffuse large B-cell lymphoma (DLBC, DLBCL) still require improvement.	Cyclophosphamide	36-52	DNA damage inducible transcript 3	Homo sapiens	95-99
34565287-1	2021	The therapeutic effects of standard cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) therapy for prevalent lymphoma diffuse large B-cell lymphoma (DLBC, DLBCL) still require improvement.	Prednisone	83-93	DNA damage inducible transcript 3	Homo sapiens	95-99
34599545-0	2021	CSC-3436 sensitizes triple negative breast cancer cells to TRAIL-induced apoptosis through ROS-mediated p38/CHOP/death receptor 5 signaling pathways.	csc-3436	0-8	DNA damage inducible transcript 3	Homo sapiens	108-112
34599545-0	2021	CSC-3436 sensitizes triple negative breast cancer cells to TRAIL-induced apoptosis through ROS-mediated p38/CHOP/death receptor 5 signaling pathways.	Reactive Oxygen Species	91-94	DNA damage inducible transcript 3	Homo sapiens	108-112
34599545-7	2021	In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways.	csc-3436	37-45	DNA damage inducible transcript 3	Homo sapiens	153-157
34599545-7	2021	In addition, the induction of DR5 by CSC-3436 was found to be dependent on the modulation of reactive oxygen species (ROS)/p38/C/EBP-homologous protein (CHOP) signaling pathways.	Reactive Oxygen Species	93-116	DNA damage inducible transcript 3	Homo sapiens	153-157
34599545-8	2021	Overall, our results indicated that CSC-3436 could potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and upregulation of DR5 via the ROS-mediated upregulation of CHOP protein.	csc-3436	36-44	DNA damage inducible transcript 3	Homo sapiens	204-208
34599545-8	2021	Overall, our results indicated that CSC-3436 could potentiate the apoptotic effects of TRAIL through down-regulation of cell survival proteins and upregulation of DR5 via the ROS-mediated upregulation of CHOP protein.	Reactive Oxygen Species	175-178	DNA damage inducible transcript 3	Homo sapiens	204-208
34710848-5	2021	In vivo, we found that inhibition of GRP78-ATF6-CHOP apoptosis signaling improved ESS symptoms, and the targeted deletion of beta-arrestin2 significantly increased saliva flow, alleviated salivary gland indices, and improved tissue integrity in the ESS model by downregulating GRP78-ATF6-CHOP apoptosis signaling.	ESS	82-85	DNA damage inducible transcript 3	Homo sapiens	48-52
34643251-10	2021	Tomentosin also induced endoplasmic reticulum stress via upregulation of cyclic AMP-dependent transcription factor ATF-4 and DNA damage-inducible transcript 3 protein genes, suggesting that in the presence of tomentosin the protective unfolded protein response signaling may induce cell apoptosis.	Cyclic AMP	73-83	DNA damage inducible transcript 3	Homo sapiens	125-166
34943000-5	2021	In vivo Dox treatment increased mitochondrial iNOS to promote ER stress as there was an increase in Bip (Grp78) response, proapoptotic CHOP (DDIT3) and ER-mediated Caspase 12 activation.	Doxorubicin	8-11	DNA damage inducible transcript 3	Homo sapiens	141-146
34797531-1	2022	Patients with high-risk diffuse large B-cell lymphoma (DLBCL) have poor outcomes following first-line cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab (R-CHOP).	Cyclophosphamide	102-118	DNA damage inducible transcript 3	Homo sapiens	175-179
34942984-5	2021	JI017 treatment increased the expression of endoplasmic reticulum (ER) stress markers, including p-PERK, p-eIF2alpha, ATF4, and CHOP, via the activation of both exosomal GRP78 and cell lysate GRP78.	ji017	0-5	DNA damage inducible transcript 3	Homo sapiens	128-132
34993544-7	2022	4-PBA attenuated TGF-beta1-induced p-eIF2alpha/eIF2alpha, CHOP, ROS generation and intergrin-beta3 expression.	4-phenylbutyric acid	0-5	DNA damage inducible transcript 3	Homo sapiens	58-62
34993544-12	2022	This study demonstrated that TGF-beta1-induced ER stress potentiates the generation of intracellular ROS to a high degree through the PERK/eIF2alpha/CHOP pathway.	Reactive Oxygen Species	101-104	DNA damage inducible transcript 3	Homo sapiens	149-153
34797531-1	2022	Patients with high-risk diffuse large B-cell lymphoma (DLBCL) have poor outcomes following first-line cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab (R-CHOP).	Doxorubicin	120-131	DNA damage inducible transcript 3	Homo sapiens	175-179
34830390-7	2021	Primary human TM cells treated with AS.IV decreased TGFbeta2 induced ECM (FN, Col-I) deposition and ER stress (KDEL, ATF4 and CHOP).	Arsenic	36-38	DNA damage inducible transcript 3	Homo sapiens	126-130
34797531-1	2022	Patients with high-risk diffuse large B-cell lymphoma (DLBCL) have poor outcomes following first-line cyclophosphamide, doxorubicin, vincristine, prednisone, and rituximab (R-CHOP).	Vincristine	133-144	DNA damage inducible transcript 3	Homo sapiens	175-179
34481877-5	2021	Furthermore, 1, 8-cineole treatment in H9C2 cardiomyocytes lowered the expressions of 78-kDa glucose-regulated protein (GRP78), p-protein kinase-like ER kinase (PERK), activation of transcription factor (ATF) 4, and ER stress effector protein C/EBP and homologous protein (CHOP).	Eucalyptol	13-25	DNA damage inducible transcript 3	Homo sapiens	243-271
34774803-11	2022	In a human intestinal organoid model exposed to hypoxia-reoxygenation, attenuation of UPR activation with integrated stress response inhibitor ISRIB strongly reduced pro-apoptotic ATF4-CHOP signaling.	2-(4-chlorophenoxy)-N-(4-(2-(4-chlorophenoxy)acetamido)cyclohexyl)acetamide	143-148	DNA damage inducible transcript 3	Homo sapiens	185-189
34764434-3	2022	We aimed to evaluate the prognostic value of BCL2 expression determined by immunohistochemistry (IHC), incorporating both the staining intensity and proportion, in patients with de novo DLBCL who received rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) as first-line treatment.	Prednisone	264-274	DNA damage inducible transcript 3	Homo sapiens	278-282
34481877-5	2021	Furthermore, 1, 8-cineole treatment in H9C2 cardiomyocytes lowered the expressions of 78-kDa glucose-regulated protein (GRP78), p-protein kinase-like ER kinase (PERK), activation of transcription factor (ATF) 4, and ER stress effector protein C/EBP and homologous protein (CHOP).	Eucalyptol	13-25	DNA damage inducible transcript 3	Homo sapiens	273-277
34481877-6	2021	These findings implied that 1, 8-cineole contribute to cardioprotection via the GRP78/CHOP pathways.	Eucalyptol	28-40	DNA damage inducible transcript 3	Homo sapiens	86-90
34605226-6	2021	Along with ER calcium release, one ER stress pathway mediated by protein kinase RNA-like ER kinase (PERK) is specifically activated, leading to increased expression of proapoptotic C/EBP-homologous protein (CHOP).	Calcium	14-21	DNA damage inducible transcript 3	Homo sapiens	181-205
34605226-6	2021	Along with ER calcium release, one ER stress pathway mediated by protein kinase RNA-like ER kinase (PERK) is specifically activated, leading to increased expression of proapoptotic C/EBP-homologous protein (CHOP).	Calcium	14-21	DNA damage inducible transcript 3	Homo sapiens	207-211
34582772-7	2021	In addition, our immunoblotting analysis highlighted that MCC1734 triggered endoplasmic reticulum (ER) stress, evidenced by the activation of p-PERK, p-eIF2alpha, ATF4 and CHOP.	mcc1734	58-65	DNA damage inducible transcript 3	Homo sapiens	172-176
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Cyclophosphamide	180-196	DNA damage inducible transcript 3	Homo sapiens	241-245
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Doxorubicin	198-209	DNA damage inducible transcript 3	Homo sapiens	241-245
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Doxorubicin	198-209	DNA damage inducible transcript 3	Homo sapiens	254-258
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Vincristine	211-222	DNA damage inducible transcript 3	Homo sapiens	241-245
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Vincristine	211-222	DNA damage inducible transcript 3	Homo sapiens	254-258
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Prednisone	227-237	DNA damage inducible transcript 3	Homo sapiens	241-245
34732441-6	2021	Moreover, high risk, defined as co-expression of BTK and either or both BCL2/MYC, independently predicted shorter progression-free survival in patients treated with rituximab plus cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) (all R-CHOP-treated patients: hazard ratio=2.565, p=0.044; R-CHOP-treated non-GCB subgroup: HR=3.833, p=0.019).	Prednisone	227-237	DNA damage inducible transcript 3	Homo sapiens	254-258
34872317-3	2021	METHODS: By retrospectively searching the hospital"s computer-database, we reviewed the records of DLBCL patients who underwent the first-line rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP)/R-CHOP-like immunochemotherapy at our institution from January 2012 to June 2019.	Prednisone	206-216	DNA damage inducible transcript 3	Homo sapiens	220-224
34606419-0	2021	Cdc25C/cdc2/cyclin B, raf/MEK/ERK and PERK/eIF2alpha/CHOP pathways are involved in forskolin-induced growth inhibition of MM.1S cells by G2/M arrest and mitochondrion-dependent apoptosis.	Colforsin	83-92	DNA damage inducible transcript 3	Homo sapiens	53-57
34606419-7	2021	Of note, we demonstrated that forskolin induced a decrease of p-C-Raf, p-MEK, p-ERK1/2 and p-p90Rsk, and an increase of p-PERK, p-eIF2alpha and CHOP, which indicated that the inhibition of Raf/MEK/ERK pathway and activation of PERK/eIF2alpha/CHOP pathway were involved, at least partially, in forskolin-induced MM.1S cells apoptosis.	Colforsin	30-39	DNA damage inducible transcript 3	Homo sapiens	144-148
34520332-7	2021	Moreover, ER stress also participated in the apoptosis induced by saikosaponin-A in HeLa cells as indicated by the upregulation of GPR78, CHOP and caspase-12 expression.	saikosaponin D	66-80	DNA damage inducible transcript 3	Homo sapiens	138-142
34594423-0	2021	NDRG4 sensitizes CRC cells to 5-FU by upregulating DDIT3 expression.	Fluorouracil	30-34	DNA damage inducible transcript 3	Homo sapiens	51-56
34520822-6	2021	Intriguingly, we established that Cd-induced ferroptosis depended on endoplasmic reticulum (ER) stress, by demonstrating that Cd activated the PERK-eIF2alpha-ATF4-CHOP pathway and that inhibition of ER stress reduced ferroptosis caused by Cd.	Cadmium	34-36	DNA damage inducible transcript 3	Homo sapiens	163-167
34520822-6	2021	Intriguingly, we established that Cd-induced ferroptosis depended on endoplasmic reticulum (ER) stress, by demonstrating that Cd activated the PERK-eIF2alpha-ATF4-CHOP pathway and that inhibition of ER stress reduced ferroptosis caused by Cd.	Cadmium	126-128	DNA damage inducible transcript 3	Homo sapiens	163-167
34075009-2	2021	MATERIAL AND METHODS: Forty-five patients who received first-line rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (R-CHOP) chemotherapy for DLBCL were included in the study.	Prednisone	124-134	DNA damage inducible transcript 3	Homo sapiens	138-142
34610523-9	2021	The patient was treated successfully with cyclophosphamide, doxorubicin, vincristine and prednisolone (mini-CHOP regimen).	Prednisolone	89-101	DNA damage inducible transcript 3	Homo sapiens	108-112
34606419-7	2021	Of note, we demonstrated that forskolin induced a decrease of p-C-Raf, p-MEK, p-ERK1/2 and p-p90Rsk, and an increase of p-PERK, p-eIF2alpha and CHOP, which indicated that the inhibition of Raf/MEK/ERK pathway and activation of PERK/eIF2alpha/CHOP pathway were involved, at least partially, in forskolin-induced MM.1S cells apoptosis.	Colforsin	30-39	DNA damage inducible transcript 3	Homo sapiens	242-246
34606419-7	2021	Of note, we demonstrated that forskolin induced a decrease of p-C-Raf, p-MEK, p-ERK1/2 and p-p90Rsk, and an increase of p-PERK, p-eIF2alpha and CHOP, which indicated that the inhibition of Raf/MEK/ERK pathway and activation of PERK/eIF2alpha/CHOP pathway were involved, at least partially, in forskolin-induced MM.1S cells apoptosis.	Colforsin	293-302	DNA damage inducible transcript 3	Homo sapiens	144-148
34606419-7	2021	Of note, we demonstrated that forskolin induced a decrease of p-C-Raf, p-MEK, p-ERK1/2 and p-p90Rsk, and an increase of p-PERK, p-eIF2alpha and CHOP, which indicated that the inhibition of Raf/MEK/ERK pathway and activation of PERK/eIF2alpha/CHOP pathway were involved, at least partially, in forskolin-induced MM.1S cells apoptosis.	Colforsin	293-302	DNA damage inducible transcript 3	Homo sapiens	242-246
34594423-3	2021	The results of the present study demonstrate that NDRG4 sensitized CRC cells to 5-FU by upregulating DNA damage inducible transcript 3 (DDIT3).	Fluorouracil	80-84	DNA damage inducible transcript 3	Homo sapiens	101-134
34594423-3	2021	The results of the present study demonstrate that NDRG4 sensitized CRC cells to 5-FU by upregulating DNA damage inducible transcript 3 (DDIT3).	Fluorouracil	80-84	DNA damage inducible transcript 3	Homo sapiens	136-141
34594423-6	2021	Mechanistic analyses revealed that NDRG4 upregulated DDIT3 expression, and that the proapoptotic effect of NDRG4 under 5-FU treatment conditions was dependent on DDIT3.	Fluorouracil	119-123	DNA damage inducible transcript 3	Homo sapiens	162-167
34594423-7	2021	These findings support the biological value of the association between NDRG4, DDIT3 and 5-FU chemosensitivity in CRC, and may advance the clinical treatment of CRC in the future.	Fluorouracil	88-92	DNA damage inducible transcript 3	Homo sapiens	78-83
34815635-2	2021	This phase 1b study evaluated the safety, pharmacokinetics, and preliminary efficacy of chidamide in combination with cyclophosphamide, doxorubicin, vincristine and prednisone (CHOP) for treatment-naive PTCL patients.	Prednisone	165-175	DNA damage inducible transcript 3	Homo sapiens	177-181
34533242-6	2021	SILAC-based quantitative proteomic analysis identified 4,461 proteins and eight proteins including C/EBP homologous protein (CHOP) were markedly decreased in cisplatin-treated HEK293 cells when exposed to rosamultin.	Cisplatin	158-167	DNA damage inducible transcript 3	Homo sapiens	99-123
34533242-6	2021	SILAC-based quantitative proteomic analysis identified 4,461 proteins and eight proteins including C/EBP homologous protein (CHOP) were markedly decreased in cisplatin-treated HEK293 cells when exposed to rosamultin.	Cisplatin	158-167	DNA damage inducible transcript 3	Homo sapiens	125-129
34533242-7	2021	Biochemical experiments further discovered that rosamultin could inhibit p38 and JNK activation, and downregulate the levels of CHOP and proteins in its upstream PERK-eIF2alpha-ATF4 signaling pathway stimulated by cisplatin or tunicamycin.	Cisplatin	214-223	DNA damage inducible transcript 3	Homo sapiens	128-132
34533242-7	2021	Biochemical experiments further discovered that rosamultin could inhibit p38 and JNK activation, and downregulate the levels of CHOP and proteins in its upstream PERK-eIF2alpha-ATF4 signaling pathway stimulated by cisplatin or tunicamycin.	Tunicamycin	227-238	DNA damage inducible transcript 3	Homo sapiens	128-132
34754325-11	2021	And it was found that IL6 was lowly expressed in the group with GlcN-treated MH7A cells, while DDIT3 was highly expressed.	Glucosamine	64-68	DNA damage inducible transcript 3	Homo sapiens	95-100
34832850-4	2021	Moreover, we found that resveratrol and curcumin in combination exerted a stronger cytotoxic effect in correlation with the induction of a stronger ER stress and the upregulation of pro-death UPR molecule CHOP.	Resveratrol	24-35	DNA damage inducible transcript 3	Homo sapiens	205-209
34834228-5	2021	We found that at a non-toxic dose, GA upregulated the expression of genes associated with the ER stress response-CHOP, sXBP1, GRP87 in both cell lines, and ATF4 predominantly in A431 cells.	gibberellic acid	35-37	DNA damage inducible transcript 3	Homo sapiens	113-117
34146628-16	2021	Mechanistically, ESV induced endoplasmic reticulum stress evidenced by the elevated expressions of GRP78 and CHOP, which accompanied by the release of calcium (Ca2+).	esv	17-20	DNA damage inducible transcript 3	Homo sapiens	109-113
34745610-0	2021	Intratumoral T-cell receptor repertoire is predictive of interim PET scan results in patients with diffuse large B-cell lymphoma treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Cyclophosphamide	152-168	DNA damage inducible transcript 3	Homo sapiens	209-213
34745610-0	2021	Intratumoral T-cell receptor repertoire is predictive of interim PET scan results in patients with diffuse large B-cell lymphoma treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Doxorubicin	169-180	DNA damage inducible transcript 3	Homo sapiens	209-213
34745610-0	2021	Intratumoral T-cell receptor repertoire is predictive of interim PET scan results in patients with diffuse large B-cell lymphoma treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Prednisolone	181-193	DNA damage inducible transcript 3	Homo sapiens	209-213
34745610-0	2021	Intratumoral T-cell receptor repertoire is predictive of interim PET scan results in patients with diffuse large B-cell lymphoma treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Vincristine	194-205	DNA damage inducible transcript 3	Homo sapiens	209-213
34745610-1	2021	Objectives: A diverse intratumoral T-cell receptor (TCR) repertoire is associated with improved survival in diffuse large B-cell lymphoma (DLBCL) treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Cyclophosphamide	169-185	DNA damage inducible transcript 3	Homo sapiens	226-230
34745610-1	2021	Objectives: A diverse intratumoral T-cell receptor (TCR) repertoire is associated with improved survival in diffuse large B-cell lymphoma (DLBCL) treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Doxorubicin	186-197	DNA damage inducible transcript 3	Homo sapiens	226-230
34745610-1	2021	Objectives: A diverse intratumoral T-cell receptor (TCR) repertoire is associated with improved survival in diffuse large B-cell lymphoma (DLBCL) treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Prednisolone	198-210	DNA damage inducible transcript 3	Homo sapiens	226-230
34745610-1	2021	Objectives: A diverse intratumoral T-cell receptor (TCR) repertoire is associated with improved survival in diffuse large B-cell lymphoma (DLBCL) treated with rituximab/cyclophosphamide/doxorubicin/prednisolone/vincristine (R-CHOP) chemoimmunotherapy.	Vincristine	211-222	DNA damage inducible transcript 3	Homo sapiens	226-230
34698138-5	2021	In addition, a substantial down-regulation of some ER stress-related genes (ATF4, sXPB1 and CHOP) was observed in the 25-30 mm AL group.	Aluminum	127-129	DNA damage inducible transcript 3	Homo sapiens	92-96
34832850-4	2021	Moreover, we found that resveratrol and curcumin in combination exerted a stronger cytotoxic effect in correlation with the induction of a stronger ER stress and the upregulation of pro-death UPR molecule CHOP.	Curcumin	40-48	DNA damage inducible transcript 3	Homo sapiens	205-209
34672241-1	2022	Anthracycline-based chemoimmunotherapy with R-CHOP is the standard treatment for diffuse large B-cell lymphoma (DLBCL) but is associated with increased risks of cardiotoxicity.	Anthracyclines	0-13	DNA damage inducible transcript 3	Homo sapiens	46-50
34668281-4	2021	Although anthracycline-based regimens such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remain the standard first-line treatment for most aggressive PTCLs, there are important variations including incorporation of novel agents, use of radiotherapy and judicious consideration of stem cell transplantation.	Anthracyclines	9-22	DNA damage inducible transcript 3	Homo sapiens	106-110
34668281-4	2021	Although anthracycline-based regimens such as cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) remain the standard first-line treatment for most aggressive PTCLs, there are important variations including incorporation of novel agents, use of radiotherapy and judicious consideration of stem cell transplantation.	Prednisone	94-104	DNA damage inducible transcript 3	Homo sapiens	106-110
34668817-1	2022	Patients with diffuse large B-cell lymphoma (DLBCL) treated with the R-CHOP regime receive a high cumulative dose of prednisone.	Prednisone	117-127	DNA damage inducible transcript 3	Homo sapiens	71-75
34664264-12	2022	AZM-mediated activation of the unfolded protein response (UPR) via the inhibition of GRP78 activity is required not only for inducing the expression of C/EBP-homologous protein (ChOP) but also for the activating sterol-regulatory element binding protein (SREBP) and its targeted genes involved in cholesterol and lipid biosynthetic processes.	Azithromycin	0-3	DNA damage inducible transcript 3	Homo sapiens	152-176
34664264-12	2022	AZM-mediated activation of the unfolded protein response (UPR) via the inhibition of GRP78 activity is required not only for inducing the expression of C/EBP-homologous protein (ChOP) but also for the activating sterol-regulatory element binding protein (SREBP) and its targeted genes involved in cholesterol and lipid biosynthetic processes.	Azithromycin	0-3	DNA damage inducible transcript 3	Homo sapiens	178-182
34358932-12	2021	AR, mTOR and DDIT3 in the PC-3 and LNCap cells were significantly upregulated with 10-6 M TPP treated.	triphenyl phosphate	90-93	DNA damage inducible transcript 3	Homo sapiens	13-18
34661507-2	2021	Therefore, we evaluated 32 patients who received rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) therapy for B-cell malignant lymphoma by analysing the changes in atherosclerosis.	Prednisolone	107-119	DNA damage inducible transcript 3	Homo sapiens	123-127
34679020-6	2021	Patulin-thiol co-treatment decreased CHOP expression and BiP and CHOP levels in HepG2 cells but did not alter BiP expression.	Sulfhydryl Compounds	8-13	DNA damage inducible transcript 3	Homo sapiens	37-41
34681736-5	2021	ROS-induced endoplasmic reticulum (ER) stress by OSMI-1 not only upregulated CHOP-DR5 signaling but also activated Jun-N-terminal kinase (JNK), resulting in a decrease in Bcl2 and the release of cytochrome c from mitochondria.	ros	0-3	DNA damage inducible transcript 3	Homo sapiens	77-81
34679020-6	2021	Patulin-thiol co-treatment decreased CHOP expression and BiP and CHOP levels in HepG2 cells but did not alter BiP expression.	Sulfhydryl Compounds	8-13	DNA damage inducible transcript 3	Homo sapiens	65-69
34214594-0	2021	Methamphetamine mediates apoptosis of vascular smooth muscle cells via the Chop-related endoplasmic reticulum stress pathway.	Methamphetamine	0-15	DNA damage inducible transcript 3	Homo sapiens	75-79
34638128-1	2022	Diffuse large B-cell lymphoma (DLBCL) is the most common B-cell malignancy with varying prognosis after the gold standard rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	181-191	DNA damage inducible transcript 3	Homo sapiens	195-199
34214594-7	2021	The results indicated that METH can induce apoptosis of vascular smooth muscle cells (VSMCs) and upregulate the expression of Chop and endoplasmic reticulum stress-related proteins.	Methamphetamine	27-31	DNA damage inducible transcript 3	Homo sapiens	126-130
34214594-10	2021	These results indicate that Chop is involved in the METH-induced endoplasmic reticulum stress and apoptosis in VSMCs and may be a potential therapeutic target for METH-induced VSMC injury.	Methamphetamine	52-56	DNA damage inducible transcript 3	Homo sapiens	28-32
34214594-10	2021	These results indicate that Chop is involved in the METH-induced endoplasmic reticulum stress and apoptosis in VSMCs and may be a potential therapeutic target for METH-induced VSMC injury.	Methamphetamine	163-167	DNA damage inducible transcript 3	Homo sapiens	28-32
34659400-8	2021	The protein levels of oxidative stress markers inducible nitric oxide synthase (iNOS) and gammaH2AX and ERS-induced apoptosis-related molecules C/EBP homologous protein (CHOP) and cleaved caspase-12 were significantly downregulated upon curcumin treatment.	Curcumin	237-245	DNA damage inducible transcript 3	Homo sapiens	144-168
34765356-4	2021	We report a case of a 65-year-old man who presented with acutely worsening dyspnoea and stridor following his fifth cycle of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy for hematological malignancy.	Cyclophosphamide	136-152	DNA damage inducible transcript 3	Homo sapiens	200-204
34765356-4	2021	We report a case of a 65-year-old man who presented with acutely worsening dyspnoea and stridor following his fifth cycle of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy for hematological malignancy.	Doxorubicin	154-165	DNA damage inducible transcript 3	Homo sapiens	200-204
34765356-4	2021	We report a case of a 65-year-old man who presented with acutely worsening dyspnoea and stridor following his fifth cycle of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy for hematological malignancy.	Vincristine	167-178	DNA damage inducible transcript 3	Homo sapiens	200-204
34765356-4	2021	We report a case of a 65-year-old man who presented with acutely worsening dyspnoea and stridor following his fifth cycle of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) chemotherapy for hematological malignancy.	Prednisolone	184-196	DNA damage inducible transcript 3	Homo sapiens	200-204
34659400-8	2021	The protein levels of oxidative stress markers inducible nitric oxide synthase (iNOS) and gammaH2AX and ERS-induced apoptosis-related molecules C/EBP homologous protein (CHOP) and cleaved caspase-12 were significantly downregulated upon curcumin treatment.	Curcumin	237-245	DNA damage inducible transcript 3	Homo sapiens	170-174
34659400-9	2021	Furthermore, curcumin administration greatly blocked the protein kinase-like endoplasmic reticulum kinase- (PERK-) eukaryotic translation initiation factor 2alpha- (eIF2alpha-) activating transcription factor 4- (ATF4-) CHOP signaling pathway.	Curcumin	13-21	DNA damage inducible transcript 3	Homo sapiens	220-224
34472704-5	2021	Treatment with c-Jun N-terminal kinase (JNK) inhibitor SP600125, JNK small interfering RNA (siRNA) and tumour necrosis factor-alpha (TNF-alpha) antibodies reversed the BTXA-induced GADD153 expression.	pyrazolanthrone	55-63	DNA damage inducible transcript 3	Homo sapiens	181-188
34520759-6	2021	Analysis of autophagy and endoplasmic reticulum stress markers showed that A-443654 successfully prevented alpha-synuclein toxicity and restored cell function in ATXN2-Q58 cells, normalizing the levels of mTOR, LC3-II, p62, STAU1, BiP and CHOP.	A 443654	75-83	DNA damage inducible transcript 3	Homo sapiens	239-243
34607978-6	2022	In addition, siRNA-mediated knockdown of CHOP attenuated shikonininduced apoptosis, as did the ER stress inhibitor TUDCA.	ursodoxicoltaurine	115-120	DNA damage inducible transcript 3	Homo sapiens	41-45
34455722-9	2021	Compared with H/R group, the expression of HIF-1alpha was evidently up-regulated, while GRP78, CHOP, capase-12 and cleaved caspase-3 expressions were all obviously downregulated in Dex+H/R group (P<0.05).	Dexmedetomidine	181-184	DNA damage inducible transcript 3	Homo sapiens	95-99
34588186-4	2022	Imeglimin upregulated the expression of endoplasmic reticulum (ER)-related molecules including Chop (Ddit3), Gadd34 (Ppp1r15a), Atf3, and Sdf2l1, and decreased eIF2alpha phosphorylation, after treatment with thapsigargin, and restored global protein synthesis in beta-cells under ER stress.	Thapsigargin	208-220	DNA damage inducible transcript 3	Homo sapiens	95-99
34588186-4	2022	Imeglimin upregulated the expression of endoplasmic reticulum (ER)-related molecules including Chop (Ddit3), Gadd34 (Ppp1r15a), Atf3, and Sdf2l1, and decreased eIF2alpha phosphorylation, after treatment with thapsigargin, and restored global protein synthesis in beta-cells under ER stress.	Thapsigargin	208-220	DNA damage inducible transcript 3	Homo sapiens	101-106
34479965-2	2021	We determined whether therapy with locked nucleic acid (LNA)-modified antisense oligonucleotides (ASOs) targeting CHOP ameliorates experimental DKD.	Oligonucleotides	80-96	DNA damage inducible transcript 3	Homo sapiens	114-118
34479965-11	2021	Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented cell death of human kidney cells in vitro Conclusions: The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi in particular at later timepoints.	Glucose	36-43	DNA damage inducible transcript 3	Homo sapiens	6-10
34479965-11	2021	Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented cell death of human kidney cells in vitro Conclusions: The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi in particular at later timepoints.	Glucose	36-43	DNA damage inducible transcript 3	Homo sapiens	52-56
34479965-11	2021	Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented cell death of human kidney cells in vitro Conclusions: The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi in particular at later timepoints.	Oligonucleotides, Antisense	130-133	DNA damage inducible transcript 3	Homo sapiens	6-10
34479965-11	2021	Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented cell death of human kidney cells in vitro Conclusions: The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi in particular at later timepoints.	Oligonucleotides, Antisense	130-133	DNA damage inducible transcript 3	Homo sapiens	52-56
34479965-11	2021	Human CHOP-ASOs efficiently reduced glucose-induced CHOP and prevented cell death of human kidney cells in vitro Conclusions: The ASO-based approach efficiently reduced renal CHOP expression in a diabetic mouse model, providing an additional benefit to an ACEi in particular at later timepoints.	Oligonucleotides, Antisense	130-133	DNA damage inducible transcript 3	Homo sapiens	175-179
34475055-8	2021	Furthermore, we identified that enhanced sensitivity to TRAIL by combination with CBUD-1001 depends on the MAPK/CHOP axis, being a key mediator of DR5.	cbud-1001	82-91	DNA damage inducible transcript 3	Homo sapiens	112-116
34229406-0	2021	Microglia-derived IL-1beta promoted neuronal apoptosis through ER stress-mediated signaling pathway PERK/eIF2alpha/ATF4/CHOP upon arsenic exposure.	Arsenic	130-137	DNA damage inducible transcript 3	Homo sapiens	120-124
34229406-6	2021	In addition, the IL-1 receptor antagonist IL-1ra diminished arsenic-induced activation of ER stress-mediated apoptotic pathway PERK/eIF2alpha/ATF4/CHOP and neuronal apoptosis.	Arsenic	60-67	DNA damage inducible transcript 3	Homo sapiens	147-151
34479965-0	2021	CHOP-ASO Ameliorates Glomerular and Tubular Damage on Top of ACE Inhibition in Diabetic Kidney Disease.	Oligonucleotides, Antisense	5-8	DNA damage inducible transcript 3	Homo sapiens	0-4
34586105-2	2021	The current first-line regimen for the treatment of DLBCL is R-CHOP, which is the combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone.	Cyclophosphamide	108-124	DNA damage inducible transcript 3	Homo sapiens	63-67
34586105-2	2021	The current first-line regimen for the treatment of DLBCL is R-CHOP, which is the combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone.	Doxorubicin	126-137	DNA damage inducible transcript 3	Homo sapiens	63-67
34586105-2	2021	The current first-line regimen for the treatment of DLBCL is R-CHOP, which is the combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone.	Vincristine	139-150	DNA damage inducible transcript 3	Homo sapiens	63-67
34586105-2	2021	The current first-line regimen for the treatment of DLBCL is R-CHOP, which is the combination of rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone.	Prednisone	155-165	DNA damage inducible transcript 3	Homo sapiens	63-67
34265889-2	2021	Chemotherapy with cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) +- rituximab has an intermediate FN risk.	Prednisone	66-76	DNA damage inducible transcript 3	Homo sapiens	78-82
34414940-7	2021	Circulating CHOP level was positively correlated with age, Cr, BUN, Cys-c, and urinary microalbumin/creatinine (UmALB/Cr).	Creatinine	59-61	DNA damage inducible transcript 3	Homo sapiens	12-16
34428285-2	2022	Promising early-phase results were reported with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) plus subcutaneous azacitidine, a hypomethylating agent.	Prednisone	108-118	DNA damage inducible transcript 3	Homo sapiens	122-126
34414940-7	2021	Circulating CHOP level was positively correlated with age, Cr, BUN, Cys-c, and urinary microalbumin/creatinine (UmALB/Cr).	Creatinine	100-110	DNA damage inducible transcript 3	Homo sapiens	12-16
34414940-7	2021	Circulating CHOP level was positively correlated with age, Cr, BUN, Cys-c, and urinary microalbumin/creatinine (UmALB/Cr).	Creatinine	118-120	DNA damage inducible transcript 3	Homo sapiens	12-16
34164906-7	2021	The expression of Beclin1, VDAC1, LC3-II, CHOP and Bip was promoted in the cells received combinatorial treatment of metformin and MALAT1 knock-down.	Metformin	117-126	DNA damage inducible transcript 3	Homo sapiens	42-46
34298014-9	2021	Furthermore, ATF4 proactively upregulated the cell death inducible genes expression, such as Chop, Chac1, and Trb3, thereby markedly reducing cell viability with 25-hydroxycholesterol.	25-hydroxycholesterol	162-183	DNA damage inducible transcript 3	Homo sapiens	93-97
34895738-7	2021	CASE SUMMARY: An 81-year-old female patient received her first cycle of R-CHOP (rituximab, cyclophosphamide, vincristine, and prednisolone) treatment after being diagnosed with high- grade B-cell lymphoma.	Cyclophosphamide	91-107	DNA damage inducible transcript 3	Homo sapiens	74-78
34895738-7	2021	CASE SUMMARY: An 81-year-old female patient received her first cycle of R-CHOP (rituximab, cyclophosphamide, vincristine, and prednisolone) treatment after being diagnosed with high- grade B-cell lymphoma.	Vincristine	109-120	DNA damage inducible transcript 3	Homo sapiens	74-78
34895738-7	2021	CASE SUMMARY: An 81-year-old female patient received her first cycle of R-CHOP (rituximab, cyclophosphamide, vincristine, and prednisolone) treatment after being diagnosed with high- grade B-cell lymphoma.	Prednisolone	126-138	DNA damage inducible transcript 3	Homo sapiens	74-78
34362493-0	2021	(Doxorubicin Hydrochloride Liposome-Based CHOP Regimen in the Initial Treatment of Elderly Patients with Diffuse Large B-Cell Lymphoma: A Retrospective Study).	Doxorubicin	1-35	DNA damage inducible transcript 3	Homo sapiens	42-46
34146894-4	2021	To this end, we detected transcription factor 6 (ATF6), the key factor of regulating lipid metabolism along with other related molecules (CHOP and GPR78) and found that curcumin significantly impaired the gene synthesis of ATF6, while CSFV infection promoted ATF6 expression.	Curcumin	169-177	DNA damage inducible transcript 3	Homo sapiens	138-142
34362493-1	2021	OBJECTIVE: To evaluate the efficacy and safety of CHOP regimen based on doxorubicin hydrochloride liposome in the initial treatment of elderly patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	72-97	DNA damage inducible transcript 3	Homo sapiens	50-54
34170142-0	2021	Efficient Synthesis of Icetexane Diterpenes and Apoptosis Inducing Effect by Upregulating BiP-ATF4-CHOP Axis in Colorectal Cells.	icetexane diterpenes	23-43	DNA damage inducible transcript 3	Homo sapiens	99-103
34254266-1	2022	PURPOSE: Comprehensive geriatric assessment (CGA) has been used to help identify elderly patients with diffuse large B-cell lymphoma (DLBCL) who were suitable for rituximab combined with CHOP therapy (cyclophosphamide, Adriamycin, vincristine, and prednisolone), but there are few reports of CGA for elderly patients with DLBCL who received R-mini-CHOP.	Cyclophosphamide	201-217	DNA damage inducible transcript 3	Homo sapiens	187-191
34336001-3	2021	Furthermore, dextromethorphan can inhibit the accumulation of GPR37 in the hippocampus of newborns caused by buprenorphine and is accompanied by the proapoptotic ER stress response that involves the procaspase-3/CHOP pathway.	Dextromethorphan	13-29	DNA damage inducible transcript 3	Homo sapiens	212-216
34426922-0	2021	Chemical Induction of Trophoblast Hypoxia by Cobalt Chloride Leads to Increased Expression of DDIT3.	cobaltous chloride	45-60	DNA damage inducible transcript 3	Homo sapiens	94-99
34472451-7	2021	Increased expressions of p-eIF2alpha and CHOP were observed in GLA-treated cells, suggesting GLA-treated cells had increased expressions of p-eIF2alpha and CHOP, which suggest endoplasmic reticulum (ER) stress.	gamma-Linolenic Acid	63-66	DNA damage inducible transcript 3	Homo sapiens	41-45
34472451-7	2021	Increased expressions of p-eIF2alpha and CHOP were observed in GLA-treated cells, suggesting GLA-treated cells had increased expressions of p-eIF2alpha and CHOP, which suggest endoplasmic reticulum (ER) stress.	gamma-Linolenic Acid	63-66	DNA damage inducible transcript 3	Homo sapiens	156-160
34472451-7	2021	Increased expressions of p-eIF2alpha and CHOP were observed in GLA-treated cells, suggesting GLA-treated cells had increased expressions of p-eIF2alpha and CHOP, which suggest endoplasmic reticulum (ER) stress.	gamma-Linolenic Acid	93-96	DNA damage inducible transcript 3	Homo sapiens	41-45
34472451-7	2021	Increased expressions of p-eIF2alpha and CHOP were observed in GLA-treated cells, suggesting GLA-treated cells had increased expressions of p-eIF2alpha and CHOP, which suggest endoplasmic reticulum (ER) stress.	gamma-Linolenic Acid	93-96	DNA damage inducible transcript 3	Homo sapiens	156-160
34306318-10	2021	Mitochondrial damage was induced by NTPAM, which was associated with enhancements of mitochondrial ROS (mtROS) and ATF4/CHOP regulation.	ntpam	36-41	DNA damage inducible transcript 3	Homo sapiens	120-124
34306318-11	2021	These results suggest that NTPAM induces HNC cell death through the upregulation of ATF4/CHOP activity by damaging mitochondria via excessive mtROS accumulation, similar to mitochondrial targeted therapy.	ntpam	27-32	DNA damage inducible transcript 3	Homo sapiens	89-93
34426922-3	2021	However, CoCl2 caused activation of the apoptosis pathway, increased the activity of effector caspases 3 and 7, and increased the expression of the unfolded protein response target DDIT3.	cobaltous chloride	9-14	DNA damage inducible transcript 3	Homo sapiens	181-186
34121033-0	2021	Spatial Analysis of Phosphatidylinositol Molecular Species in Pork Chop Tissues Using Matrix-assisted Laser Desorption/ionization-Mass Spectrometry Imaging.	Phosphatidylinositols	20-40	DNA damage inducible transcript 3	Homo sapiens	67-71
34281166-7	2021	Carfilzomib displayed potent antiproliferative effects, induced the unfolded protein response as determined by enhanced CHOP expression and ATF6 activity, and enhanced apoptosis as determined by enhanced caspase-3/7 activity.	carfilzomib	0-11	DNA damage inducible transcript 3	Homo sapiens	120-124
34258395-0	2021	Cinnabar protects serum-nutrient starvation induced apoptosis by improving intracellular oxidative stress and inhibiting the expression of CHOP and PERK.	cinnabar	0-8	DNA damage inducible transcript 3	Homo sapiens	139-143
34187946-0	2021	Vanillin oxime inhibits lung cancer cell proliferation and activates apoptosis through JNK/ERK-CHOP pathway.	Vanillin Oxime	0-14	DNA damage inducible transcript 3	Homo sapiens	95-99
34187946-10	2021	In A549 and NCI-H2170 cells vanillin oxime exposure caused significant (p < 0.05) enhancement in CHOP and DR5 mRNA expression.	Vanillin Oxime	28-42	DNA damage inducible transcript 3	Homo sapiens	97-101
34250248-3	2021	The effect of dexamethasone on proliferation inhibition, apoptosis, and ATF4-CHOP pathway in HEI-OC1 cells was examined by CCK-8 assay, flow cytometry, western blotting, and reverse transcription PCR, respectively.	Dexamethasone	14-27	DNA damage inducible transcript 3	Homo sapiens	77-81
34250248-4	2021	Results: In HEI-OC1 cells, dexamethasone was shown to significantly reduce the tunicamycin-induced expression of ATF4 and CHOP in the context of sustained viability and proliferation, a therapeutic effect that was reversible by co-treatment with a glucocorticoid antagonist.	Dexamethasone	27-40	DNA damage inducible transcript 3	Homo sapiens	122-126
34250248-4	2021	Results: In HEI-OC1 cells, dexamethasone was shown to significantly reduce the tunicamycin-induced expression of ATF4 and CHOP in the context of sustained viability and proliferation, a therapeutic effect that was reversible by co-treatment with a glucocorticoid antagonist.	Tunicamycin	79-90	DNA damage inducible transcript 3	Homo sapiens	122-126
34258395-8	2021	The protein expression levels of both CHOP and PERK were remarkably down-regulated in the cells treated with cinnabar compared to the control cells or cells treated with HgCl2.	cinnabar	109-117	DNA damage inducible transcript 3	Homo sapiens	38-42
34258395-8	2021	The protein expression levels of both CHOP and PERK were remarkably down-regulated in the cells treated with cinnabar compared to the control cells or cells treated with HgCl2.	Mercuric Chloride	170-175	DNA damage inducible transcript 3	Homo sapiens	38-42
34258395-9	2021	Overall, our data indicates that cinnabar at low concentration exerts anti-oxidative stress and anti-apoptosis effects by inhibiting the expression of the endoplasmic reticulum stress pathway proteins CHOP and PERK.	cinnabar	33-41	DNA damage inducible transcript 3	Homo sapiens	201-205
34194230-0	2021	Celastrol Modulates Multiple Signaling Pathways to Inhibit Proliferation of Pancreatic Cancer via DDIT3 and ATF3 Up-Regulation and RRM2 and MCM4 Down-Regulation.	celastrol	0-9	DNA damage inducible transcript 3	Homo sapiens	98-103
34221922-10	2021	NaAsO2 induces apoptosis in LO2 cells by activating the ERS-mediated apoptotic signaling pathway, at least partially by enhancing the methylation of H3 on the promoter regions of ERS-associated genes, including GRP78 and CHOP.	sodium arsenite	0-6	DNA damage inducible transcript 3	Homo sapiens	221-225
34183648-9	2021	Treatment with doxycycline decreased the abundance of mitochondrial encoded proteins while increasing expression of CHOP, C/EBPbeta, ClpP, and mtHsp60, markers of the mtUPR.	Doxycycline	15-26	DNA damage inducible transcript 3	Homo sapiens	116-120
34194230-9	2021	Celastrol modulated many signaling genes and its cytotoxic effect was mainly mediated via over-expression of ATF3 and DDIT3, and down-expression of RRM2 and MCM4.	celastrol	0-9	DNA damage inducible transcript 3	Homo sapiens	118-123
34306367-0	2021	CHOP overexpression sensitizes human non-small cell lung cancer cells to cisplatin treatment by Bcl-2/JNK pathway.	Cisplatin	73-82	DNA damage inducible transcript 3	Homo sapiens	0-4
34202933-5	2021	Moreover, vitamin K2 significantly decreased the expression of CHOP protein along with the levels and the nuclear localization of p-IRE1alpha, thus showing its significant role in inhibiting chronic ER stress-mediated UPR and eventually cell death.	Vitamin K 2	10-20	DNA damage inducible transcript 3	Homo sapiens	63-67
34327076-7	2021	She was treated with rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) along with intrathecal methotrexate (IT MTX)/cytarabine after CNS involvement was diagnosed.	Prednisone	80-90	DNA damage inducible transcript 3	Homo sapiens	94-98
34306367-3	2021	Herein, our study elucidated the effect of CHOP on NSCLC cells with cisplatin resistance and its mechanism.	Cisplatin	68-77	DNA damage inducible transcript 3	Homo sapiens	43-47
34306367-4	2021	In a NSCLC cell line with cisplatin-resistance, CHOP expression was decreased, compared with A549 cells.	Cisplatin	26-35	DNA damage inducible transcript 3	Homo sapiens	48-52
34306367-5	2021	Overexpression of CHOP decreased the cell viability and enhanced cell apoptosis in the cells treated with cisplatin.	Cisplatin	106-115	DNA damage inducible transcript 3	Homo sapiens	18-22
34306367-7	2021	CHOP increased the therapeutic effect of cisplatin on NSCLC cells through the Bcl-2/JNK pathway.	Cisplatin	41-50	DNA damage inducible transcript 3	Homo sapiens	0-4
34306367-8	2021	In summary, CHOP regulated cisplatin resistance in cells of NSCLC by promoting the expression of apoptotic proteins and inhibiting the Bcl-2/JNK signaling pathway, indicating the antitumor effects of CHOP.	Cisplatin	27-36	DNA damage inducible transcript 3	Homo sapiens	12-16
34306367-8	2021	In summary, CHOP regulated cisplatin resistance in cells of NSCLC by promoting the expression of apoptotic proteins and inhibiting the Bcl-2/JNK signaling pathway, indicating the antitumor effects of CHOP.	Cisplatin	27-36	DNA damage inducible transcript 3	Homo sapiens	200-204
34120620-4	2021	Unfortunately, DOX is the main cytotoxic drug in R-CHOP and it can lead to adverse reactions.	Doxorubicin	15-18	DNA damage inducible transcript 3	Homo sapiens	51-55
34088951-1	2021	The imipramine ONC201 has antiproliferative effects in several cancer cell types and activates integrated stress response pathway associated with the induction of Damage Inducible Transcript 3 (DDIT3, also known as C/EBP homologous protein or CHOP).	Imipramine	4-14	DNA damage inducible transcript 3	Homo sapiens	163-192
34179614-0	2021	Combination of Palmitic Acid and Methylseleninic Acid Induces Mitochondria-Dependent Apoptosis via Attenuation of the IRE1alpha Arm and Enhancement of CHOP in Hepatoma.	Palmitic Acid	15-28	DNA damage inducible transcript 3	Homo sapiens	151-155
34179614-0	2021	Combination of Palmitic Acid and Methylseleninic Acid Induces Mitochondria-Dependent Apoptosis via Attenuation of the IRE1alpha Arm and Enhancement of CHOP in Hepatoma.	methylselenic acid	33-53	DNA damage inducible transcript 3	Homo sapiens	151-155
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	Palmitic Acid	19-21	DNA damage inducible transcript 3	Homo sapiens	114-146
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	Palmitic Acid	19-21	DNA damage inducible transcript 3	Homo sapiens	148-152
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	methylselenic acid	26-30	DNA damage inducible transcript 3	Homo sapiens	114-146
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	methylselenic acid	26-30	DNA damage inducible transcript 3	Homo sapiens	148-152
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	Palmitic Acid	175-177	DNA damage inducible transcript 3	Homo sapiens	114-146
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	Palmitic Acid	175-177	DNA damage inducible transcript 3	Homo sapiens	148-152
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	methylselenic acid	178-182	DNA damage inducible transcript 3	Homo sapiens	114-146
34179614-7	2021	The combination of PA and MSeA attenuated the IRE1 pathway and increased the expressions of phospha-eIF2alpha and GADD153/C/EBP homologous protein (CHOP), contributing to the PA/MSeA combination-induced mitochondria-dependent apoptosis in HepG2 cells.	methylselenic acid	178-182	DNA damage inducible transcript 3	Homo sapiens	148-152
34088951-1	2021	The imipramine ONC201 has antiproliferative effects in several cancer cell types and activates integrated stress response pathway associated with the induction of Damage Inducible Transcript 3 (DDIT3, also known as C/EBP homologous protein or CHOP).	Imipramine	4-14	DNA damage inducible transcript 3	Homo sapiens	194-199
34088951-1	2021	The imipramine ONC201 has antiproliferative effects in several cancer cell types and activates integrated stress response pathway associated with the induction of Damage Inducible Transcript 3 (DDIT3, also known as C/EBP homologous protein or CHOP).	Imipramine	4-14	DNA damage inducible transcript 3	Homo sapiens	243-247
34070303-4	2021	TDA induces sustained endoplasmic reticulum stress, which triggers apoptosis through IRE1alpha/XBP1 and PERK/ATF4/CHOP pathways.	2,4-diaminotoluene	0-3	DNA damage inducible transcript 3	Homo sapiens	114-118
34105294-0	2021	DDIT3 Directs a Dual Mechanism to Balance Glycolysis and Oxidative Phosphorylation during Glutamine Deprivation.	Glutamine	90-99	DNA damage inducible transcript 3	Homo sapiens	0-5
34105294-4	2021	DDIT3 is induced during glutamine deprivation to promote glycolysis and adenosine triphosphate production via suppression of the negative glycolytic regulator TIGAR.	Glutamine	24-33	DNA damage inducible transcript 3	Homo sapiens	0-5
34105294-4	2021	DDIT3 is induced during glutamine deprivation to promote glycolysis and adenosine triphosphate production via suppression of the negative glycolytic regulator TIGAR.	Adenosine	72-81	DNA damage inducible transcript 3	Homo sapiens	0-5
34244887-13	2021	CONCLUSION: Atiprimod induced prolonged ER stress-mediated apoptosis via both activating PERK/eIF2alpha/ATF4/CHOP axis and suppressing STAT3/NF-kappaB transcription factors nuclear migration in TBNC cells.	azaspirane	12-21	DNA damage inducible transcript 3	Homo sapiens	109-113
34123711-0	2021	N-trans-Feruloyloctopamine Wakes Up BBC3, DDIT3, CDKN1A, and NOXA Signals to Accelerate HCC Cell Apoptosis.	N-feruloyloctopamine	0-26	DNA damage inducible transcript 3	Homo sapiens	42-47
34121978-6	2021	Here, we evaluated the effect of miR-30c-2-3p on controlling XBP1-CHOP-BIM and its apoptotic effects on ovarian cancer cell lines during ERS.	mir-30c-2-3p	33-45	DNA damage inducible transcript 3	Homo sapiens	66-70
34124276-1	2021	The majority of diffuse large B-cell lymphoma (DLBCL) patients develop relapsed or refractory disease after standard ruxolitinib, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy, which is partly related to a dysregulated tumor immune microenvironment.	ruxolitinib	117-128	DNA damage inducible transcript 3	Homo sapiens	192-196
34124276-1	2021	The majority of diffuse large B-cell lymphoma (DLBCL) patients develop relapsed or refractory disease after standard ruxolitinib, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy, which is partly related to a dysregulated tumor immune microenvironment.	Cyclophosphamide	130-146	DNA damage inducible transcript 3	Homo sapiens	192-196
34124276-1	2021	The majority of diffuse large B-cell lymphoma (DLBCL) patients develop relapsed or refractory disease after standard ruxolitinib, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy, which is partly related to a dysregulated tumor immune microenvironment.	Doxorubicin	148-159	DNA damage inducible transcript 3	Homo sapiens	192-196
34124276-1	2021	The majority of diffuse large B-cell lymphoma (DLBCL) patients develop relapsed or refractory disease after standard ruxolitinib, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy, which is partly related to a dysregulated tumor immune microenvironment.	Vincristine	161-172	DNA damage inducible transcript 3	Homo sapiens	192-196
34124276-1	2021	The majority of diffuse large B-cell lymphoma (DLBCL) patients develop relapsed or refractory disease after standard ruxolitinib, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) chemotherapy, which is partly related to a dysregulated tumor immune microenvironment.	Prednisone	178-188	DNA damage inducible transcript 3	Homo sapiens	192-196
35526484-4	2022	Indeed, PARP and CHK1 inhibition by AZD2461 and UCN-01, by downregulating c-Myc, reduced the expression of XBP1s, constitutively expressed in these cells, and upregulated CHOP.	AZD2461	36-43	DNA damage inducible transcript 3	Homo sapiens	171-175
34094947-11	2021	IBC (SUM149PT and SUM190PT) cells were chemosensitive to Salubrinal treatment, possibly via inhibition in OPG secretion, upregulating ATF4, and CHOP, thus ultimately driving caspase-3 mediated IBC cell death.	salubrinal	57-67	DNA damage inducible transcript 3	Homo sapiens	144-148
34150114-8	2021	The of Caspase-3, GRP78, and CHOP expression levels in the quercetin intervention group rose significantly in comparison with the blank control group (P<0.05).	Quercetin	59-68	DNA damage inducible transcript 3	Homo sapiens	29-33
34159026-5	2021	The patient was treated using rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) chemotherapy, a five-day steroid course, and one intrathecal methotrexate.	rituximab-cyclophosphamide	30-56	DNA damage inducible transcript 3	Homo sapiens	95-99
34159026-5	2021	The patient was treated using rituximab-cyclophosphamide-doxorubicin-vincristine-prednisone (R-CHOP) chemotherapy, a five-day steroid course, and one intrathecal methotrexate.	doxorubicin-vincristine-prednisone	57-91	DNA damage inducible transcript 3	Homo sapiens	95-99
34066362-2	2021	In SEPN1-depleted muscles, altered ER calcium homeostasis triggers ER stress, which induces CHOP-mediated malfunction, altering excitation-contraction coupling.	Calcium	38-45	DNA damage inducible transcript 3	Homo sapiens	92-96
35288263-8	2022	Pendulone induced the expression of ER stress-associated proteins, such as ATF4 and CHOP, which promoted the expression of death receptors.	pendulone	0-9	DNA damage inducible transcript 3	Homo sapiens	84-88
35122137-7	2022	We found that ER stress-related protein CHOP was significantly up-regulated within a short-term postmortem interval (PMI) in brain tissue of DMA samples, which may interact with a series of ER stress- and mitochondria-related protein, leading to the apoptosis of the cells.	dma	141-144	DNA damage inducible transcript 3	Homo sapiens	40-44
35122137-8	2022	It was also verified in human samples that the expression level of CHOP can sever as a potential biomarker of DMA within a specific PMI.	dma	110-113	DNA damage inducible transcript 3	Homo sapiens	67-71
35567345-10	2022	PK/PD modeling indicates that a higher concentration of nusinersen may predict an additional 5-point increase in CHOP INTEND score beyond that observed with 12 mg.	nusinersen	56-66	DNA damage inducible transcript 3	Homo sapiens	113-117
35607370-12	2022	In conclusion, downregulation of GRP78 and CHOP expression is one of the mechanisms by which TUDCA inhibits TGF-beta1-induced renal mesangial cell fibrosis.	ursodoxicoltaurine	93-98	DNA damage inducible transcript 3	Homo sapiens	43-47
35294085-6	2022	Further studies had found that beta-Elemene could increase the expression of ERS-related proteins CHOP and Calnexin in a dose-dependent manner, thereby promoting the aggregation of cleaved-caspase-3 and inducing hHSFs to undergo poptosis.	beta-elemene	31-43	DNA damage inducible transcript 3	Homo sapiens	98-102
35615997-5	2022	We showed that WO3i suppresses the expression of CHOP, a key mediator of ER stress-induced apoptosis, and the activation of apoptotic genes.	wo3i	15-19	DNA damage inducible transcript 3	Homo sapiens	49-53
35619328-4	2022	Upon AZD1775 treatment, activated PERK promotes apoptotic signaling via C/EBP-homologous protein (CHOP), while IRE1alpha-induced splicing of XBP1 (XBP1s) maintains cell survival by repressing apoptosis.	adavosertib	5-12	DNA damage inducible transcript 3	Homo sapiens	72-96
35619328-4	2022	Upon AZD1775 treatment, activated PERK promotes apoptotic signaling via C/EBP-homologous protein (CHOP), while IRE1alpha-induced splicing of XBP1 (XBP1s) maintains cell survival by repressing apoptosis.	adavosertib	5-12	DNA damage inducible transcript 3	Homo sapiens	98-102
35283426-0	2022	Gossypol induces apoptosis of human pancreatic cancer cells via CHOP/endoplasmic reticulum stress signaling pathway.	Gossypol	0-8	DNA damage inducible transcript 3	Homo sapiens	64-68
35283426-6	2022	In addition, gossypol facilitated the cleavage of caspase-3 via protein kinase RNA-like ER kinase (PERK), CHOP, and Bax/Bcl-2 upregulation in both cells, whereas the upregulation of ATF was limited to BxPC-3 cells.	Gossypol	13-21	DNA damage inducible transcript 3	Homo sapiens	106-110
35283426-8	2022	Taken together, our data suggest that gossypol may trigger apoptosis in pancreatic cancer cells via the PERK-CHOP signaling pathway.	Gossypol	38-46	DNA damage inducible transcript 3	Homo sapiens	109-113
35151835-0	2022	Glaucocalyxin A impairs tumor growth via amplification of the ATF4/CHOP/CHAC1 cascade in human oral squamous cell carcinoma.	glaucocalyxin A	0-15	DNA damage inducible transcript 3	Homo sapiens	67-71
35151835-20	2022	CONCLUSION: GLA is a promising therapeutic agent that activates the ROS-mediated ATF4/CHOP/CHAC1 axis in OSCC patients.	Reactive Oxygen Species	68-71	DNA damage inducible transcript 3	Homo sapiens	86-90
35513732-6	2022	However, sodium selenite attenuates these adverse effects, including increases in apoptotic rate, caspase 3 activity, MDA, GRP78, and CHOP expression and decreases in SELS expression in cells treated with ZEL or Thapsigargin (Tg, an ER stress agonist).	Sodium Selenite	9-24	DNA damage inducible transcript 3	Homo sapiens	134-138
35620287-6	2022	Western blot results revealed that the ER stress pathway was activated by fluoxetine, including PERK, ATF4, and CHOP, while the AKT/mTOR pathway was inhibited.	Fluoxetine	74-84	DNA damage inducible transcript 3	Homo sapiens	112-116
35579082-8	2022	Cell viability and apoptosis upon CHOP treatment were determined by MTT assay and flow cytometry, respectively.	monooxyethylene trimethylolpropane tristearate	68-71	DNA damage inducible transcript 3	Homo sapiens	34-38
35367758-6	2022	Upstream of calcium mobilization, NNC-55-0396 activated the IRE1alpha arm of the Unfolded Protein Response (UPR) resulting in the nuclear translocation of pro-apoptotic CHOP.	Calcium	12-19	DNA damage inducible transcript 3	Homo sapiens	169-173
35571237-5	2022	In vitro, miR-150-5p overexpression decreased the contents of inflammatory factors interleukin- (IL-) 6, IL-8 along with cyclooxygenase-2 (COX-2), and endoplasmic reticulum (ER) stress markers glucose-regulated protein (GRP) 78 and C/-EBP homologous protein (CHOP) and promoted cell migrate.	mir-150-5p	10-20	DNA damage inducible transcript 3	Homo sapiens	232-257
35571237-5	2022	In vitro, miR-150-5p overexpression decreased the contents of inflammatory factors interleukin- (IL-) 6, IL-8 along with cyclooxygenase-2 (COX-2), and endoplasmic reticulum (ER) stress markers glucose-regulated protein (GRP) 78 and C/-EBP homologous protein (CHOP) and promoted cell migrate.	mir-150-5p	10-20	DNA damage inducible transcript 3	Homo sapiens	259-263
35478137-2	2022	To precisely monitor ADRs, we developed a medication instruction sheet (MIS) for patients who received rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) combination therapy for non-Hodgkin"s lymphoma (NHL).	Prednisolone	162-174	DNA damage inducible transcript 3	Homo sapiens	178-182
35195784-7	2022	In conjunction, guanabenz also attenuated the AD-related oxidative stress, impaired mitochondrial functionality (MMP, cytochrome-c translocation, ATP level, and mitochondrial complex I activity), endoplasmic reticulum stress (GRP78, GADD153, cleaved caspase-12), neuronal apoptosis (Bcl-2, Bax, cleaved caspase-3), and DNA fragmentation.	Guanabenz	16-25	DNA damage inducible transcript 3	Homo sapiens	233-240
35427876-8	2022	Further experiments demonstrated that two different signaling pathways were activated by PFOA-induced ER stress and involved in PFOA toxicity: the reactive oxygen species (ROS)-dependent ERK signaling triggered trophoblast proliferation, while the ATF4-dependent C/EBP homologous protein (CHOP) signaling was the trigger of apoptosis.	3-O-(N-(p-fluorobenzenesulfonyl)carbamoyl)oleanolic acid	89-93	DNA damage inducible transcript 3	Homo sapiens	263-287
35427876-8	2022	Further experiments demonstrated that two different signaling pathways were activated by PFOA-induced ER stress and involved in PFOA toxicity: the reactive oxygen species (ROS)-dependent ERK signaling triggered trophoblast proliferation, while the ATF4-dependent C/EBP homologous protein (CHOP) signaling was the trigger of apoptosis.	3-O-(N-(p-fluorobenzenesulfonyl)carbamoyl)oleanolic acid	89-93	DNA damage inducible transcript 3	Homo sapiens	289-293
35427876-8	2022	Further experiments demonstrated that two different signaling pathways were activated by PFOA-induced ER stress and involved in PFOA toxicity: the reactive oxygen species (ROS)-dependent ERK signaling triggered trophoblast proliferation, while the ATF4-dependent C/EBP homologous protein (CHOP) signaling was the trigger of apoptosis.	Reactive Oxygen Species	172-175	DNA damage inducible transcript 3	Homo sapiens	289-293
35439009-5	2022	QN523 treatment significantly increased the expression of HSPA5, DDIT3, TRIB3, and ATF3 genes, suggesting activation of the stress response pathway.	qn523	0-5	DNA damage inducible transcript 3	Homo sapiens	65-70
35051466-0	2022	Organophosphate flame retardants induce oxidative stress and Chop/Caspase 3-related apoptosis via Sod1/p53/Map3k6/Fkbp5 in NCI-1975 cells.	Organophosphates	0-15	DNA damage inducible transcript 3	Homo sapiens	61-65
35477428-8	2022	We further confirmed that diosmin blunted oxidative stress-, inflammation-, apoptosis-, and autophagy-related factors expression induced by HG via restraining the CHOP and GRP78 expressions.	Diosmin	26-33	DNA damage inducible transcript 3	Homo sapiens	163-167
35400257-8	2022	The expression of macromolecular biomarkers indicated that 6-methoxyflavone induced apoptosis through the PERK/EIF2alpha/ATF4/CHOP pathway.	6-methoxyflavone	59-75	DNA damage inducible transcript 3	Homo sapiens	126-130
35468783-1	2022	BACKGROUND: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has been used to treat patients with diffuse large B-cell lymphoma (DLBCL) under National Health Insurance (NHI) scheme in Indonesia.	Cyclophosphamide	27-43	DNA damage inducible transcript 3	Homo sapiens	89-93
35468783-1	2022	BACKGROUND: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has been used to treat patients with diffuse large B-cell lymphoma (DLBCL) under National Health Insurance (NHI) scheme in Indonesia.	Doxorubicin	45-56	DNA damage inducible transcript 3	Homo sapiens	89-93
35468783-1	2022	BACKGROUND: Rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) has been used to treat patients with diffuse large B-cell lymphoma (DLBCL) under National Health Insurance (NHI) scheme in Indonesia.	Prednisone	75-85	DNA damage inducible transcript 3	Homo sapiens	89-93
35468783-12	2022	If we refer to the threshold three times the GDP per capita (USD 11,538), R-CHOP could thus be determined as a cost-effective therapy.	Guanosine Diphosphate	45-48	DNA damage inducible transcript 3	Homo sapiens	76-80
34995350-8	2022	R-CHOP delays of >=7 days were significantly increased with i-HD-MTX versus EOT, with 308/1573 (19.6%) i-HD-MTX treatments resulting in delay to subsequent R-CHOP (median 8 days).	Methotrexate	65-68	DNA damage inducible transcript 3	Homo sapiens	2-6
34995350-8	2022	R-CHOP delays of >=7 days were significantly increased with i-HD-MTX versus EOT, with 308/1573 (19.6%) i-HD-MTX treatments resulting in delay to subsequent R-CHOP (median 8 days).	Methotrexate	65-68	DNA damage inducible transcript 3	Homo sapiens	158-162
34995350-8	2022	R-CHOP delays of >=7 days were significantly increased with i-HD-MTX versus EOT, with 308/1573 (19.6%) i-HD-MTX treatments resulting in delay to subsequent R-CHOP (median 8 days).	Methotrexate	108-111	DNA damage inducible transcript 3	Homo sapiens	2-6
34995350-8	2022	R-CHOP delays of >=7 days were significantly increased with i-HD-MTX versus EOT, with 308/1573 (19.6%) i-HD-MTX treatments resulting in delay to subsequent R-CHOP (median 8 days).	Methotrexate	108-111	DNA damage inducible transcript 3	Homo sapiens	158-162
35395098-8	2022	Incubation of HuH-7 liver cells with THCA, which was efficiently taken up, but not through BA transporters, increased ROS production (flow cytometry), ER stress biomarkers (GRP78, CHOP and XBP1-S/XBP1-U ratio), and BAXalpha expression (RT-qPCR and immunoblot), whereas cell viability was decreased (MTT).	thca	37-41	DNA damage inducible transcript 3	Homo sapiens	180-184
35562919-4	2022	We found that the expression of the genes involved in the activation of the unfolded protein response and the pro-apoptotic transcription factor DDIT3 were markedly upregulated in patients with Sjogren"s dry-eye disease and in a human model of corneal epithelial differentiation following treatment with hyperosmotic saline.	Sodium Chloride	317-323	DNA damage inducible transcript 3	Homo sapiens	145-150
35410313-7	2022	Combinational therapies with rituximab-ibrutinib, rituximab-venetoclax and rituximab-CHOP also induced CD20 internalization which was again effectively blocked by BI-1206.	bi-1206	163-170	DNA damage inducible transcript 3	Homo sapiens	85-89
35410313-8	2022	BI-1206 significantly enhanced the in vivo anti-MCL efficacy of rituximab-ibrutinib (p = 0.05) and rituximab-venetoclax (p = 0.02), but not the rituximab-CHOP combination in JeKo-1 cell line-derived xenograft models.	bi-1206	0-7	DNA damage inducible transcript 3	Homo sapiens	154-158
35464062-15	2022	Furthermore, DDIT3 was identified as the hub gene based on PPI analysis, and ZINCOOOOO1531009 (Risedronate) was indicated to be a potential drug for DDIT3.	zincooooo1531009	77-93	DNA damage inducible transcript 3	Homo sapiens	13-18
35464062-15	2022	Furthermore, DDIT3 was identified as the hub gene based on PPI analysis, and ZINCOOOOO1531009 (Risedronate) was indicated to be a potential drug for DDIT3.	zincooooo1531009	77-93	DNA damage inducible transcript 3	Homo sapiens	149-154
35464062-15	2022	Furthermore, DDIT3 was identified as the hub gene based on PPI analysis, and ZINCOOOOO1531009 (Risedronate) was indicated to be a potential drug for DDIT3.	Risedronic Acid	95-106	DNA damage inducible transcript 3	Homo sapiens	13-18
35266887-12	2022	Propranolol treatment elevated the activity of caspase-3 and expression of bax, Wee1, GADD153 and apoptosis-inducing factor, but decreased bcl-2 which is an antiapoptotic protein.	Propranolol	0-11	DNA damage inducible transcript 3	Homo sapiens	86-93
35464062-15	2022	Furthermore, DDIT3 was identified as the hub gene based on PPI analysis, and ZINCOOOOO1531009 (Risedronate) was indicated to be a potential drug for DDIT3.	Risedronic Acid	95-106	DNA damage inducible transcript 3	Homo sapiens	149-154
35464062-17	2022	Risedronate was screened as a potential drug for BKPyVAN by targeting DDIT3.	Risedronic Acid	0-11	DNA damage inducible transcript 3	Homo sapiens	70-75
35433440-9	2022	Further detection of PERK, GRP78 and CHOP revealed that PERK signaling was upregulated by treatment with U50488h, while treatment with the PERK inhibitor GSK2656157 partially reversed the promotion of apoptosis and inhibition of cell proliferation by U50488h, indicating that endoplasmic reticulum stress is associated with its suppressing effect on HCC malignant phenotypes.	3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer	105-112	DNA damage inducible transcript 3	Homo sapiens	37-41
35101669-9	2022	Azoramide pretreatment partly alleviated tachypacing-induced calcium dyshomeostasis, ATP consumption, and accelerated apoptosis, which was likely achieved by regulating the PERK/CHOP/CaMKII pathway.	N-(2-(2-(4-chlorophenyl)-1,3-thiazol-4-yl)ethyl)butanamide	0-9	DNA damage inducible transcript 3	Homo sapiens	178-182
35101669-10	2022	Azoramide protected atrial myocytes against injury induced by high-frequency electrical stimulation by regulating ER stress, which may inhibit cell apoptosis and calcium dyshomeostasis via the PERK/CHOP/CaMKII pathway.	N-(2-(2-(4-chlorophenyl)-1,3-thiazol-4-yl)ethyl)butanamide	0-9	DNA damage inducible transcript 3	Homo sapiens	198-202
35101669-10	2022	Azoramide protected atrial myocytes against injury induced by high-frequency electrical stimulation by regulating ER stress, which may inhibit cell apoptosis and calcium dyshomeostasis via the PERK/CHOP/CaMKII pathway.	Calcium	162-169	DNA damage inducible transcript 3	Homo sapiens	198-202
35545831-9	2022	The patient received chemotherapy with cyclophosphamide, vincristine, doxorubicin, and prednisolone (CHOP protocol) for 3 cycles.	Prednisolone	87-99	DNA damage inducible transcript 3	Homo sapiens	101-105
35192143-9	2022	4-PBA treatment significantly hindered the expression of endoplasmic reticulum stress markers, such as PERK, ATF4, ATF6, p-eIF2alpha, IRE1, CHOP and XBP1, suggesting that the administration of 4-PBA was successful.	4-phenylbutyric acid	0-5	DNA damage inducible transcript 3	Homo sapiens	140-144
35573753-3	2022	We report a case of a 67-year-old woman with a story of non-Hodgkin lymphoma treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), who got a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection while being totally depleted of B cells.	Cyclophosphamide	113-129	DNA damage inducible transcript 3	Homo sapiens	92-96
35573753-3	2022	We report a case of a 67-year-old woman with a story of non-Hodgkin lymphoma treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), who got a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection while being totally depleted of B cells.	Doxorubicin	131-142	DNA damage inducible transcript 3	Homo sapiens	92-96
35573753-3	2022	We report a case of a 67-year-old woman with a story of non-Hodgkin lymphoma treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), who got a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection while being totally depleted of B cells.	Vincristine	144-155	DNA damage inducible transcript 3	Homo sapiens	92-96
35573753-3	2022	We report a case of a 67-year-old woman with a story of non-Hodgkin lymphoma treated with R-CHOP (rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone), who got a severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection while being totally depleted of B cells.	Prednisone	161-171	DNA damage inducible transcript 3	Homo sapiens	92-96
35433440-9	2022	Further detection of PERK, GRP78 and CHOP revealed that PERK signaling was upregulated by treatment with U50488h, while treatment with the PERK inhibitor GSK2656157 partially reversed the promotion of apoptosis and inhibition of cell proliferation by U50488h, indicating that endoplasmic reticulum stress is associated with its suppressing effect on HCC malignant phenotypes.	GSK2656157	154-164	DNA damage inducible transcript 3	Homo sapiens	37-41
35182797-0	2022	Gestational exposure to BDE-209 induces placental injury via the endoplasmic reticulum stress-mediated PERK/ATF4/CHOP signaling pathway.	decabromobiphenyl ether	24-31	DNA damage inducible transcript 3	Homo sapiens	113-117
35392483-3	2022	With the advent of new therapeutic options, it becomes necessary to predict responses to the standard treatment based on rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP).	Prednisone	180-190	DNA damage inducible transcript 3	Homo sapiens	194-198
35387352-5	2022	Further, the FOXO3a protein accumulated due to the blockade of autophagy flux which in turn was associated with the induction of ER stress by transcriptional upregulation of PERK-CHOP pathway, subsequently causing apoptosis due to pitavastatin treatment.	pitavastatin	231-243	DNA damage inducible transcript 3	Homo sapiens	179-183
35387352-6	2022	Taken together, pitavastatin-mediated blockade of autophagy flux caused an accumulation of FOXO3a protein, thereby leading to the induction of PERK, ultimately causing CHOP-mediated apoptosis in cancer cells.	pitavastatin	16-28	DNA damage inducible transcript 3	Homo sapiens	168-172
35434414-11	2022	Conclusions: Smaller ASA was an independent risk factor and had significant incremental value for CTRCD in patients with malignant lymphoma who received the CHOP-like regimen.	Aspirin	21-24	DNA damage inducible transcript 3	Homo sapiens	157-161
35317846-2	2022	The standard treatment for canine lymphoma is "CHOP" multiagent chemotherapy protocol consisting of Cyclophosphamide, Doxorubicin (Hydroxydaunorubicin), Vincristine (Oncovin ), and Prednisone.	Vincristine	153-164	DNA damage inducible transcript 3	Homo sapiens	47-51
35317846-2	2022	The standard treatment for canine lymphoma is "CHOP" multiagent chemotherapy protocol consisting of Cyclophosphamide, Doxorubicin (Hydroxydaunorubicin), Vincristine (Oncovin ), and Prednisone.	Prednisone	181-191	DNA damage inducible transcript 3	Homo sapiens	47-51
35297262-13	2022	The patient received treatment with mini-CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone) plus rituximab with partial response after the third cycle.	Cyclophosphamide	60-76	DNA damage inducible transcript 3	Homo sapiens	41-45
35297262-13	2022	The patient received treatment with mini-CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone) plus rituximab with partial response after the third cycle.	Doxorubicin	78-89	DNA damage inducible transcript 3	Homo sapiens	41-45
35297262-13	2022	The patient received treatment with mini-CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone) plus rituximab with partial response after the third cycle.	Vincristine	91-102	DNA damage inducible transcript 3	Homo sapiens	41-45
35297262-13	2022	The patient received treatment with mini-CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisolone) plus rituximab with partial response after the third cycle.	Prednisolone	108-120	DNA damage inducible transcript 3	Homo sapiens	41-45
35355558-8	2022	However, TUDCA treatment can alleviate the increased expression levels of BMP2, PERK ATF4, and CHOP under ox-LDL stimulation to a certain extent.	ursodoxicoltaurine	9-14	DNA damage inducible transcript 3	Homo sapiens	95-99
35451406-1	2022	ABSTRACT: Maintaining relative dose intensity (RDI) of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) improves the prognosis of patients with diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	66-82	DNA damage inducible transcript 3	Homo sapiens	128-132
35451406-1	2022	ABSTRACT: Maintaining relative dose intensity (RDI) of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) improves the prognosis of patients with diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	84-95	DNA damage inducible transcript 3	Homo sapiens	128-132
35451406-1	2022	ABSTRACT: Maintaining relative dose intensity (RDI) of rituximab, cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) improves the prognosis of patients with diffuse large B-cell lymphoma (DLBCL).	Prednisone	114-124	DNA damage inducible transcript 3	Homo sapiens	128-132
35233582-6	2022	Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01).	Tunicamycin	0-11	DNA damage inducible transcript 3	Homo sapiens	87-91
35104011-7	2022	Nrf2 deficiency enhanced the tunicamycin-mediated induction of CHOP, which was attenuated by Sirt3 overexpression.	Tunicamycin	29-40	DNA damage inducible transcript 3	Homo sapiens	63-67
35325393-7	2022	Furthermore, Rh1 induces ER stress-mediated calcium accumulation via PERK/eIF2alpha/ATF4/CHOP pathway.	Calcium	44-51	DNA damage inducible transcript 3	Homo sapiens	89-93
35486884-8	2022	Patients achieved a longer median progression-free survival with 1L rituximab-CHOP (R-CHOP) versus CHOP or rituximab, cyclophosphamide, vincristine, and prednisone (RCVP) (7.7 v 3.0 or 1.8 years, respectively).	rcvp	165-169	DNA damage inducible transcript 3	Homo sapiens	78-82
35486884-5	2022	RESULTS: Most patients with NHL received 1L chemoimmunotherapy, most commonly cyclophosphamide, doxorubicin, vincristine, and prednisone (CHOP) with/without rituximab.	Prednisone	126-136	DNA damage inducible transcript 3	Homo sapiens	138-142
35486884-8	2022	Patients achieved a longer median progression-free survival with 1L rituximab-CHOP (R-CHOP) versus CHOP or rituximab, cyclophosphamide, vincristine, and prednisone (RCVP) (7.7 v 3.0 or 1.8 years, respectively).	rcvp	165-169	DNA damage inducible transcript 3	Homo sapiens	86-90
35486884-9	2022	Use of regimens other than R-CHOP was associated with a higher risk of death/progression for patients with DLBCL (rituximab, ifosfamide, carboplatin, and etoposide/ifosfamide, carboplatin, and etoposide) and FL (CHOP).	Etoposide	154-163	DNA damage inducible transcript 3	Homo sapiens	212-216
35486884-9	2022	Use of regimens other than R-CHOP was associated with a higher risk of death/progression for patients with DLBCL (rituximab, ifosfamide, carboplatin, and etoposide/ifosfamide, carboplatin, and etoposide) and FL (CHOP).	Carboplatin	176-187	DNA damage inducible transcript 3	Homo sapiens	212-216
35212819-5	2022	Employing alveolar epithelial cells with overexpression of the terminal ER stress signaling factor Chop or the IPF-associated surfactant protein C mutation (SPCDeltaexon4) in vitro, we observed a restoration of PACS2 levels upon treatment with CPS.	Capsaicin	244-247	DNA damage inducible transcript 3	Homo sapiens	99-103
35220927-1	2022	Bendamustine plus rituximab (BR) and rituximab, cyclophosphamide, doxorubicin, vincristine and prednisolone (R-CHOP) have been shown to be effective in the treatment of indolent B-cell lymphomas (iBCL).	Prednisolone	95-107	DNA damage inducible transcript 3	Homo sapiens	111-115
35218445-8	2022	Combination treatment with prednisolone, a component of CHOP and CVP, was found to enhance ADCC sensitivity of RL cells and resistant clones and to significantly suppress tumor growth in xenograft models.	Prednisolone	27-39	DNA damage inducible transcript 3	Homo sapiens	56-60
35210509-8	2022	Seventy-two patients were treated with a cyclophosphamide, doxorubicin, vincristine, and prednisolone (CHOP-like) regimen, and six were treated with low-toxicity regimens.	Prednisolone	89-101	DNA damage inducible transcript 3	Homo sapiens	103-107
35149956-9	2022	PERK, CHOP, and the concomitant responses of quercetin in restoring the ER homeostasis in cellular organelles like mitochondria and ER, against Cu-induced toxic insults by modulating autophagic pathways.	Quercetin	45-54	DNA damage inducible transcript 3	Homo sapiens	6-10
35204594-1	2022	A 44-year-old woman presented with high (18F)FDG uptake liver lesion after six courses of R-CHOP and radiotherapy for abdominal DLBCL, which was misdiagnosed as a hepatic invasion.	Fluorodeoxyglucose F18	45-48	DNA damage inducible transcript 3	Homo sapiens	92-96
35300350-10	2021	Interestingly, lower expression of miR-27a by curcumin action enhanced the C/EBP homologous protein(CHOP) expression, leading to paraptosis.	Curcumin	46-54	DNA damage inducible transcript 3	Homo sapiens	100-104
35524380-8	2022	BzATP not only significantly increased the expression levels of CHOP, GADD34, ATF6, and HERP but also significantly decreases the XBP1 expression level in M1 macrophages.	BzATP	0-5	DNA damage inducible transcript 3	Homo sapiens	64-68
35139925-7	2022	The effects of RAM2061 and/or PI (bortezomib or carfilzomib) on markers of UPR and apoptosis were evaluated by a combination of immunoblot (ATF4, IRE1, p-eIF2a, cleaved caspases and PARP), RT-PCR (ATF4, ATF6, CHOP, PERK, IRE1) and flow cytometry (Annexin-V).	ram2061	15-22	DNA damage inducible transcript 3	Homo sapiens	209-213
35524380-9	2022	The present study showed that BzATP induces cellular stress in M1 macrophages by elevating the expression levels of UPR genes including CHOP, GADD34, ATF6, and reducing cell viability.	BzATP	30-35	DNA damage inducible transcript 3	Homo sapiens	136-140
35257357-13	2022	The treatment of psoralen resulted in an increase in ATF-6 and CHOP protein levels as well as a decrease in Bcl-2 protein level, indicating that cell apoptosis induced by psoralen was associated with ER stress.	Ficusin	17-25	DNA damage inducible transcript 3	Homo sapiens	63-67
35186752-5	2022	RNA sequencing identified 126 genes that were regulated by both FUS-DDIT3 expression and JAK1/2 inhibition using ruxolitinib.	ruxolitinib	113-124	DNA damage inducible transcript 3	Homo sapiens	68-73
34999051-11	2022	Physical binding of KDM4E to Bim and CHOP promoters decreased the response to ML324.	ML324	78-83	DNA damage inducible transcript 3	Homo sapiens	37-41
34622970-10	2022	After five cycles of cyclophosphamide + doxorubicin + vincristine + prednisolone (CHOP) chemotherapy, the patient achieved complete remission.	Vincristine	54-65	DNA damage inducible transcript 3	Homo sapiens	82-86
34622970-10	2022	After five cycles of cyclophosphamide + doxorubicin + vincristine + prednisolone (CHOP) chemotherapy, the patient achieved complete remission.	Prednisolone	68-80	DNA damage inducible transcript 3	Homo sapiens	82-86
34981454-6	2022	Interestingly, butylparaben-induced activation of apoptosis involved the upstream activation of ER stress proteins such as GRP78, CHOP, and ATF4.	butylparaben	15-27	DNA damage inducible transcript 3	Homo sapiens	130-134
35158997-5	2022	There is no definitive guideline for the treatment of PEL, although CHOP-like regimens (cyclophosphamide, doxorubicin, vincristine, and prednisone) are frequently prescribed and, given the rarity of this disease, therapeutic focus is being redirected to personalized and targeted approaches in the experimental realm.	Prednisone	136-146	DNA damage inducible transcript 3	Homo sapiens	68-72
35200638-12	2022	Western blot analysis of Hep3B cells treated with (-)-agelasidine A showed that endoplasmic reticulum (ER) stress-related proteins (GRP78, phosphorylated PERK, phosphorylated eIF2alpha, ATF4, truncated ATF6, and CHOP) were upregulated.	agelasidine A	54-67	DNA damage inducible transcript 3	Homo sapiens	212-216
34987165-7	2022	Bendamustine was a better chemotherapy backbone than CHOP either with maintenance (R-Benda-R vs R-CHOP-R, HR = 0.62; G-Benda-G vs G-CHOP-G, HR = 0.55) or without maintenance therapy (R-Benda vs R-CHOP, HR = 0.68).	Bendamustine Hydrochloride	0-12	DNA damage inducible transcript 3	Homo sapiens	98-102
34987165-7	2022	Bendamustine was a better chemotherapy backbone than CHOP either with maintenance (R-Benda-R vs R-CHOP-R, HR = 0.62; G-Benda-G vs G-CHOP-G, HR = 0.55) or without maintenance therapy (R-Benda vs R-CHOP, HR = 0.68).	Bendamustine Hydrochloride	0-12	DNA damage inducible transcript 3	Homo sapiens	196-200
34985729-8	2022	Finally, intracellular ROS production was determined using fluorescent probes (DCFH-DA).High concentrations of UA either alone or combined with LPS increased the protein levels of GRP78 and CHOP.	Uric Acid	111-113	DNA damage inducible transcript 3	Homo sapiens	190-194
35153779-5	2022	Great individual variation in the C1-trough existed among patients with mucosa-associated lymphoma (MALT), and the high C1-trough observed in patients treated with the RB regimen was associated with a better response than was obtained with R-CHOP (38.41 +- 14.13 mug/ml vs 15.49 +- 8.80 mug/ml, p = 0.0029).	Rubidium	168-170	DNA damage inducible transcript 3	Homo sapiens	242-246
35096395-6	2022	She received six cycles R-CHOP chemotherapy (rituximab, cyclophosphamide, epirubicin, vincristine, and prednisone) with complete resolution of the mass.	Cyclophosphamide	56-72	DNA damage inducible transcript 3	Homo sapiens	26-30
35096395-6	2022	She received six cycles R-CHOP chemotherapy (rituximab, cyclophosphamide, epirubicin, vincristine, and prednisone) with complete resolution of the mass.	Epirubicin	74-84	DNA damage inducible transcript 3	Homo sapiens	26-30
35096395-6	2022	She received six cycles R-CHOP chemotherapy (rituximab, cyclophosphamide, epirubicin, vincristine, and prednisone) with complete resolution of the mass.	Vincristine	86-97	DNA damage inducible transcript 3	Homo sapiens	26-30
35096395-6	2022	She received six cycles R-CHOP chemotherapy (rituximab, cyclophosphamide, epirubicin, vincristine, and prednisone) with complete resolution of the mass.	Prednisone	103-113	DNA damage inducible transcript 3	Homo sapiens	26-30
35165522-8	2022	Moreover in vitro experiments, ER stress induced by tunicamycin (TM) not only significantly increased the expression of GRP78 and CHOP, but also caused the epithelial to myofibroblast transformation (EMT) of renal tubular epithelial cells, evidenced by decreased expression of E-cadherin and increased expression of vimentin, and extracellular matrix (ECM) deposition, evidenced by increased expression of fibronectin (FN).	Tunicamycin	52-63	DNA damage inducible transcript 3	Homo sapiens	130-134
35089671-3	2022	Rituximab (Rituxan), cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the current standard of care and cures more than 60% of patients.	Doxorubicin	39-50	DNA damage inducible transcript 3	Homo sapiens	83-87
35089671-3	2022	Rituximab (Rituxan), cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) is the current standard of care and cures more than 60% of patients.	Prednisone	69-79	DNA damage inducible transcript 3	Homo sapiens	83-87
35089671-6	2022	While numerous randomized trials have failed to improve upon R-CHOP, a recent press release from the POLARIX trial (NCT03274492) suggests that adding polatuzumab vedotin (Polivy) to rituximab, cyclophosphamide, doxorubicin, and prednisone (pola-R-CHP) improves progression-free survival and may replace R-CHOP in eligible patients.	polatuzumab vedotin	150-169	DNA damage inducible transcript 3	Homo sapiens	305-309
35005770-1	2022	In this commentary, we discuss new observations stating that spliced X-box-binding protein 1 (Xbp1s)-DNA damage-inducible transcript 3 (Ddit3) promotes monocrotaline (MCT)-induced pulmonary hypertension (Jiang et al., Clinical Science (2021) 135(21), https://doi.org/10.1042/CS20210612).	Monocrotaline	152-165	DNA damage inducible transcript 3	Homo sapiens	136-141
35005770-1	2022	In this commentary, we discuss new observations stating that spliced X-box-binding protein 1 (Xbp1s)-DNA damage-inducible transcript 3 (Ddit3) promotes monocrotaline (MCT)-induced pulmonary hypertension (Jiang et al., Clinical Science (2021) 135(21), https://doi.org/10.1042/CS20210612).	Monocrotaline	167-170	DNA damage inducible transcript 3	Homo sapiens	136-141
34985729-8	2022	Finally, intracellular ROS production was determined using fluorescent probes (DCFH-DA).High concentrations of UA either alone or combined with LPS increased the protein levels of GRP78 and CHOP.	ros	23-26	DNA damage inducible transcript 3	Homo sapiens	190-194
35257357-13	2022	The treatment of psoralen resulted in an increase in ATF-6 and CHOP protein levels as well as a decrease in Bcl-2 protein level, indicating that cell apoptosis induced by psoralen was associated with ER stress.	Ficusin	171-179	DNA damage inducible transcript 3	Homo sapiens	63-67
35044836-1	2022	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) represents the standard of care for first-line treatment of diffuse large B-cell lymphoma (DLBCL).	Cyclophosphamide	24-40	DNA damage inducible transcript 3	Homo sapiens	88-92
35044836-1	2022	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) represents the standard of care for first-line treatment of diffuse large B-cell lymphoma (DLBCL).	Doxorubicin	42-53	DNA damage inducible transcript 3	Homo sapiens	88-92
35044836-1	2022	PURPOSE: Rituximab with cyclophosphamide, doxorubicin, vincristine, and prednisolone (R-CHOP) represents the standard of care for first-line treatment of diffuse large B-cell lymphoma (DLBCL).	Prednisolone	72-84	DNA damage inducible transcript 3	Homo sapiens	88-92