PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	Imatinib Mesylate	128-136	ets variant 6	Mus musculus	203-211
31178725-8	2019	However, Sta treatment partially reversed cardiac morphological and functional deteriorations, and significantly blunted cardiac fibrosis as well as Tel.	stachydrine	9-12	ets variant 6	Mus musculus	149-152
30718686-5	2019	Telmisartan-treated conditioned medium (Tel-CM) of RAW264.7 cells and of bone marrow derived macrophages (BMDM) induced the expressions of browning markers in fully differentiated white adipocytes with reduced lipid droplets, and increased oxygen consumption rate and mitochondrial biogenesis.	Oxygen	240-246	ets variant 6	Mus musculus	0-3
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	ponatinib	141-150	ets variant 6	Mus musculus	203-211
25061103-6	2014	ETV6-RUNX1-expressing cells showed a significant defect in the chemotactic response to CXCL12, caused by a block in CXCR4 signaling, as demonstrated by inhibition of CXCL12-associated calcium flux and lack of ERK phosphorylation.	Calcium	184-191	ets variant 6	Mus musculus	0-4
23955076-4	2014	To achieve B-cell-specific expression of TEL-Syk in adult mice, we used a tamoxifen-inducible Cre mouse line.	Tamoxifen	74-83	ets variant 6	Mus musculus	41-44
19100521-2	2009	Tel/PDGFRbeta results in constitutive activation of several signaling pathways and induces a myeloproliferative disease in mice, with signals via tyrosines 579/581 identified as being important for this phenotype.	Tyrosine	146-155	ets variant 6	Mus musculus	0-3
23811600-5	2013	Demonstrating the value of the assay, we identify ETV6-NTRK3 as a target of the FDA-approved drug crizotinib (Xalkori).	Crizotinib	98-108	ets variant 6	Mus musculus	50-54
23811600-6	2013	Crizotinib inhibits proliferation of ETV6-NTRK3-dependent tumor cells with nanomolar potency and induces the regression of established tumor xenografts in mice.	Crizotinib	0-10	ets variant 6	Mus musculus	37-41
22108089-5	2012	TEL-receiving Tg26 (TRTg) displayed less advanced glomerular and tubular lesions when compared with saline-receiving Tg26 (SRTg).	tg26	14-18	ets variant 6	Mus musculus	0-3
22204395-3	2011	METHODS: Oligonucleotide microarray was performed to compare mRNA changes attributable to BCR-ABL, TEL-PDGFRB and TEL-JAK2 after 1 week of activation of each fusion in Ba/F3 cell lines.	Oligonucleotides	9-24	ets variant 6	Mus musculus	99-102
22204395-4	2011	Imatinib was used to control the activation of BCR-ABL and TEL-PDGFRB, and TEL-JAK2-mediated gene expression was examined 1 week after Ba/F3-TEL-JAK2 cells were switched to factor-independent conditions.	Imatinib Mesylate	0-8	ets variant 6	Mus musculus	59-62
24339741-0	2013	ETV6/RUNX1 induces reactive oxygen species and drives the accumulation of DNA damage in B cells.	Reactive Oxygen Species	19-42	ets variant 6	Mus musculus	0-4
24339741-7	2013	Remarkably, these pro-B cell lines as well as primary bone marrow cells derived from ETV6/RUNX1 transgenic animals display elevated levels of reactive oxygen species (ROS) as tested with ETV6/RUNX1 transgenic dihydroethidium staining.	Reactive Oxygen Species	142-165	ets variant 6	Mus musculus	85-89
24339741-7	2013	Remarkably, these pro-B cell lines as well as primary bone marrow cells derived from ETV6/RUNX1 transgenic animals display elevated levels of reactive oxygen species (ROS) as tested with ETV6/RUNX1 transgenic dihydroethidium staining.	Reactive Oxygen Species	167-170	ets variant 6	Mus musculus	85-89
24339741-8	2013	In line, intracellular phospho-histone H2AX flow cytometry and comet assay revealed increased DNA damage indicating that ETV6/RUNX1 expression enhances ROS.	Reactive Oxygen Species	152-155	ets variant 6	Mus musculus	121-125
24339741-9	2013	On the basis of our data, we propose the following model: the expression of ETV6/RUNX1 creates a preleukemic clone and leads to increased ROS levels.	Reactive Oxygen Species	138-141	ets variant 6	Mus musculus	76-80
22875628-3	2013	Ruxolitinib-treated Ba/F3 cells transformed to IL3 independence by ETV6-JAK2 showed reduced proliferation and survival (IC(50) = 370 nM) compared with KG1A or Ba/F3 cells transformed by BCR-ABL1, SPBN1-FLT3 and ZMYM2-FGFR1 (IC(50) > 10 muM for all).	ruxolitinib	0-11	ets variant 6	Mus musculus	67-71
22829185-4	2011	NS-018 showed potent antiproliferative activity against cell lines expressing a constitutively activated JAK2 (the JAK2V617F or MPLW515L mutations or the TEL-JAK2 fusion gene; IC(50)=11-120 n), but showed only minimal cytotoxicity against most other hematopoietic cell lines without a constitutively activated JAK2.	NS-018	0-6	ets variant 6	Mus musculus	154-157
21572589-1	2011	A series of novel 3,5-diamino-1,2,4-triazole benzyl ureas was identified as having potent anaplastic lymphoma kinase (ALK) inhibition exemplified by 15a, 20a, and 23a, which exhibited antiproliferative IC(50) values of 70, 40, and 20 nM in Tel-ALK transformed Ba/F3 cells, respectively.	3,5-diamino-1,2,4-triazole benzyl ureas	18-57	ets variant 6	Mus musculus	240-243
19890372-7	2010	Conversely, knockdown of the endogenous miR-125b in the ETV6/RUNX1 leukemia cell line REH increased apoptosis after Doxorubicin and Staurosporine treatments.	mir-125b	40-48	ets variant 6	Mus musculus	56-60
19890372-7	2010	Conversely, knockdown of the endogenous miR-125b in the ETV6/RUNX1 leukemia cell line REH increased apoptosis after Doxorubicin and Staurosporine treatments.	Doxorubicin	116-127	ets variant 6	Mus musculus	56-60
19890372-7	2010	Conversely, knockdown of the endogenous miR-125b in the ETV6/RUNX1 leukemia cell line REH increased apoptosis after Doxorubicin and Staurosporine treatments.	Staurosporine	132-145	ets variant 6	Mus musculus	56-60
18775810-3	2008	AZ960 inhibits JAK2 kinase with a K(i) of 0.00045 microm in vitro and treatment of TEL-JAK2 driven Ba/F3 cells with AZ960 blocked STAT5 phosphorylation and potently inhibited cell proliferation (GI(50)=0.025 microm).	5-fluoro-2-(1-(4-fluorophenyl)ethylamino)-6-(5-methyl-1H-pyrazol-3-ylamino)nicotinonitrile	0-5	ets variant 6	Mus musculus	83-86
18775810-3	2008	AZ960 inhibits JAK2 kinase with a K(i) of 0.00045 microm in vitro and treatment of TEL-JAK2 driven Ba/F3 cells with AZ960 blocked STAT5 phosphorylation and potently inhibited cell proliferation (GI(50)=0.025 microm).	5-fluoro-2-(1-(4-fluorophenyl)ethylamino)-6-(5-methyl-1H-pyrazol-3-ylamino)nicotinonitrile	116-121	ets variant 6	Mus musculus	83-86
16953222-4	2007	Hck was found strongly phosphorylated in Tel-Abl-expressing Ba/F3 cells and sensitive to imatinib mesylate treatment, providing evidence that Hck is a target of Tel-Abl tyrosine kinase activity.	Imatinib Mesylate	89-106	ets variant 6	Mus musculus	161-164
17409427-5	2007	We show that ETV6-NTRK3 associates with c-Src, and that treatment with SU6656, a c-Src inhibitor, completely blocks ETV6-NTRK-transforming activity.	SU 6656	71-77	ets variant 6	Mus musculus	116-120
17409427-6	2007	Treatment of NIH3T3 cells expressing ETV6-NTRK3 with SU6656 attenuated the activation of Ras-Erk1/2 and PI3K-Akt.	SU 6656	53-59	ets variant 6	Mus musculus	37-41
17409427-5	2007	We show that ETV6-NTRK3 associates with c-Src, and that treatment with SU6656, a c-Src inhibitor, completely blocks ETV6-NTRK-transforming activity.	SU 6656	71-77	ets variant 6	Mus musculus	13-17
16953222-4	2007	Hck was found strongly phosphorylated in Tel-Abl-expressing Ba/F3 cells and sensitive to imatinib mesylate treatment, providing evidence that Hck is a target of Tel-Abl tyrosine kinase activity.	Imatinib Mesylate	89-106	ets variant 6	Mus musculus	41-44
16643438-4	2006	Similarly, transfection with BCR/ABL or TEL/PDGFRbeta leukaemogenic tyrosine kinases chronically elevated PtdIns(3,4,5)P3 levels.	phosphatidylinositol 3,4,5-triphosphate	106-121	ets variant 6	Mus musculus	40-43
15750350-0	2005	Up-regulation of glutathione biosynthesis in NIH3T3 cells transformed with the ETV6-NTRK3 gene fusion.	Glutathione	17-28	ets variant 6	Mus musculus	79-83
15729383-9	2005	When expressed in CHO cells, wild-type TEL/ARG induced the formation of fillopodia, in a fashion dependent on the C-terminal portion and intact kinase activity.	CAV protocol	18-21	ets variant 6	Mus musculus	39-42
15729383-9	2005	When expressed in CHO cells, wild-type TEL/ARG induced the formation of fillopodia, in a fashion dependent on the C-terminal portion and intact kinase activity.	Arginine	43-46	ets variant 6	Mus musculus	39-42
15729383-10	2005	Thus, these results suggest several critical domains within TEL/ARG necessary for function, and indicate that the signaling pathways necessary for viability, growth factor hyper-responsiveness and cytoskeletal reorganization are likely to be separate.	Arginine	64-67	ets variant 6	Mus musculus	60-63
15750350-3	2005	The level of glutathione (GSH) was found to be markedly increased in ETV6-NTRK3-transformed NIH3T3 cells.	Glutathione	13-24	ets variant 6	Mus musculus	69-73
15750350-3	2005	The level of glutathione (GSH) was found to be markedly increased in ETV6-NTRK3-transformed NIH3T3 cells.	Glutathione	26-29	ets variant 6	Mus musculus	69-73
15750350-7	2005	These observations imply that up-regulation of GSH biosynthesis plays a central role in ETV6-NTRK3-induced transformation.	Glutathione	47-50	ets variant 6	Mus musculus	88-92
15054045-3	2004	Alanine substitution of W593, essential for protein-protein interaction in the context of other WW domains, impaired TEL-PDGFbetaR-mediated transformation of hematopoietic cells due to inhibition of TEL-PDGFbetaR kinase activity.	Alanine	0-7	ets variant 6	Mus musculus	117-120
15044254-0	2004	Complete remission of TEL-PDGFRB-induced myeloproliferative disease in mice by receptor tyrosine kinase inhibitor SU11657.	SU 11657	114-121	ets variant 6	Mus musculus	22-25
15054045-3	2004	Alanine substitution of W593, essential for protein-protein interaction in the context of other WW domains, impaired TEL-PDGFbetaR-mediated transformation of hematopoietic cells due to inhibition of TEL-PDGFbetaR kinase activity.	Alanine	0-7	ets variant 6	Mus musculus	199-202
15044254-3	2004	SU11657 inhibited TEL/PDGFbetaR kinase activity at nanomolar concentrations and inhibited TELPDGFRB-mediated factor-independent growth in myeloblastic 32D cells.	SU 11657	0-7	ets variant 6	Mus musculus	18-21
15199413-0	2004	Stable expression of small interfering RNA sensitizes TEL-PDGFbetaR to inhibition with imatinib or rapamycin.	Imatinib Mesylate	87-95	ets variant 6	Mus musculus	54-57
15199413-0	2004	Stable expression of small interfering RNA sensitizes TEL-PDGFbetaR to inhibition with imatinib or rapamycin.	Sirolimus	99-108	ets variant 6	Mus musculus	54-57
15199413-7	2004	TPsiRNA also inhibited an imatinib-resistant TEL-PDGFbetaR mutant, and the inhibition was enhanced by siRNA in combination with PKC412, another PDGFbetaR inhibitor.	Imatinib Mesylate	26-34	ets variant 6	Mus musculus	45-48
15060146-8	2004	A mutant carrying substituted glutamates on both Ser(213) and Ser(257) functionally mimics hyperphosphorylated TEL and also shows a dominant-negative effect on TEL-induced transcriptional suppression.	Serine	62-65	ets variant 6	Mus musculus	111-114
15060146-8	2004	A mutant carrying substituted glutamates on both Ser(213) and Ser(257) functionally mimics hyperphosphorylated TEL and also shows a dominant-negative effect on TEL-induced transcriptional suppression.	Serine	62-65	ets variant 6	Mus musculus	160-163
15060146-8	2004	A mutant carrying substituted glutamates on both Ser(213) and Ser(257) functionally mimics hyperphosphorylated TEL and also shows a dominant-negative effect on TEL-induced transcriptional suppression.	Glutamates	30-40	ets variant 6	Mus musculus	111-114
15060146-10	2004	Moreover, the glutamate mutant dominantly interferes with TEL-induced erythroid differentiation in MEL cells and growth suppression in NIH 3T3 cells.	Glutamic Acid	14-23	ets variant 6	Mus musculus	58-61
15060146-8	2004	A mutant carrying substituted glutamates on both Ser(213) and Ser(257) functionally mimics hyperphosphorylated TEL and also shows a dominant-negative effect on TEL-induced transcriptional suppression.	Glutamates	30-40	ets variant 6	Mus musculus	160-163
15060146-8	2004	A mutant carrying substituted glutamates on both Ser(213) and Ser(257) functionally mimics hyperphosphorylated TEL and also shows a dominant-negative effect on TEL-induced transcriptional suppression.	Serine	49-52	ets variant 6	Mus musculus	111-114
14987801-4	2004	TEL/ABL-transformed cells displayed resistance to these DNA damaging agents as evaluated by MTT assay and the survival advantage was associated with an accelerated kinetics of DNA repair as measured by the alkaline comet assay.	monooxyethylene trimethylolpropane tristearate	92-95	ets variant 6	Mus musculus	0-7
15060146-8	2004	A mutant carrying substituted glutamates on both Ser(213) and Ser(257) functionally mimics hyperphosphorylated TEL and also shows a dominant-negative effect on TEL-induced transcriptional suppression.	Serine	49-52	ets variant 6	Mus musculus	160-163
15005341-3	2004	Treatment of these cells with doxycycline, a tetracycline analogue, rapidly induced expression of the TEL/ARG protein.	Doxycycline	30-41	ets variant 6	Mus musculus	102-105
15005341-3	2004	Treatment of these cells with doxycycline, a tetracycline analogue, rapidly induced expression of the TEL/ARG protein.	Tetracycline	45-57	ets variant 6	Mus musculus	102-105
15005341-4	2004	TEL/ARG was heavily phosphorylated on tyrosine residues and was also found to rapidly induce tyrosine phosphorylation of multiple cellular proteins, including rasGAP, CBL, STAT5, PI3K, SHP2, Dok, and SHC.	Arginine	4-7	ets variant 6	Mus musculus	0-3
15005341-4	2004	TEL/ARG was heavily phosphorylated on tyrosine residues and was also found to rapidly induce tyrosine phosphorylation of multiple cellular proteins, including rasGAP, CBL, STAT5, PI3K, SHP2, Dok, and SHC.	Tyrosine	38-46	ets variant 6	Mus musculus	0-3
15005341-4	2004	TEL/ARG was heavily phosphorylated on tyrosine residues and was also found to rapidly induce tyrosine phosphorylation of multiple cellular proteins, including rasGAP, CBL, STAT5, PI3K, SHP2, Dok, and SHC.	Tyrosine	93-101	ets variant 6	Mus musculus	0-3
15005341-5	2004	The Ba/F3-tet-TEL/ARG cells remained interleukin (IL)-3 dependent without doxycycline but with doxycycline displayed a marked reduction in cell death in the absence of IL-3.	Doxycycline	74-85	ets variant 6	Mus musculus	14-17
15005341-5	2004	The Ba/F3-tet-TEL/ARG cells remained interleukin (IL)-3 dependent without doxycycline but with doxycycline displayed a marked reduction in cell death in the absence of IL-3.	Doxycycline	95-106	ets variant 6	Mus musculus	14-17
15005341-7	2004	At least in Ba/F3 cells, although the growth rate was much lower compared to that with IL-3, TEL/ARG appeared to induce some cell proliferation as an immediate consequence.	Arginine	97-100	ets variant 6	Mus musculus	93-96
12149229-5	2002	TEL-JAK2 expression in Ba/F3 cells results in constitutive association and tyrosine phosphorylation of Shc and Ship-1 and, consequently, recruitment of Grb2 to TEL-JAK2.	Tyrosine	75-83	ets variant 6	Mus musculus	0-3
14501384-0	2003	TEL-fusion oncogenic tyrosine kinases determine leukemic cells response to idarubicin.	Idarubicin	75-85	ets variant 6	Mus musculus	0-3
14501384-3	2003	In this work we examined a role of TEL family fusion oncoproteins in the response to idarubicin.	Idarubicin	85-95	ets variant 6	Mus musculus	35-38
12527908-4	2003	Overexpressing wild-type-TEL in MEL cells enhanced differentiation induced by hexamethylene bisacetamide or dimethylsulfoxide, as judged by the increased levels of erythroid-specific delta-aminolevulinate synthase and beta-globin mRNAs.	hexamethylene bisacetamide	78-104	ets variant 6	Mus musculus	25-28
12527908-4	2003	Overexpressing wild-type-TEL in MEL cells enhanced differentiation induced by hexamethylene bisacetamide or dimethylsulfoxide, as judged by the increased levels of erythroid-specific delta-aminolevulinate synthase and beta-globin mRNAs.	Dimethyl Sulfoxide	108-125	ets variant 6	Mus musculus	25-28
12443881-3	2002	Amifostine at 14 mM decreased DNA-damaging effect of idarubicin in human lymphocytes and BaF3 cells, but increased the effect in TEL/ABL-transformed cells.	Amifostine	0-10	ets variant 6	Mus musculus	129-132
12443881-3	2002	Amifostine at 14 mM decreased DNA-damaging effect of idarubicin in human lymphocytes and BaF3 cells, but increased the effect in TEL/ABL-transformed cells.	lauric acid	133-136	ets variant 6	Mus musculus	129-132
12173038-0	2002	ETV6-NTRK3 transformation requires insulin-like growth factor 1 receptor signaling and is associated with constitutive IRS-1 tyrosine phosphorylation.	Tyrosine	125-133	ets variant 6	Mus musculus	0-4
12149229-5	2002	TEL-JAK2 expression in Ba/F3 cells results in constitutive association and tyrosine phosphorylation of Shc and Ship-1 and, consequently, recruitment of Grb2 to TEL-JAK2.	Tyrosine	75-83	ets variant 6	Mus musculus	160-163
12080468-6	2002	It is also shown that multiple signaling molecules, including PI3K, SHC, ras-GAP and CRK-L, are tyrosine phosphorylated in Ba/F3 cells that express ETV6/ARG.	Tyrosine	96-104	ets variant 6	Mus musculus	148-152
11861293-6	2002	Activation of this pathway requires the kinase activity of TEL/PDGF beta R and is inhibited by the PDGF beta R inhibitor, STI571.	Imatinib Mesylate	122-128	ets variant 6	Mus musculus	59-62
12080468-6	2002	It is also shown that multiple signaling molecules, including PI3K, SHC, ras-GAP and CRK-L, are tyrosine phosphorylated in Ba/F3 cells that express ETV6/ARG.	Arginine	153-156	ets variant 6	Mus musculus	148-152
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	Imatinib Mesylate	0-6	ets variant 6	Mus musculus	93-100
12136932-0	2002	TEL/JAK2 tyrosine kinase inhibits DNA repair in the presence of amifostine.	Amifostine	64-74	ets variant 6	Mus musculus	0-3
12136932-7	2002	Idarubicin induced DNA damage in both cell types but amifostine reduced its extent in control non-transformed BaF3 cells and enhanced it in TEL/JAK2-transformed cells.	Amifostine	53-63	ets variant 6	Mus musculus	140-143
12136932-11	2002	Amifostine could promote apoptosis or lower the threshold for apoptosis induction dependent on TEL/JAK2 activation.	Amifostine	0-10	ets variant 6	Mus musculus	95-98
11719379-2	2001	TEL/PDGFbetaR mutants have been generated that contain tyrosine-to-phenylalanine (Tyr-->Phe) substitutions at phosphorylation sites present in the native PDGFbetaR to assess the role of these sites in cell transformation by TEL/PDGFbetaR.	Tyrosine	55-63	ets variant 6	Mus musculus	0-3
11719379-2	2001	TEL/PDGFbetaR mutants have been generated that contain tyrosine-to-phenylalanine (Tyr-->Phe) substitutions at phosphorylation sites present in the native PDGFbetaR to assess the role of these sites in cell transformation by TEL/PDGFbetaR.	Phenylalanine	67-80	ets variant 6	Mus musculus	0-3
11719379-2	2001	TEL/PDGFbetaR mutants have been generated that contain tyrosine-to-phenylalanine (Tyr-->Phe) substitutions at phosphorylation sites present in the native PDGFbetaR to assess the role of these sites in cell transformation by TEL/PDGFbetaR.	Tyrosine	82-85	ets variant 6	Mus musculus	0-3
11719379-2	2001	TEL/PDGFbetaR mutants have been generated that contain tyrosine-to-phenylalanine (Tyr-->Phe) substitutions at phosphorylation sites present in the native PDGFbetaR to assess the role of these sites in cell transformation by TEL/PDGFbetaR.	Phenylalanine	91-94	ets variant 6	Mus musculus	0-3
11719379-6	2001	Hyperphosphosphorylation of phospholipase Cgamma (PLCgamma) and the p85 subunit of phosphatidylinositol 3-kinase (PI3K) requires the carboxy terminal tyrosine residues of TEL/PDGFbetaR.	Tyrosine	150-158	ets variant 6	Mus musculus	171-174
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	Imatinib Mesylate	0-6	ets variant 6	Mus musculus	93-96
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	Imatinib Mesylate	0-6	ets variant 6	Mus musculus	102-105
11290609-8	2001	STI571 inhibited tyrosine phosphorylation and cell growth of Ba/F3 cells expressing BCR/ABL, TEL/ABL, TEL/PDGFbetaR, and TEL/ARG with an IC(50) of approximately 0.5 microM in each case, but it had no effect on untransformed Ba/F3 cells growing in IL-3 or on Ba/F3 cells transformed by TEL/JAK2.	Imatinib Mesylate	0-6	ets variant 6	Mus musculus	102-105
11290609-9	2001	Culture of TEL/ARG-transfected Ba/F3 cells with IL-3 completely prevented STI571-induced apoptosis in these cells, similar to what has been observed with BCR/ABL- or TEL/ABL-transformed cells.	Imatinib Mesylate	74-80	ets variant 6	Mus musculus	11-14
11083653-1	2000	We used a mouse peritonitis model to evaluate the in vivo efficacy of telithromycin (HMR 3647) (TEL) and erythromycin (ERY) against four strains of Enterococcus faecalis and three strains of Enterococcus faecium with differing susceptibilities to TEL.	telithromycin	70-83	ets variant 6	Mus musculus	96-99
11290609-2	2001	In addition to BCR/ABL, STI571 also inhibits v-Abl, TEL/ABL, the native platelet-derived growth factor (PDGF)beta receptor, and c-KIT, but it does not inhibit SRC family kinases, c-FMS, FLT3, the epidermal growth factor receptor, or multiple other tyrosine kinases.	Imatinib Mesylate	24-30	ets variant 6	Mus musculus	52-59
11290609-4	2001	As described here, ARG has recently been implicated in the pathogenesis of leukemia as a fusion partner of TEL.	Arginine	19-22	ets variant 6	Mus musculus	107-110
11290609-6	2001	When expressed in the factor-dependent murine hematopoietic cell line Ba/F3, the TEL/ARG protein was heavily phosphorylated on tyrosine, increased tyrosine phosphorylation of multiple cellular proteins, and induced factor-independent proliferation.	Tyrosine	127-135	ets variant 6	Mus musculus	81-84
11290609-6	2001	When expressed in the factor-dependent murine hematopoietic cell line Ba/F3, the TEL/ARG protein was heavily phosphorylated on tyrosine, increased tyrosine phosphorylation of multiple cellular proteins, and induced factor-independent proliferation.	Tyrosine	147-155	ets variant 6	Mus musculus	81-84
11083653-1	2000	We used a mouse peritonitis model to evaluate the in vivo efficacy of telithromycin (HMR 3647) (TEL) and erythromycin (ERY) against four strains of Enterococcus faecalis and three strains of Enterococcus faecium with differing susceptibilities to TEL.	telithromycin	70-83	ets variant 6	Mus musculus	247-250
11021752-6	2000	Immunoblot analyses showed that JAK 2, STAT 3, STAT 5a, STAT 5b and CBL were tyrosine-phosphorylated in TEL-FLT3 expressing Ba/F3 cells in the absence of IL-3.	Tyrosine	77-85	ets variant 6	Mus musculus	104-107
10913166-3	2000	Here we show that expression of TEL in Ras-transformed NIH 3T3 cells inhibits cell growth in soft agar and in normal cultures.	Agar	98-102	ets variant 6	Mus musculus	32-35
10683371-0	2000	Fatal myeloproliferation, induced in mice by TEL/PDGFbetaR expression, depends on PDGFbetaR tyrosines 579/581.	Tyrosine	92-101	ets variant 6	Mus musculus	45-48
10845925-7	2000	Expression of a tyrosine-phosphorylated TEL-JAK2 protein and activation of STAT1 and STAT5 (signal transducer and activator of transcription) were detected in leukemic tissues.	Tyrosine	16-24	ets variant 6	Mus musculus	40-43
10361134-5	1999	Active TEL-Jak2 constructs (consisting of either Jak2 JH1 or Jak2 JH2+JH1 domain fusions) were constitutively tyrosine-phosphorylated but did not affect phosphorylation of endogeneous Jak1, Jak2, or Jak3.	Tyrosine	110-118	ets variant 6	Mus musculus	7-10
10597306-4	1999	We demonstrate that tyrosine phosphorylation of the fusion protein can be attenuated through overexpression of the TEL part of TEL-PDGF beta R, suggesting a strategy for antagonizing the signaling of TEL-PDGF beta R, and other TEL-fusion proteins containing tyrosine kinase domains.	Tyrosine	20-28	ets variant 6	Mus musculus	115-118
10597306-4	1999	We demonstrate that tyrosine phosphorylation of the fusion protein can be attenuated through overexpression of the TEL part of TEL-PDGF beta R, suggesting a strategy for antagonizing the signaling of TEL-PDGF beta R, and other TEL-fusion proteins containing tyrosine kinase domains.	Tyrosine	20-28	ets variant 6	Mus musculus	127-130
10597306-4	1999	We demonstrate that tyrosine phosphorylation of the fusion protein can be attenuated through overexpression of the TEL part of TEL-PDGF beta R, suggesting a strategy for antagonizing the signaling of TEL-PDGF beta R, and other TEL-fusion proteins containing tyrosine kinase domains.	Tyrosine	20-28	ets variant 6	Mus musculus	127-130
10597306-4	1999	We demonstrate that tyrosine phosphorylation of the fusion protein can be attenuated through overexpression of the TEL part of TEL-PDGF beta R, suggesting a strategy for antagonizing the signaling of TEL-PDGF beta R, and other TEL-fusion proteins containing tyrosine kinase domains.	Tyrosine	20-28	ets variant 6	Mus musculus	127-130
10597306-6	1999	Finally, tyrosine residues 17 and 27 in TEL-PDGF beta R was identified as autophosphorylation sites in TEL-PDGF beta R.	Tyrosine	9-17	ets variant 6	Mus musculus	40-43
10597306-6	1999	Finally, tyrosine residues 17 and 27 in TEL-PDGF beta R was identified as autophosphorylation sites in TEL-PDGF beta R.	Tyrosine	9-17	ets variant 6	Mus musculus	103-106
10702799-4	2000	Moreover, ETV6-NTRK3 has PTK activity and is autophosphorylated on tyrosine residues.	Tyrosine	67-75	ets variant 6	Mus musculus	10-14
10702799-9	2000	Deletion of the ETV6 HLH domain abolished dimer formation with either ETV6 or ETV6-NTRK3, and cells expressing this mutant protein were morphologically non-transformed and failed to grow in soft agar.	Agar	195-199	ets variant 6	Mus musculus	16-20
10361134-6	1999	TEL-Jak2 activation resulted in the constitutive tyrosine phosphorylation of Stat1, Stat3, and Stat5 as determined by detection of phosphorylation using activation-specific antibodies and by binding of each protein to a preferential GAS sequence in electrophoretic mobility shift assays.	Tyrosine	49-57	ets variant 6	Mus musculus	0-3
8962143-5	1996	In vivo, TEL/PDGF beta R was detected as a 100-kDa protein that was constitutively phosphorylated on tyrosine and transformed the murine hematopoietic cell line Ba/F3 to interleukin 3 growth factor independence.	Tyrosine	101-109	ets variant 6	Mus musculus	9-12
10029600-5	1999	Treatment of TEL/PDGFbetaR transgenic animals with a protein tyrosine kinase inhibitor with in vitro activity against PDGFbetaR (CGP57148) resulted in suppression of disease and a prolongation of survival.	Imatinib Mesylate	129-137	ets variant 6	Mus musculus	13-16
9736611-5	1998	Furthermore, all TEL/JAK2 variants strongly activated STAT 5 by phosphotyrosine Western blots and by electrophoretic mobility shift assays (EMSA).	Phosphotyrosine	64-79	ets variant 6	Mus musculus	17-20
9653143-8	1998	Further, treatment with the proteasome inhibitor Z-IE(O-t-Bu)A-leucinal suppressed IL-3 and TEL/PDGFRbeta-dependent survival.	z-ie	49-53	ets variant 6	Mus musculus	92-95
34864570-5	2022	Especially, SIJ1263 is 80-fold more potent (GI50 = 24 nM) on TEL-FGFR4 V550E Ba/F3 cells than BLU9931, which suggests that SIJ1263 would be effective for overriding drug resistance.	sij1263	12-19	ets variant 6	Mus musculus	61-64
34864570-5	2022	Especially, SIJ1263 is 80-fold more potent (GI50 = 24 nM) on TEL-FGFR4 V550E Ba/F3 cells than BLU9931, which suggests that SIJ1263 would be effective for overriding drug resistance.	sij1263	123-130	ets variant 6	Mus musculus	61-64
35436119-7	2022	Furthermore, 17a and 17b exhibited remarkable efficacies in TEL-V555M-FGFR3 Ba/F3 xenograft mouse model and 17a is more efficacious than infigratinib.	infigratinib	137-149	ets variant 6	Mus musculus	60-63
35182957-8	2022	RESULTS AND DISCUSSION: The results suggest that combinatorial treatment of CDDP and renin-angiotensin system inhibitors, particularly ENA and TEL, may exacerbate CDDP-induced nephrotoxicity.	Cisplatin	76-80	ets variant 6	Mus musculus	143-146
35182957-8	2022	RESULTS AND DISCUSSION: The results suggest that combinatorial treatment of CDDP and renin-angiotensin system inhibitors, particularly ENA and TEL, may exacerbate CDDP-induced nephrotoxicity.	Cisplatin	163-167	ets variant 6	Mus musculus	143-146