PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
12808051-6	2003	Conversely, cells carrying a mutation in the Kar2 ATPase domain, in which Kar2 poorly dissociated from Ire1 even in the presence of tunicamycin, a potent inducer of ER stress, were unable to activate the pathway.	Tunicamycin	132-143	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	45-49
12578559-10	2003	However, AE2 expressed in the presence of the glycosylation inhibitor, tunicamycin, was not glycosylated, yet retained 85 +/- 8% of anion-transport activity.	Tunicamycin	71-82	NBPF member 3	Homo sapiens	9-12
12727195-4	2003	Here, we report that the mRNA of lectin ERGIC-53, a cargo receptor for the transport of glycoproteins from ER to ERGIC, and of its related protein VIP36 is induced by the known inducers of ER stress, tunicamycin and thapsigargin.	Tunicamycin	200-211	lectin, mannose binding 1	Homo sapiens	40-48
12727195-4	2003	Here, we report that the mRNA of lectin ERGIC-53, a cargo receptor for the transport of glycoproteins from ER to ERGIC, and of its related protein VIP36 is induced by the known inducers of ER stress, tunicamycin and thapsigargin.	Tunicamycin	200-211	lectin, mannose binding 2	Homo sapiens	147-152
12754298-4	2003	Cells in which ARMER was overexpressed exhibited protection from multiple apoptotic inducers including serum starvation, doxorubicin, UV irradiation, tumor necrosis factor alpha, and the ER stressors brefeldin A, tunicamycin, and thapsigargin.	Tunicamycin	213-224	ADP ribosylation factor like GTPase 6 interacting protein 1	Homo sapiens	15-20
12634852-5	2003	Inhibition of insulin-receptor processing using tunicamycin suggests that the basal interaction occurs during insulin-receptor biosynthesis in the ER.	Tunicamycin	48-59	insulin receptor	Homo sapiens	14-30
12634852-5	2003	Inhibition of insulin-receptor processing using tunicamycin suggests that the basal interaction occurs during insulin-receptor biosynthesis in the ER.	Tunicamycin	48-59	insulin receptor	Homo sapiens	110-126
12235182-2	2002	Substituting Asn residue with Gln at the single glycosylation site within apoB-17 (N(158)) decreased its secretion efficiency to a level equivalent to that of wild-type apoB-17 treated with tunicamycin, but had little effect on its synthesis or intracellular distribution.	Tunicamycin	190-201	apolipoprotein B	Homo sapiens	74-78
12943552-3	2003	The influence of N-glycosylation on AtXylT activity has been evaluated using either tunicamycin or mutagenesis of potential N-glycosylation sites.	Tunicamycin	84-95	beta-1,2-xylosyltransferase	Arabidopsis thaliana	36-42
12486168-6	2002	Moreover, AIGP1 gene expression in cultured neurons is specifically induced by the endoplasmic reticulum (ER)-Golgi stressors tunicamycin and brefeldin A.	Tunicamycin	126-137	serine incorporator 3	Homo sapiens	10-15
12228224-6	2002	Insulin-like growth factor-1, okadaic acid, calyculin A, and lithium also protected cells from two other inducers of ER stress, tunicamycin and brefeldin A.	Tunicamycin	128-139	insulin like growth factor 1	Homo sapiens	0-28
12175333-10	2002	Furthermore, soluble Protein A-CST expressed in the presence of tunicamycin was almost inactive, and accumulated in transfected cells.	Tunicamycin	64-75	galactose-3-O-sulfotransferase 1	Mus musculus	31-34
12409609-6	2002	To our knowledge, this is the first report of (i) visualization of the activation of Bid by proteolytic cleavage, with direct observation of the cleavage of YFP-Bid-CFP in the cytoplasm and subsequent translocation of the cleaved Bid to mitochondria and (ii) the absence of Abeta- or tunicamycin-mediated significant activation of caspase 8 in individual living cells.	Tunicamycin	284-295	BH3 interacting domain death agonist	Homo sapiens	85-88
12409609-6	2002	To our knowledge, this is the first report of (i) visualization of the activation of Bid by proteolytic cleavage, with direct observation of the cleavage of YFP-Bid-CFP in the cytoplasm and subsequent translocation of the cleaved Bid to mitochondria and (ii) the absence of Abeta- or tunicamycin-mediated significant activation of caspase 8 in individual living cells.	Tunicamycin	284-295	BH3 interacting domain death agonist	Homo sapiens	161-164
12409609-6	2002	To our knowledge, this is the first report of (i) visualization of the activation of Bid by proteolytic cleavage, with direct observation of the cleavage of YFP-Bid-CFP in the cytoplasm and subsequent translocation of the cleaved Bid to mitochondria and (ii) the absence of Abeta- or tunicamycin-mediated significant activation of caspase 8 in individual living cells.	Tunicamycin	284-295	BH3 interacting domain death agonist	Homo sapiens	161-164
12410842-9	2002	Furthermore, trr1 mutants are resistant to tunicamycin, consistent with their high UPR.	Tunicamycin	43-54	thioredoxin-disulfide reductase TRR1	Saccharomyces cerevisiae S288C	13-17
12488460-6	2003	Digestion of immunoprecipitated TPP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with tunicamycin reduced the molecular mass of TPP I proenzyme by approximately 10 kDa, which indicates that all five potential N-glycosylation sites in TPP I are utilized.	Tunicamycin	135-146	tripeptidyl peptidase 1	Homo sapiens	32-37
12488460-6	2003	Digestion of immunoprecipitated TPP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with tunicamycin reduced the molecular mass of TPP I proenzyme by approximately 10 kDa, which indicates that all five potential N-glycosylation sites in TPP I are utilized.	Tunicamycin	135-146	tripeptidyl peptidase 1	Homo sapiens	177-182
12488460-6	2003	Digestion of immunoprecipitated TPP I proenzyme with both N-glycosidase F and endoglycosidase H as well as treatment of the cells with tunicamycin reduced the molecular mass of TPP I proenzyme by approximately 10 kDa, which indicates that all five potential N-glycosylation sites in TPP I are utilized.	Tunicamycin	135-146	tripeptidyl peptidase 1	Homo sapiens	177-182
12556489-2	2003	In this report, we show that the expression of human GADD34 in cultured cells reversed eIF-2 alpha phosphorylation induced by thapsigargin and tunicamycin, agents that promote protein unfolding in the endoplasmic reticulum (ER).	Tunicamycin	143-154	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	53-59
12556489-2	2003	In this report, we show that the expression of human GADD34 in cultured cells reversed eIF-2 alpha phosphorylation induced by thapsigargin and tunicamycin, agents that promote protein unfolding in the endoplasmic reticulum (ER).	Tunicamycin	143-154	eukaryotic translation initiation factor 2A	Homo sapiens	87-98
12535667-2	2003	In transgenic plants, tunicamycin stimulated expression of a reporter gene under the control of the BiP promoter and promoter analysis identified a 24 bp sequence crucial to this induction.	Tunicamycin	22-33	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	100-103
12845220-6	2003	Overproduction of fibronectin and tenascin by HMCs was normalized by tunicamycin and brefeldin A.	Tunicamycin	69-80	fibronectin 1	Homo sapiens	18-29
12845220-6	2003	Overproduction of fibronectin and tenascin by HMCs was normalized by tunicamycin and brefeldin A.	Tunicamycin	69-80	tenascin C	Homo sapiens	34-42
12845220-6	2003	Overproduction of fibronectin and tenascin by HMCs was normalized by tunicamycin and brefeldin A.	Tunicamycin	69-80	MKKS centrosomal shuttling protein	Homo sapiens	46-50
12845220-7	2003	Similarly, when HMCs were exposed to exogenous TGF-beta, the increase in fibronectin was reversed by tunicamycin and brefeldin A.	Tunicamycin	101-112	MKKS centrosomal shuttling protein	Homo sapiens	16-20
12845220-7	2003	Similarly, when HMCs were exposed to exogenous TGF-beta, the increase in fibronectin was reversed by tunicamycin and brefeldin A.	Tunicamycin	101-112	transforming growth factor beta 1	Homo sapiens	47-55
12845220-7	2003	Similarly, when HMCs were exposed to exogenous TGF-beta, the increase in fibronectin was reversed by tunicamycin and brefeldin A.	Tunicamycin	101-112	fibronectin 1	Homo sapiens	73-84
14643758-4	2003	Treatment with SAC protected these cells against Abeta- and tunicamycin-induced neuronal death, which is mediated predominantly through caspase-12-dependent pathway in a concentration-dependent manner.	Tunicamycin	60-71	caspase 12	Rattus norvegicus	136-146
12384508-7	2002	The affinity toward FXa could be restored when the mutants were expressed in the presence of tunicamycin to inhibit glycosylation, indicating the lost FXa affinity to be caused by the added carbohydrates.	Tunicamycin	93-104	coagulation factor X	Homo sapiens	20-23
12384508-7	2002	The affinity toward FXa could be restored when the mutants were expressed in the presence of tunicamycin to inhibit glycosylation, indicating the lost FXa affinity to be caused by the added carbohydrates.	Tunicamycin	93-104	coagulation factor X	Homo sapiens	151-154
12515321-0	2002	Effect of 2-fluoropalmitate, cerulenin and tunicamycin on the palmitoylation and intracellular translocation of myelin proteolipid protein.	Tunicamycin	43-54	proteolipid protein 1	Rattus norvegicus	112-138
12147617-11	2002	Glucose deprivation or treatment of ARPE-19 cells with tunicamycin, brefeldin A, the calcium ionophore A23187, or thapsigargin increased the expression of VEGF mRNA in these cells by 8- to 10-fold.	Tunicamycin	55-66	vascular endothelial growth factor A	Homo sapiens	155-159
12081137-3	2002	Cells treated with tunicamycin produced only a 25 kDa band, representing a deglycosylated form of PrP.	Tunicamycin	19-30	prion protein	Homo sapiens	98-101
11991954-11	2002	Synthesis of the 74-kDa NFIC was also inhibited in this setting by tunicamycin.	Tunicamycin	67-78	nuclear factor I/C	Mus musculus	24-28
12058017-6	2002	Deletion of COD1 also impaired ER function, causing constitutive activation of the unfolded protein response, hypersensitivity to the glycosylation inhibitor tunicamycin, and synthetic lethality with deletion of the unfolded protein response regulator HAC1.	Tunicamycin	158-169	uncharacterized protein	Drosophila melanogaster	12-16
11877404-9	2002	The mobility of wt-CFTR and DeltaF508-CFTR was reduced by maneuvers that alter CFTR processing or interactions with molecular chaperones, including tunicamycin, geldanamycin, and lactacystin.	Tunicamycin	148-159	cystic fibrosis transmembrane conductance regulator	Cricetulus griseus	19-23
12021180-5	2002	Cycloheximide treatment, at a dose able to profoundly inhibit protein synthesis in FRTL-5 cells, obliterated the decrease in the level of the inhibitory subunit I kappa B alpha produced by thapsigargin and tunicamycin.	Tunicamycin	206-217	NFKB inhibitor alpha	Rattus norvegicus	161-176
11877404-9	2002	The mobility of wt-CFTR and DeltaF508-CFTR was reduced by maneuvers that alter CFTR processing or interactions with molecular chaperones, including tunicamycin, geldanamycin, and lactacystin.	Tunicamycin	148-159	cystic fibrosis transmembrane conductance regulator	Cricetulus griseus	38-42
11877404-9	2002	The mobility of wt-CFTR and DeltaF508-CFTR was reduced by maneuvers that alter CFTR processing or interactions with molecular chaperones, including tunicamycin, geldanamycin, and lactacystin.	Tunicamycin	148-159	cystic fibrosis transmembrane conductance regulator	Cricetulus griseus	38-42
11961028-6	2002	It was further shown that this glycosylation process is highly sensitive to inhibition by tunicamycin, which is a naturally occurring antibiotic, leading to retention of nonglycosylated nephrin molecules in the endoplasmic reticulum.	Tunicamycin	90-101	NPHS1 adhesion molecule, nephrin	Homo sapiens	186-193
11867635-7	2002	M2BP-1,2 expressed in tunicamycin-treated cells contained no glycosyl residues, indicating that O-glycosylation is not occurring.	Tunicamycin	22-33	galectin 3 binding protein	Homo sapiens	0-4
11961028-5	2002	When cells were treated with the N-glycosylation inhibitor, tunicamycin, the molecular weight of nephrin was decreased to a single immunoband of 150 kD, indicating that the shift in the electrophoretic migration of nephrin is due to N-linked carbohydrate moieties.	Tunicamycin	60-71	NPHS1 adhesion molecule, nephrin	Homo sapiens	97-104
11559706-6	2001	FPR-C126W differed from FPR-WT and FPR-F110S in migration on SDS-polyacrylamide gels and tunicamycin-sensitive glycosylation.	Tunicamycin	89-100	formyl peptide receptor 1	Homo sapiens	0-3
11961028-5	2002	When cells were treated with the N-glycosylation inhibitor, tunicamycin, the molecular weight of nephrin was decreased to a single immunoband of 150 kD, indicating that the shift in the electrophoretic migration of nephrin is due to N-linked carbohydrate moieties.	Tunicamycin	60-71	NPHS1 adhesion molecule, nephrin	Homo sapiens	215-222
11914074-2	2002	We found that the alpha(1B)-AR undergoes N-linked glycosylation as demonstrated by its sensitivity to endoglycosidases and by the effect of tunicamycin on receptor maturation.	Tunicamycin	140-151	adrenoceptor alpha 1B	Homo sapiens	28-30
11952786-10	2002	Tunicamycin inhibited N-linked glycosylation of Ac45 and interfered with the cleavage process, suggesting that Ac45 needs proper folding for the cleavage to occur.	Tunicamycin	0-11	ATPase H+ transporting accessory protein 1	Homo sapiens	48-52
11952786-10	2002	Tunicamycin inhibited N-linked glycosylation of Ac45 and interfered with the cleavage process, suggesting that Ac45 needs proper folding for the cleavage to occur.	Tunicamycin	0-11	ATPase H+ transporting accessory protein 1	Homo sapiens	111-115
11595658-2	2001	Cells expressing CRFR1 were treated with tunicamycin to block receptor glycosylation.	Tunicamycin	41-52	corticotropin releasing hormone receptor 1	Homo sapiens	17-22
11791712-7	2001	The spf1 disruptant also showed increased expression of Kar2p and sensitivity to tunicamycin.	Tunicamycin	81-92	ion-transporting P-type ATPase SPF1	Saccharomyces cerevisiae S288C	4-8
11837675-1	2001	The expression of the ischemia-responsive protein (irp94) was enhanced by endoplasmic reticulum (ER) stress inducing drugs such as brefeldin A (BFA), calcium ionophor A23187, dithiothreitol (DTT) and tunicamycin in fisher rat thyroid epithelial cell line (FRTL-5 cells).	Tunicamycin	200-211	heat shock protein family A (Hsp70) member 4	Rattus norvegicus	51-56
11837675-2	2001	In particular, irp94 mRNA expression was increased dose dependently by tunicamycin, and there was increased irp94 expression when the cells were incubated with the thyroid-stimulating hormone (TSH) together.	Tunicamycin	71-82	heat shock protein family A (Hsp70) member 4	Rattus norvegicus	15-20
11544325-5	2001	Although these mutants were expressed on the cell surface and maintained its ability to associate with human TLR4, these mutations or tunicamycin treatment substantially impaired the ability of MD-2 to complement TLR4-mediated activation of NF-kappaB by LPS.	Tunicamycin	134-145	lymphocyte antigen 96	Homo sapiens	194-198
11557602-3	2001	Wound repair stimulated by epidermal growth factor was substantially attenuated by 10(-7) M tunicamycin (TM), an N-glycosylation inhibitor, but not by the inhibitors deoxymannojirimycin or castanospermine.	Tunicamycin	92-103	epidermal growth factor	Homo sapiens	27-50
11557602-3	2001	Wound repair stimulated by epidermal growth factor was substantially attenuated by 10(-7) M tunicamycin (TM), an N-glycosylation inhibitor, but not by the inhibitors deoxymannojirimycin or castanospermine.	Tunicamycin	105-107	epidermal growth factor	Homo sapiens	27-50
11606310-10	2001	(b) Inhibiting receptor glycosylation in HEK293 cells with tunicamycin enabled tryptase-mediated PAR(2) activation.	Tunicamycin	59-70	tryptase alpha/beta 1	Rattus norvegicus	79-87
11606310-10	2001	(b) Inhibiting receptor glycosylation in HEK293 cells with tunicamycin enabled tryptase-mediated PAR(2) activation.	Tunicamycin	59-70	F2R like trypsin receptor 1	Homo sapiens	97-103
11590221-5	2001	Tunicamycin significantly reduced cell-associated PAF-AH activity and inhibited enzyme secretion; but it did not alter the ratio of secreted to cell-associated enzyme (1.8 at 6 h and 3.1 at 24 h), suggesting that glycosylation is not essential for PAF-AH secretion.	Tunicamycin	0-11	phospholipase A2 group VII	Homo sapiens	50-56
11544325-5	2001	Although these mutants were expressed on the cell surface and maintained its ability to associate with human TLR4, these mutations or tunicamycin treatment substantially impaired the ability of MD-2 to complement TLR4-mediated activation of NF-kappaB by LPS.	Tunicamycin	134-145	toll like receptor 4	Homo sapiens	213-217
11544325-5	2001	Although these mutants were expressed on the cell surface and maintained its ability to associate with human TLR4, these mutations or tunicamycin treatment substantially impaired the ability of MD-2 to complement TLR4-mediated activation of NF-kappaB by LPS.	Tunicamycin	134-145	interferon regulatory factor 6	Homo sapiens	254-257
11261789-8	2001	Furthermore, inhibition of glycosylation of these Tf-1beta2 cells by tunicamycin treatment yields a standard 39-kDa molecule recognized on western blot with anti-gamma c antibody, as seen for the standard 64-kDa isoform of gamma c.	Tunicamycin	69-80	interleukin 2 receptor subunit gamma	Homo sapiens	162-169
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	nuclear factor kappa B subunit 1	Homo sapiens	36-45
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
11360202-5	2001	Moreover, p65-/- fibroblasts were killed more efficiently by calcium ionopore and tunicamycin but not hydrogen peroxide compared to wild type fibroblasts.	Tunicamycin	82-93	RELA proto-oncogene, NF-kB subunit	Homo sapiens	10-13
11360202-6	2001	We also show that parthenolide, a NF-kappaB inhibitor, sensitizes breast cancer cells to tunicamycin.	Tunicamycin	89-100	nuclear factor kappa B subunit 1	Homo sapiens	34-43
11509666-5	2001	The results also demonstrate that induction of ER stress with calcium ionophore A23187, brefeldin A, or tunicamycin is associated with translocation of ER-associated c-Abl to mitochondria.	Tunicamycin	104-115	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	166-171
11328816-7	2001	In the ceramidase overexpressing HEK293 cells, 133-kDa (Golgi-form) and 113-kDa (endoplasmic reticulum-form) Myc-tagged ceramidases were detected, whereas these two proteins were converted to a 87-kDa protein concomitantly with loss of activity when expressed in the presence of tunicamycin, indicating that the N-glycosylation process is indispensable for the expression of the enzyme activity.	Tunicamycin	279-290	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	109-112
11451447-14	2001	In contrast, nonglycosylated PAC1 receptors produced by tunicamycin treatment of the transfected COS-7 cells showed a 30-fold lower affinity for PACAP-27 and were capable of signal transduction with 30--50-fold lower potency as compared with the glycosylated PAC1 receptors.	Tunicamycin	56-67	adenylate cyclase activating polypeptide 1	Rattus norvegicus	145-150
11478581-1	2001	Using flow cytometry or immunoprecipitation analysis in cells chronically infected with HIV-1 IIIB Supt-1, we noticed an additive effect of tunicamycin and low molecular weight dextran (LMDS) on the binding of the G3-4 monoclonal antibody to monomeric and oligomeric forms of glycoprotein 120 (gp120).	Tunicamycin	140-151	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	294-299
11478581-2	2001	The inhibition of glycosylation by tunicamycin reduced the number of monomeric and oligomeric forms of gp120.	Tunicamycin	35-46	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	103-108
11389975-2	2001	RAMP proteins modify the glycosylation status of CRLR and determine their receptor specificity; when treated with tunicamycin, a glycosylation inhibitor, CHO-K1 cells constitutively expressing both RAMP2 and CRLR lost the capacity to bind adrenomedullin.	Tunicamycin	114-125	calcitonin receptor like receptor	Homo sapiens	49-53
11389975-2	2001	RAMP proteins modify the glycosylation status of CRLR and determine their receptor specificity; when treated with tunicamycin, a glycosylation inhibitor, CHO-K1 cells constitutively expressing both RAMP2 and CRLR lost the capacity to bind adrenomedullin.	Tunicamycin	114-125	receptor activity-modifying protein 2	Cricetulus griseus	198-203
11389975-2	2001	RAMP proteins modify the glycosylation status of CRLR and determine their receptor specificity; when treated with tunicamycin, a glycosylation inhibitor, CHO-K1 cells constitutively expressing both RAMP2 and CRLR lost the capacity to bind adrenomedullin.	Tunicamycin	114-125	calcitonin receptor like receptor	Homo sapiens	208-212
11389975-4	2001	Whichever RAMP protein was co-expressing with CRLR, the ligand binding was sensitive to tunicamycin.	Tunicamycin	88-99	calcitonin receptor like receptor	Homo sapiens	46-50
11261789-8	2001	Furthermore, inhibition of glycosylation of these Tf-1beta2 cells by tunicamycin treatment yields a standard 39-kDa molecule recognized on western blot with anti-gamma c antibody, as seen for the standard 64-kDa isoform of gamma c.	Tunicamycin	69-80	interleukin 2 receptor subunit gamma	Homo sapiens	223-230
11226227-8	2001	Characteristic aspects of the cyt1 phenotype, including radial swelling and accumulation of callose, can be mimicked with the inhibitor of N-glycosylation, tunicamycin.	Tunicamycin	156-167	Glucose-1-phosphate adenylyltransferase family protein	Arabidopsis thaliana	30-34
11181082-4	2001	Inhibition of glycosylation by tunicamycin also abolished cathepsin K maturation.	Tunicamycin	31-42	cathepsin K	Homo sapiens	58-69
11171045-0	2001	Tunicamycin induces ubiquitination and degradation of apolipoprotein B in HepG2 cells.	Tunicamycin	0-11	apolipoprotein B	Homo sapiens	54-70
11171045-4	2001	The present study was undertaken to address the question of whether the inhibition of N-linked glycosylation with tunicamycin would interfere with apoB-100 production.	Tunicamycin	114-125	apolipoprotein B	Homo sapiens	147-155
11171045-5	2001	We demonstrated that the treatment of HepG2 cells with tunicamycin decreased the net production of apoB-100 by enhancing co-translational degradation of the protein.	Tunicamycin	55-66	apolipoprotein B	Homo sapiens	99-107
11171045-7	2001	Because lactacystin only partly reversed the effects of tunicamycin on apoB biogenesis, tunicamycin seemed also to induce apoB co-translational degradation in HepG2 cells by one or more non-proteasomal pathways.	Tunicamycin	88-99	apolipoprotein B	Homo sapiens	122-126
11171045-8	2001	Furthermore, tunicamycin increased apoB ubiquitination approx.	Tunicamycin	13-24	apolipoprotein B	Homo sapiens	35-39
11171045-11	2001	Thus the tunicamycin-mediated inhibition of N-linked glycosylation interferes with the production of apoB-100 that is mediated by both proteasomal and non-proteasomal pathways.	Tunicamycin	9-20	apolipoprotein B	Homo sapiens	101-109
11162531-5	2001	In a murine hepatocellular carcinoma cell line, Sdf2l1 was strongly induced by tunicamycin and a calcium ionophore, A23187, and weakly induced by heat stress but was not induced by cycloheximide.	Tunicamycin	79-90	stromal cell-derived factor 2-like 1	Mus musculus	48-54
11345535-7	2001	In addition, 7D5 immunoprecipitated the approximately 58 kDa unglycosylated gp91phox protein from solubilized membrane fractions of tunicamycin-treated PLB-985 granulocytes, indicating that glycans were not required for 7D5 binding.	Tunicamycin	132-143	cytochrome b-245 beta chain	Homo sapiens	76-84
11134314-2	2001	The results reveal that in this cell system, the precursor is efficiently cleaved and the resulting G1 and G2 glycoproteins are transported from the endoplasmic reticulum (ER) to the Golgi complex, where they are retained, a process that could be blocked by tunicamycin.	Tunicamycin	258-269	proline rich protein BstNI subfamily 3	Homo sapiens	100-109
11024053-8	2001	Treatment with tunicamycin abolished any differences in beta-catenin phosphorylation for the mock vis a vis the GnT-lll transfectants.	Tunicamycin	15-26	catenin (cadherin associated protein), beta 1	Mus musculus	56-68
11024053-8	2001	Treatment with tunicamycin abolished any differences in beta-catenin phosphorylation for the mock vis a vis the GnT-lll transfectants.	Tunicamycin	15-26	glucosaminyl (N-acetyl) transferase family member 7	Mus musculus	112-115
11119727-3	2000	Tunicamycin dose-dependently inhibited the glycosylation of a myc-tagged hCRLR and in parallel specific [(125)I]CGRP and -ADM binding.	Tunicamycin	0-11	calcitonin receptor like receptor	Homo sapiens	73-78
11104692-6	2000	Palmitoylation of LPC was found to be sensitive to the protein palmitoyltransferase inhibitor tunicamycin but not cerulenin.	Tunicamycin	94-105	proprotein convertase subtilisin/kexin type 7	Homo sapiens	18-21
11010973-8	2000	Pretreatment of NIH 3T3 cells with UVC markedly attenuates the subsequent induction of CHOP mRNA by the cellular stress activators methylmethane sulfate, tunicamycin, glucose deprivation, and methionine deprivation for as long as at least 16 h. This inhibitory effect of UVC on CHOP expression in response to stress is independent of the presence or absence of p53 and does not involve mRNA degradation as opposed to the UVC effect that inhibits p21 expression seen only in the absence of p53.	Tunicamycin	154-165	DNA-damage inducible transcript 3	Mus musculus	87-91
11119727-3	2000	Tunicamycin dose-dependently inhibited the glycosylation of a myc-tagged hCRLR and in parallel specific [(125)I]CGRP and -ADM binding.	Tunicamycin	0-11	calcitonin related polypeptide alpha	Homo sapiens	112-116
11119727-3	2000	Tunicamycin dose-dependently inhibited the glycosylation of a myc-tagged hCRLR and in parallel specific [(125)I]CGRP and -ADM binding.	Tunicamycin	0-11	adrenomedullin	Homo sapiens	122-125
11046064-7	2000	The expressed CCR2B was found to be N:-glycosylated, as N:-glycosidase F treatment of the receptor or growth of the cells in tunicamycin reduced the receptor size to the same level, from 50 to 45 kDa.	Tunicamycin	125-136	C-C motif chemokine receptor 2	Homo sapiens	14-19
11089547-13	2000	Likewise, a decrease in glucose consumption (-50%) after treatment of cells with tunicamycin was accompanied by a decrease (-70% vs. control) in the membrane expression of a 50-kDa form of Glut-1 and an increase in its unglycosylated 41-kDa form.	Tunicamycin	81-92	solute carrier family 2 member 1	Rattus norvegicus	189-195
11069764-8	2000	In the presence of tunicamycin, NPP3 was not N-glycosylated.	Tunicamycin	19-30	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	32-36
11105962-0	2000	Axonal and neuronal amyloid precursor protein immunoreactivity in the brains of guinea pigs given tunicamycin.	Tunicamycin	98-109	amyloid-beta A4 protein	Cavia porcellus	20-45
11105962-1	2000	Amyloid precursor protein (APP) immunocytochemistry was used to study axonal and neuronal changes in guinea pig brains exposed to tunicamycin.	Tunicamycin	130-141	amyloid-beta A4 protein	Cavia porcellus	0-25
11041857-6	2000	Activity measurements of CD39L4 isolated from tunicamycin-treated, transiently transfected COS-7 cells indicate that glycosylation is not required for full ADPase activity.	Tunicamycin	46-57	ectonucleoside triphosphate diphosphohydrolase 5 (inactive)	Homo sapiens	25-31
10725401-4	2000	Tunicamycin inhibition experiments showed that the apical polarity of VEGF(165) was independent of N-glycosylation.	Tunicamycin	0-11	vascular endothelial growth factor A	Homo sapiens	70-74
10922362-4	2000	mRNA expression of Herp was strongly up-regulated by inducers of ER stress, including mercaptoethanol, tunicamycin, A23187, and thapsigargin.	Tunicamycin	103-114	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	19-23
10801872-6	2000	Treatment with tunicamycin and N-glycosidase F led to a BACE derivative with a molecular weight corresponding to an unmodified version.	Tunicamycin	15-26	beta-secretase 1	Homo sapiens	56-60
11027576-2	2000	It has a mutation in the DAD1 gene and enters apoptosis at the restrictive temperature of 39 degrees C. The defect of Dad1p causes a loss of N-linked glycosylation; therefore, it was thought that an inhibition of N-linked glycosylation induced apoptosis.However, tunicamycin, a potent inhibitor of N-linked glycosylation, had not caused apoptosis in wild-type BHK21 cells.	Tunicamycin	263-274	dolichyl-diphosphooligosaccharide--protein glycosyltransferase subunit DAD1	Mesocricetus auratus	25-29
11027576-2	2000	It has a mutation in the DAD1 gene and enters apoptosis at the restrictive temperature of 39 degrees C. The defect of Dad1p causes a loss of N-linked glycosylation; therefore, it was thought that an inhibition of N-linked glycosylation induced apoptosis.However, tunicamycin, a potent inhibitor of N-linked glycosylation, had not caused apoptosis in wild-type BHK21 cells.	Tunicamycin	263-274	dolichyl-diphosphooligosaccharide--protein glycosyltransferase subunit DAD1	Mesocricetus auratus	118-123
10993946-2	2000	In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice.	Tunicamycin	20-31	prion protein	Mus musculus	59-65
10993946-2	2000	In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice.	Tunicamycin	20-31	sodium channel, voltage-gated, type II, alpha	Mus musculus	107-112
10993946-2	2000	In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice.	Tunicamycin	20-31	prion protein	Mus musculus	186-193
10993946-2	2000	In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice.	Tunicamycin	20-31	prion protein	Mus musculus	207-213
10993946-2	2000	In earlier studies, tunicamycin prevented glycosylation of PrP(C) in scrapie-infected mouse neuroblastoma (ScN2a) cells but it was still expressed on the cell surface and converted into PrP(Sc); mutation of PrP(C) at glycosylation consensus sites (T182A, T198A) produced low steady-state levels of PrP that were insufficient to propagate prions in transgenic mice.	Tunicamycin	20-31	prion protein	Mus musculus	59-62
11000257-2	2000	These viruses use the related sodium-phosphate symporters Pit1 and Pit2, respectively, as receptors in nonhamster cells, and evidence has suggested that the corresponding transporters of CHO cells may be masked by tunicamycin-sensitive secreted inhibitors.	Tunicamycin	214-225	sodium-dependent phosphate transporter 2	Cricetulus griseus	67-71
11000257-4	2000	Moreover, expression of E36 Pit2 in CHO cells conferred tunicamycin-independent susceptibilities to both viruses.	Tunicamycin	56-67	sodium-dependent phosphate transporter 2	Cricetulus griseus	28-32
10973810-2	2000	When J774.1 cells were pretreated with tunicamycin, their granulocytin-dependent TNF-alpha production was greatly reduced.	Tunicamycin	39-50	tumor necrosis factor	Mus musculus	81-90
10988254-4	2000	Tunicamycin treatment completely abolished hFucTIII enzyme activity while castanospermine treatment diminished hFucTIII enzyme activity to approximately 40% of the activity of the native enzyme.	Tunicamycin	0-11	fucosyltransferase 3 (Lewis blood group)	Homo sapiens	43-51
10799532-2	2000	In fact, the glycosylation inhibitor tunicamycin induces dephosphorylation of mammalian BiP.	Tunicamycin	37-48	heat shock protein family A (Hsp70) member 5	Homo sapiens	88-91
10799532-5	2000	In contrast to tunicamycin treatment, water stress condition stimulated phosphorylation of BiP species in soybean cultured cells and stressed leaves.	Tunicamycin	15-26	ER-binding immunoglobulin protein BIP2	Glycine max	91-94
10799532-7	2000	We also compared the induction of the soybean BiP gene family, which consists of at least four members designated soyBiPA, soyBiPB, soyBiPC, and soyBiPD, by tunicamycin and osmotic stress.	Tunicamycin	157-168	ER-binding immunoglobulin protein BIP2	Glycine max	46-49
10799532-8	2000	Although all soybean BiP genes were induced by tunicamycin, just the soyBiPA RNA was up-regulated by osmotic stress.	Tunicamycin	47-58	ER-binding immunoglobulin protein BIP2	Glycine max	21-24
10971580-3	2000	HumHtrA2 is upregulated in mammalian cells in response to stress induced by both heat shock and tunicamycin treatment.	Tunicamycin	96-107	HtrA serine peptidase 2	Homo sapiens	0-8
10971580-7	2000	HumHtrA2 cleaves beta-casein with an inhibitor profile similar to that previously described for E. coli HtrA, in addition to an increase in beta-casein turnover when the assay temperature is raised from 37 to 45 degrees C. The biochemical and sequence similarities between humHtrA2 and its bacterial homologues, in conjunction with its nuclear location and upregulation in response to tunicamycin and heat shock suggest that it is involved in mammalian stress response pathways.	Tunicamycin	385-396	HtrA serine peptidase 2	Homo sapiens	0-8
10971580-7	2000	HumHtrA2 cleaves beta-casein with an inhibitor profile similar to that previously described for E. coli HtrA, in addition to an increase in beta-casein turnover when the assay temperature is raised from 37 to 45 degrees C. The biochemical and sequence similarities between humHtrA2 and its bacterial homologues, in conjunction with its nuclear location and upregulation in response to tunicamycin and heat shock suggest that it is involved in mammalian stress response pathways.	Tunicamycin	385-396	HtrA serine peptidase 1	Homo sapiens	3-7
10933718-9	2000	Thus, we infer that the tunicamycin-dependent infection of mouse cells by RD114 and type D retroviruses is caused by deglycosylation of mASCT1, which unmasks previously buried sites for viral interactions.	Tunicamycin	24-35	solute carrier family 1 (glutamate/neutral amino acid transporter), member 4	Mus musculus	136-142
10788525-5	2000	Moreover, p22(phox) coprecipitated with unglycosylated gp91(phox) primary translation product made in the presence of tunicamycin, suggesting that heterodimer formation does not require glycosylation.	Tunicamycin	118-129	calcineurin like EF-hand protein 1	Homo sapiens	10-13
10771098-3	2000	In Sf21 insect cells, overexpression of canine GRP94 led to the appearance of a multiplet of three or more molecular-mass isoforms which was reduced to a single mobility form following treatment of cells with tunicamycin, suggesting stable accumulations of consecutively modified protein.	Tunicamycin	209-220	heat shock protein 90 beta family member 1	Canis lupus familiaris	47-52
10753675-7	2000	Tunicamycin reversed the polarity of secretion of CgA to the basolateral side.	Tunicamycin	0-11	chromogranin A	Bos taurus	50-53
10760948-3	2000	This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, calcium ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells.	Tunicamycin	188-199	heat shock protein family A (Hsp70) member 5	Homo sapiens	77-82
10760948-3	2000	This article characterizes the different biological features associated with GRP78 induction by two kinds of stress agents, calcium ionophore, ionomycin (IM), and glycosylation inhibitor, tunicamycin (TM), focusing on the association with apoptosis in human prostate cancer cells.	Tunicamycin	201-203	heat shock protein family A (Hsp70) member 5	Homo sapiens	77-82
10727211-7	2000	Treating the transfected cells with tunicamycin inhibited the secretion and LAO activity of the recombinant apoxin I.	Tunicamycin	36-47	interleukin 4 induced 1	Homo sapiens	76-79
10692464-4	2000	Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1.	Tunicamycin	61-72	tumor necrosis factor	Bos taurus	79-106
10692464-4	2000	Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1.	Tunicamycin	61-72	oxidized low density lipoprotein receptor 1	Bos taurus	191-196
10692464-4	2000	Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1.	Tunicamycin	61-72	oxidized low density lipoprotein receptor 1	Bos taurus	198-204
10692464-4	2000	Furthermore, when treated with an N-glycosylation inhibitor, tunicamycin, both tumor necrosis factor-alpha-activated bovine aortic endothelial cells and CHO-K1 cells stably expressing bovine LOX-1 (BLOX-1-CHO) exclusively produced a 32-kDa deglycosylated form of LOX-1.	Tunicamycin	61-72	oxidized low density lipoprotein receptor 1	Bos taurus	199-204
11201795-4	2000	Pretreatment of this stable clones with tunicamycin, a potent inhibitor of N-glycosylation, caused the appearance of unglycosylated Trk core protein.	Tunicamycin	40-51	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	132-135
10708769-5	2000	Treatment with the glycosylation inhibitor tunicamycin both enhances the synthesis of Mif1 mRNA and protein.	Tunicamycin	43-54	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	86-90
10708769-6	2000	The Mif1 5" flanking region contains a functional ER stress-responsive element which is sufficient for induction by tunicamycin.	Tunicamycin	116-127	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	4-8
10808272-6	2000	The pIgR molecule (molecular mass 100 kDa) after complete deglycosylation by tunicamycin treatment was still able to bind to pIgA, indicating that N-glycosylation of pIgR is not necessary for pIgA-pIgR binding.	Tunicamycin	77-88	polymeric immunoglobulin receptor	Mus musculus	4-8
10888037-4	2000	In this study we show that inhibition of N-linked glycosylation using tunicamycin or the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor lovastatin resulted in down-regulation of IGF-1R at the cell surface in Ewing"s sarcoma cell lines (RD-ES and ES-1 cells).	Tunicamycin	70-81	insulin like growth factor 1 receptor	Homo sapiens	199-205
10721463-2	2000	We observed that the inhibition of glycosylation by high concentrations of tunicamycin results in the reduction of an oligomeric gp120 on the surface of infected MoIT 4 cells as well as the decrease in the concentration of a monomeric form in the cytoplasm.	Tunicamycin	75-86	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	129-134
10761711-3	2000	Immunoprecipitation studies of human tumor cell lines revealed that FU-MK-1 recognizes a monomeric membrane glycoprotein with two forms, 40 kDa (major form) and 42 kDa (minor form), and with a molecular mass of 35 kDa following treatment with the N-glycosylation inhibitor tunicamycin.	Tunicamycin	273-284	epithelial cell adhesion molecule	Homo sapiens	71-75
10949666-9	2000	Accumulation of an immunopositive cell specific asparagine-linked (N-linked) glycoprotein, Factor VIII:C in the absence of Glc3Man9GlcNAc2-PP-Dol in tunicamycin treated cells has been proposed as an apoptotic triggering mechanism under the current experimental conditions.	Tunicamycin	149-160	coagulation factor VIII	Bos taurus	91-102
10714394-8	2000	Similarly, under suboptimal conditions, a synergistic effect was obtained with tunicamycin and PMA: each one alone was ineffective but in combination they induced the acquisition of HA binding by the lymphoma cells, while their CD44 expression was not enhanced.	Tunicamycin	79-90	CD44 molecule (Indian blood group)	Homo sapiens	228-232
10569245-10	1999	The tunicamycin sensitivity of (delta)ire1 cells was also suppressed by extra expression of KAR2, suggesting that BiP plays a principal role in protecting cell growth against misfolded proteins accumulated in the ER.	Tunicamycin	4-15	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	92-96
10561463-5	1999	Furthermore sThy-1 lacking glycosylation could be produced with the inhibitor tunicamycin but in contrast cell surface expression of unglycosylated GPI anchored Thy-1 could not be obtained.	Tunicamycin	78-89	thy-1 membrane glycoprotein	Cricetulus griseus	13-18
10517826-1	1999	The cytotoxic drug tunicamycin kills cells because it is a specific inhibitor of UDP-N-acetylglucosamine:dolichol phosphate N-acetylglucosamine-1-P transferase (GPT), an enzyme that catalyzes the initial step of the biosynthesis of dolichol-linked oligosaccharides.	Tunicamycin	19-30	UDP-glcnac-adolichol phosphate glcnac-1-p-transferase	Arabidopsis thaliana	161-164
10517826-4	1999	Cells that are treated with tunicamycin normally experience an unfolded protein response and induce genes that encode endoplasmic reticulum chaperones such as the binding protein (BiP).	Tunicamycin	28-39	binding protein	Arabidopsis thaliana	163-178
10517826-4	1999	Cells that are treated with tunicamycin normally experience an unfolded protein response and induce genes that encode endoplasmic reticulum chaperones such as the binding protein (BiP).	Tunicamycin	28-39	binding protein	Arabidopsis thaliana	180-183
10517826-9	1999	These observations suggest that excess GPT activity obviates the normal unfolded protein response that cells experience when exposed to tunicamycin.	Tunicamycin	136-147	UDP-glcnac-adolichol phosphate glcnac-1-p-transferase	Arabidopsis thaliana	39-42
10514258-7	1999	When the N-glycosylation was completely blocked with the addition of tunicamycin to the culture, the secretion of hG-CSF and hGH was decreased to a negligible level although the other host-derived proteins were well secreted to the culture broth regardless of the presence of tunicamycin.	Tunicamycin	69-80	colony stimulating factor 3	Homo sapiens	114-120
10514258-7	1999	When the N-glycosylation was completely blocked with the addition of tunicamycin to the culture, the secretion of hG-CSF and hGH was decreased to a negligible level although the other host-derived proteins were well secreted to the culture broth regardless of the presence of tunicamycin.	Tunicamycin	276-287	colony stimulating factor 3	Homo sapiens	114-120
10484609-6	1999	Inhibition of N-linked glycosylation with tunicamycin (TM) prevented secretion of HL enzyme activity and protein mass.	Tunicamycin	42-53	lipase C, hepatic type	Homo sapiens	82-84
10415113-6	1999	In HA-1 cells, adapt78 mRNA was induced by the calcium ionophore A23187, 2-deoxyglucose, brefeldin A, tunicamycin, thapsigargin, and cyclopiazonic acid, with thapsigargin being the most potent inducer (7.3-fold).	Tunicamycin	102-113	regulator of calcineurin 1	Homo sapiens	15-22
10417322-10	1999	Treatment with tunicamycin (TUN) diminished the binding of MUC2 to CRT, suggesting a requirement for initial N-glycan addition during this process.	Tunicamycin	15-26	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	59-63
10417322-10	1999	Treatment with tunicamycin (TUN) diminished the binding of MUC2 to CRT, suggesting a requirement for initial N-glycan addition during this process.	Tunicamycin	15-26	calreticulin	Homo sapiens	67-70
10503534-5	1999	The T. reesei pdi1 promoter has two possible unfolded protein response (UPR) elements and it was shown by treatments with dithiothreitol and tunicamycin that the gene is under the control of the UPR pathway.	Tunicamycin	141-152	protein disulfide isomerase PDI1	Saccharomyces cerevisiae S288C	14-18
10398368-7	1999	Bacteriophage displaying CTLA-4 with somatostatin in CDR3 (CTLA-4R-Som3) specifically bound somatostatin receptors on transfected CHO-K1 cells pre-incubated with 1 microg/ml tunicamycin to remove receptor glycosylation.	Tunicamycin	174-185	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	25-31
10398368-7	1999	Bacteriophage displaying CTLA-4 with somatostatin in CDR3 (CTLA-4R-Som3) specifically bound somatostatin receptors on transfected CHO-K1 cells pre-incubated with 1 microg/ml tunicamycin to remove receptor glycosylation.	Tunicamycin	174-185	CDR3	Homo sapiens	53-57
10419504-4	1999	Tunicamycin treatment resulted in a 140-kDa protein, the deduced size of NPC1, suggesting that NPC1 is N-glycosylated.	Tunicamycin	0-11	NPC intracellular cholesterol transporter 1	Cricetulus griseus	73-77
10419504-4	1999	Tunicamycin treatment resulted in a 140-kDa protein, the deduced size of NPC1, suggesting that NPC1 is N-glycosylated.	Tunicamycin	0-11	NPC intracellular cholesterol transporter 1	Cricetulus griseus	95-99
10411905-3	1999	Cyclin D1 protein synthesis was rapidly inhibited by tunicamycin treatment.	Tunicamycin	53-64	cyclin D1	Homo sapiens	0-9
10411905-6	1999	Enforced overexpression of cyclin D1 in tunicamycin-treated cells maintained cyclin D- and E-dependent kinase activities and kept cells in cycle in the face of a fully activated UPR.	Tunicamycin	40-51	cyclin D1	Homo sapiens	27-36
10395686-4	1999	Pulse-chase experiments and treatment of cells with brefeldin A and/or tunicamycin showed that IL-16 is secreted despite the absence of a signal peptide, but with a signal peptide IL-16 is processed through the endoplasmic reticulum-golgi pathway and is glycosylated.	Tunicamycin	71-82	interleukin 16	Homo sapiens	95-100
10542372-3	1999	When mouse blastocysts were exposed to the alkylating agent MMS, the metabolic inhibitor sodium arsenite or an inhibitor of protein glycosylation tunicamycin, levels of the CHOP-10 mRNA were increased by two- to threefold relative to the mRNA for beta-actin.	Tunicamycin	146-157	DNA-damage inducible transcript 3	Mus musculus	173-180
10542372-9	1999	The results suggest that there is a link between the extent of glycoprotein synthesis and the sensitivity of CHOP-10 to tunicamycin.	Tunicamycin	120-131	DNA-damage inducible transcript 3	Mus musculus	109-116
10537138-3	1999	Through functional analysis of the hSR-transfected cells cultured in the presence of various glycosylation inhibitors, it was found that tunicamycin and castanospermine were able to significantly reduce the secretin-stimulated cAMP response.	Tunicamycin	137-148	HSR	Homo sapiens	35-38
10537138-3	1999	Through functional analysis of the hSR-transfected cells cultured in the presence of various glycosylation inhibitors, it was found that tunicamycin and castanospermine were able to significantly reduce the secretin-stimulated cAMP response.	Tunicamycin	137-148	secretin	Homo sapiens	207-215
10536042-5	1999	In exploring structure-function relationships among N-glycans, and since tunicamycin has various reported biochemical activities; we have generated a germline deletion in the mouse GPT gene.	Tunicamycin	73-84	glutamic pyruvic transaminase, soluble	Mus musculus	181-184
10574586-7	1999	By expressing chimeric rFII/hFII constructs in tunicamycin-treated HEK293 cells, it was shown that the kringle 2 structure of prothrombin was responsible for this difference.	Tunicamycin	47-58	coagulation factor II, thrombin	Homo sapiens	126-137
10569245-10	1999	The tunicamycin sensitivity of (delta)ire1 cells was also suppressed by extra expression of KAR2, suggesting that BiP plays a principal role in protecting cell growth against misfolded proteins accumulated in the ER.	Tunicamycin	4-15	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	38-42
10222064-5	1999	Cycloheximide (protein synthesis inhibitor), tunicamycin (N-linked glycosylation inhibitor), and beta-d-xyloside (chondroitin sulfation inhibitor) all inhibited IL-4-mediated downregulation of TNFalpha-induced monocyte HA binding.	Tunicamycin	45-56	interleukin 4	Homo sapiens	161-165
10482549-4	1999	(i) The U(L)3 proteins forming all six bands were present in lysates of cells infected with wild-type virus and treated with tunicamycin or monensin or in cells infected with the mutant lacking the gene encoding the U(S)3 protein kinase.	Tunicamycin	125-136	nuclear protein UL3	Human alphaherpesvirus 1	8-13
10222064-5	1999	Cycloheximide (protein synthesis inhibitor), tunicamycin (N-linked glycosylation inhibitor), and beta-d-xyloside (chondroitin sulfation inhibitor) all inhibited IL-4-mediated downregulation of TNFalpha-induced monocyte HA binding.	Tunicamycin	45-56	tumor necrosis factor	Homo sapiens	193-201
10424404-6	1999	Interestingly, while the majority of the breast cancer cell lines can respond to tunicamycin- and thapsigargin-induced stress by increasing the steady state levels of grp94 and grp78 transcripts, the induction at the GRP protein level is variable and does not always correspond with the transcript level.	Tunicamycin	81-92	heat shock protein 90 beta family member 1	Homo sapiens	167-172
10208935-7	1999	An important shift in the relative mobility of gp250 in SDS-PAGE was observed after tunicamycin treatment of infected cells labeled with [3H]glucosamine, confirming the presence of N-linked sugars on gp250.	Tunicamycin	84-95	sortilin related receptor 1	Homo sapiens	47-52
10328552-4	1999	The MBL binding to Colo205 cells was more strongly reduced by the pretreatment of the cells with an O-linked glycosylation inhibitor, benzyl-2-acetamide-2-deoxy-alpha-galactopyranoside (Bz-alpha-GalNAc), rather than an N-linked glycosylation inhibitor, tunicamycin.	Tunicamycin	253-264	mannose binding lectin 2	Homo sapiens	4-7
10229326-1	1999	To elucidate the role of N-glycosylation in the functional activity of the universal glucose transporter, Glut-1, we investigated effects of the N-glycosylation inhibitor, tunicamycin, on glucose transport by human leukemic cell lines K562, U937 and HL60.	Tunicamycin	172-183	solute carrier family 2 member 1	Homo sapiens	106-112
10024536-15	1999	RA-treated P19 cells were about 4-fold more resistant to tunicamycin, a fungal antibiotic which inhibits GPT, than were control cells.	Tunicamycin	57-68	glutamic pyruvic transaminase, soluble	Mus musculus	105-108
10024536-17	1999	4-fold increased resistance to tunicamycin compared with activity in membranes from untreated control cells, demonstrating that resistance to tunicamycin is correlated with induced GPT activity.	Tunicamycin	31-42	glutamic pyruvic transaminase, soluble	Mus musculus	181-184
10024536-17	1999	4-fold increased resistance to tunicamycin compared with activity in membranes from untreated control cells, demonstrating that resistance to tunicamycin is correlated with induced GPT activity.	Tunicamycin	142-153	glutamic pyruvic transaminase, soluble	Mus musculus	181-184
10424404-6	1999	Interestingly, while the majority of the breast cancer cell lines can respond to tunicamycin- and thapsigargin-induced stress by increasing the steady state levels of grp94 and grp78 transcripts, the induction at the GRP protein level is variable and does not always correspond with the transcript level.	Tunicamycin	81-92	heat shock protein family A (Hsp70) member 5	Homo sapiens	177-182
10424404-6	1999	Interestingly, while the majority of the breast cancer cell lines can respond to tunicamycin- and thapsigargin-induced stress by increasing the steady state levels of grp94 and grp78 transcripts, the induction at the GRP protein level is variable and does not always correspond with the transcript level.	Tunicamycin	81-92	gastrin releasing peptide	Homo sapiens	217-220
10367750-4	1999	METHODS: We generated the GRP-inducing culture conditions by exposing cells to 2-deoxyglucose (2DG), calcium ionophore A23187 and tunicamycin, and examined cellular sensitivity to cisplatin and carboplatin under these conditions.	Tunicamycin	130-141	gastrin releasing peptide	Homo sapiens	26-29
10225275-3	1999	Inhibition of N-linked glycosylation by tunicamycin revealed that NS1 synthesised in MVE-infected C6/36 cells was derived from two polypeptide backbones of 39 kDa (NS1(o)) and 47 kDa (NS1").	Tunicamycin	40-51	influenza virus NS1A binding protein	Homo sapiens	66-69
9925876-7	1999	Tunicamycin, an inhibitor of N-linked glycosylation, blocked normal surface membrane expression of a HERG-green fluorescent protein (GFP) fusion protein (HERGGFP) transiently expressed in human embryonic kidney (HEK 293) cells imaged with confocal microscopy.	Tunicamycin	0-11	potassium voltage-gated channel subfamily H member 2	Homo sapiens	101-105
9931016-4	1999	The ecto-apyrase was also expressed in the presence of tunicamycin, which completely prevented N-linked glycosylation, resulting in a nonglycosylated core protein devoid of ATP and ADP hydrolyzing activity.	Tunicamycin	55-66	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	4-16
9931016-7	1999	The glycosylated ecto-apyrase exists as a homodimer in situ as assessed by both size-exclusion chromatography of detergent-solubilized ecto-apyrase and cross-linking of membrane-bound ecto-apyrase, in contrast to the enzymatically deglycosylated ecto-apyrase and the tunicamycin-treated ecto-apyrase.	Tunicamycin	267-278	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	17-29
10073711-4	1999	The inclusion of tunicamycin during these time-course experiments suggested that EGT is glycosylated.	Tunicamycin	17-28	ecdysteroid UDP-glucosyl transferase	Autographa californica nucleopolyhedrovirus	81-84
9880569-6	1999	In contrast, inhibition of glycosylation of P69, by tunicamycin treatment of the insect cells, produced an enzymatically inactive protein.	Tunicamycin	52-63	islet cell autoantigen 1	Homo sapiens	44-47
9878696-6	1999	The antibiotic tunicamycin completely inhibited GPT activity at a concentration of 100-200 ng ml(-1) and an IC50 of 40 ng ml(-1), but had little effect on the other two enzymes.	Tunicamycin	15-26	glutamic--pyruvic transaminase	Homo sapiens	48-51
9854035-4	1999	Secretion of alpha1-antitrypsin, an unrelated N-glycoprotein, was also inhibited by monensin, BFA and tunicamycin, but not by CCCP, castanospermine or N-methyldeoxynojirimycin.	Tunicamycin	102-113	serpin family A member 1	Homo sapiens	13-31
10402670-5	1999	Tunicamycin and A23187, the calcium ionophore, enhanced BiP mRNA accumulation first at the neurula stage, while heat shock induced BiP mRNA accumulation first at the gastrula stage.	Tunicamycin	0-11	heat shock 70 kDa protein 5b	Xenopus laevis	56-59
10025674-8	1999	Tunicamycin prevented calcium toxicity; gel electrophoresis studies showed that this protection was likely due to degradation of the NR1 subunit.	Tunicamycin	0-11	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	133-136
9837919-4	1998	Inhibition of acquisition of N-linked oligosaccharides by tunicamycin treatment in CHO cells stably expressing TSHR produced nonglycosylated TSHR, which was totally nonfunctional.	Tunicamycin	58-69	thyrotropin receptor	Cricetulus griseus	111-115
10461108-3	1999	MDCK cells (2 x 10(6) cells/well) were cultured to a confluent state, and the binding of OPN to the cellular surface was then inhibited by adding one of the following 4 substances: human OPN polyclonal antibody, thrombin, cyclic Arg-Gly-Asp (RGD) peptides and tunicamycin.	Tunicamycin	260-271	secreted phosphoprotein 1	Canis lupus familiaris	89-92
9922157-11	1998	Finally, a comparison of cleavage site selection in the presence and absence of tunicamycin treatment showed that N-glycosylation of certain mutant forms of CSF-1(256) sterically interfered with protease accessibility, which in turn had an effect on the selection of the site used for cleavage.	Tunicamycin	80-91	colony stimulating factor 1	Homo sapiens	157-162
9837919-4	1998	Inhibition of acquisition of N-linked oligosaccharides by tunicamycin treatment in CHO cells stably expressing TSHR produced nonglycosylated TSHR, which was totally nonfunctional.	Tunicamycin	58-69	thyrotropin receptor	Cricetulus griseus	141-145
9820151-7	1998	Sp1 is O-glycosylated while PEF-1 appears to have a novel type of glycosylation, as shown by the interaction with pokeweed lectin and by the inhibition of this interaction by tunicamycin.	Tunicamycin	175-186	penta-EF-hand domain containing 1	Homo sapiens	28-33
9832151-2	1998	The glycosylation inhibitor tunicamycin induced a dose-dependent decrease in the rVMAT1-mediated uptake of [3H]serotonin.	Tunicamycin	28-39	solute carrier family 18 member A1	Rattus norvegicus	81-87
10049651-10	1998	Northern blot analysis revealed that RTP mRNA expression was induced in HUVECs treated with not only homocysteine but also 2-mercaptoethanol and tunicamycin, both of which are known to induce ER stress.	Tunicamycin	145-156	N-myc downstream regulated 1	Homo sapiens	37-40
10100886-0	1998	Effect of cycloheximide and tunicamycin on the gonadotrophin-releasing hormone stimulated distal glycosylation of luteinizing hormone by rat pituitary cells.	Tunicamycin	28-39	gonadotropin releasing hormone 1	Homo sapiens	47-78
9778359-6	1998	In this study, we focused on the consequences of removing N-linked glycosylation from the P2X2 receptor by using two different approaches, tunicamycin treatment or site-directed mutagenesis.	Tunicamycin	139-150	purinergic receptor P2X 2	Homo sapiens	90-94
9778359-9	1998	Cell surface labeling with biotin or indirect immunofluorescence revealed that the expression of the nonglycosylated receptors produced by either tunicamycin or site-directed mutagenesis is greatly reduced at the cell surface, indicating that the nonglycosylated P2X2 receptors are retained inside the cell.	Tunicamycin	146-157	purinergic receptor P2X 2	Homo sapiens	263-267
9767079-2	1998	Treatment of cells expressing wild-type RFC with tunicamycin (0-3 microg) resulted in a progressive shift of the approximately 85 kDa RFC on western blots to 65 kDa.	Tunicamycin	49-60	solute carrier family 19 member 1	Homo sapiens	40-43
9767079-2	1998	Treatment of cells expressing wild-type RFC with tunicamycin (0-3 microg) resulted in a progressive shift of the approximately 85 kDa RFC on western blots to 65 kDa.	Tunicamycin	49-60	solute carrier family 19 member 1	Homo sapiens	134-137
9767079-3	1998	At 3 microg/ml tunicamycin, the nearly complete loss of glycosylated RFC was accompanied by a approximately 25% decreased rate of methotrexate uptake.	Tunicamycin	15-26	solute carrier family 19 member 1	Homo sapiens	69-72
10100886-2	1998	In the present report, we have further examined the GnRH-induced [3H]Gal-LH synthesis and release by treating anterior pituitary cells with polypeptide synthesis and glycosylation inhibitors (cycloheximide and tunicamycin, respectively).	Tunicamycin	210-221	gonadotropin releasing hormone 1	Homo sapiens	52-56
10100886-8	1998	Addition of tunicamycin to the pituitary cells inhibited the rates of synthesis and release of [3H]Man-LH which had been induced by GnRH, without altering those of [14C]Leu-LH.	Tunicamycin	12-23	gonadotropin releasing hormone 1	Homo sapiens	132-136
9751510-10	1998	Complete inhibition of hTPO N-glycosylation with tunicamycin led to a 95% decrease in hTPO at the plasma membrane and, thus, to a decrease in enzymatic activity at the cell surface, emphasizing the role of N-glycans in the intracellular trafficking of hTPO.	Tunicamycin	49-60	thyroid peroxidase	Homo sapiens	23-27
9751510-10	1998	Complete inhibition of hTPO N-glycosylation with tunicamycin led to a 95% decrease in hTPO at the plasma membrane and, thus, to a decrease in enzymatic activity at the cell surface, emphasizing the role of N-glycans in the intracellular trafficking of hTPO.	Tunicamycin	49-60	thyroid peroxidase	Homo sapiens	86-90
9751510-10	1998	Complete inhibition of hTPO N-glycosylation with tunicamycin led to a 95% decrease in hTPO at the plasma membrane and, thus, to a decrease in enzymatic activity at the cell surface, emphasizing the role of N-glycans in the intracellular trafficking of hTPO.	Tunicamycin	49-60	thyroid peroxidase	Homo sapiens	86-90
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	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	47-51
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	76-81
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	82-85
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
9835451-2	1998	Inhibition of N-linked glycosylation by tunicamycin, which has previously been shown to block the translocation of IGF-1R to the cell surface, blocked cell growth and/or induced cell death in these cell lines.	Tunicamycin	40-51	insulin like growth factor 1 receptor	Homo sapiens	115-121
10049651-9	1998	It encoded a novel protein with 394 amino acids, which was termed RTP (reducing agent and tunicamycin-responsive protein).	Tunicamycin	90-101	N-myc downstream regulated 1	Homo sapiens	66-69
9545520-5	1998	The expression of grp78 is constitutive and can be enhanced by starvation, treatment with tunicamycin, the calcium ionophore A23187 or elevated temperatures (40 degrees C).	Tunicamycin	90-101	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	18-23
9727361-7	1998	Immunoblot analyses revealed that in WT10 cells, 34% of AQP2 is glycosylated, which was reduced to 2% after tunicamycin treatment.	Tunicamycin	108-119	aquaporin 2	Canis lupus familiaris	56-60
9727361-10	1998	However, in tunicamycin-treated WT10 cells, all AQP2 in the apical membrane was unglycosylated, whereas in untreated cells 30% of AQP2 in the apical membrane was glycosylated.	Tunicamycin	12-23	aquaporin 2	Canis lupus familiaris	48-52
9727361-10	1998	However, in tunicamycin-treated WT10 cells, all AQP2 in the apical membrane was unglycosylated, whereas in untreated cells 30% of AQP2 in the apical membrane was glycosylated.	Tunicamycin	12-23	aquaporin 2	Canis lupus familiaris	130-134
9668061-4	1998	Inhibition of N-glycosylation with tunicamycin treatment slowed down the rate of dimerization and introduced further oligomerization of the MUC2 apomucin in the endoplasmic reticulum.	Tunicamycin	35-46	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	140-144
9668061-6	1998	The non-N-glycosylated species of the MUC2 mucin were retained in the endoplasmic reticulum because no O-glycosylated species were precipitated after inhibition by tunicamycin.	Tunicamycin	164-175	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	38-42
9668061-6	1998	The non-N-glycosylated species of the MUC2 mucin were retained in the endoplasmic reticulum because no O-glycosylated species were precipitated after inhibition by tunicamycin.	Tunicamycin	164-175	LOC100508689	Homo sapiens	43-48
9660831-6	1998	The study of the secretion of HBe derived from C-terminal-truncated precursors demonstrates that the tunicamycin-sensitive secretion absolutely requires a part of the C-terminal region that is removed to form mature HBe, indicating that the cellular tunicamycin-sensitive protein increases the efficiency of the intracellular transport of P22.	Tunicamycin	101-112	calcineurin like EF-hand protein 1	Homo sapiens	339-342
9660831-6	1998	The study of the secretion of HBe derived from C-terminal-truncated precursors demonstrates that the tunicamycin-sensitive secretion absolutely requires a part of the C-terminal region that is removed to form mature HBe, indicating that the cellular tunicamycin-sensitive protein increases the efficiency of the intracellular transport of P22.	Tunicamycin	250-261	calcineurin like EF-hand protein 1	Homo sapiens	339-342
9654121-3	1998	First, stable K562 transfectants expressing human B7-1 were treated with the N-glycosylation inhibitor tunicamycin.	Tunicamycin	103-114	CD80 molecule	Homo sapiens	50-54
9654121-5	1998	Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor.	Tunicamycin	68-79	CD80 molecule	Homo sapiens	60-64
9654121-5	1998	Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor.	Tunicamycin	68-79	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	124-130
9654121-5	1998	Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor.	Tunicamycin	68-79	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	165-171
9654121-5	1998	Significantly, the non-glycosylated cell surface-associated B7-1 on tunicamycin-treated cells retained the capacity to bind CTLA-4 x Ig, a soluble derivative of the CTLA-4(CD152) counter-receptor.	Tunicamycin	68-79	cytotoxic T-lymphocyte associated protein 4	Homo sapiens	172-177
9692865-7	1998	Moreover, tunicamycin treatment revealed the core form of pIgR had a molecular mass of approximately 100 kDa.	Tunicamycin	10-21	polymeric immunoglobulin receptor	Mus musculus	58-62
9557657-7	1998	Treatment of AGMK and cr5 cells with tunicamycin reduced binding of protective monoclonal Ab (MAb) 190/4, which suggested that N-glycans are required for binding of MAb 190/4 to havcr-1.	Tunicamycin	37-48	hepatitis A virus cellular receptor 1	Homo sapiens	178-185
9492298-2	1998	ERp29 was induced to high levels in the rat hepatoma cells under metabolic stress conditions known to cause an aberrant accumulation of proteins in the ER [(e.g. culture in presence of the Ca2+ ionophore A23187, inhibitors of Ca2+-ATPase (thapsigargin), intracellular protein transport (brefeldin A), or protein N-glycosylation (tunicamycin)].	Tunicamycin	329-340	endoplasmic reticulum protein 29	Rattus norvegicus	0-5
9531536-6	1998	It entailed exposing mice with defined chop genotypes to a single sublethal intraperitoneal injection of tunicamycin and resulted in a severe illness characterized by transient renal insufficiency.	Tunicamycin	105-116	DNA-damage inducible transcript 3	Mus musculus	39-43
9507013-12	1998	rPLD1 bound to concanavalin A-Sepharose beads, and its electrophoretic mobility was altered by treatment with endoglycosidase F. The amount of PLD bound to the beads was decreased in a concentration-dependent manner when tunicamycin was added to the Sf9 expression system.	Tunicamycin	221-232	phospholipase D1	Rattus norvegicus	0-5
9507013-12	1998	rPLD1 bound to concanavalin A-Sepharose beads, and its electrophoretic mobility was altered by treatment with endoglycosidase F. The amount of PLD bound to the beads was decreased in a concentration-dependent manner when tunicamycin was added to the Sf9 expression system.	Tunicamycin	221-232	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	1-4
9507013-13	1998	Tunicamycin also decreased membrane localization of rPLD1.	Tunicamycin	0-11	phospholipase D1	Rattus norvegicus	52-57
9492298-5	1998	In rat hepatoma cells ERp29 was found to be associated with the abundant molecular chaperone/stress protein BiP/GRP78 and this interaction was significantly enhanced after treatment with tunicamycin and A23187.	Tunicamycin	187-198	endoplasmic reticulum protein 29	Rattus norvegicus	22-27
9492298-5	1998	In rat hepatoma cells ERp29 was found to be associated with the abundant molecular chaperone/stress protein BiP/GRP78 and this interaction was significantly enhanced after treatment with tunicamycin and A23187.	Tunicamycin	187-198	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	108-111
9492298-5	1998	In rat hepatoma cells ERp29 was found to be associated with the abundant molecular chaperone/stress protein BiP/GRP78 and this interaction was significantly enhanced after treatment with tunicamycin and A23187.	Tunicamycin	187-198	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	112-117
10353723-5	1998	ER stress induced calreticulin expression in response to either thapsigargin or tunicamycin was equivalent in these cells to that seen in control, nontransfected cells, leading us to conclude that calreticulin is unlikely be involved in its own induction.	Tunicamycin	80-91	calreticulin	Homo sapiens	18-30
9422791-5	1998	The aglycosylated fragment CCP2-ap-SPag was also expressed by using tunicamycin.	Tunicamycin	68-79	AGBL carboxypeptidase 2	Homo sapiens	27-31
10353723-6	1998	Levels of the mRNA encoding the fusion protein were also increased by tunicamycin, but not thapsigargin, suggesting that, in agreement with our previous observations, inhibition of N-linked glycosylation may increase the stability of calreticulin mRNA.	Tunicamycin	70-81	calreticulin	Homo sapiens	234-246
9701462-12	1998	RTP mRNA was also observed in unstimulated cells and induced by not only homocysteine but also 2-mercaptoethanol and tunicamycin.	Tunicamycin	117-128	N-myc downstream regulated 1	Homo sapiens	0-3
9388233-6	1997	The latter results were obtained also when BiP was overexpressed not via transfection but as a response to ER stress by tunicamycin.	Tunicamycin	120-131	heat shock protein family A (Hsp70) member 5	Homo sapiens	43-46
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
9415709-5	1997	Moreover, both chemical depalmitoylation by hydroxylamine and inhibition of palmitoyl-CoA transferase in vivo by tunicamycin treatment incresed the reconstitutive activity of detergent extracts and eliminated the differences between native and opioid-dependent cells, indicating that the increase in stimulatory activity is due to depalmitoylation of Gs alpha.	Tunicamycin	113-124	GNAS complex locus	Homo sapiens	351-359
9409741-5	1997	The grp78-K8/18 association is induced by culturing cells in the presence of tunicamycin or after glucose starvation.	Tunicamycin	77-88	heat shock protein family A (Hsp70) member 5	Homo sapiens	4-9
9409741-5	1997	The grp78-K8/18 association is induced by culturing cells in the presence of tunicamycin or after glucose starvation.	Tunicamycin	77-88	keratin 8	Homo sapiens	10-15
9367877-6	1997	Both thapsigargin, and tunicamycin, increased calreticulin secretion from the cells, although this might be due to more than simply saturation of KDEL receptor binding.	Tunicamycin	23-34	calreticulin	Homo sapiens	46-58
9367877-6	1997	Both thapsigargin, and tunicamycin, increased calreticulin secretion from the cells, although this might be due to more than simply saturation of KDEL receptor binding.	Tunicamycin	23-34	KDEL endoplasmic reticulum protein retention receptor 1	Homo sapiens	146-159
9409285-7	1997	Alterations in apoB conformation and their impact on degradation were also investigated by using DTT and by inhibiting N-linked glycosylation with tunicamycin.	Tunicamycin	147-158	apolipoprotein B	Homo sapiens	15-19
9409285-11	1997	In tunicamycin-treated cells, DTT further accelerated the degradation of unglycosylated apoB.	Tunicamycin	3-14	apolipoprotein B	Homo sapiens	88-92
18982490-6	1997	The expressed UDPGT was a glycoprotein as indicated by electrophoretic mobility shift in Mr approximately 3,000-4,000 when expressed in the presence of tunicamycin.	Tunicamycin	152-163	UDP glucuronosyltransferase family 1 member A4	Homo sapiens	14-19
9388239-10	1997	Altered glycosylation generated the new beta1 integrin form since integrin core beta1-chain proteins of the same molecular weight were yielded in Ki-ras, Ha-ras, and control transfectants after removal of sugar residues with endoglycosidase F or following tunicamycin treatment to inhibit glycosylation.	Tunicamycin	256-267	integrin subunit beta 1	Homo sapiens	40-54
9376679-3	1997	To study the roles of N-glycosylation in the GnT-III function, rat GnT-III was expressed in COS-1 cells under tunicamycin or castanospermine treatment.	Tunicamycin	110-121	beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase	Rattus norvegicus	67-74
9376679-4	1997	The tunicamycin-treated GnT-III, which was not N-glycosylated, had almost no activity.	Tunicamycin	4-15	beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase	Homo sapiens	24-31
9376679-10	1997	The null glycosylation mutant had no activity, corresponding to the case of tunicamycin-treated wild-type GnT-III.	Tunicamycin	76-87	beta-1,4-mannosyl-glycoprotein 4-beta-N-acetylglucosaminyltransferase	Homo sapiens	106-113
9261166-5	1997	We report that PrP molecules mutated at Thr182 alone or at both Thr182 and Thr198 [corrected] fail to reach the cell surface after synthesis, but that those mutated at Thr198 [corrected] or synthesized in the presence of tunicamycin can be detected on the plasma membrane.	Tunicamycin	221-232	prion protein	Mus musculus	15-18
9268304-6	1997	Prior heat shock did not protect cells from IDAM but pretreatment with trans-4,5-dihydroxy-1,2-dithiane (DTTox), thapsigargin, or tunicamycin enhanced expression of the endoplasmic reticulum (ER) chaperones GRP78 and GRP94 and rendered cells tolerant to IDAM.	Tunicamycin	130-141	heat shock protein family A (Hsp70) member 5	Sus scrofa	207-212
9268304-6	1997	Prior heat shock did not protect cells from IDAM but pretreatment with trans-4,5-dihydroxy-1,2-dithiane (DTTox), thapsigargin, or tunicamycin enhanced expression of the endoplasmic reticulum (ER) chaperones GRP78 and GRP94 and rendered cells tolerant to IDAM.	Tunicamycin	130-141	heat shock protein 90 beta family member 1	Sus scrofa	217-222
9237560-9	1997	There were a number of precursor TNF isoforms that were unchanged upon tunicamycin treatment and these presumably reflect protein modifications other than glycosylation.	Tunicamycin	71-82	tumor necrosis factor	Mus musculus	33-36
9271078-6	1997	Cells that were Ca2+ depleted for 2 h slowly secreted an abnormal slightly smaller complex oligosaccharide form of alpha1-antitrypsin at approximately the same rate as the non-glycosylated protein generated by treatment with tunicamycin.	Tunicamycin	225-236	serpin family A member 1	Homo sapiens	115-133
9241531-4	1997	Here, by means of cytofluorimetric analysis evidence is provided, that the induction of APN surface expression is partially resistent to the action of the inhibitors of protein biosynthesis, puromycin and cycloheximide, and is not prevented by tunicamycin, an inhibitor of glycosylation.	Tunicamycin	244-255	alanyl aminopeptidase, membrane	Homo sapiens	88-91
9149128-2	1997	Here we report that MDR cells are hypersensitive to the N-linked glycosylation inhibitor tunicamycin, which induces partial inhibition of GLUT-1 glycosylation and diminishes GLUT-1-mediated transport.	Tunicamycin	89-100	solute carrier family 2 member 1	Homo sapiens	138-144
9149128-2	1997	Here we report that MDR cells are hypersensitive to the N-linked glycosylation inhibitor tunicamycin, which induces partial inhibition of GLUT-1 glycosylation and diminishes GLUT-1-mediated transport.	Tunicamycin	89-100	solute carrier family 2 member 1	Homo sapiens	174-180
9139799-7	1997	In addition, tunicamycin-derived, nonglycosylated LHRs were present at the cell surface and exhibited a phenotype consistent with mature receptors due to their capability to mediate hCG-stimulated cAMP production as well as bind oLH with high affinity.	Tunicamycin	13-24	hypertrichosis 2 (generalised, congenital)	Homo sapiens	182-185
9112387-6	1997	Flow cytometric analysis showed decreased expression of the hCaR on the cell membrane in tunicamycin-treated cells.	Tunicamycin	89-100	CXADR Ig-like cell adhesion molecule	Homo sapiens	60-64
9112387-8	1997	Tunicamycin treatment of cells, transfected with a mutant hCaR complementary DNA containing a nonsense codon at position 599 preceding the 1st transmembrane domain, blocked the secretion of a 95-kDa protein, representing the amino-terminal extracellular domain, into the medium.	Tunicamycin	0-11	CXADR Ig-like cell adhesion molecule	Homo sapiens	58-62
9145315-5	1997	Inhibition of the N-glycosylation pathway by tunicamycin resulted in a decreased ETSA-B21 signal on the cell membrane.	Tunicamycin	45-56	cytohesin 1	Homo sapiens	86-89
9102228-11	1997	Inhibition of N-linked glycosylation with tunicamycin resulted in decreased HA binding of cells bearing an active CD44 receptor.	Tunicamycin	42-53	CD44 molecule (Indian blood group)	Homo sapiens	114-118
9089636-4	1997	Using a temperature-sensitive RNA polymerase II mutant, we demonstrate that increased stability was the primary determinant of higher ALG7 mRNA abundance in response to glucose limitation or treatment with tunicamycin.	Tunicamycin	206-217	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Saccharomyces cerevisiae S288C	134-138
8972186-7	1997	The Y-box proteins can repress the inducibility of the grp78 core element mediated by treatment of cells with A23187, thapsigargin, and tunicamycin.	Tunicamycin	136-147	heat shock protein family A (Hsp70) member 5	Homo sapiens	55-60
9110380-6	1997	Tunicamycin elicited a 2.4- and 2.7-fold increase in IAPP mRNA levels in the low and high glucose media, respectively; however, it did not change insulin mRNA.	Tunicamycin	0-11	islet amyloid polypeptide	Homo sapiens	53-57
8995369-9	1997	Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55.	Tunicamycin	79-90	neuroplastin	Homo sapiens	27-31
8995369-9	1997	Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55.	Tunicamycin	79-90	neuroplastin	Homo sapiens	36-40
9020069-5	1997	Northern blot analysis revealed that induction of ORP150 in U373 cells was not limited to hypoxia but also observed by 2-deoxyglucose or tunicamycin treatment.	Tunicamycin	137-148	hypoxia up-regulated 1	Homo sapiens	50-56
9111868-15	1997	In many, but not in all cases, CD44 does not bind HA unless it is stimulated by phorbol esters, activated by agonistic anti-CD44 antibody, or deglycosylated (e.g., by tunicamycin).	Tunicamycin	167-178	CD44 molecule (Indian blood group)	Homo sapiens	31-35
9038234-4	1997	However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells.	Tunicamycin	78-89	heat shock protein 5	Mus musculus	9-14
9038234-4	1997	However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells.	Tunicamycin	78-89	heat shock protein 90, beta (Grp94), member 1	Mus musculus	15-20
9038234-4	1997	However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells.	Tunicamycin	78-89	heat shock protein 5	Mus musculus	130-135
9038234-4	1997	However, grp78/grp94 transcription was induced by the glycosylation inhibitor tunicamycin, suggesting that there are at least two grp78/grp94 signaling pathways, one in response to TG-induced endoplasmic reticulum Ca2+ pool depletion, which is inoperable in WEHI7.2 cells, and one in response to glycosylation inhibition, which is operable in WEHI7.2 cells.	Tunicamycin	78-89	heat shock protein 90, beta (Grp94), member 1	Mus musculus	136-141
9030589-7	1997	Interestingly, even nonglycosylated GM2AP is delivered to the lysosome, as shown by tunicamycin treatment and subcellular fractionation.	Tunicamycin	84-95	ganglioside GM2 activator	Homo sapiens	36-41
9159886-5	1997	Northern hybridization analysis demonstrated that BiP mRNA was present constitutively in the Xenopus A6 kidney epithelial cell line and that BiP mRNA levels could be enhanced by treatment of the cells with galactose-free media, 2-deoxyglucose, 2-deoxygalactose, glucosamine, tunicamycin, heat shock, dithiothreitol, and the calcium ionophore, A23187.	Tunicamycin	275-286	heat shock protein family A (Hsp70) member 5 L homeolog	Xenopus laevis	50-53
9159886-5	1997	Northern hybridization analysis demonstrated that BiP mRNA was present constitutively in the Xenopus A6 kidney epithelial cell line and that BiP mRNA levels could be enhanced by treatment of the cells with galactose-free media, 2-deoxyglucose, 2-deoxygalactose, glucosamine, tunicamycin, heat shock, dithiothreitol, and the calcium ionophore, A23187.	Tunicamycin	275-286	heat shock protein family A (Hsp70) member 5 L homeolog	Xenopus laevis	141-144
9006956-6	1997	The same complex of the four putative chaperones with Tg was observed in cells treated with tunicamycin, indicating that these four ER chaperones stably associate with Tg when it is misfolded/misassembled due to inhibition of its glycosylation.	Tunicamycin	92-103	thyroglobulin	Rattus norvegicus	54-56
9006956-6	1997	The same complex of the four putative chaperones with Tg was observed in cells treated with tunicamycin, indicating that these four ER chaperones stably associate with Tg when it is misfolded/misassembled due to inhibition of its glycosylation.	Tunicamycin	92-103	thyroglobulin	Rattus norvegicus	168-170
9473774-4	1997	Nonrestricted CD45 epitopes were not affected by the sialyl acid cleavage with sodium metaperiodate or neuraminidase, but were sensitive to both, tunicamycin, the N-glycosylation inhibitor and monensin, an inhibitor of protein transport through the Golgi compartment.	Tunicamycin	146-157	protein tyrosine phosphatase receptor type C	Homo sapiens	14-18
8961954-6	1996	Inhibition of N-glycosylation with an optimized concentration of tunicamycin yielded completely nonglycosylated hPTH/PTHrP receptor (approximately 60 kDa).	Tunicamycin	65-76	parathyroid hormone	Homo sapiens	112-116
8961954-6	1996	Inhibition of N-glycosylation with an optimized concentration of tunicamycin yielded completely nonglycosylated hPTH/PTHrP receptor (approximately 60 kDa).	Tunicamycin	65-76	parathyroid hormone like hormone	Homo sapiens	117-122
8961954-10	1996	The molecular weight (approximately 60000) of the band representing the photo-cross-linked, nonglycosylated receptor (obtained from the tunicamycin-treated HEK-293/C-21 cells) was similar to that of the deglycosylated photo-cross-linked receptor (obtained by enzymatic treatment with Endoglycosidase-F/N-glycosidase-F).	Tunicamycin	136-147	TBL1X/Y related 1	Homo sapiens	164-168
8973632-7	1996	Inhibition of N-glycosylation by tunicamycin dramatically reduced the expression of IFN-gamma, but did not block its secretion.	Tunicamycin	33-44	interferon gamma	Homo sapiens	84-93
8700133-2	1996	The use of hNET-specific antibodies and the membrane-impermeant biotinylating reagent sulfosuccinimidobiotin establishes that treatment of stably transfected LLC-PK1 cells with tunicamycin depletes surface membranes of mature hNET glycoproteins, which is consistent with a failure of less stable, nonglycosylated subunits to replenish surface compartments.	Tunicamycin	177-188	solute carrier family 6 member 2	Homo sapiens	11-15
8995369-9	1997	Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55.	Tunicamycin	79-90	neuroplastin	Homo sapiens	185-189
8995369-9	1997	Furthermore, expression of gp65 and gp55 cDNAs in human 293 cells treated with tunicamycin results in the production of unglycosylated core proteins of identical size to deglycosylated gp65 and gp55.	Tunicamycin	79-90	neuroplastin	Homo sapiens	194-198
8987625-4	1996	Synthesis of the recombinant proteins in the absence and presence of tunicamycin revealed that both E1 and E2 were glycosylated with apparent molecular weights of 52 kDa and 37 kDa, respectively.	Tunicamycin	69-80	small nucleolar RNA, H/ACA box 73A	Homo sapiens	100-109
8794367-5	1996	Tunicamycin treatment, which inhibits N-glycosylation, increased the rate of migration of the UL37 protein to 68 kDa, verifying its modification by N-glycosylation in HCMV-infected cells.	Tunicamycin	0-11	envelope glycoprotein UL37	Human betaherpesvirus 5	94-98
8888624-2	1996	In Arabidopsis seedlings, accumulation of transcripts for BiP was induced not only by inhibition of the N-glycosylation of proteins by tunicamycin but also by inhibition of the processing of N-linked glycans by castanospermine.	Tunicamycin	135-146	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	58-61
8837730-0	1996	Inhibition by tunicamycin of mucin synthesis, not morphological changes, in epidermis during retinol-induced mucous metaplasia of chick embryonic cultured skin.	Tunicamycin	14-25	mucin 2, oligomeric mucus/gel-forming	Gallus gallus	29-34
8837730-4	1996	RESULTS: Tunicamycin, which prevents the formation of N-glycans and inhibits maturation or morphological organization of various epithelial cells, irreversibly inhibited the synthesis of sulfated glycoproteins (O-glycans, mucin) in the epidermis only when applied to retinol-pretreated skin.	Tunicamycin	9-20	mucin 2, oligomeric mucus/gel-forming	Gallus gallus	222-227
8837730-7	1996	CONCLUSION: These results suggest that tunicamycin did not prevent morphological changes induced by retinol but inhibited mucin synthesis by a direct action on the epidermis of retinol-pretreated skin.	Tunicamycin	39-50	mucin 2, oligomeric mucus/gel-forming	Gallus gallus	122-127
8837730-8	1996	Because in some cell-line mucin precursors contain high mannose N-linked oligosaccharides side chains, tunicamycin may have inhibited mucin synthesis.	Tunicamycin	103-114	mucin 2, oligomeric mucus/gel-forming	Gallus gallus	26-31
8837730-8	1996	Because in some cell-line mucin precursors contain high mannose N-linked oligosaccharides side chains, tunicamycin may have inhibited mucin synthesis.	Tunicamycin	103-114	mucin 2, oligomeric mucus/gel-forming	Gallus gallus	134-139
8939898-13	1996	RTP mRNA was also observed in unstimulated cells and induced by not only homocysteine but also 2-mercaptoethanol and tunicamycin.	Tunicamycin	117-128	N-myc downstream regulated 1	Homo sapiens	0-3
8922392-18	1996	Tunicamycin treatment inhibits HA binding by CD44v and at the same time destroys oligomerization.	Tunicamycin	0-11	CD44 molecule (Indian blood group)	Rattus norvegicus	45-50
8887673-8	1996	Like KAR2, SSI1 is induced both in the presence of tunicamycin and in a kar2-159 mutant strain, conditions which lead to an accumulation of unfolded proteins in the ER.	Tunicamycin	51-62	Hsp70 family chaperone LHS1	Saccharomyces cerevisiae S288C	11-15
8932376-1	1996	The Saccharomyces cerevisiae IRE1 gene, encoding a putative receptor-type protein kinase, is known to be required for inositol prototrophy and for the induction of a chaperon molecule, BiP, encoded by KAR2, under stress conditions such as tunicamycin addition.	Tunicamycin	239-250	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	29-33
8932376-1	1996	The Saccharomyces cerevisiae IRE1 gene, encoding a putative receptor-type protein kinase, is known to be required for inositol prototrophy and for the induction of a chaperon molecule, BiP, encoded by KAR2, under stress conditions such as tunicamycin addition.	Tunicamycin	239-250	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	201-205
8932376-4	1996	Introduction of IRE2/HAC1 into the ire1 mutant clearly restored the expression of KAR2 upon tunicamycin treatment.	Tunicamycin	92-103	transcription factor HAC1	Saccharomyces cerevisiae S288C	21-25
8932376-4	1996	Introduction of IRE2/HAC1 into the ire1 mutant clearly restored the expression of KAR2 upon tunicamycin treatment.	Tunicamycin	92-103	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	35-39
8932376-4	1996	Introduction of IRE2/HAC1 into the ire1 mutant clearly restored the expression of KAR2 upon tunicamycin treatment.	Tunicamycin	92-103	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	82-86
8932376-5	1996	ire2/hac1-disrupted yeast cells showed not only the inositol auxotrophic phenotype but also the tunicamycin sensitivity, and failed to induce the expression of KAR2.	Tunicamycin	96-107	transcription factor HAC1	Saccharomyces cerevisiae S288C	5-9
8918549-7	1996	Complete inhibition of the binding of these glycoprotein precursors to calnexin by tunicamycin or castanospermine indicates the importance of partially trimmed N-linked oligosaccharides for their association.	Tunicamycin	83-94	calnexin	Homo sapiens	71-79
8700133-2	1996	The use of hNET-specific antibodies and the membrane-impermeant biotinylating reagent sulfosuccinimidobiotin establishes that treatment of stably transfected LLC-PK1 cells with tunicamycin depletes surface membranes of mature hNET glycoproteins, which is consistent with a failure of less stable, nonglycosylated subunits to replenish surface compartments.	Tunicamycin	177-188	solute carrier family 6 member 2	Homo sapiens	226-230
8828806-4	1996	Tunicamycin (0.01 ng/ml) when added to the incubation media together with glucose prevented the decrease in Ca2+ATPase activity.	Tunicamycin	0-11	carbonic anhydrase 2	Homo sapiens	108-118
8837227-7	1996	Analysis of GPC synthesis in the presence of tunicamycin revealed that the unglycosylated GPC appeared as two polypeptides of 43 and 46 kDa.	Tunicamycin	45-56	glycophorin C (Gerbich blood group)	Homo sapiens	90-93
8654361-4	1996	Our studies indicate that LHS1 is regulated by the unfolded protein response pathway, as evidenced by its transcriptional induction in cells treated with tunicamycin, and in various mutants defective in precursor processing (sec11-7, sec53-6 and sec59-1).	Tunicamycin	154-165	Hsp70 family chaperone LHS1	Saccharomyces cerevisiae S288C	26-30
8648261-5	1996	Northern hybridization of poly(A)+ RNA from LLC-PK1 cells illustrated that in tunicamycin-treated cells, NHE-3 mRNA expression increased threefold over control cells.	Tunicamycin	78-89	solute carrier family 9 member A3	Sus scrofa	105-110
8648261-8	1996	NHE-3 immunoblots of whole cell extract from tunicamycin-treated cells showed that in addition to the 95 kd protein, an 87 kd band was also detected.	Tunicamycin	45-56	solute carrier family 9 member A3	Sus scrofa	0-5
12232600-0	1996	The Effect of Tunicamycin on the Interaction of Fibronectin and HT1080 Cells.	Tunicamycin	14-25	fibronectin 1	Homo sapiens	48-59
8645293-4	1996	Other stress inducers, tunicamycin, A23187, and heat shock, which caused an accumulation of unfolded proteins, also induced the PDI mRNA, indicating that the unfolded protein accumulation response induces PDI gene expression.	Tunicamycin	23-34	prolyl 4-hydroxylase subunit beta	Homo sapiens	128-131
8645293-4	1996	Other stress inducers, tunicamycin, A23187, and heat shock, which caused an accumulation of unfolded proteins, also induced the PDI mRNA, indicating that the unfolded protein accumulation response induces PDI gene expression.	Tunicamycin	23-34	prolyl 4-hydroxylase subunit beta	Homo sapiens	205-208
8593668-7	1996	Using quantitative electron-microscopic immunocytochemistry, the lysosomal contents of SGP-1 were shown to increase significantly after the administration of tunicamycin in vivo.	Tunicamycin	158-169	prosaposin	Rattus norvegicus	87-92
8601595-3	1996	Our results show that treatment of a panel of human cell lines which constitutively express CD44 with the inhibitor of N-linked glycosylation tunicamycin results in the loss of attachment of these cells to hyaluronate-coated substrate.	Tunicamycin	142-153	CD44 molecule (Indian blood group)	Homo sapiens	92-96
8546698-3	1996	Photoaffinity labelling of cell-surface AT2 receptors revealed that PC-12 cells grown in the presence of tunicamycin expressed, in addition to the previously described 140 kDa receptor, lower-molecular-mass receptors of 63 kDa, 47 kDa and 32 kDa.	Tunicamycin	105-116	angiotensin II receptor, type 2	Rattus norvegicus	40-43
8546698-6	1996	Both receptor forms exhibited a high affinity for angiotensin II, although a slight decrease (of about 2-fold) was consistently observed on tunicamycin-treated cells as compared with control cells.	Tunicamycin	140-151	angiotensinogen	Rattus norvegicus	50-64
8546698-9	1996	In conclusion, the stepwise action of tunicamycin suggests the presence of at least three N-linked oligosaccharide side chains on the AT2 receptor of PC-12 cells.	Tunicamycin	38-49	angiotensin II receptor, type 2	Rattus norvegicus	134-137
8818631-8	1996	Exposure of cell monolayers to tunicamycin, an inhibitor of protein glycosylation, mimicked the effect of NO2 exposure on expression of GRP-78.	Tunicamycin	31-42	heat shock protein family A (Hsp70) member 5	Homo sapiens	136-142
8846915-7	1996	Tunicamycin treatment experiments, biochemical fractionation and extraction experiments, and proteinase K protection experiments collectively indicate that Axl2p is an integral membrane glycoprotein at the plasma membrane.	Tunicamycin	0-11	Axl2p	Saccharomyces cerevisiae S288C	156-161
8635486-5	1996	The PDGF-induced IGF-1R expression was suppressed in the presence of tunicamycin, an inhibitor of N-linked glycosylation.	Tunicamycin	69-80	insulin like growth factor 1 receptor	Homo sapiens	17-23
8576245-8	1996	In contrast, co-treatment with the classical GRP inducers thapsigargin and tunicamycin produced only simple additive increases in grp78 promoter activity.	Tunicamycin	75-86	gastrin releasing peptide	Rattus norvegicus	45-48
8576245-8	1996	In contrast, co-treatment with the classical GRP inducers thapsigargin and tunicamycin produced only simple additive increases in grp78 promoter activity.	Tunicamycin	75-86	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	130-135
8636209-8	1996	In contrast, treatment of T cells with tunicamycin suggested that N-linked glycosylation of CD3 delta is required for TCR assembly.	Tunicamycin	39-50	CD3 delta subunit of T-cell receptor complex	Homo sapiens	92-101
8636209-8	1996	In contrast, treatment of T cells with tunicamycin suggested that N-linked glycosylation of CD3 delta is required for TCR assembly.	Tunicamycin	39-50	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	118-121
7592677-3	1995	Tunicamycin, an N-glycosylation inhibitor, markedly inhibited GM-CSF binding, GM-CSF-induced deoxyglucose uptake, and protein tyrosine phosphorylation in HL-60(eos) cells but did not affect cell surface expression of the alpha subunit as detected by an anti-alpha subunit monoclonal antibody.	Tunicamycin	0-11	colony stimulating factor 2	Homo sapiens	62-68
7492299-5	1995	SDS/PAGE of rhLF expressed in the presence of tunicamycin revealed a protein with the same M(r) as that of enzymically deglycosylated natural hLF.	Tunicamycin	46-57	HLF transcription factor, PAR bZIP family member	Homo sapiens	13-16
8750891-9	1995	The 5-HT2C receptor cell line (3T3/2C) was grown in the presence of tunicamycin to metabolically inhibit N-linked glycosylation.	Tunicamycin	68-79	5-hydroxytryptamine receptor 2C	Rattus norvegicus	4-10
7500048-5	1995	To examine this issue, we have directly explored the binding of calnexin to both Ii truncation mutants lacking the typical sites of N-glycosylation or Ii produced in cells treated with tunicamycin to prevent glycan addition.	Tunicamycin	185-196	calnexin	Mus musculus	64-72
7492303-8	1995	Tunicamycin or treatment with endoglucosidase H reduced the molecular mass of hypertonicity-induced Cox-2 by 5 kDa.	Tunicamycin	0-11	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	100-105
7592880-3	1995	Tunicamycin also induced biochemical changes in Cx43 protein; the level increased, and a considerable fraction became phosphorylated and Triton X-100 insoluble, in contrast to untreated cells where Cx43 was non-phosphorylated and Triton X-100 soluble.	Tunicamycin	0-11	gap junction protein alpha 1	Homo sapiens	48-52
7592677-3	1995	Tunicamycin, an N-glycosylation inhibitor, markedly inhibited GM-CSF binding, GM-CSF-induced deoxyglucose uptake, and protein tyrosine phosphorylation in HL-60(eos) cells but did not affect cell surface expression of the alpha subunit as detected by an anti-alpha subunit monoclonal antibody.	Tunicamycin	0-11	colony stimulating factor 2	Homo sapiens	78-84
7666502-3	1995	Treatment with the N glycosylation inhibitor tunicamycin converted the two SPI-3 proteins to a single 40-kDa protein, close to the size of 42 kDa predicted from the DNA sequence, suggesting that the SPI-3 protein, unlike the other two orthopoxvirus serpins, is a glycoprotein.	Tunicamycin	45-56	serpin family B member 6	Homo sapiens	75-80
7666502-3	1995	Treatment with the N glycosylation inhibitor tunicamycin converted the two SPI-3 proteins to a single 40-kDa protein, close to the size of 42 kDa predicted from the DNA sequence, suggesting that the SPI-3 protein, unlike the other two orthopoxvirus serpins, is a glycoprotein.	Tunicamycin	45-56	serpin family B member 6	Homo sapiens	199-204
7665231-6	1995	Incubation of NCI-H1688 cells with tunicamycin or cleavage of carbohydrate residues of NCI-H1688 or MCF-7/AdrVp membrane proteins with PNGase F leads to the appearance of a sharp 35-kDa band reactive with anti-P-95 antisera.	Tunicamycin	35-46	nibrin	Homo sapiens	210-214
7776966-12	1995	Similarly, when cells expressing the wild type FSHR were treated with tunicamycin to prevent N-linked glycosylation, the resulting nonglycosylated FSHR was not able to bind FSH.	Tunicamycin	70-81	follicle stimulating hormone receptor	Homo sapiens	47-51
7665923-11	1995	Pulse-chase experiments revealed that gp80 is synthesized from a 55-kD precursor molecule, the maturation of which was prevented by treating cells with tunicamycin.	Tunicamycin	152-163	interleukin 6 receptor	Homo sapiens	38-42
7543138-9	1995	Furthermore, culture in tunicamycin for 2-3 d converted parental and inducible cell lines into cells showing constitutive CD44-mediated HA binding.	Tunicamycin	24-35	CD44 antigen	Mus musculus	122-126
7619064-7	1995	Pretreatment of the cells with tunicamycin to inhibit the first step of N-glycosylation led to intracellular accumulation of immature rLCAT (approximately 46-48 kDa) and a marked reduction in enzyme secreted.	Tunicamycin	31-42	lecithin cholesterol acyltransferase	Rattus norvegicus	134-139
7876241-2	1995	Most proteins that calnexin binds are N-glycosylated, and treatment of cells with tunicamycin or inhibitors of initial glucose trimming steps interferes with calnexin binding.	Tunicamycin	82-93	calnexin	Homo sapiens	19-27
7876241-2	1995	Most proteins that calnexin binds are N-glycosylated, and treatment of cells with tunicamycin or inhibitors of initial glucose trimming steps interferes with calnexin binding.	Tunicamycin	82-93	calnexin	Homo sapiens	158-166
7876246-5	1995	Nonglycosylated MPO precursors synthesized in the presence of tunicamycin did not interact with CRT.	Tunicamycin	62-73	myeloperoxidase	Homo sapiens	16-19
7867726-9	1995	These bands likely represent differently glycosylated forms of the two RET primary products (117 and 122 kDa) detected in tunicamycin-treated cells.	Tunicamycin	122-133	ret proto-oncogene	Homo sapiens	71-74
7543137-5	1995	Treatment of the nonbinding clone with tunicamycin reduced the size of the protein and allowed the cells to recognize HA via CD44.	Tunicamycin	39-50	CD44 antigen	Cricetulus griseus	125-129
12242382-7	1995	Treating plants with tunicamycin, a drug that blocks N-glycosylation in the ER, or with cold shock, known to block secretory protein transport, led to a marked accumulation of aERD2 and aSAR1 transcripts.	Tunicamycin	21-32	ER lumen protein retaining receptor family protein	Arabidopsis thaliana	176-181
12242382-7	1995	Treating plants with tunicamycin, a drug that blocks N-glycosylation in the ER, or with cold shock, known to block secretory protein transport, led to a marked accumulation of aERD2 and aSAR1 transcripts.	Tunicamycin	21-32	secretion-associated RAS super family 2	Arabidopsis thaliana	186-191
7663166-5	1995	Tunicamycin treatment of infected cells resulted in a mobility shift of OSF-2 (approximately 90-kDa band) on Western blots.	Tunicamycin	0-11	periostin, osteoblast specific factor	Mus musculus	72-77
7744857-3	1995	On the basis of tunicamycin sensitivity, both GLUT1 species arose from a common protein migrating at 36 kDa.	Tunicamycin	16-27	solute carrier family 2 (facilitated glucose transporter), member 1	Mus musculus	46-51
7658166-10	1995	Treatment of COS1 cells with tunicamycin for 24 h had the same effect on wild type hLPL processing and edoplasmic reticulum distribution.	Tunicamycin	29-40	lipoprotein lipase	Homo sapiens	83-87
7721836-6	1995	Tunicamycin treatment of transfected COS-7 cells as well as peptide-N-glycosidase F digestion of the transporter converted the 58-kDa species to a 50-kDa form, indicating that the latter represents the hNET core protein.	Tunicamycin	0-11	solute carrier family 6 member 2	Homo sapiens	202-206
7710927-0	1995	Inhibition of N-linked glycosylation of P-glycoprotein by tunicamycin results in a reduced multidrug resistance phenotype.	Tunicamycin	58-69	ATP binding cassette subfamily B member 1	Homo sapiens	40-54
7710927-3	1995	Incubation of clone A cells with tunicamycin for different periods resulted in a time-dependent increase in daunorubicin accumulation, reflecting a reduction in P-gp function.	Tunicamycin	33-44	ATP binding cassette subfamily B member 1	Homo sapiens	161-165
7710927-5	1995	Reduction in surface-associated P-gp following exposure to tunicamycin was established by FACS analysis, Western blot analysis and immunoprecipitation of surface-iodinated P-gp.	Tunicamycin	59-70	ATP binding cassette subfamily B member 1	Homo sapiens	32-36
7710927-5	1995	Reduction in surface-associated P-gp following exposure to tunicamycin was established by FACS analysis, Western blot analysis and immunoprecipitation of surface-iodinated P-gp.	Tunicamycin	59-70	ATP binding cassette subfamily B member 1	Homo sapiens	172-176
7776966-12	1995	Similarly, when cells expressing the wild type FSHR were treated with tunicamycin to prevent N-linked glycosylation, the resulting nonglycosylated FSHR was not able to bind FSH.	Tunicamycin	70-81	follicle stimulating hormone receptor	Homo sapiens	147-151
7720792-0	1995	Tunicamycin potently inhibits tumor necrosis factor-induced hepatocyte apoptosis.	Tunicamycin	0-11	tumor necrosis factor	Mus musculus	30-51
7832797-0	1995	Tunicamycin inhibits the expression of functional thrombin receptors on human T-lymphoblastoid cells.	Tunicamycin	0-11	coagulation factor II, thrombin	Homo sapiens	50-58
7832797-2	1995	In the present report we investigated the effect of tunicamycin, a specific inhibitor of N-linked glycosylation, on the expression and function of the thrombin receptor on human T-lymphoblastoid cells.	Tunicamycin	52-63	coagulation factor II, thrombin	Homo sapiens	151-159
7832797-3	1995	We found that tunicamycin selectively inhibited thrombin-induced Ca2+ mobilization in a dose-dependent manner while the same response triggered by anti-CD3 antibody was unchanged in these cells.	Tunicamycin	14-25	coagulation factor II, thrombin	Homo sapiens	48-56
7832797-4	1995	Surface expression of the thrombin receptor, as assessed by immunofluorescence staining using two different antibodies, was strongly decreased in the presence of tunicamycin.	Tunicamycin	162-173	coagulation factor II, thrombin	Homo sapiens	26-34
7720792-1	1995	The protein glycosylation inhibitor tunicamycin protected male BALB/c mice from tumor necrosis factor alpha-induced liver failure.	Tunicamycin	36-47	tumor necrosis factor	Mus musculus	80-101
7720792-2	1995	Tunicamycin also inhibited tumor necrosis factor-induced cell death in primary hepatocyte cultures with a median inhibitory concentration of 8 nM, but not in the tumor cell line WEHI 164 clone 13.	Tunicamycin	0-11	tumor necrosis factor	Mus musculus	27-48
8548206-6	1995	Tunicamycin diminished the formation of leukocyte IFN, but the decrease in titre of this IFN is due to the inhibition of protein synthesis.	Tunicamycin	0-11	interferon alpha 1	Homo sapiens	50-53
7811745-4	1995	LPL in cells treated with tunicamycin, preventing the transfer of N-linked oligosaccharide chain, was unglycosylated (51 kDa) and inactive.	Tunicamycin	26-37	lipoprotein lipase	Homo sapiens	0-3
8548206-6	1995	Tunicamycin diminished the formation of leukocyte IFN, but the decrease in titre of this IFN is due to the inhibition of protein synthesis.	Tunicamycin	0-11	interferon alpha 1	Homo sapiens	89-92
7873794-3	1994	This study was undertaken to investigate the internalization of Sertoli-derived SGP-2 and synthesis of an endogenous efferent duct form of SGP-2 by nonciliated cells targeted to their secondary lysosomes on animals whose efferent ducts were ligated and/or received injections of tunicamycin.	Tunicamycin	279-290	clusterin	Homo sapiens	139-144
7808470-1	1994	A gene which overexpresses a 36-kDa protein (p36) in tunicamycin-resistant Leishmania was mapped by transfection and overexpression to the upstream region of the drug maker in the extrachromosomal amplicon.	Tunicamycin	53-64	annexin A2	Homo sapiens	45-48
8044801-10	1994	Treatment of DCC-expressing cells with tunicamycin decreased the apparent molecular weight of the immunoreactive proteins, establishing that DCC is a glycoprotein.	Tunicamycin	39-50	DCC netrin 1 receptor	Homo sapiens	13-16
8044801-10	1994	Treatment of DCC-expressing cells with tunicamycin decreased the apparent molecular weight of the immunoreactive proteins, establishing that DCC is a glycoprotein.	Tunicamycin	39-50	DCC netrin 1 receptor	Homo sapiens	141-144
7710927-6	1995	In addition, immunoprecipitation of P-gp from 32P-orthophosphate-labelled cells demonstrated reduced phosphorylation of P-gp associated with tunicamycin exposure.	Tunicamycin	141-152	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
7710927-6	1995	In addition, immunoprecipitation of P-gp from 32P-orthophosphate-labelled cells demonstrated reduced phosphorylation of P-gp associated with tunicamycin exposure.	Tunicamycin	141-152	ATP binding cassette subfamily B member 1	Homo sapiens	120-124
7875740-5	1994	Treatment of CD4+ cell lines with tunicamycin resulted in the appearance of a 47,000 MW band for both allelic forms indicating that the difference in M(r) is due to glycosylation.	Tunicamycin	34-45	CD4 molecule	Bos taurus	13-16
7895167-3	1994	Treatment of H-2Dd+ target cells with tunicamycin prevents their binding to Ly-49A+ cells and renders them susceptible to lysis by Ly-49A+ NK cells.	Tunicamycin	38-49	killer cell lectin-like receptor, subfamily A, member 1	Mus musculus	76-82
7895167-3	1994	Treatment of H-2Dd+ target cells with tunicamycin prevents their binding to Ly-49A+ cells and renders them susceptible to lysis by Ly-49A+ NK cells.	Tunicamycin	38-49	killer cell lectin-like receptor, subfamily A, member 1	Mus musculus	131-137
7877727-0	1994	Tunicamycin inhibits prostaglandin F2 alpha receptor-mediated phosphoinositide hydrolysis in cultured rat astrocytes.	Tunicamycin	0-11	prostaglandin F receptor	Rattus norvegicus	21-52
7999029-5	1994	Both the mature and non-mature forms of the G-CSFR appear to be N-glycosylated, as determined by glycanase digestion and inhibition of glycosylation by tunicamycin.	Tunicamycin	152-163	colony stimulating factor 3 receptor (granulocyte)	Mus musculus	44-50
7526846-1	1994	In order to determine whether the endoplasmic reticulum (ER) luminal FK506-binding protein, FKBP13, shares properties of ER molecular chaperones, MDCK cells were treated with either tunicamycin or Ca2+ ionophores.	Tunicamycin	182-193	FKBP prolyl isomerase 2	Homo sapiens	92-98
7526846-2	1994	By Northern-blot analysis, tunicamycin resulted in a 2-fold rise in FKBP13 mRNA, whereas ionophores (A23187 and ionomycin) caused a more impressive rise in FKBP13 mRNA (up to 5-fold with ionomycin).	Tunicamycin	27-38	FKBP prolyl isomerase 2	Homo sapiens	68-74
7523405-10	1994	The expression of the serotonin transporter in tunicamycin-treated Sf9 cells resulted in low levels of ligand binding activity (0.2 pmol/mg) but unchanged Kd.	Tunicamycin	47-58	solute carrier family 6 member 4	Rattus norvegicus	22-43
7972488-4	1994	The signal peptide is cleaved at the same position as in maize and the mature protein undergoes tunicamycin-sensitive glycosylation, yielding a product with the same mobility on SDS-PAGE as authentic maize ABP1.	Tunicamycin	96-107	auxin-binding protein 1	Zea mays	206-210
8163533-7	1994	PNGase F digestion of extracts prepared from LLC-NET- and hNET-transfected HeLa cells convert all immunoreactive species to a 46-kDa form, equivalent to that observed following incubation of whole cells with the glycosylation inhibitor tunicamycin.	Tunicamycin	236-247	solute carrier family 6 member 2	Homo sapiens	58-62
8188375-7	1994	The effects on grp78 expression of heat shock and tunicamycin treatment, the latter of which specifically stimulates mammalian grp78, were investigated.	Tunicamycin	50-61	heat shock protein family A (Hsp70) member 5	Homo sapiens	15-20
8188375-8	1994	While the level of the grp78 protein remained constant under all circumstances, grp78 mRNA was unaffected by heat shock but induced fivefold by tunicamycin.	Tunicamycin	144-155	heat shock protein family A (Hsp70) member 5	Homo sapiens	80-85
8089706-2	1994	Under conditions which block the addition of opsin to outer segments, various lipids continue to be synthesized and transported to the outer segment in the presence of monensin, puromycin, brefeldin A, tunicamycin and several general metabolic inhibitors.	Tunicamycin	202-213	rhodopsin, gene2 L homeolog	Xenopus laevis	45-50
8038169-6	1994	Its levels were correlated with RCK1 current amplitudes (IRCK1) and upon incubation of the cRNA-injected oocytes with tunicamycin, its molecular weight was decreased and at the same time IRCK1 was reduced.	Tunicamycin	118-129	potassium voltage-gated channel subfamily A member 1	Rattus norvegicus	32-36
8006041-5	1994	Monensin or tunicamycin treatment resulted in a shift of the 27-29-kDa human CR-1 protein to 24 kDa and 20 kDa, respectively.	Tunicamycin	12-23	teratocarcinoma-derived growth factor 1	Mus musculus	77-81
7515860-6	1994	Expression of sLe(a) and sLe(x) antigens and binding to E-selectin were reduced by pre-treatment of SW1990 cells with the O-linked glycosylation inhibitor benzyl-alpha-GalNAc but not with the N-linked glycosylation inhibitor tunicamycin.	Tunicamycin	225-236	selectin E	Homo sapiens	56-66
7515913-5	1994	Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction.	Tunicamycin	0-11	complement C3d receptor 2	Homo sapiens	25-29
7515913-5	1994	Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction.	Tunicamycin	0-11	Fc epsilon receptor II	Homo sapiens	87-91
7515913-5	1994	Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction.	Tunicamycin	0-11	Fc epsilon receptor II	Homo sapiens	181-185
7515913-5	1994	Tunicamycin treatment of CD21-transfected K562 cells strongly inhibited the binding of CD23-liposomes, suggesting that an N-linked sugar, present on SCRs 5 to 8, is involved in the CD23/CD21 interaction.	Tunicamycin	0-11	complement C3d receptor 2	Homo sapiens	186-190
8163533-9	1994	On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool.	Tunicamycin	113-124	solute carrier family 6 member 2	Homo sapiens	90-93
8163533-9	1994	On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool.	Tunicamycin	113-124	solute carrier family 6 member 2	Homo sapiens	184-188
8163533-9	1994	On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool.	Tunicamycin	113-124	solute carrier family 6 member 2	Homo sapiens	185-188
8163533-9	1994	On the other hand, NE transport and antagonist ([125I]RTI-55) binding assays on whole LLC-NET cells treated with tunicamycin reveal a pronounced reduction in NE transport activity and hNET membrane density paralleled by an inability of NET proteins to replenish the higher M(r) hNET pool.	Tunicamycin	113-124	solute carrier family 6 member 2	Homo sapiens	278-282
7909499-3	1994	Prevention of post-translational addition of N-linked oligosaccharides by treatment of the resistant cells with tunicamycin resulted in a dramatic enhancement in LAK cell cytotoxicity which was partially inhibited by antibodies against LFA-1 and ICAM-1.	Tunicamycin	112-123	alpha kinase 1	Homo sapiens	162-165
7909499-3	1994	Prevention of post-translational addition of N-linked oligosaccharides by treatment of the resistant cells with tunicamycin resulted in a dramatic enhancement in LAK cell cytotoxicity which was partially inhibited by antibodies against LFA-1 and ICAM-1.	Tunicamycin	112-123	integrin subunit alpha L	Homo sapiens	236-241
7909499-3	1994	Prevention of post-translational addition of N-linked oligosaccharides by treatment of the resistant cells with tunicamycin resulted in a dramatic enhancement in LAK cell cytotoxicity which was partially inhibited by antibodies against LFA-1 and ICAM-1.	Tunicamycin	112-123	intercellular adhesion molecule 1	Homo sapiens	246-252
7909499-5	1994	Tunicamycin treatment caused a decrease in the molecular weight of ICAM-1 from approximately 95,000 to 50,000 Da.	Tunicamycin	0-11	intercellular adhesion molecule 1	Homo sapiens	67-73
8155721-2	1994	43% of 35S-labeled LPL subunits in tunicamycin (TUN)-treated cells did not bind to a heparin-Sepharose column and 46% was eluted with 0.6 M NaCl.	Tunicamycin	35-46	lipoprotein lipase	Homo sapiens	19-22
8138587-3	1994	Sensitivity to tunicamycin indicated that N-linked post-translational modifications to this 43 kDa core species generated the full complement of 50 kDa (intermediate) and 52 kDa (mature) p52(PAI-1) glycosylated isoforms.	Tunicamycin	15-26	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	187-190
8138587-3	1994	Sensitivity to tunicamycin indicated that N-linked post-translational modifications to this 43 kDa core species generated the full complement of 50 kDa (intermediate) and 52 kDa (mature) p52(PAI-1) glycosylated isoforms.	Tunicamycin	15-26	serpin family E member 1	Rattus norvegicus	191-196
8027512-9	1994	The Golgi apparatus inhibitors monensin, swainsonine and tunicamycin enhanced ricin toxicity, as evidenced by shortened survival times.	Tunicamycin	57-68	ricin	Ricinus communis	78-83
8132654-13	1994	Interestingly, degradation of unglycosylated apoB, detected in tunicamycin-pretreated cells, occurred earlier, resulted in generation of additional fragments, and was largely uninhibited by ALLN.	Tunicamycin	63-74	apolipoprotein B	Homo sapiens	45-49
8032172-3	1994	Stable transfection studies show that GRP78 transcription is also regulated by ethanol and that ethanol also potentiates GRP78 induction by classical inducing agents such as tunicamycin.	Tunicamycin	174-185	heat shock protein 5	Mus musculus	121-126
8110797-7	1994	Inhibition of N-glycosylation by tunicamycin also increased the binding of monoclonal antibody LRB 200 to hepatocyte apoB.	Tunicamycin	33-44	apolipoprotein B	Rattus norvegicus	117-121
8110187-10	1994	The trypsin-resistant MUC2 fragment contained N-linked carbohydrate, as indicated by a decrease in size as a result of peptidyl N-glycosidase digestion or tunicamycin treatment of HM3 cells.	Tunicamycin	155-166	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	22-26
8110187-10	1994	The trypsin-resistant MUC2 fragment contained N-linked carbohydrate, as indicated by a decrease in size as a result of peptidyl N-glycosidase digestion or tunicamycin treatment of HM3 cells.	Tunicamycin	155-166	cholinergic receptor muscarinic 3	Homo sapiens	180-183
8114674-4	1994	Enzymatically active recombinant hPGHS-1 and hPGHS-2 were present as glycosylated proteins in the microsomal fraction prepared from infected cells, whereas recombinant hPGHS-1 and hPGHS-2 prepared from the microsomal fraction of cells treated with tunicamycin, an inhibitor of N-linked glycosylation, were enzymatically inactive.	Tunicamycin	248-259	prostaglandin-endoperoxide synthase 1	Homo sapiens	33-40
7979996-4	1994	The recombinant E2 protein appeared to be glycosylated since it was susceptible to tunicamycin.	Tunicamycin	83-94	ubiquitin conjugating enzyme E2 B	Homo sapiens	16-26
8011427-3	1994	We show here that (1) in CHO-Y2 cells, basal endocytosis, like insulin-induced internalization, was markedly altered despite normal receptor turnover and (2) in both CHO-R and CHO-Y2 cells, basal receptor endocytosis was altered by tunicamycin, an inhibitor of protein N-glycosylation, whereas insulin-induced internalization was not.	Tunicamycin	232-243	insulin	Cricetulus griseus	63-70
8227155-5	1993	Immunoprecipitation with anti-flg antibody followed by electrophoresis produced a band of 90 Kd in tunicamycin-treated cells expressing the mutant as well as the wild-type receptors, indicating that the inhibition of binding was not due to defective expression of the protein.	Tunicamycin	99-110	filaggrin	Homo sapiens	30-33
7994083-9	1994	Growth of cells in the presence of tunicamycin demonstrates that both P190 and P70 are glycosylated, with the deglycosylated forms migrating in polyacrylamide gels as proteins of 165 kDa and 45 kDa, respectively.	Tunicamycin	35-46	annexin A6	Homo sapiens	79-82
7937345-3	1994	Tunicamycin pretreatment concentration-dependently decreased GLP-1 binding to RINm5F cells due to a decreased receptor number without change of receptor affinity.	Tunicamycin	0-11	glucagon	Rattus norvegicus	61-66
7516308-7	1993	Furthermore, isoproterenol stimulation of protein glycosylation by exogenous dolichyl monophosphate and its inhibition by tunicamycin (GlcNAc-1P transferase inhibitor) supported the concept that isoproterenol specifically stimulated protein N-glycosylation event(s) in the cell.	Tunicamycin	122-133	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	135-156
7935356-11	1993	Tunicamycin, an inhibitor of co-translational transfer of core oligosaccharide, provoked rapid phosphorylation of eIF-2 alpha and inhibition of translational initiation whereas sugar analog inhibitors of glycoprotein processing did neither.	Tunicamycin	0-11	eukaryotic translation initiation factor 2A	Rattus norvegicus	114-125
8477700-6	1993	In addition, inhibition of PiM and PiZ alpha 1-AT glycosylation and secretion by tunicamycin did not result in the accumulation of the protein, but instead in its rapid lag-free degradation.	Tunicamycin	81-92	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	27-30
8212855-10	1993	Moreover tunicamycin treatment of cells infected with the virus indicated that p32 was glycosylated.	Tunicamycin	9-20	inhibitor of growth family member 2	Homo sapiens	79-82
8337817-5	1993	Using myxoma virus and recombinant vaccinia virus constructs for experiments with tunicamycin and peptide N-glycosidase F, it is shown that the secreted SERP1 protein is modified by N-linked glycosylation.	Tunicamycin	82-93	stress associated endoplasmic reticulum protein 1	Homo sapiens	153-158
8099781-2	1993	(i) Tunicamycin completely inhibited mannose incorporation into Thy-1.	Tunicamycin	4-15	Thy-1 cell surface antigen	Rattus norvegicus	64-69
8223708-11	1993	Two inhibitors of MPR-mediated enzyme transport, tunicamycin and chloroquine, were used.	Tunicamycin	49-60	progesterone receptor membrane component 1	Rattus norvegicus	18-21
8388383-8	1993	1) Tunicamycin treatment of wild type u-PAR-expressing cells.	Tunicamycin	3-14	plasminogen activator, urokinase receptor	Homo sapiens	38-43
8486673-9	1993	Rat CRP acquired the ability to bind to phosphorylcholine-Sepharose and to form the dimeric and oligomeric species prior to acquiring resistance to endo H. Studies using tunicamycin revealed that the N-linked oligosaccharide present in rat CRP was not required for formation of its dimeric component, oligomerization, ability to bind to phosphorylcholine, or secretion.	Tunicamycin	170-181	C-reactive protein	Rattus norvegicus	4-7
8490167-0	1993	Effect of tunicamycin treatment on ligand binding to the erythropoietin receptor: conversion from two classes of binding sites to a single class.	Tunicamycin	10-21	erythropoietin receptor	Mesocricetus auratus	57-80
8490167-4	1993	Scatchard plots of baby hamster kidney (BHK) cells that had been engineered to express cloned mouse EPO-R were also biphasic and the plots of cells cultured with tunicamycin became a single phase with high-affinity sites.	Tunicamycin	162-173	erythropoietin receptor	Mus musculus	100-105
8490167-8	1993	BHK cells that expressed mutant EPO-R showed biphasic Scatchard plots that were converted to single-phase plots with only high-affinity sites by tunicamycin treatment.	Tunicamycin	145-156	erythropoietin receptor	Mesocricetus auratus	32-37
8319938-3	1993	However, when the receptor was subjected to deglycosylation by treatment with tunicamycin, the receptors of the KMT-17 and MRK-49F cells gave the same molecular mass of 225K, indicating that the difference in molecular mass between two cell lines resulted from the different oligosaccharide sizes.	Tunicamycin	78-89	ciliogenesis associated kinase 1	Rattus norvegicus	123-126
8397508-6	1993	Inhibition of N-glycosylation with tunicamycin caused a dramatic intracellular degradation of these convertases within the endoplasmic reticulum, with the net effect of a reduction in the available activity of PC1 and PC2.	Tunicamycin	35-46	proprotein convertase subtilisin/kexin type 1	Rattus norvegicus	210-213
8397508-6	1993	Inhibition of N-glycosylation with tunicamycin caused a dramatic intracellular degradation of these convertases within the endoplasmic reticulum, with the net effect of a reduction in the available activity of PC1 and PC2.	Tunicamycin	35-46	proprotein convertase subtilisin/kexin type 2	Rattus norvegicus	218-221
7690438-7	1993	Inhibition of N-linked glycosylation by tunicamycin resulted in the production of identical-sized nascent L-selectin by normal and CLL cells.	Tunicamycin	40-51	selectin L	Homo sapiens	106-116
7686870-2	1993	The recombinant NS1 protein (re-NS1) produced in infected insect cells was localized on the cell surface and was apparently glycosylated, because it was susceptible to treatment with both tunicamycin and N-glycanase.	Tunicamycin	188-199	protein tyrosine phosphatase non-receptor type 11	Homo sapiens	16-19
7686870-2	1993	The recombinant NS1 protein (re-NS1) produced in infected insect cells was localized on the cell surface and was apparently glycosylated, because it was susceptible to treatment with both tunicamycin and N-glycanase.	Tunicamycin	188-199	polyglutamine binding protein 1	Homo sapiens	29-35
8222275-7	1993	Tunicamycin (0.3-3.0 micrograms/l) increased the percentage of Hex B in the medium, whereas an increased release of Hex was noted only after 48 h. Tunicamycin is known to enhance the secretion of N-linked oligosaccharide-free forms of lysosomal enzymes.	Tunicamycin	0-11	O-GlcNAcase	Homo sapiens	63-66
8222275-7	1993	Tunicamycin (0.3-3.0 micrograms/l) increased the percentage of Hex B in the medium, whereas an increased release of Hex was noted only after 48 h. Tunicamycin is known to enhance the secretion of N-linked oligosaccharide-free forms of lysosomal enzymes.	Tunicamycin	147-158	O-GlcNAcase	Homo sapiens	63-66
8222275-7	1993	Tunicamycin (0.3-3.0 micrograms/l) increased the percentage of Hex B in the medium, whereas an increased release of Hex was noted only after 48 h. Tunicamycin is known to enhance the secretion of N-linked oligosaccharide-free forms of lysosomal enzymes.	Tunicamycin	147-158	O-GlcNAcase	Homo sapiens	116-119
7685904-3	1993	FKB2 mRNA levels are elevated in cells blocked in N-glycosylation--i.e., in wild-type cells treated with tunicamycin and in the sec53-6 mutant grown at the nonpermissive temperature.	Tunicamycin	105-116	peptidylprolyl isomerase family protein FPR2	Saccharomyces cerevisiae S288C	0-4
8315416-1	1993	Tunicamycin inhibits the dolichol pathway for N-linked glycosylation of proteins, including photoreceptor opsin, and causes a buildup of tubulo-vesicular profiles in the intersegmental space between photoreceptor rod inner and outer segments associated with disruption of new disc assembly.	Tunicamycin	0-11	rhodopsin, gene2 L homeolog	Xenopus laevis	106-111
8484745-1	1993	By culturing with tunicamycin A1, an inhibitor of N-glycosylation, or by sialidase digestion, mouse monocytic cells P388D1 were induced to carry out Fc receptor-mediated phagocytosis of IgG-coated sheep red blood cells.	Tunicamycin	18-29	Fc receptor	Mus musculus	149-160
8477700-6	1993	In addition, inhibition of PiM and PiZ alpha 1-AT glycosylation and secretion by tunicamycin did not result in the accumulation of the protein, but instead in its rapid lag-free degradation.	Tunicamycin	81-92	serpin family A member 1	Homo sapiens	39-49
8141920-4	1993	The spot for transferrin shifted to the more basic isoforms by treatment for 3 hr with monensin or tunicamycin.	Tunicamycin	99-110	transferrin	Rattus norvegicus	13-24
7679747-9	1993	(iii) The UL10 protein in cells treated with tunicamycin formed a single band (apparent M(r) of 47,000) reactive with the anti-UL10 antibody, indicating that the 47,000-M(r) protein was a precursor of N-glycosylated, more slowly migrating forms of UL10.	Tunicamycin	45-56	envelope glycoprotein M	Human alphaherpesvirus 1	10-14
7679747-9	1993	(iii) The UL10 protein in cells treated with tunicamycin formed a single band (apparent M(r) of 47,000) reactive with the anti-UL10 antibody, indicating that the 47,000-M(r) protein was a precursor of N-glycosylated, more slowly migrating forms of UL10.	Tunicamycin	45-56	envelope glycoprotein M	Human alphaherpesvirus 1	127-131
7679747-9	1993	(iii) The UL10 protein in cells treated with tunicamycin formed a single band (apparent M(r) of 47,000) reactive with the anti-UL10 antibody, indicating that the 47,000-M(r) protein was a precursor of N-glycosylated, more slowly migrating forms of UL10.	Tunicamycin	45-56	envelope glycoprotein M	Human alphaherpesvirus 1	127-131
8431454-6	1993	Adding tunicamycin or deoxymannojirimycin to the TGF-beta 1-treated and untreated cells caused these 55 and 65 kDa glucose transporters to migrate as one band at 40-43 kDa.	Tunicamycin	7-18	transforming growth factor, beta 1	Mus musculus	49-59
8464905-3	1993	Tunicamycin and pulse-chase experiments revealed that the mature protein was processed by N-linked glycosylation of a 145-kDa erbB-3 core polypeptide.	Tunicamycin	0-11	erb-b2 receptor tyrosine kinase 3	Homo sapiens	126-132
8454000-3	1993	Treatment of the cells with tunicamycin caused a rapid decrease in GRP78 phosphorylation within 2 to 4 h in both cell types prior to GRP78 induction.	Tunicamycin	28-39	heat shock protein family A (Hsp70) member 5	Homo sapiens	67-72
8454000-3	1993	Treatment of the cells with tunicamycin caused a rapid decrease in GRP78 phosphorylation within 2 to 4 h in both cell types prior to GRP78 induction.	Tunicamycin	28-39	heat shock protein family A (Hsp70) member 5	Homo sapiens	133-138
8454000-4	1993	Following a longer period of tunicamycin treatment, GRP78 phosphorylation recovered gradually in parallel with the accumulation of newly synthesized GRP78.	Tunicamycin	29-40	heat shock protein family A (Hsp70) member 5	Homo sapiens	52-57
8454000-4	1993	Following a longer period of tunicamycin treatment, GRP78 phosphorylation recovered gradually in parallel with the accumulation of newly synthesized GRP78.	Tunicamycin	29-40	heat shock protein family A (Hsp70) member 5	Homo sapiens	149-154
8454000-5	1993	The half-life of GRP78 was over 24 h and similar in both normal and transformed cells either with or without tunicamycin treatment.	Tunicamycin	109-120	heat shock protein family A (Hsp70) member 5	Homo sapiens	17-22
8454000-6	1993	In contrast, the half-life of phosphate groups incorporated into GRP78 was about 120 min in both types of cells in the absence of tunicamycin treatment.	Tunicamycin	130-141	heat shock protein family A (Hsp70) member 5	Homo sapiens	65-70
8093618-7	1993	The addition of high concentrations of tunicamycin to 293-GC-C cells also reduced the M(r) to 120,000, indicating that GC-C is an N-linked glycoprotein.	Tunicamycin	39-50	guanylate cyclase 2C	Homo sapiens	58-62
8093618-7	1993	The addition of high concentrations of tunicamycin to 293-GC-C cells also reduced the M(r) to 120,000, indicating that GC-C is an N-linked glycoprotein.	Tunicamycin	39-50	guanylate cyclase 2C	Homo sapiens	119-123
8430814-7	1993	Treatment of fetal rabbit lung explants with inhibitors of oligosaccharide addition (tunicamycin) and processing (castanospermine), which act within the endoplasmic reticulum, significantly reduced the rate of transport of newly synthesized SP-A to lamellar bodies.	Tunicamycin	85-96	pulmonary surfactant-associated protein A	Oryctolagus cuniculus	241-245
8476209-6	1993	Upon addition of tunicamycin, to cycling cells the progression through G1 was blocked in a similar way to that following HMG CoA reductase inhibition.	Tunicamycin	17-28	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	121-138
8416385-3	1993	Nonglycosylated forms of gp120 generated either by deletion of the signal sequence of HIV-1 gp120 or by synthesis in the presence of tunicamycin failed to bind to CD4.	Tunicamycin	133-144	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	25-30
1450177-9	1992	Inhibition of LPL secretion by tunicamycin in both peritoneal macrophages and J774.1 cells prevented a hypertriglyceridemic very low density lipoprotein-induced triglyceride accumulation, an effect that was counteracted by addition of exogenous LPL.	Tunicamycin	31-42	lipoprotein lipase	Mus musculus	14-17
1450177-9	1992	Inhibition of LPL secretion by tunicamycin in both peritoneal macrophages and J774.1 cells prevented a hypertriglyceridemic very low density lipoprotein-induced triglyceride accumulation, an effect that was counteracted by addition of exogenous LPL.	Tunicamycin	31-42	lipoprotein lipase	Mus musculus	245-248
1479287-4	1992	LPL catalytic activity from the heparin-releasable fraction of adipocytes was inhibited by more than 70%, with similar decreases in LPL mass, when cells were cultured for 24 h in the presence of either tunicamycin or castanospermine.	Tunicamycin	202-213	lipoprotein lipase	Rattus norvegicus	0-3
1479287-7	1992	The appearance of 35S-labeled LPL in the medium was blocked by treatment of cells with tunicamycin and castanospermine, whereas secretion was not affected by DMJ or swainsonine.	Tunicamycin	87-98	lipoprotein lipase	Rattus norvegicus	30-33
1479287-9	1992	The unglycosylated [35S]LPL that was synthesized in the presence of tunicamycin demonstrated essentially no intracellular degradation.	Tunicamycin	68-79	lipoprotein lipase	Rattus norvegicus	24-27
1359965-10	1992	By contrast, inhibition of N-glycosylation with tunicamycin resulted into rapid degradation of non-N-glycosylated DPP IV molecules in both cell types.	Tunicamycin	48-59	dipeptidylpeptidase 4	Rattus norvegicus	114-120
1425427-2	1992	Proenkephalin is synthesized in both N-glycosylated and unglycosylated forms, as demonstrated by treatment with tunicamycin.	Tunicamycin	112-123	proenkephalin	Rattus norvegicus	0-13
24178389-7	1992	Treatment of cells with tunicamycin, which inhibits N-glycosylation, and digestion of the (35)S-labelled processing intermediates with endoglycosidase H indicate that beta-1,3-glucanase has a single N-glycan attached to the C-terminal extension.	Tunicamycin	24-35	glucan endo-1,3-beta-glucosidase, acidic-like	Nicotiana tabacum	167-185
1375936-9	1992	Growth of HL60 cells in tunicamycin inhibited the ability of these cells to support P-selectin-mediated binding and, to a lesser extent, E-selectin-mediated binding.	Tunicamycin	24-35	selectin P	Homo sapiens	84-94
1387671-7	1992	Treatment of AcMCP 1-infected Sf-21 cells with tunicamycin resulted in reduced production of the 21- and 23-kDa proteins and an increase in 16- to 18-kDa products, the predicted size range of uncleaved and nonglycosylated rat MCP 1.	Tunicamycin	47-58	C-C motif chemokine ligand 2	Rattus norvegicus	15-20
1505923-7	1992	By inhibition of the N-glycosylation using tunicamycin, rat C1-esterase inhibitor was identified as a glycoprotein.	Tunicamycin	43-54	complement C1s	Rattus norvegicus	60-71
1398755-3	1992	In this study we show that tunicamycin-treated cells release small CD23 fragments with a MW of 16,000.	Tunicamycin	27-38	Fc epsilon receptor II	Homo sapiens	67-71
1386872-4	1992	Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand.	Tunicamycin	10-21	Fc epsilon receptor II	Homo sapiens	37-41
1386872-4	1992	Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand.	Tunicamycin	10-21	Fc epsilon receptor II	Homo sapiens	109-113
1386872-4	1992	Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand.	Tunicamycin	10-21	Fc epsilon receptor II	Homo sapiens	109-113
1386872-4	1992	Moreover, tunicamycin treatment of a CD23-binding cell line, RPMI 8226, significantly reduced the binding of CD23 incorporated into fluorescent liposomes, and a sugar, fucose-1-phosphate, was found to inhibit CD23-liposome binding to RPMI 8226 cells, suggesting the contribution of sugar structures on the CD23 ligand.	Tunicamycin	10-21	Fc epsilon receptor II	Homo sapiens	109-113
1515555-7	1992	Production of TNF but not F2 was inhibited when the cells were cultured with tunicamycin and PDB.	Tunicamycin	77-88	tumor necrosis factor	Homo sapiens	14-17
1318394-9	1992	Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide.	Tunicamycin	98-109	carcinoembryonic antigen-related cell adhesion molecule 1	Mus musculus	21-25
1318394-9	1992	Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide.	Tunicamycin	98-109	carcinoembryonic antigen-related cell adhesion molecule 1	Mus musculus	52-56
1318394-9	1992	Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide.	Tunicamycin	98-109	carcinoembryonic antigen-related cell adhesion molecule 1	Mus musculus	52-56
1318394-9	1992	Nonglycosylated core MHVR proteins were made in Vac-MHVR-infected BHK-21 cells in the presence of tunicamycin by in vitro translation of MHVR mRNA in a rabbit reticulocyte cell-free system in the absence of microsomal membranes and by expression of an N-terminal deletion clone of MHVR lacking its signal peptide.	Tunicamycin	98-109	carcinoembryonic antigen-related cell adhesion molecule 1	Mus musculus	52-56
1344885-0	1992	Bean homologs of the mammalian glucose-regulated proteins: induction by tunicamycin and interaction with newly synthesized seed storage proteins in the endoplasmic reticulum.	Tunicamycin	72-83	brain expressed associated with NEDD4 1	Homo sapiens	0-4
1344885-1	1992	Treatment of developing bean cotyledons with the inhibitor of N-glycosylation tunicamycin enhanced the synthesis of at least two polypeptides with molecular mass 78 kDa and 97 kDa.	Tunicamycin	78-89	brain expressed associated with NEDD4 1	Homo sapiens	24-28
1344885-5	1992	When newly synthesized storage glycoproteins phaseolin, phytohemagglutinin or alpha-amylase inhibitor were immunoprecipitated from an ER preparation of tunicamycin-treated tissue, the GRP78 homolog was always co-precipitated.	Tunicamycin	152-163	heat shock protein family A (Hsp70) member 5	Homo sapiens	184-189
1356290-7	1992	In addition, ICAM-1 proteins expressed in the presence of tunicamycin also retained their virus binding capability.	Tunicamycin	58-69	intercellular adhesion molecule 1	Homo sapiens	13-19
1596569-3	1992	Synthesis of this protein could also be induced by tunicamycin, suggesting that it might be the 78-Kd glucose-regulated protein (GRP78).	Tunicamycin	51-62	heat shock protein 5	Mus musculus	129-134
1420307-7	1992	Glycosylation of the intrinsic factor was demonstrated by lectin binding to the recombinant protein separated on SDS-PAGE, and by a shift in apparent molecular mass from 47 kDa to 43 kDa following treatment of Sf9 cells with tunicamycin.	Tunicamycin	225-236	cobalamin binding intrinsic factor	Homo sapiens	21-37
1325440-2	1992	Overproduction of BiP/Kar2 protein was achieved by the cloning of the KAR2 gene on multicopy plasmids and the treatment of cells harboring the cloned KAR2 gene with tunicamycin.	Tunicamycin	165-176	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	22-26
1325440-2	1992	Overproduction of BiP/Kar2 protein was achieved by the cloning of the KAR2 gene on multicopy plasmids and the treatment of cells harboring the cloned KAR2 gene with tunicamycin.	Tunicamycin	165-176	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	150-154
1423514-3	1992	Immunogold labelling of ultrathin sections from tunicamycin-treated rats revealed that, in about 5% of vasopressin neurones, the accretions could be immunogold-labelled for vasopressin and its associated neurophysin.	Tunicamycin	48-59	arginine vasopressin	Rattus norvegicus	103-114
1423514-3	1992	Immunogold labelling of ultrathin sections from tunicamycin-treated rats revealed that, in about 5% of vasopressin neurones, the accretions could be immunogold-labelled for vasopressin and its associated neurophysin.	Tunicamycin	48-59	arginine vasopressin	Rattus norvegicus	173-184
1506413-2	1992	Expression of the glucose regulated proteins (GRP78 and GRP94) is greatly increased after cells are exposed to stress agents (including A23187 and tunicamycin) which inhibit ER function.	Tunicamycin	147-158	heat shock protein family A (Hsp70) member 5	Homo sapiens	46-51
1506413-2	1992	Expression of the glucose regulated proteins (GRP78 and GRP94) is greatly increased after cells are exposed to stress agents (including A23187 and tunicamycin) which inhibit ER function.	Tunicamycin	147-158	heat shock protein 90 beta family member 1	Homo sapiens	56-61
1506413-6	1992	The increased accumulation of GRP78 mRNA after exposure of cells to either thapsigargin, brefeldin A, AIF4-, A23187, or tunicamycin can be blocked by pre-incubation in cycloheximide.	Tunicamycin	120-131	heat shock protein family A (Hsp70) member 5	Homo sapiens	30-35
1583718-5	1992	Metabolic labelling of gp41 with [3H]GlcNAc occurred in the presence of tunicamycin.	Tunicamycin	72-83	occlusion-derived virus glycoprotein	Autographa californica nucleopolyhedrovirus	23-27
1315744-5	1992	It had been assumed that this cDNA, termed TRG for tunicamycin resistance gene, encoded GPT enzyme.	Tunicamycin	51-62	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Cricetulus griseus	88-91
1521926-0	1992	Tunicamycin inhibits function and expression of the high-affinity IL-2 receptor in a murine IL-2-dependent cell line.	Tunicamycin	0-11	interleukin 2	Mus musculus	66-70
1521926-0	1992	Tunicamycin inhibits function and expression of the high-affinity IL-2 receptor in a murine IL-2-dependent cell line.	Tunicamycin	0-11	interleukin 2	Mus musculus	92-96
1521926-4	1992	Inhibition of proliferation by tunicamycin was accompanied by an inhibition of binding of 125I-IL-2 to its high-affinity receptor.	Tunicamycin	31-42	interleukin 2	Mus musculus	95-99
1373378-5	1992	GRP78 overexpressing cells treated with tunicamycin or A23187 exhibited a reduced induction of endogenous GRP78 and GRP94 mRNAs compared to wild-type CHO cells.	Tunicamycin	40-51	endoplasmic reticulum chaperone BiP	Cricetulus griseus	0-5
1373378-5	1992	GRP78 overexpressing cells treated with tunicamycin or A23187 exhibited a reduced induction of endogenous GRP78 and GRP94 mRNAs compared to wild-type CHO cells.	Tunicamycin	40-51	endoplasmic reticulum chaperone BiP	Cricetulus griseus	106-111
1723541-7	1991	Culture of RC-2A cells in the presence of tunicamycin (after removal of surface antigens by pronase) blocked re-expression of the epitopes recognised by all 3 mAb suggesting that they involve N-linked glycosylation.	Tunicamycin	42-53	paired box 5	Homo sapiens	153-158
1371789-7	1992	In biosynthetic studies, all four anti-Fc alpha R antibodies and the IgA ligand bound a single 32-kDa core protein present in tunicamycin-treated cells, and the exceptional antibody again recognized molecules with relatively restricted glycosylation in the nontreated cells.	Tunicamycin	126-137	Fc alpha receptor	Homo sapiens	39-49
1735447-6	1992	When N-glycosylation was inhibited in prb1-Ala519 mutant cells by tunicamycin, a smaller molecule of about 71 kDa appeared consistent with single N-glycosylation and signal-sequence cleavage of the translocated mutant PrB molecule in the endoplasmic reticulum.	Tunicamycin	66-77	proteinase B	Saccharomyces cerevisiae S288C	38-42
1601876-6	1992	In vivo synthesis studies in the presence and absence of tunicamycin, an inhibitor of N-linked glycosylation, indicate that pro-P34 is 47 kDa.	Tunicamycin	57-68	P34 probable thiol protease	Glycine max	128-131
1540178-5	1992	Preincubation of the transfected cells with the N-glycosylation inhibitor tunicamycin resulted in the conversion of the 47 kDa VEGF homodimer into a smaller, deglycosylated form of 42 kDa.	Tunicamycin	74-85	vascular endothelial growth factor A	Homo sapiens	127-131
1531639-2	1992	Cell treatment with the N-glycosylation inhibitor tunicamycin generated unglycosylated CD45 polypeptides of 130 and 140 kDa.	Tunicamycin	50-61	protein tyrosine phosphatase receptor type C	Homo sapiens	87-91
1531639-3	1992	Immunofluorescence flow cytometry and Scatchard techniques revealed that CD45 cell surface expression was decreased in a time- and dose-dependent manner upon tunicamycin incubation.	Tunicamycin	158-169	protein tyrosine phosphatase receptor type C	Homo sapiens	73-77
1531639-4	1992	Moreover, a remarkable decrease in CD45 phosphatase activity was detected in tunicamycin-treated cells, which correlated with the diminished CD45 cell surface expression.	Tunicamycin	77-88	protein tyrosine phosphatase receptor type C	Homo sapiens	35-39
1531639-4	1992	Moreover, a remarkable decrease in CD45 phosphatase activity was detected in tunicamycin-treated cells, which correlated with the diminished CD45 cell surface expression.	Tunicamycin	77-88	protein tyrosine phosphatase receptor type C	Homo sapiens	141-145
1576204-4	1992	Tunicamycin treatment, monitored by lectin-induced aggregation, drastically diminished cell adhesion to laminin and fibronectin, whereas cell binding to collagen IV was not affected.	Tunicamycin	0-11	fibronectin 1	Homo sapiens	116-127
1624059-2	1992	Tunicamycin-induced expression of the chimeric gene during Xenopus development was similar to the pattern of endogenous GRP78 protein synthesis, with expression first being detected at gastrula and increasing at least until the tailbud stage.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5 L homeolog	Xenopus laevis	120-125
1624059-3	1992	Deletion analysis of the rat GRP78 promoter revealed that sequences between -154 and -130 were necessary for full tunicamycin-inducible and constitutive expression of the fusion gene.	Tunicamycin	114-125	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	29-34
1660878-2	1991	In the presence of tunicamycin cathepsin D was synthesized as an unglycosylated 43-kDa proenzyme which was proteolytically processed via a 39-kDa intermediate to a 28-kDa mature form.	Tunicamycin	19-30	cathepsin D	Homo sapiens	31-42
1662699-4	1991	In tumour cells, U90 is located principally in the plasma membrane fraction and cannot be induced by heat shock, glucose starvation, or treatment with tunicamycin or calcium ionophore.	Tunicamycin	151-162	small Cajal body-specific RNA 7	Homo sapiens	17-20
1656972-4	1991	Cells treated with tunicamycin (6.25 ng/ml) for 24 h lost approximately 35% of their high-affinity thrombin binding sites, yet binding of receptor monoclonal antibody TR-9 was not affected, indicating that the receptor was present in the membrane, but unable to bind thrombin.	Tunicamycin	19-30	coagulation factor II	Mus musculus	99-107
1656972-4	1991	Cells treated with tunicamycin (6.25 ng/ml) for 24 h lost approximately 35% of their high-affinity thrombin binding sites, yet binding of receptor monoclonal antibody TR-9 was not affected, indicating that the receptor was present in the membrane, but unable to bind thrombin.	Tunicamycin	19-30	coagulation factor II	Mus musculus	267-275
1924389-4	1991	By using N-glycosidase F, tunicamycin, and specific antibodies produced in both chicken and rabbit, we demonstrate that PlGF, derived from transfected COS-1 cells, is actually N-glycosylated and secreted into the medium.	Tunicamycin	26-37	placental growth factor	Homo sapiens	120-124
1937047-6	1991	The inhibition of the hGHR-ED secretion by treatment with tunicamycin suggests that glycosylation is important for secretion.	Tunicamycin	58-69	growth hormone receptor	Homo sapiens	22-26
1930196-6	1991	When glycosylation was prevented by tunicamycin, individual bands of nonglycosylated vascular permeability factor were also secreted at equivalent rates, but much more slowly (approximately 60 min) than native glycoprotein.	Tunicamycin	36-47	vascular endothelial growth factor A	Homo sapiens	85-113
1833390-4	1991	GP85 is then incorporated into the plasma membrane where its turnover rate is relatively slow, a t1/2 of approximately 8 h. Following tunicamycin treatment, we have detected two other precursor proteins: p42 which is unglycosylated and p58 which is O-glycosylated.	Tunicamycin	134-145	erythrocyte membrane protein band 4.2	Homo sapiens	204-207
1833390-4	1991	GP85 is then incorporated into the plasma membrane where its turnover rate is relatively slow, a t1/2 of approximately 8 h. Following tunicamycin treatment, we have detected two other precursor proteins: p42 which is unglycosylated and p58 which is O-glycosylated.	Tunicamycin	134-145	cyclin dependent kinase 11B	Homo sapiens	236-239
1915351-10	1991	Adaptation of phosphate transport in NBL-1 cells to low-phosphate medium was abolished by tunicamycin, an inhibitor of protein glycosylation, indicating that the transporter in these cells, like that in bovine BBMV, is a <protein-id="337919">glycoprotein.	Tunicamycin	90-101	NBL1, DAN family BMP antagonist	Canis lupus familiaris	37-42
1910317-7	1991	In the presence of inducers of Grp78 synthesis, such as ionomycin, tunicamycin, or 2-deoxyglucose, there was a large increase in the level of Grp78 in the cells but a decrease in the amount of phosphorylated protein.	Tunicamycin	67-78	heat shock protein family A (Hsp70) member 5	Bos taurus	31-36
1910317-7	1991	In the presence of inducers of Grp78 synthesis, such as ionomycin, tunicamycin, or 2-deoxyglucose, there was a large increase in the level of Grp78 in the cells but a decrease in the amount of phosphorylated protein.	Tunicamycin	67-78	heat shock protein family A (Hsp70) member 5	Bos taurus	142-147
1654885-3	1991	The most pronounced effects on VIP binding were obtained with tunicamycin and deoxymannojirimycin, which respectively caused 80% and 67% inhibition.	Tunicamycin	62-73	vasoactive intestinal peptide	Homo sapiens	31-34
1654885-6	1991	In contrast, tunicamycin and castanospermine caused decreases in the cell-surface number of functional VIP receptors without affecting affinity.	Tunicamycin	13-24	vasoactive intestinal peptide	Homo sapiens	103-106
1654885-8	1991	When compared with their counterpart synthesized in control cells, VIP-binding proteins produced by deoxymannojirimycin- or swainsonine-treated cells were smaller in size and exhibited the expected sensitivity to Endo H. No modification in the apparent molecular mass was observed in the presence of either castanospermine or tunicamycin.	Tunicamycin	326-337	vasoactive intestinal peptide	Homo sapiens	67-70
1908097-3	1991	In order to determine the relationship between active renin heterogeneity and differences in composition or attachment of oligosaccharides, two separate experiments were performed: (i) Tunicamycin, which interferes with normal glycosylation processing, increased the proportion of relatively basic renin forms secreted into the incubation media by rat renal cortical slices.	Tunicamycin	185-196	renin	Rattus norvegicus	298-303
1831351-7	1991	Complete blocking of the glycosylation of lipoprotein lipase with tunicamycin (1 microgram/ml) for 24 h resulted in synthesis of an inactive non-secretable form of lipase with a smaller subunit (Mr 51,000-52,000).	Tunicamycin	66-77	lipoprotein lipase	Mus musculus	42-60
1831351-7	1991	Complete blocking of the glycosylation of lipoprotein lipase with tunicamycin (1 microgram/ml) for 24 h resulted in synthesis of an inactive non-secretable form of lipase with a smaller subunit (Mr 51,000-52,000).	Tunicamycin	66-77	lipase, endothelial	Mus musculus	54-60
1831351-8	1991	Immunofluorescent studies showed that unglycosylated lipase in tunicamycin-treated cells was retained in the endoplasmic reticulum.	Tunicamycin	63-74	lipase, endothelial	Mus musculus	53-59
2017192-4	1991	Glc-fed cells that have been tunicamycin treated contain principally the 38,000 Mr GLUT-1 polypeptide, which is found predominantly in intracellular membrane fractions.	Tunicamycin	29-40	solute carrier family 2 member 1	Rattus norvegicus	83-89
1713450-4	1991	When the transfected CHO cells are treated with tunicamycin a single 29 kDa hIGFBP-3 protein is observed.	Tunicamycin	48-59	insulin like growth factor binding protein 3	Homo sapiens	76-84
2061316-10	1991	Inhibition of N-linked glycosylation by tunicamycin causes a complete block in intracellular Tg transport by inducing the formation of biologically irreversible aggregates, suggesting that glycosylation of Tg serves to prevent denaturation of the secretory protein within the ER lumen.	Tunicamycin	40-51	thyroglobulin	Homo sapiens	93-95
1716973-10	1991	Tunicamycin blocked de novo glycosylation and led to reduced surface recognition of the CD22 antigen.	Tunicamycin	0-11	CD22 molecule	Homo sapiens	88-92
1711069-2	1991	FMC46 detects an epitope of the leukocyte adhesion molecule-1 (LAM-1), a member of the selecting family (LAM-1, Endothelial Leukocyte Adhesion Molecular-1 (ELAM-1), and Granule Membrane Protein-140 (GMP-140), that is expressed on LAM-1-transfected cell lines, is a glycosylation epitope based on its loss after culture in tunicamycin, and is closely related to the LAM-1.2 epitope.	Tunicamycin	322-333	selectin L	Homo sapiens	32-61
1711069-2	1991	FMC46 detects an epitope of the leukocyte adhesion molecule-1 (LAM-1), a member of the selecting family (LAM-1, Endothelial Leukocyte Adhesion Molecular-1 (ELAM-1), and Granule Membrane Protein-140 (GMP-140), that is expressed on LAM-1-transfected cell lines, is a glycosylation epitope based on its loss after culture in tunicamycin, and is closely related to the LAM-1.2 epitope.	Tunicamycin	322-333	selectin L	Homo sapiens	63-68
1658176-8	1991	Tunicamycin treatment of cells resulted in an unglycosylated doublet comprised of one single chain and one cleaved form of apoJ.	Tunicamycin	0-11	clusterin	Homo sapiens	123-127
1897978-2	1991	From the results of tunicamycin treatment and N-glycosidase F digestion, it was demonstrated that Namalwa-derived hGM-CSF was highly glycosylated at two potential N-glycosylation sites and several O-glycosylation sites as previously shown for naturally occurring hGM-CSF.	Tunicamycin	20-31	colony stimulating factor 2	Homo sapiens	114-121
1840923-6	1991	In addition, both b-70 polypeptides can be induced in maize cell cultures with tunicamycin treatment.	Tunicamycin	79-90	luminal-binding protein 2	Zea mays	18-22
2004604-4	1991	Forty-eight percent of recombinant proenkephalin was glycosylated; glycosylation could be entirely prevented by the addition of tunicamycin.	Tunicamycin	128-139	proenkephalin	Rattus norvegicus	35-48
1850168-4	1991	Similarly, inhibition of N-linked glycosylation by tunicamycin during viral infection of cell monolayers altered their ability to induce IFN alpha.	Tunicamycin	51-62	interferon alpha 1	Homo sapiens	137-146
1672608-7	1991	In the presence of tunicamycin, a 120 kDa form of P-gp was synthesized and this form was no longer processed.	Tunicamycin	19-30	ATP binding cassette subfamily B member 1	Homo sapiens	50-54
1672608-8	1991	Treating the 125 kDa precursor form with endo-beta-N-acetylglucosaminidase H (Endo H) and the 140 kDa mature form with N-glycanase diminished the molecular size of P-gp to that of the tunicamycin-treated form.	Tunicamycin	184-195	ATP binding cassette subfamily B member 1	Homo sapiens	164-168
1705556-5	1991	The epitopes are protein and not carbohydrate as both monoclonals were able to precipitate deglycosylated CD13 from tunicamycin- and monensin-treated cells and o-glycanase-treated purified CD13.	Tunicamycin	116-127	alanyl aminopeptidase, membrane	Homo sapiens	106-110
1824944-8	1991	After treatment with tunicamycin, the transfectants secreted unglycosylated 18-kDa polypeptides which could also bind IgE.	Tunicamycin	21-32	immunoglobulin heavy constant epsilon	Homo sapiens	118-121
1703479-4	1991	Ligand blotting using [125I]IGF-I revealed a major IGFBP of 40,000 mol wt, and treatment of the cells with tunicamycin reduced the mol wt of this protein to about 32,000. mRNA from Swiss 3T3 cells hybridized to a 32P-labeled oligonucleotide (50-mer) complementary to rat IGFBP-3.	Tunicamycin	107-118	insulin-like growth factor binding protein 3	Rattus norvegicus	271-278
1710120-10	1991	ICAM-1 levels, as measured by surface labeling of C32 cells with FITC CD54 monoclonal antibody, were decreased in cells treated with tunicamycin.	Tunicamycin	133-144	intercellular adhesion molecule 1	Homo sapiens	0-6
1710120-10	1991	ICAM-1 levels, as measured by surface labeling of C32 cells with FITC CD54 monoclonal antibody, were decreased in cells treated with tunicamycin.	Tunicamycin	133-144	intercellular adhesion molecule 1	Homo sapiens	70-74
1850937-5	1991	The inhibitory effect of tunicamycin on Ad5 DNA replication was much reduced in 293 cells which provide E1a gene products in trans.	Tunicamycin	25-36	Alzheimer disease, familial, type 5	Homo sapiens	40-43
1850937-7	1991	These results suggest that tunicamycin inhibits a glycosylation event induced by the early gene products of Ad5 and SV40 viruses during the early phase of infection.	Tunicamycin	27-38	Alzheimer disease, familial, type 5	Homo sapiens	108-111
2025645-7	1991	GLUT1 protein, detected on immunoblots, accumulated 10- to 20-fold in response to all glycosylation inhibitors, with apparent molecular masses of 40 kDa after glucose deprivation, 42 kDa after 2-deoxyglucose and 38 kDa after glucosamine or tunicamycin treatments, compared to 45-50 kDa in glucose-fed cells.	Tunicamycin	240-251	solute carrier family 2 member 1	Rattus norvegicus	0-5
1708210-7	1991	The SP-D translation product migrated faster than the major cellular form of SP-D but approximately 1 kDa slower than cellular SP-D synthesized in the presence of 2,2"-dipyridyl plus tunicamycin.	Tunicamycin	183-194	surfactant protein D	Rattus norvegicus	4-8
1916065-2	1991	The 78-kDa polypeptide was tentatively identified as glucose-regulated protein (GRP) 78 on the basis of molecular mass, pl (5.2), and tunicamycin inducibility, which took place upon treating embryos after the midblastula transition (MBT).	Tunicamycin	134-145	heat shock protein family A (Hsp70) member 5 L homeolog	Xenopus laevis	53-87
1916065-5	1991	A comparison of tunicamycin-induced polypeptide synthesis in Xenopus embryos, A6 cell line, and white blood cells by 2D-PAGE and fluorography revealed three spots in the GRP78 region of the gel.	Tunicamycin	16-27	heat shock protein family A (Hsp70) member 5 L homeolog	Xenopus laevis	170-175
1706526-7	1991	This was tested by subjecting L8 myocytes and NIH 3T3 fibroblasts to glucose starvation or exposure to the calcium ionophore A23187, 2-mercaptoethanol, or tunicamycin, all known to increase GRP levels.	Tunicamycin	155-166	gastrin releasing peptide	Rattus norvegicus	190-193
1847926-8	1991	Nonglycosylated MPR 46 synthesized in the presence of tunicamycin, thus preserving the asparagine residues, had a normal stability and high affinity binding.	Tunicamycin	54-65	mannose-6-phosphate receptor, cation dependent	Homo sapiens	16-22
1705558-7	1991	The cDNA sequence is continuous across the junction between the 135- and 80-kD components, and a single 170-kD Ng-CAM polypeptide was isolated from tunicamycin-treated cells.	Tunicamycin	148-159	L1 cell adhesion molecule	Gallus gallus	111-117
1645456-13	1991	In addition, affinity cross-linking experiments showed that [125I]IGF-II also bound to the unglycosylated receptor precursor that accumulated in the tunicamycin-treated cells, and the binding affinity of IGF-II for this species was indistinguishable from the binding affinity of IGF-II for the mature receptor.	Tunicamycin	149-160	insulin like growth factor 2	Homo sapiens	66-72
1645456-13	1991	In addition, affinity cross-linking experiments showed that [125I]IGF-II also bound to the unglycosylated receptor precursor that accumulated in the tunicamycin-treated cells, and the binding affinity of IGF-II for this species was indistinguishable from the binding affinity of IGF-II for the mature receptor.	Tunicamycin	149-160	insulin like growth factor 2	Homo sapiens	204-210
1645456-13	1991	In addition, affinity cross-linking experiments showed that [125I]IGF-II also bound to the unglycosylated receptor precursor that accumulated in the tunicamycin-treated cells, and the binding affinity of IGF-II for this species was indistinguishable from the binding affinity of IGF-II for the mature receptor.	Tunicamycin	149-160	insulin like growth factor 2	Homo sapiens	204-210
2000222-3	1991	When the neuroblastoma cells were treated with tunicamycin, a protein with an apparent molecular weight of 120 kd, which is consistent with that of the c-ret protein predicted from the cDNA sequence, appeared on immunoblots.	Tunicamycin	47-58	ret proto-oncogene	Homo sapiens	154-157
1985932-4	1991	Adipocytes cultured with Trans35S-label and tunicamycin produced an LPL species of 52,000 daltons, but tunicamycin abolished the incorporation of 35SO4 into LPL.	Tunicamycin	44-55	lipoprotein lipase	Gallus gallus	68-71
1985932-4	1991	Adipocytes cultured with Trans35S-label and tunicamycin produced an LPL species of 52,000 daltons, but tunicamycin abolished the incorporation of 35SO4 into LPL.	Tunicamycin	103-114	lipoprotein lipase	Gallus gallus	157-160
2254345-6	1990	ERp72 mRNA and, to a lesser degree, PDI mRNA were induced by treatment of Chinese hamster ovary cells with tunicamycin or A23187.	Tunicamycin	107-118	protein disulfide-isomerase	Cricetulus griseus	36-39
2265706-4	1990	The overexpressed pool of non-ADP-ribosylated GRP78 synthesized during tunicamycin treatment was available for ADP-ribosylation during subsequent amino acid starvation, especially in the absence of tunicamycin.	Tunicamycin	71-82	heat shock protein 5	Mus musculus	46-51
2265706-4	1990	The overexpressed pool of non-ADP-ribosylated GRP78 synthesized during tunicamycin treatment was available for ADP-ribosylation during subsequent amino acid starvation, especially in the absence of tunicamycin.	Tunicamycin	198-209	heat shock protein 5	Mus musculus	46-51
1702721-3	1990	Incubation of K-562 cells with the N-glycosylation inhibitor tunicamycin blocked carbohydrate processing during biosynthesis of CD45 proteins, generating unglycosylated polypeptides similar in size to those resulting from digestion of CD45 proteins with a mixture of both N- and O-glycanases.	Tunicamycin	61-72	protein tyrosine phosphatase receptor type C	Homo sapiens	128-132
1702721-3	1990	Incubation of K-562 cells with the N-glycosylation inhibitor tunicamycin blocked carbohydrate processing during biosynthesis of CD45 proteins, generating unglycosylated polypeptides similar in size to those resulting from digestion of CD45 proteins with a mixture of both N- and O-glycanases.	Tunicamycin	61-72	protein tyrosine phosphatase receptor type C	Homo sapiens	235-239
2269328-3	1990	Furthermore, presentation of the insulin fragment as well as presentation of ovalbumin (OVA) was inhibited by treatment of APC with chloroquine, cerulenin or tunicamycin.	Tunicamycin	158-169	insulin	Homo sapiens	33-40
2258708-5	1990	Immunodepletion, biosynthetic labeling, and tunicamycin treatment confirm that the protein encoded by gene 37 in Qa-1b mice is Qa-1.2.	Tunicamycin	44-55	histocompatibility 2, T region locus 23	Mus musculus	113-118
2258708-5	1990	Immunodepletion, biosynthetic labeling, and tunicamycin treatment confirm that the protein encoded by gene 37 in Qa-1b mice is Qa-1.2.	Tunicamycin	44-55	histocompatibility 2, T region locus 23	Mus musculus	113-117
2173269-6	1990	A 16-kDa product was detected, while in cells infected in the presence of tunicamycin, the immunoprecipitated product had a mobility on SDS-polyacrylamide gels of approximately 6 kDa, indicating that the SFGF gene product is extensively post-transcriptionally modified.	Tunicamycin	74-85	gp010L	Rabbit fibroma virus	204-208
1700792-1	1990	We have isolated a portion of the uridine diphosphate N-acetyl-D-glucosamine:dolichol phosphate N-acetyl-glucosamine-1-phosphate transferase gene (GTR2) from the genome of a tunicamycin-resistant clonal Chinese hamster ovary cell line, 3E11.	Tunicamycin	174-185	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Cricetulus griseus	147-151
2243109-2	1990	Biosynthetic experiments with articular chondrocytes in the presence of tunicamycin, an inhibitor of N-linked oligosaccharide synthesis, demonstrated a specific inhibition of [35S]SO4 incorporation into fibromodulin.	Tunicamycin	72-83	fibromodulin	Bos taurus	203-215
2246236-13	1990	The expression of functional vEGF receptors was inhibited when the cells were preincubated with tunicamycin, indicating that glycosylation of the receptor is important for the expression of functional vEGF receptors.	Tunicamycin	96-107	vascular endothelial growth factor A	Bos taurus	29-33
2246236-13	1990	The expression of functional vEGF receptors was inhibited when the cells were preincubated with tunicamycin, indicating that glycosylation of the receptor is important for the expression of functional vEGF receptors.	Tunicamycin	96-107	vascular endothelial growth factor A	Bos taurus	201-205
2171700-10	1990	Third, synthesis of 35S-labeled 46-Kd cell surface receptor protein was inhibited when the cells were grown in the presence of tunicamycin, while the synthesis of the 36-Kd species was unaffected.	Tunicamycin	127-138	CD177 molecule	Homo sapiens	38-59
2174119-4	1990	Aglycosylated anti-NIP IgG3 antibody has been produced by cell growth in the presence of the antibiotic tunicamycin.	Tunicamycin	104-115	immunoglobulin heavy constant gamma 3 (G3m marker)	Homo sapiens	23-27
2076345-10	1990	Nonglycosylated gp120 or gp160 delta proteins from tunicamycin-treated cultures did immunoprecipitate with anti-HIV-1 antiserum but did not interact with CD4.	Tunicamycin	51-62	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	16-21
2076345-10	1990	Nonglycosylated gp120 or gp160 delta proteins from tunicamycin-treated cultures did immunoprecipitate with anti-HIV-1 antiserum but did not interact with CD4.	Tunicamycin	51-62	glutamyl aminopeptidase	Homo sapiens	25-30
2150412-3	1990	Secretion of hepatic lipase activity was abolished by tunicamycin, castanospermine, and N-methyldeoxynojirimycin.	Tunicamycin	54-65	lipase C, hepatic type	Rattus norvegicus	13-27
2168959-4	1990	Treatment of AcPVR-infected cells with tunicamycin revealed that the PVR is a glycoprotein containing N-glycosidic linkages and that carbohydrate accounts for nearly 50% of its molecular weight as estimated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis.	Tunicamycin	39-50	PVR cell adhesion molecule	Homo sapiens	15-18
2094823-3	1990	In the presence of tunicamycin, an antibiotic which inhibits protein glycosylation, the cellular amount of the hydrophobic DE 16S AChE is increased.	Tunicamycin	19-30	acetylcholinesterase	Rattus norvegicus	130-134
2386935-7	1990	The size distribution of O-linked oligosaccharides in ASGP-1 from tunicamycin-treated versus control MAT-B1 cells is indistinguishable, as determined by Bio-Gel P-4 chromatography following alkaline-borohydride treatment.	Tunicamycin	66-77	mucin 4, cell surface associated	Rattus norvegicus	54-60
2386935-9	1990	Tunicamycin-treated cells, consistent with the reduced expression of ASGP-1, are significantly more susceptible to natural killer cell-mediated lysis, when compared to untreated controls.	Tunicamycin	0-11	mucin 4, cell surface associated	Rattus norvegicus	69-75
1715769-3	1990	Oligosaccharide analysis of recombinant IL 6 utilizing tunicamycin and endoglycosidases revealed O- and N-linked glycosylation that is comparable to that of natural IL 6 derived from human monocytes and fibroblasts.	Tunicamycin	55-66	interleukin 6	Homo sapiens	40-44
2386799-4	1990	6-d-old human monocytes have stores of mRNA for linear release of LPL up to 24 h. Enzyme activity in cells and in culture medium was almost completely inhibited by 24 h treatment with tunicamycin, an inhibitor of glycosylation.	Tunicamycin	184-195	lipoprotein lipase	Homo sapiens	66-69
2116966-4	1990	When human and Ren1 renins were expressed in oocytes treated with tunicamycin, both were secreted efficiently.	Tunicamycin	66-77	renin 1 structural	Mus musculus	15-19
2353452-5	1990	Endoglycosidase F treatment or labeling in the presence of tunicamycin suggests that YF prM and NS1 each have two N-linked oligosaccharides.	Tunicamycin	59-70	influenza virus NS1A binding protein	Homo sapiens	96-99
2318146-0	1990	Effects of tunicamycin on growth hormone binding in rat adipocytes.	Tunicamycin	11-22	gonadotropin releasing hormone receptor	Rattus norvegicus	26-40
2404451-8	1990	Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells.	Tunicamycin	7-18	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	67-73
2111144-5	1990	Inhibition of de novo glycosylation by tunicamycin impaired the secretion of M-type alpha 1-antitrypsin by about 75% whereas inhibition of oligosaccharide processing by the mannosidase II inhibitor swainsonine did not alter the secretion of M-type alpha 1-antitrypsin.	Tunicamycin	39-50	serpin family A member 1	Homo sapiens	84-103
2111144-7	1990	Even unglycosylated alpha 1-antitrypsin secreted by human monocytes treated with tunicamycin formed a complex with elastase.	Tunicamycin	81-92	serpin family A member 1	Homo sapiens	20-39
2303708-1	1990	Effect of tunicamycin on the glycosylation of IL-5 and the biologic activity of deglycosylated IL-5.	Tunicamycin	10-21	interleukin 5	Mus musculus	46-50
2303708-9	1990	Furthermore, deglycosylated rIL-5 that had been translated in the presence of tunicamycin showed very limited heterogeneity by two-dimensional gel electrophoresis (first dimension, nonequilibrium pH gradient electrophoresis; second dimension, SDS-PAGE).	Tunicamycin	78-89	interleukin 5	Rattus norvegicus	28-33
2303708-15	1990	Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions.	Tunicamycin	49-60	interleukin 5	Rattus norvegicus	15-20
2303708-15	1990	Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions.	Tunicamycin	49-60	interleukin 5	Mus musculus	16-20
2303708-15	1990	Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions.	Tunicamycin	49-60	interleukin 5	Rattus norvegicus	91-95
2303708-15	1990	Deglycosylated rIL-5 that had been obtained from tunicamycin-treated oocytes could bind to IL-5-responding cells (T88-M), which express both high- and low-affinity IL-5 receptors, as efficient as intact rIL-5 under high-affinity conditions.	Tunicamycin	49-60	interleukin 5	Rattus norvegicus	203-208
1690264-5	1990	In the presence of tunicamycin gp120 was no longer detectable and a non-glycosylated precursor of 75K was found instead.	Tunicamycin	19-30	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	31-36
2156003-8	1990	Experiments utilizing tunicamycin, endoglycosidase H and glycopeptidase F revealed that p130 and p40 exhibited properties characteristic of glycoproteins.	Tunicamycin	22-33	nucleolar and coiled-body phosphoprotein 1	Homo sapiens	88-92
2404451-8	1990	Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells.	Tunicamycin	7-18	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	235-241
2404451-8	1990	Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells.	Tunicamycin	7-18	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	235-241
2404451-8	1990	Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells.	Tunicamycin	264-275	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	67-73
2404451-8	1990	Adding tunicamycin to the culture medium of cells transfected with GM-CSF(del) also yielded a single non-N-glycosylated species of about 18 kDa, but secretion was at a significantly lower level than either the 29-kDa hyperglycosylated GM-CSF(del) protein from non-tunicamycin-treated cells or the 18-kDa non-N-glycosylated full-length GM-CSF from tunicamycin-treated cells.	Tunicamycin	264-275	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	67-73
2132545-9	1990	Tunicamycin, an inhibitor of glycosylation of proteins, reduced UVB light effect on the SS-A/Ro and SS-B/La antigen"s expression.	Tunicamycin	0-11	tripartite motif containing 21	Homo sapiens	88-95
2132545-9	1990	Tunicamycin, an inhibitor of glycosylation of proteins, reduced UVB light effect on the SS-A/Ro and SS-B/La antigen"s expression.	Tunicamycin	0-11	small RNA binding exonuclease protection factor La	Homo sapiens	100-104
2333387-3	1990	Furthermore, addition of 0.1 microgram mL-1 tunicamycin to the incubation medium virtually eliminated incorporation of glucose into the protein bands but had no effect on the pattern or rate of incorporation of labelled amino acids in parallel experiments.	Tunicamycin	44-55	L1 cell adhesion molecule	Mus musculus	39-43
1694435-7	1990	This heterogeneity probably is a result of differences in glycosylation of LBP since pretreatment of the hepatocytes with tunicamycin results in accumulation of a single polypeptide with an apparent mass of 50 kD in SDS-PAGE.	Tunicamycin	122-133	lipopolysaccharide-binding protein	Oryctolagus cuniculus	75-78
657267-3	1978	Tunicamycin inhibited the incorporation of 3H-mannose into CSP by 92--98% and 14C-glucosamine by 84--96%, whereas total protein synthesis was decreased by only 15--45%.	Tunicamycin	0-11	DnaJ heat shock protein family (Hsp40) member C5	Mus musculus	59-62
657267-4	1978	Tunicamycin treatment decreased total amounts of CSP by approximately 50--65%, with equal decreases in CSP occurring on the cell surface and in culture medium, whereas intracellular pools of CSP were not substantially affected.	Tunicamycin	0-11	DnaJ heat shock protein family (Hsp40) member C5	Mus musculus	49-52
657267-4	1978	Tunicamycin treatment decreased total amounts of CSP by approximately 50--65%, with equal decreases in CSP occurring on the cell surface and in culture medium, whereas intracellular pools of CSP were not substantially affected.	Tunicamycin	0-11	DnaJ heat shock protein family (Hsp40) member C5	Mus musculus	103-106
657267-4	1978	Tunicamycin treatment decreased total amounts of CSP by approximately 50--65%, with equal decreases in CSP occurring on the cell surface and in culture medium, whereas intracellular pools of CSP were not substantially affected.	Tunicamycin	0-11	DnaJ heat shock protein family (Hsp40) member C5	Mus musculus	103-106
33798597-8	2021	In addition, we have found that treatment of SH-SY5Y cells with imipramine in combination of either thapsigargin or tunicamycin is associated with the alteration of ER stress-induced IRE1alpha-XBP1 signalling.	Tunicamycin	116-127	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	183-192
657267-8	1978	We examined the mechanism of the decrease in CSP after tunicamycin treatment.	Tunicamycin	55-66	DnaJ heat shock protein family (Hsp40) member C5	Mus musculus	45-48
33798597-8	2021	In addition, we have found that treatment of SH-SY5Y cells with imipramine in combination of either thapsigargin or tunicamycin is associated with the alteration of ER stress-induced IRE1alpha-XBP1 signalling.	Tunicamycin	116-127	X-box binding protein 1	Homo sapiens	193-197
657267-10	1978	Tunicamycin had only a slight effect on the initial times and rates of CSP appearance on the cell surface; some apparent intracellular redistribution of CSP was detected by immunofluorescence.	Tunicamycin	0-11	DnaJ heat shock protein family (Hsp40) member C5	Mus musculus	71-74
33798597-9	2021	Despite potentiation of ER stress-induced XBP1 splicing, imipramine suppresses both thapsigargin- and tunicamycin-induced expression of Hrd1.	Tunicamycin	102-113	synoviolin 1	Homo sapiens	136-140
657267-11	1978	The major effect of tunicamycin treatment was to accelerate the rate of degradation of CSP 2--3 fold.	Tunicamycin	20-31	DnaJ heat shock protein family (Hsp40) member C5	Mus musculus	87-90
34744019-5	2022	Tunicamycin treatment of S. cervi worms revealed that the expression of GRP94 is associated with ER stress.	Tunicamycin	0-11	heat shock protein 90 beta family member 1	Bos taurus	72-77
33822017-9	2021	In HT-29 cells, tunicamycin-induced ER stress triggered AGR2 intracellular expression and its secretion.	Tunicamycin	16-27	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	56-60
33803345-3	2021	On the other hand, treatment with tunicamycin (Tm) shifted the molecular weight of the full-length CREB3L2 protein downward but abolished CREB3 protein expression.	Tunicamycin	34-45	cAMP responsive element binding protein 3 like 2	Homo sapiens	99-106
33803345-3	2021	On the other hand, treatment with tunicamycin (Tm) shifted the molecular weight of the full-length CREB3L2 protein downward but abolished CREB3 protein expression.	Tunicamycin	34-45	cAMP responsive element binding protein 3	Homo sapiens	99-104
33031913-4	2021	CHOP was induced in both strains after incubation with tunicamycin, indicating both strains have competent endoplasmic reticulum stress pathways.	Tunicamycin	55-66	DNA-damage inducible transcript 3	Mus musculus	0-4
33235302-8	2020	ALA pre-treatment significantly reduced the expression of ER stress markers namely, GRP78, XBP1, sXBP1 and ATF4 in response to tunicamycin.	Tunicamycin	127-138	heat shock protein family A (Hsp70) member 5	Homo sapiens	84-89
33235302-8	2020	ALA pre-treatment significantly reduced the expression of ER stress markers namely, GRP78, XBP1, sXBP1 and ATF4 in response to tunicamycin.	Tunicamycin	127-138	X-box binding protein 1	Homo sapiens	91-95
33235302-8	2020	ALA pre-treatment significantly reduced the expression of ER stress markers namely, GRP78, XBP1, sXBP1 and ATF4 in response to tunicamycin.	Tunicamycin	127-138	activating transcription factor 4	Homo sapiens	107-111
33235302-9	2020	In functional assays, ALA treatment abrogated significantly the tunicamycin-mediated transcriptional activation of ATF6 while it enhanced the insulin-stimulated glucose uptake and Glut4 translocation.	Tunicamycin	64-75	activating transcription factor 6	Homo sapiens	115-119
33235302-10	2020	Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress.	Tunicamycin	91-102	DnaJ heat shock protein family (Hsp40) member B3	Homo sapiens	28-34
33235302-10	2020	Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress.	Tunicamycin	91-102	DnaJ heat shock protein family (Hsp40) member B3	Homo sapiens	143-149
33235302-10	2020	Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress.	Tunicamycin	186-197	DnaJ heat shock protein family (Hsp40) member B3	Homo sapiens	28-34
33235302-10	2020	Silencing the expression of DNAJB3 but not HSP72 abolished the protective effect of ALA on tunicamycin-induced ER stress, suggesting thus that DNAJB3 is a key mediator of ALA-alleviated tunicamycin-induced ER stress.	Tunicamycin	186-197	DnaJ heat shock protein family (Hsp40) member B3	Homo sapiens	143-149
19322020-7	2009	Finally, chemical endoplasmic reticulum (ER) stress inducers, thapsigargin, tunicamycin, and brefeldin A, dose-dependently increased both mRNA and protein expressions of NF-L, and, its expression was specific to BIP-positive rBMSCs.	Tunicamycin	76-87	neurofilament light chain	Rattus norvegicus	170-174
19322020-7	2009	Finally, chemical endoplasmic reticulum (ER) stress inducers, thapsigargin, tunicamycin, and brefeldin A, dose-dependently increased both mRNA and protein expressions of NF-L, and, its expression was specific to BIP-positive rBMSCs.	Tunicamycin	76-87	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	212-215
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
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	65-93
34973349-9	2022	In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced.	Tunicamycin	54-65	X-box binding protein 1	Homo sapiens	162-166
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	95-100
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
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	caspase 3	Homo sapiens	147-156
34923100-6	2022	The total and nuclear NRF2 protein expression was also induced in porcine oocytes following H2O2 and tunicamycin (Tm) exposure.	Tunicamycin	101-112	NFE2 like bZIP transcription factor 2	Homo sapiens	22-26
34923100-6	2022	The total and nuclear NRF2 protein expression was also induced in porcine oocytes following H2O2 and tunicamycin (Tm) exposure.	Tunicamycin	114-116	NFE2 like bZIP transcription factor 2	Homo sapiens	22-26
34937426-7	2022	Finally, we determined the effect of tunicamycin, a pharmacological inhibitor of N-linked glycosylation, and targeted mutations in Asn residues on SLC17A4 function.	Tunicamycin	37-48	solute carrier family 17 member 4	Homo sapiens	147-154
34979291-9	2021	Tunicamycin administration caused significant increase of the expression level of genes related to ER stress and UPR, such as CHOP, Grp78 and ATF6, but the berberine pre-treatment could significantly downregulate the expression level of these genes.	Tunicamycin	0-11	DNA-damage inducible transcript 3	Mus musculus	126-130
34979291-9	2021	Tunicamycin administration caused significant increase of the expression level of genes related to ER stress and UPR, such as CHOP, Grp78 and ATF6, but the berberine pre-treatment could significantly downregulate the expression level of these genes.	Tunicamycin	0-11	heat shock protein 5	Mus musculus	132-137
34979291-9	2021	Tunicamycin administration caused significant increase of the expression level of genes related to ER stress and UPR, such as CHOP, Grp78 and ATF6, but the berberine pre-treatment could significantly downregulate the expression level of these genes.	Tunicamycin	0-11	activating transcription factor 6	Mus musculus	142-146
34968413-6	2022	AGB1 has previously been shown to control a distinct UPR pathway independently of IRE1 when treated with an ER stress inducer tunicamycin.	Tunicamycin	126-137	GTP binding protein beta 1	Arabidopsis thaliana	0-4
34937426-12	2022	Immunoblot studies on lysates of transfected cells cultured in absence or presence of tunicamycin indicated that SLC17A4 is subject to N-linked glycosylation.	Tunicamycin	86-97	solute carrier family 17 member 4	Homo sapiens	113-120
34494876-7	2021	The elimination of N-glycosylation by tunicamycin (TM) treatment, or mutagenesis, showed that N-glycosylation is critical for the proper cell surface expression of ACE2 but not for its carboxiprotease activity.	Tunicamycin	38-49	angiotensin converting enzyme 2	Homo sapiens	164-168
34847196-11	2021	Expression of the pro-apoptotic protein CHOP was induced with TM, and not inhibited by vorinostat.	Tunicamycin	62-64	DNA-damage inducible transcript 3	Mus musculus	40-44
34832960-7	2021	IFN-beta expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-beta expression.	Tunicamycin	51-62	interferon alpha	Mus musculus	0-8
34832960-7	2021	IFN-beta expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-beta expression.	Tunicamycin	51-62	DEAD/H box helicase 58	Mus musculus	156-161
34832960-7	2021	IFN-beta expression induced by ER stress inducers, tunicamycin and thapsigargin, was abolished in RIG-I-deficient hepatocytes and macrophages, showing that RIG-I is required for ER stress-induced IFN-beta expression.	Tunicamycin	51-62	interferon alpha	Mus musculus	196-204
34973349-9	2022	In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced.	Tunicamycin	54-65	sirtuin 4	Homo sapiens	3-8
34973349-9	2022	In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced.	Tunicamycin	54-65	activating transcription factor 6	Homo sapiens	115-119
34973349-9	2022	In SIRT4-silenced cells, when treated with 2.5 mug/ml Tunicamycin for 16 hours, the increase in the expressions of ATF6, GRP78 and the ratio of spliced/unspliced XBP1 mRNA were reduced.	Tunicamycin	54-65	heat shock protein family A (Hsp70) member 5	Homo sapiens	121-126
34831215-4	2021	AIMS: The objective of this study was to investigate the effects of N-glycosylation inhibitors (tunicamycin or 2-deoxy-D-glucose) or the histone deacetylase inhibitor valproic acid (VPA) on FLT3-ITD localization and downstream activity.	Tunicamycin	96-107	FMS-like tyrosine kinase 3	Mus musculus	190-194
34831215-10	2021	RESULTS: The susceptibility of FLT3-ITD-expressing cells to 17-AAG after pre-treatment with tunicamycin or 2-deoxy-D-glucose was demonstrated.	Tunicamycin	92-103	fms related receptor tyrosine kinase 3	Homo sapiens	31-35
34831215-10	2021	RESULTS: The susceptibility of FLT3-ITD-expressing cells to 17-AAG after pre-treatment with tunicamycin or 2-deoxy-D-glucose was demonstrated.	Tunicamycin	92-103	N-methylpurine DNA glycosylase	Homo sapiens	63-66
34831215-11	2021	Importantly, in Ba/F3 cells that were stably expressing distinct FLT3-ITD variants that were located either in the juxtamembrane domain (JMD) or in the tyrosine kinase 1 domain (TKD1), response to the sequential treatments with tunicamycin and 17-AAG varied between individual FLT3-ITD motifs without dependence on the localization of the ITD.	Tunicamycin	228-239	FMS-like tyrosine kinase 3	Mus musculus	65-69
34831215-12	2021	In all of the FLT3-ITD cell lines that were investigated, incubation with tunicamycin was accompanied by intracellular retention of FLT3-ITD due to the inhibition of glycosylation.	Tunicamycin	74-85	FMS-like tyrosine kinase 3	Mus musculus	14-18
34831215-12	2021	In all of the FLT3-ITD cell lines that were investigated, incubation with tunicamycin was accompanied by intracellular retention of FLT3-ITD due to the inhibition of glycosylation.	Tunicamycin	74-85	FMS-like tyrosine kinase 3	Mus musculus	132-136
34831215-14	2021	The allocation of FLT3 to different cellular compartments that was induced by tunicamycin, 2-deoxy-D-glucose, or VPA resulted in the activation of distinct downstream signaling pathways.	Tunicamycin	78-89	FMS-like tyrosine kinase 3	Mus musculus	18-22
34618053-5	2021	Loss-of-function of NRP1 and NRP2 results in decreased tolerance to the ER stress inducer tunicamycin (TM), accelerating cell death.	Tunicamycin	90-101	NAP1-related protein 1	Arabidopsis thaliana	20-24
34618053-5	2021	Loss-of-function of NRP1 and NRP2 results in decreased tolerance to the ER stress inducer tunicamycin (TM), accelerating cell death.	Tunicamycin	90-101	NAP1-related protein 2	Arabidopsis thaliana	29-33
34636989-5	2021	We also verified the identified XBP1-dependent genes with specific silencing of this transcription factor during pharmacological ER stress induction with both an N-linked glycosylation inhibitor (tunicamycin) and a non-competitive inhibitor of the sarco/endoplasmic reticulum Ca2+ ATPase (SERCA) (thapsigargin).	Tunicamycin	196-207	X-box binding protein 1	Homo sapiens	32-36
34725321-7	2021	Using thapsigargin and tunicamycin to induce acute ER stress, we identified the transcription factor C/EBPdelta (CEBPD) as a mediator of PERK signaling to secretion of tumor promoting chemokines.	Tunicamycin	23-34	CCAAT enhancer binding protein delta	Homo sapiens	101-111
34725321-7	2021	Using thapsigargin and tunicamycin to induce acute ER stress, we identified the transcription factor C/EBPdelta (CEBPD) as a mediator of PERK signaling to secretion of tumor promoting chemokines.	Tunicamycin	23-34	CCAAT enhancer binding protein delta	Homo sapiens	113-118
34725321-7	2021	Using thapsigargin and tunicamycin to induce acute ER stress, we identified the transcription factor C/EBPdelta (CEBPD) as a mediator of PERK signaling to secretion of tumor promoting chemokines.	Tunicamycin	23-34	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	137-141
34601014-12	2021	Also, tunicamycin blocked sevoflurane-induced downregulation of IRE1-JNK-beclin1 signaling pathway.	Tunicamycin	6-17	mitogen-activated protein kinase 8	Rattus norvegicus	69-72
34601014-12	2021	Also, tunicamycin blocked sevoflurane-induced downregulation of IRE1-JNK-beclin1 signaling pathway.	Tunicamycin	6-17	beclin 1	Rattus norvegicus	73-80
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	mitogen-activated protein kinase 14	Homo sapiens	73-76
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	mitogen-activated protein kinase 8	Homo sapiens	81-84
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
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	162-166
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	eukaryotic translation initiation factor 2A	Homo sapiens	167-176
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	activating transcription factor 4	Homo sapiens	177-181
34494876-7	2021	The elimination of N-glycosylation by tunicamycin (TM) treatment, or mutagenesis, showed that N-glycosylation is critical for the proper cell surface expression of ACE2 but not for its carboxiprotease activity.	Tunicamycin	51-53	angiotensin converting enzyme 2	Homo sapiens	164-168
34700340-4	2022	For HBECs and A549 cells, atmospheric pressure cold plasma was able to alleviate tunicamycin-induced cell proliferation inhibition, inflammation and oxidant stress, and enhance nuclear factor-erythroid-2-related factor 2 (NRF2) pathway activation.	Tunicamycin	81-92	NFE2 like bZIP transcription factor 2	Homo sapiens	177-220
34716302-7	2021	PERK inhibitor ameliorated autophagy, fibrotic protein expression and apoptosis in TM-treated cells, indicating a role of the PERK/eIF2alpha pathway in autophagy activation during ER stress.	Tunicamycin	83-85	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	0-4
34716302-7	2021	PERK inhibitor ameliorated autophagy, fibrotic protein expression and apoptosis in TM-treated cells, indicating a role of the PERK/eIF2alpha pathway in autophagy activation during ER stress.	Tunicamycin	83-85	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	126-130
34716302-7	2021	PERK inhibitor ameliorated autophagy, fibrotic protein expression and apoptosis in TM-treated cells, indicating a role of the PERK/eIF2alpha pathway in autophagy activation during ER stress.	Tunicamycin	83-85	eukaryotic translation initiation factor 2A	Homo sapiens	131-140
34778390-11	2021	Moreover, treatment with the ER Stress inducer tunicamycin promoted VKORC1L1, but not VKORC1 expression.	Tunicamycin	47-58	vitamin K epoxide reductase complex, subunit 1-like 1	Mus musculus	68-76
34700340-4	2022	For HBECs and A549 cells, atmospheric pressure cold plasma was able to alleviate tunicamycin-induced cell proliferation inhibition, inflammation and oxidant stress, and enhance nuclear factor-erythroid-2-related factor 2 (NRF2) pathway activation.	Tunicamycin	81-92	NFE2 like bZIP transcription factor 2	Homo sapiens	222-226
34700340-5	2022	Moreover, NRF2/ARE (anti-oxidant response elements) pathway was involved in the regulation of atmospheric pressure cold plasma on tunicamycin-induced oxidative stress.	Tunicamycin	130-141	NFE2 like bZIP transcription factor 2	Homo sapiens	10-14
34759791-8	2021	Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels.	Tunicamycin	14-16	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	58-62
34759791-8	2021	Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels.	Tunicamycin	14-16	heat shock protein 5	Mus musculus	64-69
34759791-8	2021	Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels.	Tunicamycin	14-16	activating transcription factor 6	Mus musculus	71-75
34759791-8	2021	Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels.	Tunicamycin	14-16	X-box binding protein 1	Mus musculus	77-81
34759791-8	2021	Additionally, TM treatment resulted in markedly increased PERK, GRP78, ATF6, XBP1, and CHOP protein expression levels.	Tunicamycin	14-16	DNA-damage inducible transcript 3	Mus musculus	87-91
34759791-9	2021	On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment.	Tunicamycin	88-90	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	35-39
34759791-9	2021	On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment.	Tunicamycin	88-90	heat shock protein 5	Mus musculus	41-46
34759791-9	2021	On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment.	Tunicamycin	88-90	X-box binding protein 1	Mus musculus	48-52
34759791-9	2021	On the contrary, the expression of PERK, GRP78, XBP1, and CHOP was obviously reduced in TM-induced bEnd.3 cells after ESC treatment.	Tunicamycin	88-90	DNA-damage inducible transcript 3	Mus musculus	58-62
34681705-7	2021	Using qPCR to analyze the unfolded protein response genes, we observed that loss of S1R led to decreased levels of IRE1 and PERK-related effectors and increased over-expression of most of the effectors after a tunicamycin challenge.	Tunicamycin	210-221	sigma non-opioid intracellular receptor 1	Danio rerio	84-87
34681705-8	2021	Finally, S1R deficiency led to alterations in mitochondria bioenergetics with decreased in basal, ATP-linked and non-mitochondrial respiration and following tunicamycin challenge.	Tunicamycin	157-168	sigma non-opioid intracellular receptor 1	Danio rerio	9-12
34153400-7	2021	Meanwhile, Lapatinib resistant HER2-positive breast cancer cells (LapR) display lower basal expression levels of UPR genes and enhanced tolerance to EnR stress with attenuated response to Brefeldin A and Tunicamycin.	Tunicamycin	204-215	erb-b2 receptor tyrosine kinase 2	Homo sapiens	31-35
34712218-8	2021	Furthermore, tunicamycin stimulation and PKR overexpression activated NF-kappaB and interferon response at the early stage of PRRSV infection, thus reinforcing the expression of type I interferons and proinflammatory cytokines and leading to inhibition of PRRSV.	Tunicamycin	13-24	nuclear factor kappa B subunit 1	Homo sapiens	70-79
34671436-7	2021	The results of protein analysis showed that the levels of BIP, p-AMPK, and cleaved-caspase3 in the TM group increased significantly, while the levels decreased after ghrelin pretreatment.	Tunicamycin	99-101	heat shock protein 5	Mus musculus	58-61
34837678-12	2021	The cells treated with 150 and 300 muM doses of TMAO for 24 hours showed a significant elevation in the protein and/or mRNA levels of TLR4 when compared to normal control or tunicamycin-treated cells.	Tunicamycin	174-185	toll-like receptor 4	Mus musculus	134-138
34549824-3	2021	To this end, we generated Creld2-deficient mice and induced UPR by injection of tunicamycin.	Tunicamycin	80-91	cysteine-rich with EGF-like domains 2	Mus musculus	26-32
34386060-5	2021	Notably, restoration of the ATG5-dependent autophagy in DU145 cells significantly increased the cytotoxic effects of the chemotherapeutic drugs, docetaxel and valproic acid, and the endoplasmic reticulum stress inducers, brefeldin A, tunicamycin and thapsigargin.	Tunicamycin	234-245	autophagy related 5	Homo sapiens	28-32
34604209-4	2021	In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2.	Tunicamycin	43-54	heat shock protein family A (Hsp70) member 5	Homo sapiens	197-202
34604209-4	2021	In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2.	Tunicamycin	43-54	BCL2 associated X, apoptosis regulator	Homo sapiens	238-241
34604209-4	2021	In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2.	Tunicamycin	43-54	BCL2 apoptosis regulator	Homo sapiens	305-310
34604209-5	2021	Our findings indicate that tunicamycin can induce HSCs apoptosis through calpain-2/Ca2+-dependent ERS pathway.	Tunicamycin	27-38	calpain 2	Homo sapiens	73-82
34521445-10	2021	In addition, overexpression of KCNQ1OT1/XIST partly abolished the inhibitory effects of XBP-1u knockdown or tunicamycin, an activator of endoplasmic reticulum stress, on CRC cell viability loss and apoptosis.	Tunicamycin	108-119	KCNQ1 overlapping transcript 1	Mus musculus	31-39
34521445-10	2021	In addition, overexpression of KCNQ1OT1/XIST partly abolished the inhibitory effects of XBP-1u knockdown or tunicamycin, an activator of endoplasmic reticulum stress, on CRC cell viability loss and apoptosis.	Tunicamycin	108-119	inactive X specific transcripts	Mus musculus	40-44
34378991-6	2021	We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1.	Tunicamycin	181-192	CREB regulated transcription coactivator 1	Mus musculus	33-39
34378991-6	2021	We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1.	Tunicamycin	181-192	activating transcription factor 4	Mus musculus	50-54
34378991-6	2021	We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1.	Tunicamycin	181-192	activating transcription factor 4	Mus musculus	140-144
34378991-6	2021	We further demonstrated that the mTORC1-dependent ATF4 activation is an integral signaling event of unfolded protein response (UPR) as both ATF4 activation and NNMT upregulation by tunicamycin, a well-documented endoplasmic reticulum (ER) stress inducer, are blunted when hepatocytes were pretreated with Torin1.	Tunicamycin	181-192	nicotinamide N-methyltransferase	Mus musculus	160-164
34786210-5	2021	Activation of ER stress positively correlated with PKM2 expression both in HCC tissue samples and tunicamycin (TM)-induced HCC cell lines.	Tunicamycin	98-109	pyruvate kinase M1/2	Homo sapiens	51-55
34786210-5	2021	Activation of ER stress positively correlated with PKM2 expression both in HCC tissue samples and tunicamycin (TM)-induced HCC cell lines.	Tunicamycin	111-113	pyruvate kinase M1/2	Homo sapiens	51-55
34533126-2	2021	Methods With the expression level of glucose regulated protein 78 (GRP78) as an indicator to explore the optimal concentration and time, a cell model of tunicamycin-induced ERS in HSC-T6 cells was established.	Tunicamycin	153-164	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	37-65
34533126-2	2021	Methods With the expression level of glucose regulated protein 78 (GRP78) as an indicator to explore the optimal concentration and time, a cell model of tunicamycin-induced ERS in HSC-T6 cells was established.	Tunicamycin	153-164	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	67-72
34533126-5	2021	Compared with the control group and treatment group with DMSO, the treatment group with 1 mug/mL of tunicamycin had no significant change in cell proliferation, but the expression of alpha-SMA was up-regulated with the apoptosis increased, the proportion of G1 phase cells was significantly increased and that of S phase cells decreased, the ERS induced apoptosis related signal proteins CHOP and caspase-12 were significantly up-regulated, and the expression of cyclin D1 was significantly down-regulated.	Tunicamycin	100-111	DNA-damage inducible transcript 3	Rattus norvegicus	388-392
34533126-5	2021	Compared with the control group and treatment group with DMSO, the treatment group with 1 mug/mL of tunicamycin had no significant change in cell proliferation, but the expression of alpha-SMA was up-regulated with the apoptosis increased, the proportion of G1 phase cells was significantly increased and that of S phase cells decreased, the ERS induced apoptosis related signal proteins CHOP and caspase-12 were significantly up-regulated, and the expression of cyclin D1 was significantly down-regulated.	Tunicamycin	100-111	caspase 12	Rattus norvegicus	397-407
34533126-5	2021	Compared with the control group and treatment group with DMSO, the treatment group with 1 mug/mL of tunicamycin had no significant change in cell proliferation, but the expression of alpha-SMA was up-regulated with the apoptosis increased, the proportion of G1 phase cells was significantly increased and that of S phase cells decreased, the ERS induced apoptosis related signal proteins CHOP and caspase-12 were significantly up-regulated, and the expression of cyclin D1 was significantly down-regulated.	Tunicamycin	100-111	cyclin D1	Rattus norvegicus	463-472
34121978-10	2021	Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays.	Tunicamycin	47-58	annexin A5	Homo sapiens	113-122
34448454-3	2021	We find that mutants in the intraflagellar transport protein gene osm-3 were significantly protected from tunicamycin-induced ER stress.	Tunicamycin	106-117	Osmotic avoidance abnormal protein 3	Caenorhabditis elegans	66-71
34448454-6	2021	Expression of P-glycoprotein (PGP) xenobiotic detoxification genes was elevated in osm-3 mutants and their knockdown or inhibition with verapamil suppressed tunicamycin resistance.	Tunicamycin	157-168	Osmotic avoidance abnormal protein 3	Caenorhabditis elegans	83-88
34436503-5	2021	Meanwhile, tunicamycin-induced ER stress blocked the TGF-beta/Smad signaling pathway.	Tunicamycin	11-22	transforming growth factor alpha	Homo sapiens	53-61
34415333-7	2021	Ex vivo treatment of mesenteric arteries with an AMPK agonist (A769662) or a PPARdelta agonist (GW1516) improved the impaired EDR in DMO and reversed the tunicamycin-induced ER stress, ROS production, and EDR impairment in mesenteric arteries from CMO.	Tunicamycin	154-165	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	49-53
34336161-0	2021	Tunicamycin-Induced Endoplasmic Reticulum Stress Promotes Breast Cancer Cell MDA-MB-231 Apoptosis through Inhibiting Wnt/beta-Catenin Signaling Pathway.	Tunicamycin	0-11	catenin beta 1	Homo sapiens	121-133
34336161-8	2021	Besides, tunicamycin dose dependently inhibited both Wnt/beta-catenin pathway and cells viability.	Tunicamycin	9-20	catenin beta 1	Homo sapiens	57-69
34299151-8	2021	In conclusion, PAR2-induced TF synthesis in HTECs is enhanced by culture in high concentrations of glucose and suppressed by inhibiting either PAR2 activation (I-191), glycolysis (2DOG) or glycosylation (tunicamycin).	Tunicamycin	204-215	F2R like trypsin receptor 1	Homo sapiens	15-19
34322380-12	2021	Besides, some compounds (such as the Acetaminophen, Urethane and Tunicamycin) were predicted for curing breast cancer via targeting MRPL12, MRPL13 and POP1 simultaneously.	Tunicamycin	65-76	mitochondrial ribosomal protein L12	Homo sapiens	132-138
34322380-12	2021	Besides, some compounds (such as the Acetaminophen, Urethane and Tunicamycin) were predicted for curing breast cancer via targeting MRPL12, MRPL13 and POP1 simultaneously.	Tunicamycin	65-76	mitochondrial ribosomal protein L13	Homo sapiens	140-146
34322380-12	2021	Besides, some compounds (such as the Acetaminophen, Urethane and Tunicamycin) were predicted for curing breast cancer via targeting MRPL12, MRPL13 and POP1 simultaneously.	Tunicamycin	65-76	POP1 homolog, ribonuclease P/MRP subunit	Homo sapiens	151-155
34229656-5	2021	METHODS: To investigate changes in ER stress response genes, we treated LRRK2-wild type and LRRK2-G2019S astrocytes with tunicamycin, an ER stress-inducing agent, and performed gene expression profiling with microarrays.	Tunicamycin	121-132	leucine-rich repeat kinase 2	Mus musculus	72-77
34229656-5	2021	METHODS: To investigate changes in ER stress response genes, we treated LRRK2-wild type and LRRK2-G2019S astrocytes with tunicamycin, an ER stress-inducing agent, and performed gene expression profiling with microarrays.	Tunicamycin	121-132	leucine-rich repeat kinase 2	Mus musculus	92-97
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
34079010-6	2021	Hence, although levels of spliced XBP1 and CHOP mRNA and ATF4 protein increase with Ipom-F, the accompanying increase in the levels of ER lumenal BiP and GRP94 seen with tunicamycin are not observed.	Tunicamycin	170-181	X-box binding protein 1	Homo sapiens	34-38
34079010-6	2021	Hence, although levels of spliced XBP1 and CHOP mRNA and ATF4 protein increase with Ipom-F, the accompanying increase in the levels of ER lumenal BiP and GRP94 seen with tunicamycin are not observed.	Tunicamycin	170-181	heat shock protein family A (Hsp70) member 5	Homo sapiens	146-149
34079010-6	2021	Hence, although levels of spliced XBP1 and CHOP mRNA and ATF4 protein increase with Ipom-F, the accompanying increase in the levels of ER lumenal BiP and GRP94 seen with tunicamycin are not observed.	Tunicamycin	170-181	heat shock protein 90 beta family member 1	Homo sapiens	154-159
34077277-4	2021	The current study aimed to investigate the effect of imoxin (IMX), a selective PKR inhibitor, on tunicamycin (TN)-induced promotion of ER stress and suppression of insulin signaling in C2C12 myotubes.	Tunicamycin	97-108	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	79-82
34077277-4	2021	The current study aimed to investigate the effect of imoxin (IMX), a selective PKR inhibitor, on tunicamycin (TN)-induced promotion of ER stress and suppression of insulin signaling in C2C12 myotubes.	Tunicamycin	110-112	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	79-82
34077277-11	2021	These findings suggest that IMX may protect against TN-induced skeletal muscle ER stress and insulin resistance, which are potentially mediated by PKR.	Tunicamycin	52-54	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	147-150
34260993-9	2021	CAE suppressed the bleomycin or TM-induced increases in ER-stress biomarker, BiP, and PERK pathway proteins, resulting in a decrease in ER stress in mouse lung tissues and A549 cells, respectively.	Tunicamycin	32-34	heat shock protein 5	Mus musculus	77-80
34260993-9	2021	CAE suppressed the bleomycin or TM-induced increases in ER-stress biomarker, BiP, and PERK pathway proteins, resulting in a decrease in ER stress in mouse lung tissues and A549 cells, respectively.	Tunicamycin	32-34	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	86-90
34260993-10	2021	Additionally, CAE treatment suppressed the bleomycin or TM-induced increase in the ER-stress downstream proteins, activating ATF3 and increased the levels of PINK1 in AEC IIs, both in vivo and in vitro.	Tunicamycin	56-58	activating transcription factor 3	Mus musculus	125-129
34260993-10	2021	Additionally, CAE treatment suppressed the bleomycin or TM-induced increase in the ER-stress downstream proteins, activating ATF3 and increased the levels of PINK1 in AEC IIs, both in vivo and in vitro.	Tunicamycin	56-58	PTEN induced putative kinase 1	Mus musculus	158-163
34139004-4	2021	We also find an attenuation of glucose induced increase of alpha-E catenin when hexosamine biosynthesis pathway is inhibited either with glutamine depletion or with the drugs azaserine and tunicamycin.	Tunicamycin	189-200	catenin alpha 1	Homo sapiens	59-74
34322482-5	2021	Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro.	Tunicamycin	36-47	epiregulin	Homo sapiens	16-18
34322482-5	2021	Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro.	Tunicamycin	36-47	microRNA 494	Homo sapiens	126-133
34322482-5	2021	Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro.	Tunicamycin	49-52	epiregulin	Homo sapiens	16-18
34322482-5	2021	Pharmacological ER stress inducers (tunicamycin (TCN) and thapsigargin) and hyperglycemia robustly increase the expression of miR-494 in vitro.	Tunicamycin	49-52	microRNA 494	Homo sapiens	126-133
34322482-7	2021	Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to TCN in endothelial cells and increases cell viability.	Tunicamycin	99-102	microRNA 494	Homo sapiens	14-21
34322482-7	2021	Surprisingly, miR-494 pretreatment dampens the induction and magnitude of ER stress in response to TCN in endothelial cells and increases cell viability.	Tunicamycin	99-102	epiregulin	Homo sapiens	74-76
34143952-7	2021	Furthermore, analysis of the unfolded protein response showed a reduced increase in EIF2AK3 (PERK) expression upon stimulation with tunicamycin as compared to controls, suggesting an impaired unfolded protein response.	Tunicamycin	132-143	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	84-91
34143952-7	2021	Furthermore, analysis of the unfolded protein response showed a reduced increase in EIF2AK3 (PERK) expression upon stimulation with tunicamycin as compared to controls, suggesting an impaired unfolded protein response.	Tunicamycin	132-143	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	93-97
34086738-5	2021	In MIN6 beta cells, HSPGs, HS and HPSE were reduced following treatment with pharmacological inducers of ER stress (thapsigargin or tunicamycin).	Tunicamycin	132-143	heparanase	Mus musculus	34-38
34199510-4	2021	Downregulation of microtubule acetylation using shRNA or CRSIPR/Cas9 techniques targeting ATAT1, which encodes alpha-tubulin N-acetyltransferase (alphaTAT1), resulted in the upregulation of ER stress markers, changes in ER morphology, and enhanced tunicamycin-induced UPR signaling in cancer cells.	Tunicamycin	248-259	alpha tubulin acetyltransferase 1	Homo sapiens	90-95
34199510-4	2021	Downregulation of microtubule acetylation using shRNA or CRSIPR/Cas9 techniques targeting ATAT1, which encodes alpha-tubulin N-acetyltransferase (alphaTAT1), resulted in the upregulation of ER stress markers, changes in ER morphology, and enhanced tunicamycin-induced UPR signaling in cancer cells.	Tunicamycin	248-259	alpha tubulin acetyltransferase 1	Homo sapiens	146-155
34199510-5	2021	A set of genes involved in cancer progression, especially focal adhesion genes, were downregulated in both ATAT1-knockout and tunicamycin-treated cells, whereas ATAT1 overexpression restored the gene expression inhibited by tunicamycin.	Tunicamycin	224-235	alpha tubulin acetyltransferase 1	Homo sapiens	161-166
34121978-10	2021	Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays.	Tunicamycin	47-58	caspase 3	Homo sapiens	145-162
34121978-10	2021	Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays.	Tunicamycin	60-62	annexin A5	Homo sapiens	113-122
34121978-10	2021	Cell viability and apoptosis in STF-083010 and Tunicamycin (Tm) co-treated cells were evaluated using BrdU, MTT, Annexin V-FITC/PI staining, and caspase-12 and -3 activities assays.	Tunicamycin	60-62	caspase 3	Homo sapiens	145-162
34237462-12	2021	The mutant AGR2 showed reduced capacity to bind MUC2 and alleviate tunicamycin-induced ER stress.	Tunicamycin	67-78	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	11-15
35467485-4	2022	Top six better performing drugs, binding affinity for dpagt1 at the range of -17.63 to -20.40 kcal/mol, than the reference ligand (tunicamycin; -14.86 kcal/mol) were obtained at the end of structure-based-pharmacophore- and virtual-screening and "induced fit" docking calculations.	Tunicamycin	131-142	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	54-60
35421744-4	2022	Using ET receptor Never ripe (Nr) mutants, a significant role of ET in tunicamycin (Tm)-induced ER stress sensing and signaling was confirmed based on the changes in the expression levels of SlIRE1b and SlBiP.	Tunicamycin	71-82	BEL1-like homeodomain protein 2	Solanum lycopersicum	203-208
35421744-4	2022	Using ET receptor Never ripe (Nr) mutants, a significant role of ET in tunicamycin (Tm)-induced ER stress sensing and signaling was confirmed based on the changes in the expression levels of SlIRE1b and SlBiP.	Tunicamycin	84-86	BEL1-like homeodomain protein 2	Solanum lycopersicum	203-208
35398613-7	2022	The cells treated with A23187 or tunicamycin exhibited the activation of calpain-5 and truncation of caspase-4.	Tunicamycin	33-44	calpain 5	Homo sapiens	73-82
35398613-7	2022	The cells treated with A23187 or tunicamycin exhibited the activation of calpain-5 and truncation of caspase-4.	Tunicamycin	33-44	caspase 4	Homo sapiens	101-110
35304860-4	2022	Control and IRE1alpha knockout (KO) GECs were incubated with tunicamycin to induce ER stress and subjected to proteomic analysis.	Tunicamycin	61-72	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	12-21
35304860-6	2022	Tunicamycin enhanced expression of Sec23B and the reticulophagy adaptor reticulon-3-long (RTN3L) in control, but not IRE1alpha KO GECs.	Tunicamycin	0-11	SEC23 homolog B, COPII coat complex component	Mus musculus	35-41
35304860-6	2022	Tunicamycin enhanced expression of Sec23B and the reticulophagy adaptor reticulon-3-long (RTN3L) in control, but not IRE1alpha KO GECs.	Tunicamycin	0-11	reticulon 3	Mus musculus	72-83
35304860-8	2022	Tunicamycin stimulated colocalization of autophagosomes with Sec23B and RTN3L in an IRE1alpha-dependent manner.	Tunicamycin	0-11	SEC23 homolog B, COPII coat complex component	Mus musculus	61-67
35304860-8	2022	Tunicamycin stimulated colocalization of autophagosomes with Sec23B and RTN3L in an IRE1alpha-dependent manner.	Tunicamycin	0-11	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	84-93
35304860-10	2022	Degradation of RTN3L and collagen IV increased in response to tunicamycin, and the turnover was blocked by deletion of IRE1alpha; thus, the IRE1alpha pathway promotes RTN3L-mediated reticulophagy and collagen IV may be an IRE1alpha-dependent reticulophagy substrate.	Tunicamycin	62-73	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	140-149
35304860-10	2022	Degradation of RTN3L and collagen IV increased in response to tunicamycin, and the turnover was blocked by deletion of IRE1alpha; thus, the IRE1alpha pathway promotes RTN3L-mediated reticulophagy and collagen IV may be an IRE1alpha-dependent reticulophagy substrate.	Tunicamycin	62-73	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	222-231
35194770-3	2022	METHODS: IL-1beta and two additional ER stress activators, palmitate and tunicamycin were applied to evaluate the expression level miR-25 by Taqman  RT-PCR.	Tunicamycin	73-84	microRNA 25	Homo sapiens	131-137
35194770-8	2022	Expression levels of miR-25 were significantly upregulated with the treatment of IL-1beta, palmitate or tunicamycin in both INS-1 cells and human islets.	Tunicamycin	104-115	microRNA 25	Rattus norvegicus	21-27
35339509-13	2022	Importin alpha4 expression was increased in the nuclear insoluble fraction after incubation with tunicamycin or hydrogen peroxide.	Tunicamycin	97-108	karyopherin (importin) alpha 3	Mus musculus	0-15
35325747-8	2022	Moreover, this method is competent to monitor changed states of PTK7-specific sialylation induced by tunicamycin.	Tunicamycin	101-112	protein tyrosine kinase 7 (inactive)	Homo sapiens	64-68
35603939-11	2022	In HCT116 cells, tunicamycin increased the expression of Grp78, Gro-alpha and IL-8 in a concentration-dependent manner.	Tunicamycin	17-28	heat shock protein family A (Hsp70) member 5	Homo sapiens	57-62
35603939-11	2022	In HCT116 cells, tunicamycin increased the expression of Grp78, Gro-alpha and IL-8 in a concentration-dependent manner.	Tunicamycin	17-28	C-X-C motif chemokine ligand 1	Homo sapiens	64-73
35603939-11	2022	In HCT116 cells, tunicamycin increased the expression of Grp78, Gro-alpha and IL-8 in a concentration-dependent manner.	Tunicamycin	17-28	C-X-C motif chemokine ligand 8	Homo sapiens	78-82
35603939-12	2022	Furthermore, p38 MAPK inhibitor significantly inhibited the upregulation of Gro-alpha and IL-8 induced by tunicamycin.	Tunicamycin	106-117	C-X-C motif chemokine ligand 1	Homo sapiens	76-85
35603939-12	2022	Furthermore, p38 MAPK inhibitor significantly inhibited the upregulation of Gro-alpha and IL-8 induced by tunicamycin.	Tunicamycin	106-117	C-X-C motif chemokine ligand 8	Homo sapiens	90-94
35390453-8	2022	Tunicamycin, an ER stress inducer, increased ERdj5 levels.	Tunicamycin	0-11	DnaJ heat shock protein family (Hsp40) member C10	Mus musculus	45-50
35500653-7	2022	Furthermore, ablation of IRE1alpha phosphorylation at Ser724 exacerbated ER stress-induced hepatic steatosis in Tunicamycin-treated Ern1S724A/S724A mice.	Tunicamycin	112-123	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	25-34
35500653-7	2022	Furthermore, ablation of IRE1alpha phosphorylation at Ser724 exacerbated ER stress-induced hepatic steatosis in Tunicamycin-treated Ern1S724A/S724A mice.	Tunicamycin	112-123	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	132-136
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	21-32	heat shock protein 1B	Mus musculus	183-188
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	21-32	heat shock protein 5	Mus musculus	207-212
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	21-32	heat shock protein 9	Mus musculus	219-224
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	21-32	heat shock protein family A (Hsp70) member 9	Rattus norvegicus	226-231
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	34-36	heat shock protein 1B	Mus musculus	183-188
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	34-36	heat shock protein 5	Mus musculus	207-212
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	34-36	heat shock protein 9	Mus musculus	219-224
35344886-6	2022	After treatment with tunicamycin (TM), an ER stress agonist, mass spectrometry (MS) identified several known ER stress and calmodulin proteins, including heat shock protein family A (HSP70) member (HSPA) 5 (GRP78)) and HSPA9 (GRP75, glucose-regulated protein 75).	Tunicamycin	34-36	heat shock protein family A (Hsp70) member 9	Rattus norvegicus	226-231
35597864-0	2022	The yeast two-component SLN1 branch of the HOG pathway and the scaffolding activity of Pbs2 modulate the response to endoplasmic reticulum stress induced by tunicamycin.	Tunicamycin	157-168	histidine kinase	Saccharomyces cerevisiae S288C	24-28
35597864-0	2022	The yeast two-component SLN1 branch of the HOG pathway and the scaffolding activity of Pbs2 modulate the response to endoplasmic reticulum stress induced by tunicamycin.	Tunicamycin	157-168	mitogen-activated protein kinase kinase PBS2	Saccharomyces cerevisiae S288C	87-91
35594368-0	2022	Concise Synthesis of Tunicamycin V and Discovery of a Cytostatic DPAGT1 Inhibitor.	Tunicamycin	21-32	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	65-71
35579911-6	2022	We discovered that PD patients with high amounts of PDIA6 and HYOU1 proteins were more sensitive to endoplasmic reticulum stress, in particular to tunicamycin.	Tunicamycin	147-158	protein disulfide isomerase family A member 6	Homo sapiens	52-57
35579911-6	2022	We discovered that PD patients with high amounts of PDIA6 and HYOU1 proteins were more sensitive to endoplasmic reticulum stress, in particular to tunicamycin.	Tunicamycin	147-158	hypoxia up-regulated 1	Homo sapiens	62-67
35513574-6	2022	Sptlc2 was upregulated and ceramide levels were elevated by tunicamycin in the livers of C57BL/6J wild-type mice.	Tunicamycin	60-71	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	0-6
35348185-5	2022	After treating with the ER-stress inducer tunicamycin, cell viability was investigated by performing Cell Counting Kit-8, TUNEL and western blotting assays, which revealed that CTRP9 increased the activity of HTR8/SVneo cells induced by HG through the alleviation of ER stress.	Tunicamycin	42-53	C1q and TNF related 9	Homo sapiens	177-182
35514983-4	2022	We found that microglia release nanomolar levels of calreticulin when inflammatory-activated with lipopolysaccharide, when endoplasmic reticulum stress was induced by tunicamycin, or when cell death was induced by staurosporine, and that neurons release calreticulin when crushed.	Tunicamycin	167-178	calreticulin	Homo sapiens	52-64
35428325-4	2022	RESULTS: Palmitate- or tunicamycin-induced ER stress resulted in PGC-1alpha downregulation and enhanced expression of activating transcription factor 4 (ATF4) in human myotubes and mouse skeletal muscle.	Tunicamycin	23-34	PPARG coactivator 1 alpha	Homo sapiens	65-75
35428325-4	2022	RESULTS: Palmitate- or tunicamycin-induced ER stress resulted in PGC-1alpha downregulation and enhanced expression of activating transcription factor 4 (ATF4) in human myotubes and mouse skeletal muscle.	Tunicamycin	23-34	activating transcription factor 4	Homo sapiens	118-151
35428325-4	2022	RESULTS: Palmitate- or tunicamycin-induced ER stress resulted in PGC-1alpha downregulation and enhanced expression of activating transcription factor 4 (ATF4) in human myotubes and mouse skeletal muscle.	Tunicamycin	23-34	activating transcription factor 4	Homo sapiens	153-157
35428325-5	2022	Overexpression of ATF4 decreased basal PCG-1alpha expression, whereas ATF4 knockdown abrogated the reduction of PCG-1alpha caused by tunicamycin in myotubes.	Tunicamycin	133-144	activating transcription factor 4	Mus musculus	70-74
35428325-8	2022	Moreover, siRNA against S6 kinase, an mTORC1 downstream target, prevented the reduction in the expression of CRTC2 and PGC-1alpha caused by the ER stressor tunicamycin.	Tunicamycin	156-167	CREB regulated transcription coactivator 2	Homo sapiens	109-114
35428325-8	2022	Moreover, siRNA against S6 kinase, an mTORC1 downstream target, prevented the reduction in the expression of CRTC2 and PGC-1alpha caused by the ER stressor tunicamycin.	Tunicamycin	156-167	PPARG coactivator 1 alpha	Homo sapiens	119-129
35492579-5	2022	Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets.	Tunicamycin	110-112	tumor necrosis factor	Sus scrofa	74-83
35492579-5	2022	Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets.	Tunicamycin	110-112	interleukin 6	Sus scrofa	88-92
35492579-5	2022	Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets.	Tunicamycin	110-112	interleukin 6	Sus scrofa	161-165
35492579-5	2022	Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets.	Tunicamycin	110-112	C-reactive protein	Sus scrofa	170-173
35492579-5	2022	Furthermore, the concentrations of the proinflammatory cytokines, namely, TNF-alpha and IL-6 were elevated in TM-treated piglet livers, and the plasma levels of IL-6 and CRP were also higher, indicating the occurrence of inflammation in TM-treated piglets.	Tunicamycin	237-239	interleukin 6	Sus scrofa	161-165
35330105-6	2022	Tunicamycin treatment significantly increased the levels of serum ALT and AST and hepatic triglycerides.	Tunicamycin	0-11	glutamic pyruvic transaminase, soluble	Mus musculus	66-69
35454076-9	2022	We tested a small biological molecule, Tunicamycin, that blocks a specific step of the protein N-glycosylation pathway in the endoplasmic reticulum (ER), i.e., the catalytic activity of N-acetylglusosaminyl 1-phosphate transferase (GPT).	Tunicamycin	39-50	glutamic--pyruvic transaminase	Homo sapiens	232-235
35019714-7	2022	Tunicamycin treatment confirmed p44 as glycosylated form of p41.	Tunicamycin	0-11	erythrocyte membrane protein band 4.1	Homo sapiens	60-63
35456517-11	2022	In the presence of tunicamycin, an ER stress inducer, DDIT3 expression increased in Pcsk6-deficient H9c2 cells but reduced in PCSK6-overexpressing cells.	Tunicamycin	19-30	DNA-damage inducible transcript 3	Rattus norvegicus	54-59
35456517-11	2022	In the presence of tunicamycin, an ER stress inducer, DDIT3 expression increased in Pcsk6-deficient H9c2 cells but reduced in PCSK6-overexpressing cells.	Tunicamycin	19-30	proprotein convertase subtilisin/kexin type 6	Rattus norvegicus	84-89
35456517-11	2022	In the presence of tunicamycin, an ER stress inducer, DDIT3 expression increased in Pcsk6-deficient H9c2 cells but reduced in PCSK6-overexpressing cells.	Tunicamycin	19-30	proprotein convertase subtilisin/kexin type 6	Rattus norvegicus	126-131
35273242-6	2022	In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2.	Tunicamycin	13-24	C-X-C motif chemokine ligand 8	Homo sapiens	65-68
35273242-6	2022	In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2.	Tunicamycin	13-24	C-X-C motif chemokine ligand 1	Homo sapiens	70-75
35273242-6	2022	In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2.	Tunicamycin	13-24	C-X-C motif chemokine ligand 2	Homo sapiens	81-86
35273242-6	2022	In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2.	Tunicamycin	13-24	valosin containing protein	Homo sapiens	125-128
35273242-6	2022	In contrast, tunicamycin-induced ER stress resulted in increased IL8, CXCL1, and CXCL2 production in cells with knockdown of VCP, while enhanced expression of these proinflammatory molecules was abolished upon knockout of NOD2.	Tunicamycin	13-24	nucleotide binding oligomerization domain containing 2	Homo sapiens	222-226
35350536-6	2022	Pak2 overexpression enhances the XBP1-Hrd1 UPR axis and ameliorates tunicamycin induced cardiac apoptosis and dysfunction in mice.	Tunicamycin	68-79	p21 (RAC1) activated kinase 2	Mus musculus	0-4
35233582-0	2022	The role of GRP78 in oxidative stress induced by tunicamycin in trabecular meshwork cells.	Tunicamycin	49-60	heat shock protein family A (Hsp70) member 5	Homo sapiens	12-17
35233582-1	2022	OBJECTIVE: To clarify the regulatory effect of GRP-78 induced by tunicamycin on endoplasmic reticulum (ER) stress.	Tunicamycin	65-76	heat shock protein family A (Hsp70) member 5	Homo sapiens	47-53
35233582-2	2022	METHODS: Tunicamycin was used to induce ER stress in trabecular meshwork cells (HTMC and GTM3).	Tunicamycin	9-20	glutathione S-transferase mu 3	Homo sapiens	89-93
35233582-4	2022	RESULTS: Tunicamycin could significantly increase the ROS content and the apoptosis rate in HTMC and GTM3 (p<0.01).	Tunicamycin	9-20	glutathione S-transferase mu 3	Homo sapiens	101-105
35233582-6	2022	Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01).	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	51-56
35233582-6	2022	Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01).	Tunicamycin	0-11	voltage dependent anion channel 1	Homo sapiens	57-62
35233582-6	2022	Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01).	Tunicamycin	0-11	activating transcription factor 4	Homo sapiens	64-68
35233582-6	2022	Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01).	Tunicamycin	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	70-74
35233582-6	2022	Tunicamycin can also increase expression levels of GRP78,VDAC1, ATF4, PERK, eIF2a, and CHOP (p<0.01).	Tunicamycin	0-11	eukaryotic translation initiation factor 2 subunit alpha	Homo sapiens	76-81
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
35233582-10	2022	CONCLUSION: Tunicamycin induces oxidative stress in trabecular meshwork cells, and the increase in GRP78 expression can protect the cells during ER stress by regulating eIF2.	Tunicamycin	12-23	heat shock protein family A (Hsp70) member 5	Homo sapiens	99-104
35233582-10	2022	CONCLUSION: Tunicamycin induces oxidative stress in trabecular meshwork cells, and the increase in GRP78 expression can protect the cells during ER stress by regulating eIF2.	Tunicamycin	12-23	eukaryotic translation initiation factor 2 subunit alpha	Homo sapiens	169-173
35104011-6	2022	In tunicamycin-induced ER stress conditions and liver injury animal models following ER stress, NRF2 levels were highly correlated with SIRT3.	Tunicamycin	3-14	NFE2 like bZIP transcription factor 2	Homo sapiens	96-100
35104011-7	2022	Nrf2 deficiency enhanced the tunicamycin-mediated induction of CHOP, which was attenuated by Sirt3 overexpression.	Tunicamycin	29-40	NFE2 like bZIP transcription factor 2	Homo sapiens	0-4
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
35104011-7	2022	Nrf2 deficiency enhanced the tunicamycin-mediated induction of CHOP, which was attenuated by Sirt3 overexpression.	Tunicamycin	29-40	sirtuin 3	Homo sapiens	93-98
35104011-8	2022	Further, Sirt3 delivery to hepatocytes in Nrf2 knockout mice prevented tunicamycin from increasing mortality by decreasing ER stress.	Tunicamycin	71-82	sirtuin 3	Mus musculus	9-14
35104011-8	2022	Further, Sirt3 delivery to hepatocytes in Nrf2 knockout mice prevented tunicamycin from increasing mortality by decreasing ER stress.	Tunicamycin	71-82	nuclear factor, erythroid derived 2, like 2	Mus musculus	42-46
35330105-6	2022	Tunicamycin treatment significantly increased the levels of serum ALT and AST and hepatic triglycerides.	Tunicamycin	0-11	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	74-77
35159364-7	2022	Furthermore, tunicamycin suppresses the association of C53 with the centrosome.	Tunicamycin	13-24	CDK5 regulatory subunit associated protein 3	Homo sapiens	55-58
35222844-6	2022	Remarkably, the nucleoside antibiotic tunicamycin, which targets UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosaminephosphotransferase (ALG7) and N-glycosylation in other organisms, induces a delayed-death effect and inhibits parasite growth during the second IDC after treatment.	Tunicamycin	38-49	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	147-151
2514095-2	1989	We have investigated the structural and functional properties of the transferrin receptor from murine plasmacytoma cells (NS-1 cells) treated with the glycosylation inhibitor, tunicamycin and the glycosylation-processing inhibitors, swainsonine and castanospermine.	Tunicamycin	176-187	transferrin	Mus musculus	69-80
35226981-10	2022	In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment.	Tunicamycin	118-120	transforming growth factor beta receptor 2	Homo sapiens	31-42
35226981-10	2022	In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment.	Tunicamycin	118-120	SMAD family member 2	Homo sapiens	47-54
35226981-10	2022	In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment.	Tunicamycin	118-120	transforming growth factor beta receptor 2	Homo sapiens	69-80
35226981-10	2022	In addition, the expression of TGF-betaRII and Smad2/3, and mRNAs of TGF-betaRII and Smad3 were also decreased by the TM treatment.	Tunicamycin	118-120	SMAD family member 3	Homo sapiens	85-90
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	120-125
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
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	cadherin 1	Homo sapiens	277-287
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	vimentin	Homo sapiens	316-324
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	fibronectin 1	Homo sapiens	406-417
35162959-7	2022	We also find that, in response to tunicamycin-induced ER stress, miR-16-5p suppression decreases apoptosis, inflammation and cardiac damage via activating the ATF6-mediated cytoprotective pathway.	Tunicamycin	34-45	activating transcription factor 6	Homo sapiens	159-163
35053376-9	2022	LCN2 knockout cells showed enhanced and sustained activation of unfolded protein response proteins when treated with tunicamycin or cultured under glucose deprivation.	Tunicamycin	117-128	lipocalin 2	Homo sapiens	0-4
35370192-5	2022	The usefulness of tunicamycin as antibacterial agents is limited by off-target inhibition of human UDP-N-acetylglucosamine (GlcNAc): polyprenol phosphate translocase (GPT).	Tunicamycin	18-29	glutamic--pyruvic transaminase	Homo sapiens	167-170
35370192-7	2022	Next, the minimum structural requirements for tunicamycin V for MraY inhibition were established by systematic structure-activity relationship studies with truncated analogs of tunicamycin V. Our collaborative study elucidated a crystal structure of human GPT in complex with tunicamycin.	Tunicamycin	46-57	glutamic--pyruvic transaminase	Homo sapiens	256-259
35370192-7	2022	Next, the minimum structural requirements for tunicamycin V for MraY inhibition were established by systematic structure-activity relationship studies with truncated analogs of tunicamycin V. Our collaborative study elucidated a crystal structure of human GPT in complex with tunicamycin.	Tunicamycin	177-188	glutamic--pyruvic transaminase	Homo sapiens	256-259
35370192-7	2022	Next, the minimum structural requirements for tunicamycin V for MraY inhibition were established by systematic structure-activity relationship studies with truncated analogs of tunicamycin V. Our collaborative study elucidated a crystal structure of human GPT in complex with tunicamycin.	Tunicamycin	276-287	glutamic--pyruvic transaminase	Homo sapiens	256-259
2514095-7	1989	Incubation of NS-1 cells with tunicamycin resulted in a shift in the apparent molecular mass of the transferrin receptor from 96 kDa and 94 kDa to approximately 82 kDa.	Tunicamycin	30-41	transferrin	Mus musculus	100-111
2514095-17	1989	The non-glycosylated receptor from tunicamycin-treated cells appears to bind transferrin as demonstrated by interaction with transferrin-Sepharose.	Tunicamycin	35-46	transferrin	Mus musculus	77-88
2514095-17	1989	The non-glycosylated receptor from tunicamycin-treated cells appears to bind transferrin as demonstrated by interaction with transferrin-Sepharose.	Tunicamycin	35-46	transferrin	Mus musculus	125-136
2513184-5	1989	Inhibition of N-linked glycosylation by treatment with tunicamycin, 2-deoxy-D-glucose or glucosamine stimulated the synthesis of non-ADP-ribosylated GRP78 up to sixfold with relatively little effect on its ADP-ribosylation.	Tunicamycin	55-66	heat shock protein 5	Mus musculus	149-154
2590385-5	1989	Neuraminidase and tunicamycin treatment demonstrated that the GH receptor on F442A preadipocytes is a sialo-glycoprotein with N-linked carbohydrate chains.	Tunicamycin	18-29	growth hormone receptor	Mus musculus	62-73
2481822-8	1989	Analysis of biosynthetically labeled CD6 in the presence of tunicamycin revealed a reduction in mol.	Tunicamycin	60-71	CD6 molecule	Homo sapiens	37-40
2676595-4	1989	In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin.	Tunicamycin	89-100	chitobiosyldiphosphodolichol beta-1,4 mannosyltransferase	Saccharomyces cerevisiae S288C	186-190
2789018-5	1989	In the presence of tunicamycin, IL-6 is secreted exclusively in the O-glycosylated form, whereas in the presence of cycloheximide the pathway leading to both N- and O-glycosylation is dominant.	Tunicamycin	19-30	interleukin 6	Homo sapiens	32-36
2570611-9	1989	Cells treated with tunicamycin produced a 120 kDa form of P-glycoprotein which was no longer processed but showed stability similar to that of the mature 140-150 kDa form.	Tunicamycin	19-30	ATP binding cassette subfamily B member 1	Homo sapiens	58-72
2676595-4	1989	In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin.	Tunicamycin	89-100	GDP-Man:Man(1)GlcNAc(2)-PP-dolichol alpha-1,3-mannosyltransferase	Saccharomyces cerevisiae S288C	195-199
2676595-4	1989	In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin.	Tunicamycin	250-261	chitobiosyldiphosphodolichol beta-1,4 mannosyltransferase	Saccharomyces cerevisiae S288C	186-190
2676595-4	1989	In addition, labeling of the wild-type yeast cells with [3H]palmitate in the presence of tunicamycin revealed the incorporation of [3H]palmitate into the same five bands as found in the alg1 and alg2 mutants at the non-permissive temperature without tunicamycin.	Tunicamycin	250-261	GDP-Man:Man(1)GlcNAc(2)-PP-dolichol alpha-1,3-mannosyltransferase	Saccharomyces cerevisiae S288C	195-199
2692828-5	1989	Tunicamycin blocked the appearance of such accumulations, suggesting that glycosylation is involved in the transport of nascent BuChE molecules to the oocyte"s surface.	Tunicamycin	0-11	butyrylcholinesterase like L homeolog	Xenopus laevis	128-133
2760068-13	1989	Furthermore, tunicamycin shifted the synthesis of PLP-A by placental explants from the Mr 29,000 and 33,000 forms to the Mr 25,000 species.	Tunicamycin	13-24	prolactin family 4, subfamily A, member 1	Rattus norvegicus	50-55
16666984-7	1989	The molecular weight of these polypeptides is reduced by treatment with glycopeptidase F but not with endoglycosidase H. Treatment of the suspension cultures with tunicamycin also leads to reduction in the molecular weight of the chitinase bands.	Tunicamycin	163-174	endochitinase A	Nicotiana tabacum	230-239
2474541-2	1989	In the presence of tunicamycin, keratinocytes incorporated [3H]glucosamine into a vitamin A-regulated acidic 53-kDa component of the cytoskeleton which was identified as cytokeratin 13 by one- and two-dimensional immunoblotting with specific monoclonal antibodies.	Tunicamycin	19-30	keratin 13	Homo sapiens	170-184
2492635-6	1989	The carbohydrate side-chains are essential for the stability of fibroblast PS beta G, because PS beta G synthesis in these fibroblasts could not be detected in the presence of tunicamycin, a protein glycosylation inhibitor which did not affect PS beta G mRNA expression.	Tunicamycin	176-187	protein S (beta) pseudogene	Homo sapiens	75-82
2618551-4	1989	PAA of HL-60 cells pre-cultured in the presence of tunicamycin (0.1-1.0 microgram/ml) to inhibit glycosylation decreased after neuraminidase treatment.	Tunicamycin	51-62	neuraminidase 1	Homo sapiens	127-140
2677679-2	1989	Tunicamycin, a nucleoside antibiotic which prevents the formation of the dolichol intermediate necessary for oligosaccharide addition of the nascent polypeptide chain, appeared to block secretory exit and led to an increase in the cellular associated, nonglycosylated pro-TGF-beta 1 form.	Tunicamycin	0-11	transforming growth factor beta-1 proprotein	Cricetulus griseus	272-282
2525840-4	1989	In experiments in which infected cells were treated with tunicamycin it was shown that the glycosylation of NS1 was not required for either the dimerization or the membrane association.	Tunicamycin	57-68	influenza virus NS1A binding protein	Homo sapiens	108-111
2722854-7	1989	This nonglycosylated receptor was also capable of dimer formation; however, much less of it reached the cell surface than the fully glycosylated form, although both untreated and tunicamycin-grown cells appeared to synthesize transferrin receptors at similar rates.	Tunicamycin	179-190	transferrin	Homo sapiens	226-237
2722854-8	1989	Although the number of receptor molecules/cell was similar in control and tunicamycin-treated cells, the nonglycosylated receptors exhibited a much lower affinity for transferrin than those of untreated cells; in contrast, when receptors were purified by immunoprecipitation and digested with bacterial alkaline phosphatase, no difference was observed between the affinity of these receptors and undigested immunoprecipitated receptors.	Tunicamycin	74-85	transferrin	Homo sapiens	167-178
2545067-0	1989	Tunicamycin modulates binding of 125I-erythropoietin to Friend erythroleukemia cells.	Tunicamycin	0-11	erythropoietin	Mus musculus	38-52
2545067-2	1989	Neuraminidase treatment of B8 cells did not affect the specific binding of erythropoietin, but tunicamycin treatment caused a 2.5 to 4-fold increase in the amount of 125I-erythropoietin binding.	Tunicamycin	95-106	erythropoietin	Mus musculus	171-185
2463989-10	1989	Tunicamycin-treated HEL cells synthesized three to four precursors of 80-92 kDa, suggesting the possibility of heterogeneity of GMP-140 at the protein level.	Tunicamycin	0-11	selectin P	Homo sapiens	128-135
2536232-0	1989	Effects of lectins and tunicamycin on cAMP response to parathyroid hormone.	Tunicamycin	23-34	parathyroid hormone	Rattus norvegicus	55-74
2531019-3	1989	This rapidly excreted fraction exhibits a low density on rubidium chloride gradients characteristic of poorly sialylated and poorly iodinated thyroglobulin, comigrating on rubidium chloride gradients with thyroglobulin isolated from tunicamycin treated glands.	Tunicamycin	233-244	thyroglobulin	Homo sapiens	142-155
2531019-3	1989	This rapidly excreted fraction exhibits a low density on rubidium chloride gradients characteristic of poorly sialylated and poorly iodinated thyroglobulin, comigrating on rubidium chloride gradients with thyroglobulin isolated from tunicamycin treated glands.	Tunicamycin	233-244	thyroglobulin	Homo sapiens	205-218
2498325-9	1989	Studies with tunicamycin indicated that this apoE was N-glycosylated at Asn194.	Tunicamycin	13-24	apolipoprotein E	Homo sapiens	45-49
2722801-1	1989	Tunicamycin, a specific inhibitor of N-glycosylation, was used to study the function of asparagine-linked oligosaccharides of the low density lipoprotein (LDL) receptor in cultured human skin fibroblasts.	Tunicamycin	0-11	low density lipoprotein receptor	Homo sapiens	130-168
2722801-7	1989	However, the LDL receptor produced in tunicamycin-treated cells was smaller in molecular size, and it exhibited an about 50% lower binding capacity when compared with its counterpart synthesized in control cells.	Tunicamycin	38-49	low density lipoprotein receptor	Homo sapiens	13-25
2471524-1	1989	Previous studies in this laboratory (1) have shown that tunicamycin-treatment inhibits the secretion of three secretory glycoproteins--alpha 2-macroglobulin, ceruloplasmin, and alpha 1-protease inhibitor in human hepatoma (Hep G2) cell cultures.	Tunicamycin	56-67	alpha-2-macroglobulin	Homo sapiens	135-156
2471524-1	1989	Previous studies in this laboratory (1) have shown that tunicamycin-treatment inhibits the secretion of three secretory glycoproteins--alpha 2-macroglobulin, ceruloplasmin, and alpha 1-protease inhibitor in human hepatoma (Hep G2) cell cultures.	Tunicamycin	56-67	ceruloplasmin	Homo sapiens	158-171
2471524-1	1989	Previous studies in this laboratory (1) have shown that tunicamycin-treatment inhibits the secretion of three secretory glycoproteins--alpha 2-macroglobulin, ceruloplasmin, and alpha 1-protease inhibitor in human hepatoma (Hep G2) cell cultures.	Tunicamycin	56-67	serpin family A member 1	Homo sapiens	177-203
2471524-3	1989	Using percoll density gradient centrifugation, we found that tunicamycin-treatment markedly inhibited the transport of alpha 2-macroglobulin, ceruloplasmin and alpha 1-protease inhibitor from the rough endoplasmic reticulum.	Tunicamycin	61-72	alpha-2-macroglobulin	Homo sapiens	119-140
2471524-3	1989	Using percoll density gradient centrifugation, we found that tunicamycin-treatment markedly inhibited the transport of alpha 2-macroglobulin, ceruloplasmin and alpha 1-protease inhibitor from the rough endoplasmic reticulum.	Tunicamycin	61-72	ceruloplasmin	Homo sapiens	142-155
2471524-3	1989	Using percoll density gradient centrifugation, we found that tunicamycin-treatment markedly inhibited the transport of alpha 2-macroglobulin, ceruloplasmin and alpha 1-protease inhibitor from the rough endoplasmic reticulum.	Tunicamycin	61-72	serpin family A member 1	Homo sapiens	160-186
2523818-8	1989	Incubation of monocytes with tunicamycin and 1-deoxymynnojirimycin and treatment of IL-6 with endoglucosaminidase H suggested that the 27.5 kDa form of IL-6 carries at least one N-linked complex-type oligosaccharide chain.	Tunicamycin	29-40	interleukin 6	Homo sapiens	152-156
2538234-9	1989	As a result of inhibition of glycosylation by the antibiotic tunicamycin, a fourth intracellular TAP (P58) and a third extracellular TAP (P60) were found.	Tunicamycin	61-72	sequestosome 1	Homo sapiens	138-141
2644281-5	1989	When cells were cultured in the presence of tunicamycin, a 49-kDa form of LPL was synthesized by the cells but was not secreted.	Tunicamycin	44-55	lipoprotein lipase	Rattus norvegicus	74-77
2644281-6	1989	In addition, LPL activity was reduced by 90% when glycosylation was blocked by either tunicamycin or glucose deprivation.	Tunicamycin	86-97	lipoprotein lipase	Rattus norvegicus	13-16
2564824-6	1989	mAb 12-15 was also reactive with the tunicamycin-treated form of the CD2 antigen suggesting that the cross-reactive epitope was of protein nature.	Tunicamycin	37-48	CD2 antigen	Mus musculus	69-72
2494430-9	1989	Treatment of Sf9 cells with tunicamycin, but not with inhibitors of oligosaccharide processing, prevented the appearance of t-PA in the extracellular medium.	Tunicamycin	28-39	chromosome 20 open reading frame 181	Homo sapiens	124-128
2718627-4	1989	The calculated molecular mass (64 kDa) of the protein is in good agreement with that of the unglycosylated HN protein (63 kDa) identified in tunicamycin treated mumps virus infected cells (Herrler and Compans, 1983).	Tunicamycin	141-152	hemagglutinin-neuraminidase	Mumps orthorubulavirus	107-109
2848842-2	1988	The first step in the assembly of the dolichol-linked oligosaccharides required for asparagine-linked glycosylation in eukaryotes is catalyzed by a tunicamycin-sensitive, dolichol phosphate-dependent N-acetylglucosamine-1-phosphate transferase (GPT).	Tunicamycin	148-159	alanine aminotransferase 1	Cricetulus griseus	245-248
3198612-1	1988	A protein doublet (Mr = 135,000/130,000) was found to coprecipitate with an unglycosylated form of the transferrin receptor in tunicamycin-treated A431 cells.	Tunicamycin	127-138	transferrin receptor	Homo sapiens	103-123
2903742-1	1988	Tunicamycin, a known inhibitor of the lipid-dependent glycosylation of proteins, was used in vivo to study the biosynthesis of rat intestinal brush border membrane aminopeptidase N and dipeptidyl aminopeptidase IV.	Tunicamycin	0-11	alanyl aminopeptidase, membrane	Rattus norvegicus	164-180
2903742-5	1988	In addition, there were decreased levels of assayable aminopeptidase N, dipeptidyl aminopeptidase IV and disaccharidase activity in intestinal mucosal cell homogenates and brush border membranes of tunicamycin-treated rats.	Tunicamycin	198-209	alanyl aminopeptidase, membrane	Rattus norvegicus	54-70
2903742-6	1988	Though tunicamycin decreased incorporation of newly synthesized aminopeptidase N and dipeptidyl aminopeptidase IV protein into brush border membranes by 70-75%, the newly synthesized enzyme that was incorporated was indistinguishable from that of controls.	Tunicamycin	7-18	alanyl aminopeptidase, membrane	Rattus norvegicus	64-80
3063258-5	1988	The extent of co-translational glycosylation was measured by treating the cells with tunicamycin; in the presence of this inhibitor, a 74 kDa aglyco-CEA was produced and was still recognized by the antibody.	Tunicamycin	85-96	CEA cell adhesion molecule 3	Homo sapiens	149-152
2905169-6	1988	Tunicamycin treatment blocks the conversion of the precursor to the mature form, and removal of N-linked oligosaccharides with Endo F reduces the relative molecular weight of P-glycoprotein to 140K.	Tunicamycin	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	175-189
3262613-6	1988	Treatment with either tunicamycin or N-glycanase resulted in IL-3 running as one band with Mr 16,000, corresponding to its 140-amino acid polypeptide chain.	Tunicamycin	22-33	interleukin 3	Mus musculus	61-65
3382684-0	1988	Tunicamycin-treated rat heart cell cultures synthesize an inactive nonreleasable lipoprotein lipase.	Tunicamycin	0-11	lipoprotein lipase	Rattus norvegicus	81-99
3141784-1	1988	The importance of carbohydrate in the secretion of immunoglobulin A (IgA) has previously been suggested by results of studies with tunicamycin, which prevents N-linked glycosylation of all cell glycoproteins.	Tunicamycin	131-142	immunoglobulin heavy constant alpha	Mus musculus	51-73
2844594-1	1988	(Na,K)ATPase from Torpedo californica was expressed in Xenopus laevis oocytes in the presence of tunicamycin by injecting mRNAs for the alpha- and beta-subunits derived from the cloned cDNAs into the oocytes.	Tunicamycin	97-108	ATPase Na+/K+ transporting subunit beta 1 L homeolog	Xenopus laevis	1-12
3372529-14	1988	We identified two putative precursors of hsp47 using an in vitro translation/processing system and tunicamycin: one is a 42-kDa primary translation product and the second is a 41-kDa polypeptide lacking signal peptide and carbohydrate moieties.	Tunicamycin	99-110	serpin family H member 1	Gallus gallus	41-46
3047151-7	1988	Glycosylation of Sec12p during biogenesis is indicated by an electrophoretic mobility shift of the protein that is influenced by tunicamycin and by imposition of an independent secretory pathway block.	Tunicamycin	129-140	Sar family guanine nucleotide exchange factor SEC12	Saccharomyces cerevisiae S288C	17-23
3149275-2	1988	The EGF receptor of NA cells synthesized in the presence of tunicamycin had an apparent molecular weight of 130,000.	Tunicamycin	60-71	epidermal growth factor receptor	Homo sapiens	4-16
3137261-3	1988	The induction of ICAM-1 by these cytokines was neutralized by cytokine-specific antisera as well as some steroids and the glycosylation inhibitor, tunicamycin.	Tunicamycin	147-158	intercellular adhesion molecule 1	Homo sapiens	17-23
2456347-4	1988	Therefore, we examined the effect of tunicamycin (TM), an inhibitor of asparagine-linked glycosylation and ganglioside biosynthesis, on the expression of Hh-1 determinants in H-2b/Hh-1b lymphomas.	Tunicamycin	37-48	hemopoietic histocompatibility	Mus musculus	154-158
2456347-4	1988	Therefore, we examined the effect of tunicamycin (TM), an inhibitor of asparagine-linked glycosylation and ganglioside biosynthesis, on the expression of Hh-1 determinants in H-2b/Hh-1b lymphomas.	Tunicamycin	50-52	hemopoietic histocompatibility	Mus musculus	154-158
3042455-1	1988	Tyrosine sulfation of entactin was studied by labeling of 3T3-L1 adipocytes with [35S]methionine or H2 35SO4 in the presence or absence of tunicamycin or monensin.	Tunicamycin	139-150	nidogen 1	Homo sapiens	22-30
3042455-4	1988	Inhibition of co-translational transfer of N-linked oligosaccharides by tunicamycin produced EN1 and EN3 as intracellular species, and EN3 was sulfated and secreted.	Tunicamycin	72-83	engrailed homeobox 1	Homo sapiens	93-96
3259951-4	1988	Under conditions where treatment of CD4+ human acute lymphoblastic leukemia cells (CEM-CM3 cells) with the glycosylation inhibitor tunicamycin decreased surface expression of CD4 in a time- and concentration-dependent manner, the surface expression of several other glycoproteins was unaffected.	Tunicamycin	131-142	CD4 molecule	Homo sapiens	36-39
3259951-4	1988	Under conditions where treatment of CD4+ human acute lymphoblastic leukemia cells (CEM-CM3 cells) with the glycosylation inhibitor tunicamycin decreased surface expression of CD4 in a time- and concentration-dependent manner, the surface expression of several other glycoproteins was unaffected.	Tunicamycin	131-142	CD4 molecule	Homo sapiens	175-178
3259951-5	1988	Incubation with tunicamycin for 48 h inhibited mannose incorporation by 98%, caused a 76% decrease in CD4 surface expression as judged by flow cytometry, and had little effect on methionine incorporation.	Tunicamycin	16-27	CD4 molecule	Homo sapiens	102-105
3259951-6	1988	Scatchard analysis showed a decrease in the total number of CD4 molecules on the cell surface from 17,000 to 8,900 after 24 h of tunicamycin treatment.	Tunicamycin	129-140	CD4 molecule	Homo sapiens	60-63
3259951-7	1988	Immunoprecipitation of metabolically labeled CD4 revealed the presence of an unglycosylated precursor in tunicamycin-treated cells.	Tunicamycin	105-116	CD4 molecule	Homo sapiens	45-48
3177093-1	1988	We have investigated the effect of tunicamycin-C2, which specifically inhibits glycosylation of proteins but not their synthesis, in the induction of crystal-induced chemotactic factor (CCF) in human neutrophils by monosodium urate crystals.	Tunicamycin	35-46	paired like homeodomain 1	Homo sapiens	150-184
3177093-1	1988	We have investigated the effect of tunicamycin-C2, which specifically inhibits glycosylation of proteins but not their synthesis, in the induction of crystal-induced chemotactic factor (CCF) in human neutrophils by monosodium urate crystals.	Tunicamycin	35-46	paired like homeodomain 1	Homo sapiens	186-189
3046935-7	1988	The in vitro phenotype of sec53 could be mimicked by isolating rough microsomes from wild-type cells that had been grown for 1 h in the presence of tunicamycin.	Tunicamycin	148-159	phosphomannomutase SEC53	Saccharomyces cerevisiae S288C	26-31
3150971-4	1988	Like others (Volpe &amp; Goldberg, 1983), we found that tunicamycin inhibited the activity of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMG-CoA), which constitutes the ratelimiting step in the biosynthesis of cholesterol and isoprenoid derivatives, by catalysing the reduction of HMG-CoA to mevalonate, and it has been suggested that it plays a role in the control of cell proliferation and in tumour transformation.	Tunicamycin	56-67	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	Mus musculus	94-141
3150971-4	1988	Like others (Volpe &amp; Goldberg, 1983), we found that tunicamycin inhibited the activity of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMG-CoA), which constitutes the ratelimiting step in the biosynthesis of cholesterol and isoprenoid derivatives, by catalysing the reduction of HMG-CoA to mevalonate, and it has been suggested that it plays a role in the control of cell proliferation and in tumour transformation.	Tunicamycin	56-67	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	Mus musculus	143-150
3150971-4	1988	Like others (Volpe &amp; Goldberg, 1983), we found that tunicamycin inhibited the activity of 3-hydroxy-3-methylglutaryl coenzyme-A reductase (HMG-CoA), which constitutes the ratelimiting step in the biosynthesis of cholesterol and isoprenoid derivatives, by catalysing the reduction of HMG-CoA to mevalonate, and it has been suggested that it plays a role in the control of cell proliferation and in tumour transformation.	Tunicamycin	56-67	3-hydroxy-3-methylglutaryl-Coenzyme A reductase	Mus musculus	287-294
3382684-3	1988	Treatment of the cultures with 5 micrograms/ml tunicamycin caused almost complete loss of lipoprotein lipase activity in all three compartments.	Tunicamycin	47-58	lipoprotein lipase	Rattus norvegicus	90-108
2452086-12	1988	The inhibition of N-glycosylation by tunicamycin abolished the effect of interleukin-6 on the secretion of alpha 2-macroglobulin, indicating a possible role of interleukin-6 on N-glycosylation.	Tunicamycin	37-48	interleukin 6	Homo sapiens	73-86
3366781-0	1988	Characterization of the transferrin receptor in tunicamycin-treated A431 cells.	Tunicamycin	48-59	transferrin receptor	Homo sapiens	24-44
3366781-2	1988	In this study, the functional and structural properties of the transferrin receptor from tunicamycin-treated A431 cells were examined.	Tunicamycin	89-100	transferrin	Homo sapiens	63-74
3234361-4	1988	The SP-A synthesized under these conditions showed a shift in apparent molecular weight to 27,000 and 29,000 compared to 29,000 and 31,000 for SP-A synthesized in the presence of tunicamycin alone.	Tunicamycin	179-190	surfactant protein A2	Homo sapiens	4-8
3234361-4	1988	The SP-A synthesized under these conditions showed a shift in apparent molecular weight to 27,000 and 29,000 compared to 29,000 and 31,000 for SP-A synthesized in the presence of tunicamycin alone.	Tunicamycin	179-190	surfactant protein A2	Homo sapiens	143-147
2452086-12	1988	The inhibition of N-glycosylation by tunicamycin abolished the effect of interleukin-6 on the secretion of alpha 2-macroglobulin, indicating a possible role of interleukin-6 on N-glycosylation.	Tunicamycin	37-48	alpha-2-macroglobulin	Homo sapiens	107-128
3339713-2	1988	Pulse-chase, tunicamycin treatment, and carbohydrate trimming experiments revealed that VGF is synthesized as a 19-kilodalton (kDa) precursor which is rapidly modified to a high-mannose-type 22-kDa protein.	Tunicamycin	13-24	VGF nerve growth factor inducible	Homo sapiens	88-91
3258589-7	1988	P3.58 molecules precipitated from tunicamycin-treated cells were identical in all cell types, suggesting that the variation observed is due to variable N-glycosylation.	Tunicamycin	34-45	intercellular adhesion molecule 1	Homo sapiens	0-5
3131023-3	1988	In addition, the processing of the EGF receptor and its intracellular transport was analyzed by distinguishing cell surface receptors from intracellular receptors and by treating cells with inhibitors such as tunicamycin, monensin and brefeldin A.	Tunicamycin	209-220	epidermal growth factor receptor	Homo sapiens	35-47
3367907-7	1988	Unglycosylated NB, expressed either in influenza B virus-infected cells treated with tunicamycin or in cells expressing the NB mutant lacking both N-linked glycosylation sites, was expressed at the cell surface, indicating that NB does not require carbohydrate addition for transport.	Tunicamycin	85-96	NUBP iron-sulfur cluster assembly factor 1, cytosolic	Homo sapiens	15-17
3131023-7	1988	In A431 cells, the truncated EGF receptor was generated from a protein of Mr 60,000 through tunicamycin- and monensin-sensitive glycosylation.	Tunicamycin	92-103	epidermal growth factor receptor	Homo sapiens	29-41
2968956-6	1988	When the FcE receptor-positive RPMI-1788 cells are treated with tunicamycin and then with papain, a suppressor factor(s) for human IgE synthesis is released.	Tunicamycin	64-75	ferrochelatase	Homo sapiens	9-12
3057191-2	1988	As in normal fibroblasts the EGF receptor from MDA-MB-231 cells was synthesized from a Mr = 160,000 precursor and tunicamycin treatment of cells resulted in accumulation of a Mr = 130,000 polypeptide.	Tunicamycin	114-125	epidermal growth factor receptor	Homo sapiens	29-41
3128509-3	1988	NCA components synthesized by three tumor cell lines, QGP-1 (pancreas), HLC-1 (lung) and CAOV-2 (ovary) showed slightly different migration patterns on SDS-PAGE, but the molecular weights of their unglycosylated peptides synthesized in the presence of tunicamycin were all found to be 35K.	Tunicamycin	252-263	CEA cell adhesion molecule 3	Homo sapiens	0-3
3671295-7	1987	Tunicamycin, an inhibitor of glycosylation of proteins, blocked the glycosylation of nascent ovalbumin molecules at a concentration of 5 micrograms/mL in the medium.	Tunicamycin	0-11	ovalbumin	Coturnix japonica	93-102
2823941-4	1987	In addition it was found that the secretion of erythropoietin was almost completely abrogated by tunicamycin, an inhibitor of N-linked glycosylation.	Tunicamycin	97-108	erythropoietin	Homo sapiens	47-61
2823941-5	1987	This effect of tunicamycin was also observed in a permanently transfected cell line that secretes erythropoietin in large quantities.	Tunicamycin	15-26	erythropoietin	Homo sapiens	98-112
3121640-7	1987	Tunicamycin could in fact mimic the effect of a temperature shift on the biosynthesis of EGF receptor, but it did not have the same rapid effect on DNA synthesis and cell cycle progression.	Tunicamycin	0-11	epidermal growth factor receptor	Homo sapiens	89-101
3445230-4	1987	Optimal transport of TF to the plasma membrane and shedding in membrane vesicles required glycosylation as judged by partial inhibition of this process by the tunicamycin homologues B2 and C2.	Tunicamycin	159-170	coagulation factor III, tissue factor	Homo sapiens	21-23
3681266-8	1987	The glycosylated E1 (gp26, gp25) proteins arose as a result of O-linked glycosylation of p23/E1 as indicated by the resistance of these species to tunicamycin.	Tunicamycin	147-158	prostaglandin E synthase 3	Homo sapiens	89-95
2443498-4	1987	In tunicamycin-treated cells, the initial precursor is similar in size (Mr = 24,000) to deglycosylated GPA from human erythrocytes.	Tunicamycin	3-14	glycophorin A (MNS blood group)	Homo sapiens	103-106
3040864-4	1987	All three forms of the Ki-1 antigen possess a tunicamycin-sensitive 6-kDa N-linked carbohydrate moiety.	Tunicamycin	46-57	TNF receptor superfamily member 8	Homo sapiens	23-35
2822343-0	1987	Effect of tunicamycin on the biosynthesis of human fibroblast collagenase.	Tunicamycin	10-21	matrix metallopeptidase 1	Homo sapiens	51-73
2440862-4	1987	Tunicamycin prevents approximately 50% of the phosphate from being incorporated into FRTL-5 cell thyroglobulin.	Tunicamycin	0-11	thyroglobulin	Rattus norvegicus	97-110
3499144-12	1987	In the presence of tunicamycin an unglycosylated alpha 1-inhibitor3 with an apparent Mr of 154,000 was found in cells and in the medium.	Tunicamycin	19-30	alpha-1-inhibitor III	Rattus norvegicus	49-67
3499144-13	1987	In a pulse-chase experiment it was shown that inhibition of glycosylation by tunicamycin resulted in a marked delay of secretion of alpha 1-inhibitor3.	Tunicamycin	77-88	alpha-1-inhibitor III	Rattus norvegicus	132-150
3115291-4	1987	Experiments with tunicamycin and endoglycosidase H demonstrated that sialophorin contains N-linked carbohydrate (approximately two units per molecule) and is therefore an N,O-glycoprotein.	Tunicamycin	17-28	sialophorin	Homo sapiens	69-80
3115291-5	1987	Pulse-labeling of tunicamycin-treated CEM cells together with immunoprecipitation provided the means to isolate the [35S]-methionine-labeled polypeptide core of sialophorin and determine its molecular weight (58,000).	Tunicamycin	18-29	sialophorin	Homo sapiens	161-172
3108266-8	1987	The glycosylation of GPIIb-IIIa was examined in megakaryocytes by metabolic labeling in the presence of tunicamycin, monensin, or treatment with endoglycosidase H. The polypeptide backbones of the GPIIb and the GPIIIa have molecular masses of 120 and 90 kD, respectively.	Tunicamycin	104-115	integrin subunit alpha 2b	Homo sapiens	21-26
2438387-6	1987	Quantitative electroimmunoblotting for myelin basic protein (MBP) in the CNS of tunicamycin-treated young adult rats indicated that, as in acute EAE, no extensive demyelination had occurred.	Tunicamycin	80-91	myelin basic protein	Rattus norvegicus	39-59
2438387-6	1987	Quantitative electroimmunoblotting for myelin basic protein (MBP) in the CNS of tunicamycin-treated young adult rats indicated that, as in acute EAE, no extensive demyelination had occurred.	Tunicamycin	80-91	myelin basic protein	Rattus norvegicus	61-64
3104330-10	1987	A 47,000-dalton form of hepatic lipase was immunoisolated from cell lysates only after tunicamycin treatment and could be generated from the secreted 59,000-dalton enzyme by prolonged endoglycosidase digestion.	Tunicamycin	87-98	lipase C, hepatic type	Rattus norvegicus	24-38
2435722-9	1987	In a pulse-chase experiment using tunicamycin to block N-glycosylation, alpha 1-macroglobulin secretion was totally inhibited.	Tunicamycin	34-45	pregnancy-zone protein	Rattus norvegicus	72-93
3104330-12	1987	Further, an intracellular 47,000-dalton precursor peptide can be identified after tunicamycin treatment, which may represent the hepatic lipase polypeptide, presumably after removal of its signal sequence; a 53,000-dalton partially glycosylated peptide exists as a major precursor form in the cell; and the mature 59,000-dalton hepatic lipase is present in the hepatocyte, but it is rapidly secreted.	Tunicamycin	82-93	lipase C, hepatic type	Rattus norvegicus	129-143
3104330-12	1987	Further, an intracellular 47,000-dalton precursor peptide can be identified after tunicamycin treatment, which may represent the hepatic lipase polypeptide, presumably after removal of its signal sequence; a 53,000-dalton partially glycosylated peptide exists as a major precursor form in the cell; and the mature 59,000-dalton hepatic lipase is present in the hepatocyte, but it is rapidly secreted.	Tunicamycin	82-93	lipase C, hepatic type	Rattus norvegicus	328-342
3301649-2	1987	Cell-surface expression of transfected H-2Db in the B2m deficient cell line R1E was completely abolished by the drug tunicamycin (Tm).	Tunicamycin	117-128	beta-2 microglobulin	Mus musculus	52-55
2950522-4	1987	Tunicamycin-resistant cells contain amplified DNA, which hybridizes in proportion to the cells" degree of drug resistance with Alg 7, a cloned DNA probe apparently encoding yeast N-acetylglucosaminyltransferase.	Tunicamycin	0-11	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Saccharomyces cerevisiae S288C	127-132
3803451-4	1987	Peptide mapping analysis and pulse-chase experiments revealed that p45 A is a precursor of polypeptides p45 B, C, D. Tunicamycin treatment inhibits the synthesis of all four polypeptides but a new related protein appears, p-p45, the unglycosylated precursor.	Tunicamycin	117-128	nuclear factor, erythroid derived 2	Mus musculus	67-70
3803451-4	1987	Peptide mapping analysis and pulse-chase experiments revealed that p45 A is a precursor of polypeptides p45 B, C, D. Tunicamycin treatment inhibits the synthesis of all four polypeptides but a new related protein appears, p-p45, the unglycosylated precursor.	Tunicamycin	117-128	nuclear factor, erythroid derived 2	Mus musculus	104-107
3803451-4	1987	Peptide mapping analysis and pulse-chase experiments revealed that p45 A is a precursor of polypeptides p45 B, C, D. Tunicamycin treatment inhibits the synthesis of all four polypeptides but a new related protein appears, p-p45, the unglycosylated precursor.	Tunicamycin	117-128	nuclear factor, erythroid derived 2	Mus musculus	104-107
3803451-5	1987	In the presence of tunicamycin, p-p45 is also found in the medium, demonstrating that glycosylation is not essential for the secretion.	Tunicamycin	19-30	nuclear factor, erythroid derived 2	Mus musculus	34-37
3305909-3	1987	Tunicamycin, an inhibitor of N-linked oligosaccharide addition, blocks acquisition of both EGF and insulin binding activity.	Tunicamycin	0-11	insulin	Homo sapiens	99-106
3475645-1	1987	The activity and intracellular distribution of catalase was studied in culture human myeloid leukemia cells before and after induction of differentiation with tunicamycin.	Tunicamycin	159-170	catalase	Homo sapiens	47-55
3497327-6	1987	In contrast, T cells treated with tunicamycin released IgE-suppressing factors capable of inhibiting the IgE-potentiating activity of TCS derived from untreated T cells.	Tunicamycin	34-45	immunoglobulin heavy constant epsilon	Homo sapiens	55-58
3497327-6	1987	In contrast, T cells treated with tunicamycin released IgE-suppressing factors capable of inhibiting the IgE-potentiating activity of TCS derived from untreated T cells.	Tunicamycin	34-45	immunoglobulin heavy constant epsilon	Homo sapiens	105-108
3475645-5	1987	Induction of differentiation with tunicamycin decreased high activity of catalase in cultured leukemic cells.	Tunicamycin	34-45	catalase	Homo sapiens	73-81
3099750-6	1986	In the presence of tunicamycin, a compound that blocks the formation of N-asparagine-linked oligosaccharide chains, a decrease in Mr of both secreted and intracellular major forms is observed, indicating that secreted and intracellular C1 Inh contain N-linked oligosaccharide units.	Tunicamycin	19-30	serpin family G member 1	Homo sapiens	236-242
3039288-8	1986	Furthermore, non-glycosylated t-PA synthesized in the presence of tunicamycin was secreted efficiently and was indistinguishable in specific activity from glycosylated t-PAs.	Tunicamycin	66-77	plasminogen activator, tissue type	Homo sapiens	30-34
3490480-9	1986	Activation is blocked by tunicamycin and is markedly slowed (t 1/2 = 120 min) by 1-deoxynojirimycin, an inhibitor of glucosidase I.	Tunicamycin	25-36	mannosyl-oligosaccharide glucosidase	Homo sapiens	117-130
3535799-8	1986	Specific 125I-insulin binding was increased by glucose refeeding of glucose-starved cells and this change in binding was inhibited by tunicamycin and cycloheximide.	Tunicamycin	134-145	insulin	Homo sapiens	14-21
3771139-3	1986	Incubation of Xenopus retinas with tunicamycin has been shown to block the glycosylation of opsin, the rod visual pigment apoglycoprotein, with concomitant accumulation of vesicular membrane material in the compartment between the rod inner and outer segments (i.e., the intersegmental space) (Fliesler et al, J Cell Biol 100:574-587, 1985).	Tunicamycin	35-46	rhodopsin, gene2 L homeolog	Xenopus laevis	92-97
3771140-3	1986	Tunicamycin (TM), a selective inhibitor of dolichylphosphate-dependent oligosaccharide biosynthesis, effectively blocks glycosylation, but not synthesis, of opsin, the rod visual pigment apoglycoprotein.	Tunicamycin	0-11	rhodopsin, gene2 L homeolog	Xenopus laevis	157-162
3771140-3	1986	Tunicamycin (TM), a selective inhibitor of dolichylphosphate-dependent oligosaccharide biosynthesis, effectively blocks glycosylation, but not synthesis, of opsin, the rod visual pigment apoglycoprotein.	Tunicamycin	13-15	rhodopsin, gene2 L homeolog	Xenopus laevis	157-162
2946699-2	1986	Tunicamycin was used to produce carbohydrate-depleted fibronectin; it was synthesized by cultured fibroblasts.	Tunicamycin	0-11	fibronectin 1	Homo sapiens	54-65
3093061-8	1986	Tunicamycin-treated B16-F10 cells exhibited poor adhesion to substrate-adsorbed fibronectin and laminin, whereas both castanospermine- and swainsonine-treated cells possessed near normal adhesive capacity; furthermore, the initial rate of loss of tunicamycin-treated cells from the lungs of mice was substantially greater than either control, castanospermine- or swainsonine-treated cells.	Tunicamycin	0-11	fibronectin 1	Mus musculus	80-91
3021451-5	1986	Culturing the cells in the presence of varying concentrations of tunicamycin, an inhibitor of N-glycosylation, revealed six species of 5"-nucleotidase after sodium dodecyl sulfate/polyacrylamide electrophoresis.	Tunicamycin	65-76	5' nucleotidase, ecto	Rattus norvegicus	135-150
2874833-7	1986	Tunicamycin also reduced lysyl oxidase activity in the medium and to a lesser extent in the cell layer, but the effective dose, 1-10 micrograms/ml, also inhibited the incorporation of [3H]leucine into total protein.	Tunicamycin	0-11	lysyl oxidase	Homo sapiens	25-38
3753016-8	1986	Pulse-labeling in the presence of tunicamycin yielded a 42,000-Da form of LAMP-1, which was converted within 30 min to a 43,000-Da molecule.	Tunicamycin	34-45	lysosomal-associated membrane protein 1	Mus musculus	74-80
3768962-2	1986	To study the role of the sugar moieties of this adhesion molecule, we tested the effect of tunicamycin on aggregation mediated by E-cadherin of teratocarcinoma cells.	Tunicamycin	91-102	cadherin 1	Homo sapiens	130-140
3768962-3	1986	Immunoblot analysis using a monoclonal antibody to E-cadherin showed that in cells treated with tunicamycin this adhesion molecule is converted into two forms with MW of 118,000 and 131,000.	Tunicamycin	96-107	cadherin 1	Homo sapiens	51-61
3768962-4	1986	The smaller one was exposed on the cell surface and showed a trypsin sensitivity characteristic to E-cadherin, suggesting that this is the peptide moiety of E-cadherin whose glycosylation with N-linked oligosaccharides was blocked by tunicamycin.	Tunicamycin	234-245	cadherin 1	Homo sapiens	99-109
3768962-4	1986	The smaller one was exposed on the cell surface and showed a trypsin sensitivity characteristic to E-cadherin, suggesting that this is the peptide moiety of E-cadherin whose glycosylation with N-linked oligosaccharides was blocked by tunicamycin.	Tunicamycin	234-245	cadherin 1	Homo sapiens	157-167
3768962-6	1986	These tunicamycin-treated cells aggregated in a Ca2+-dependent manner, and the aggregation was inhibited by a monoclonal antibody to E-cadherin.	Tunicamycin	6-17	cadherin 1	Homo sapiens	133-143
2427577-7	1986	All three forms of DAF were approximately 3000 lower in Mr in the presence of tunicamycin.	Tunicamycin	78-89	CD55 molecule (Cromer blood group)	Homo sapiens	19-22
3541907-10	1986	Cell-surface immunodetectable lipoprotein lipase amounts were decreased significantly when cells were incubated in the presence of either colchicine or tunicamycin.	Tunicamycin	152-163	lipoprotein lipase	Homo sapiens	30-48
3733260-0	1986	Effect of tunicamycin on synthesis and secretion of carcinoembryonic antigen by human colonic adenocarcinoma cells.	Tunicamycin	10-21	CEA cell adhesion molecule 3	Homo sapiens	52-76
3733260-1	1986	The effect of the glycosylation inhibitor, tunicamycin, on synthesis and secretion of the membrane-associated glycoprotein carcinoembryonic antigen (CEA), was studied in the LS174T human colon cancer cell line.	Tunicamycin	43-54	CEA cell adhesion molecule 3	Homo sapiens	123-147
3733260-1	1986	The effect of the glycosylation inhibitor, tunicamycin, on synthesis and secretion of the membrane-associated glycoprotein carcinoembryonic antigen (CEA), was studied in the LS174T human colon cancer cell line.	Tunicamycin	43-54	CEA cell adhesion molecule 3	Homo sapiens	149-152
3733260-4	1986	However, in the tunicamycin-treated cells several forms of CEA with lower MWs and representing molecules with decreased glycosylation could be detected in addition to the original CEA molecule of 200 kDa present in control cells.	Tunicamycin	16-27	CEA cell adhesion molecule 3	Homo sapiens	59-62
3733260-4	1986	However, in the tunicamycin-treated cells several forms of CEA with lower MWs and representing molecules with decreased glycosylation could be detected in addition to the original CEA molecule of 200 kDa present in control cells.	Tunicamycin	16-27	CEA cell adhesion molecule 3	Homo sapiens	180-183
3733260-5	1986	The rates of synthesis, secretion and turnover of the lower-molecular-weight forms of poorly glycosylated CEA that appear after tunicamycin treatment are similar to those of CEA in control cells.	Tunicamycin	128-139	CEA cell adhesion molecule 3	Homo sapiens	106-109
2429661-0	1986	Inhibition of overall protein and RNA synthesis as a mechanism for the tunicamycin induced decrease in cytochrome P-450 in rat hepatocytes.	Tunicamycin	71-82	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	103-119
2429661-1	1986	In rat hepatocytes maintained in culture, cytochrome P-450 and NADPH cytochrome c reductase activities were decreased by tunicamycin in a dose and time dependent fashion.	Tunicamycin	121-132	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	42-58
2429661-3	1986	Tunicamycin decreased L-[35S] methionine incorporation into many proteins, including a 52 kDa cytochrome P-450 isozyme.	Tunicamycin	0-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	94-110
2429661-5	1986	These results indicate that tunicamycin decreased cytochrome P-450 levels in hepatocytes by inhibiting protein and RNA synthesis.	Tunicamycin	28-39	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-66
3094838-1	1986	Effects of the intraocular injection of three inhibitors of glycosylation (tunicamycin, castanospermine, and swainsonine) on the rhodopsin content and the integrity of disc membranes in frog retina were studied.	Tunicamycin	75-86	rhodopsin	Homo sapiens	129-138
3094838-2	1986	The administration of 10 or 100 micrograms of tunicamycin resulted in a 78% loss of rhodopsin in the frog retina which also exhibited a significant reduction in the length of photoreceptor outer segments (as examined under light microscope).	Tunicamycin	46-57	rhodopsin	Homo sapiens	84-93
3094838-3	1986	This suggests that the synthesis and/or insertion of rhodopsin into the disc membrane is inhibited by tunicamycin.	Tunicamycin	102-113	rhodopsin	Homo sapiens	53-62
3522736-5	1986	The glycosylation of Mac-1 was examined by both translation in vitro in the presence of dog pancreas microsomes and by biosynthesis in vivo and treatment with tunicamycin, endoglycosidase H, and the deglycosylating agent trifluoromethane sulfonic acid.	Tunicamycin	159-170	integrin alpha M	Mus musculus	21-26
3016293-5	1986	When PRV-infected Vero cells were incubated in the presence of tunicamycin, the gp50 that was produced had an identical molecular weight to that produced in the absence of drug.	Tunicamycin	63-74	tumor associated calcium signal transducer 2	Homo sapiens	80-84
3800894-5	1986	We show here that two-dimensional gel patterns of PSP-A similar to that of the primary translation products are obtained by incorporation of [35S]methionine in the presence of tunicamycin or by N-glycanase digestion of the 32-36 kDa group.	Tunicamycin	176-187	surfactant protein A2	Homo sapiens	50-55
3099750-11	1986	The underglycosylated C1 Inh secreted in presence of tunicamycin is still reactive with purified C1s.	Tunicamycin	53-64	serpin family G member 1	Homo sapiens	22-28
2939068-8	1986	In the presence of tunicamycin, each of the CR1 allelic products is 25,000 lower in Mr than the glycosylated receptor.	Tunicamycin	19-30	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	44-47
2939068-11	1986	Nonglycosylated CR1 synthesized in the presence of tunicamycin had twice the turnover rate of glycosylated CR1.	Tunicamycin	51-62	complement C3b/C4b receptor 1 (Knops blood group)	Homo sapiens	16-19
2878363-8	1986	p185 and the EGF receptor had distinct electrophoretic mobilities when synthesized under normal culture conditions or in the presence of tunicamycin.	Tunicamycin	137-148	epidermal growth factor receptor	Rattus norvegicus	13-25
3011561-0	1986	Tunicamycin sensitivity of prolactin, insulin and epidermal growth factor receptors in rat liver plasmalemma.	Tunicamycin	0-11	prolactin	Rattus norvegicus	27-36
3011561-0	1986	Tunicamycin sensitivity of prolactin, insulin and epidermal growth factor receptors in rat liver plasmalemma.	Tunicamycin	0-11	epidermal growth factor like 1	Rattus norvegicus	50-73
3011561-1	1986	We have used the glycosylation inhibitor tunicamycin to assess the stability of the receptors for prolactin, insulin and epidermal growth factor (EGF) in rat liver cell membrane.	Tunicamycin	41-52	prolactin	Rattus norvegicus	98-107
3011561-2	1986	Direct binding studies on liver plasmalemma fractions which were isolated from tunicamycin-treated rats revealed a rapid loss of prolactin receptors (t1/2 approximately 35 min) with a more prolonged half-life for insulin (10 h) and EGF receptors (8 h).	Tunicamycin	79-90	prolactin	Rattus norvegicus	129-138
3011561-2	1986	Direct binding studies on liver plasmalemma fractions which were isolated from tunicamycin-treated rats revealed a rapid loss of prolactin receptors (t1/2 approximately 35 min) with a more prolonged half-life for insulin (10 h) and EGF receptors (8 h).	Tunicamycin	79-90	epidermal growth factor like 1	Rattus norvegicus	232-235
3955081-3	1986	In the presence of tunicamycin, an inhibitor of N-glycosylation, the secretion of angiotensinogen as well as total protein and albumin secretion were diminished.	Tunicamycin	19-30	angiotensinogen	Rattus norvegicus	82-97
3081330-11	1986	In contrast, in the presence of tunicamycin, the predominant intracellular form of TBG had an apparent mol wt of 44K (TBG3).	Tunicamycin	32-43	serpin family A member 7	Homo sapiens	83-86
3082891-2	1986	Treatment of human umbilical vein endothelial cells with tunicamycin inhibited N-linked glycosylation of nascent vWf and the resulting pro-vWf monomers failed to dimerize.	Tunicamycin	57-68	von Willebrand factor	Homo sapiens	113-116
3082891-2	1986	Treatment of human umbilical vein endothelial cells with tunicamycin inhibited N-linked glycosylation of nascent vWf and the resulting pro-vWf monomers failed to dimerize.	Tunicamycin	57-68	von Willebrand factor	Homo sapiens	139-142
3086086-9	1986	Synaptophysin is N-glycosylated, since cultivation of the rat phaeochromocytoma cell line PC12 in the presence of tunicamycin reduced its mol.	Tunicamycin	114-125	synaptophysin	Rattus norvegicus	0-13
3510667-5	1986	The repletion of lipoprotein lipase content was studied in these cells maintained in the presence of tunicamycin after cycloheximide removal.	Tunicamycin	101-112	lipoprotein lipase	Mus musculus	17-35
3510667-10	1986	An inactive form of lipoprotein lipase from tunicamycin-treated cells was detected by competition experiments with mature active lipoprotein lipase for the binding to immobilized antilipoprotein lipase antibodies, as well as by immunofluorescence staining.	Tunicamycin	44-55	lipoprotein lipase	Mus musculus	20-38
3510667-10	1986	An inactive form of lipoprotein lipase from tunicamycin-treated cells was detected by competition experiments with mature active lipoprotein lipase for the binding to immobilized antilipoprotein lipase antibodies, as well as by immunofluorescence staining.	Tunicamycin	44-55	lipoprotein lipase	Mus musculus	129-147
3510667-13	1986	Despite this lack of activation, the lipoprotein lipase molecule was able to migrate intracellularily and to undergo secretion after heparin stimulation of the tunicamycin-treated cells.	Tunicamycin	160-171	lipoprotein lipase	Mus musculus	37-55
4052441-0	1985	Importance of the different steps of glycosylation for the activity and secretion of lipoprotein lipase in rat preadipocytes studied with monensin and tunicamycin.	Tunicamycin	151-162	lipoprotein lipase	Rattus norvegicus	85-103
2418827-3	1986	When the cells were treated with tunicamycin the unglycosylated alpha 2-macroglobulin subunit exhibited a molecular weight of 160,000.	Tunicamycin	33-44	alpha-2-macroglobulin	Homo sapiens	64-85
3510136-3	1986	Insulin receptor turnover was estimated by measurement of insulin binding after inhibition of synthesis of functional receptors with tunicamycin (0.5 micrograms/ml).	Tunicamycin	133-144	insulin receptor	Homo sapiens	0-16
3510136-6	1986	The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1).	Tunicamycin	83-94	insulin	Homo sapiens	42-49
3510136-6	1986	The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1).	Tunicamycin	83-94	insulin	Homo sapiens	118-125
3510136-6	1986	The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1).	Tunicamycin	83-94	insulin	Homo sapiens	118-125
3510136-6	1986	The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1).	Tunicamycin	150-161	insulin	Homo sapiens	42-49
3510136-6	1986	The t1/2 of disappearance of cell surface insulin binding capacity determined with tunicamycin was 8.0 h. Addition of insulin (1000 ng/ml) or AIRA to tunicamycin reduced the t1/2 to 2.6 h (insulin), 2.2 h (patient B10), and 2.0 h (patient 1).	Tunicamycin	150-161	ectonucleotide pyrophosphatase/phosphodiesterase 3	Homo sapiens	214-217
3007151-8	1986	Results from digestion with endoglycosidase H, incubation with tunicamycin and metabolic labelling with [3H]mannose indicated that myeloperoxidase contained high mannose oligosaccharide side chains.	Tunicamycin	63-74	myeloperoxidase	Homo sapiens	131-146
3023826-2	1986	When grown in the presence of tunicamycin, both cells expressed a receptor-related species p135, the presumptive aglycosylated form of the biosynthetic precursor, gp145, of the mature form of the receptor, gp165, expressed at the cell surface.	Tunicamycin	30-41	dynactin subunit 1	Homo sapiens	91-95
3023826-3	1986	Two additional receptor-related species, p115 and p70, were detected when A431, but not Hep 3B, cells were treated with tunicamycin.	Tunicamycin	120-131	USO1 vesicle transport factor	Homo sapiens	41-45
3023826-3	1986	Two additional receptor-related species, p115 and p70, were detected when A431, but not Hep 3B, cells were treated with tunicamycin.	Tunicamycin	120-131	ubiquitin associated and SH3 domain containing B	Homo sapiens	50-53
2422549-7	1986	When macrophages were induced in the presence of tunicamycin, only one activity of a molecular weight of about 19,000 dalton was found which again was neutralized by anti-interferon-beta.	Tunicamycin	49-60	interferon beta 1, fibroblast	Mus musculus	171-186
3905815-6	1985	The post-translational modification which, despite the removal of signal peptide, resulted in an increase in apparent Mr, reflects the glycosylation as examined using Xenopus oocytes microinjected with renin mRNA in the presence of tunicamycin, an inhibitor of protein glycosylation.	Tunicamycin	232-243	LOW QUALITY PROTEIN: renin	Oryctolagus cuniculus	202-207
3937276-5	1985	The possible role of N-linked oligosaccharides for the biological activity of t-PA was studied using t-PA secreted by melanoma cells in the presence of tunicamycin, an inhibitor of N-glycosylation.	Tunicamycin	152-163	plasminogen activator, tissue type	Homo sapiens	78-82
4066700-4	1985	The biosynthesis of PP63 was studied in vitro in a cell-free system and in intact hepatocytes incubated with or without tunicamycin.	Tunicamycin	120-131	alpha-2-HS-glycoprotein	Rattus norvegicus	20-24
4066700-12	1985	PP63 secretion was altered by tunicamycin.	Tunicamycin	30-41	alpha-2-HS-glycoprotein	Rattus norvegicus	0-4
4052441-5	1985	Addition of tunicamycin (5 micrograms/ml) for 24 h caused a 30-50% reduction in immunoadsorbable lipoprotein lipase, but the enzyme activity was reduced by 90%.	Tunicamycin	12-23	lipoprotein lipase	Rattus norvegicus	97-115
4052441-9	1985	The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium.	Tunicamycin	121-132	lipoprotein lipase	Rattus norvegicus	169-187
4052441-9	1985	The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium.	Tunicamycin	121-132	lipoprotein lipase	Rattus norvegicus	198-216
4052441-9	1985	The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium.	Tunicamycin	121-132	lipoprotein lipase	Rattus norvegicus	198-216
4052441-9	1985	The present results indicate that: the presence of asparagine-linked oligosaccharide (formation of which is inhibited by tunicamycin) is mandatory for the expression of lipoprotein lipase activity; lipoprotein lipase is active also in a high mannose form; and terminal glycosylation and oligosaccharide processing, which is inhibited by monensin, may be important for the appearance of heparin-releasable lipoprotein lipase and secretion of lipoprotein lipase into the medium.	Tunicamycin	121-132	lipoprotein lipase	Rattus norvegicus	198-216
3936778-5	1985	Proliferation of the IL 2-dependent CTLL cells was normal in the presence of Swainsonine but strongly impaired in the presence of Tunicamycin.	Tunicamycin	130-141	interleukin 2	Mus musculus	21-25
3934016-4	1985	N-Glycosylation of secreted angiotensinogen was inhibited using tunicamycin.	Tunicamycin	64-75	angiotensinogen	Homo sapiens	28-43
4046741-0	1985	Inhibition of protein synthesis: a basis for tunicamycin-induced decrease in rat liver cytochrome P-450.	Tunicamycin	45-56	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	87-103
3000457-4	1985	Thus, treatment of 3T3-L1 adipocytes with tunicamycin caused the loss of cellular insulin binding activity and the accumulation of an inactive aglyco-proreceptor.	Tunicamycin	42-53	insulin	Homo sapiens	82-89
3161943-5	1985	The Ly-m20.2 molecules of tissues and clonal cell lines exhibit size and charge heterogeneity that can be eliminated by the complete removal of N-linked sugars with the enzyme endo-F or by inhibiting glycosylation with tunicamycin.	Tunicamycin	219-230	Fc receptor, IgG, low affinity IIb	Mus musculus	4-10
4079938-5	1985	The BW5147 T200 molecule is 3000 daltons larger than the molecule expressed by the transfected L-cell, a size difference due to glycosylation moieties, since treatment of the molecules with Endoglycosidase F or treatment of cells with tunicamycin yields T200 molecules of the same size from the 2 cell sources.	Tunicamycin	235-246	protein tyrosine phosphatase, receptor type, C	Mus musculus	11-15
3931637-3	1985	The predominant intracellular form was not susceptible to digestion by neuraminidase but was sensitive to endoglycosidase treatment, which digested it to a species with a molecular weight comparable to that of the sole hemopexin species produced by tunicamycin-treated hepatocytes and that produced by in vitro translation.	Tunicamycin	249-260	hemopexin	Rattus norvegicus	219-228
4031826-6	1985	Tunicamycin treatment results in the synthesis of a 70K protein (p70) which incorporates [3H]glucosamine and [3H]fucose but not [3H]mannose.	Tunicamycin	0-11	ubiquitin associated and SH3 domain containing B	Homo sapiens	65-68
3894594-8	1985	If the cultures are treated with tunicamycin, the astrocytes produce fibronectin that is unglycosylated, as shown by [3H]glucosamine labeling, and is neither sulfated nor phosphorylated as indicated by [35S]O4 and [32P]O4 labeling studies.	Tunicamycin	33-44	fibronectin 1	Homo sapiens	69-80
3927903-3	1985	We show that native, undenatured calcitonin is an active substrate for oligosaccharyltransferase and that glycosylation of calcitonin by the transferase is inhibited by tunicamycin.	Tunicamycin	169-180	calcitonin related polypeptide alpha	Homo sapiens	33-43
3927903-3	1985	We show that native, undenatured calcitonin is an active substrate for oligosaccharyltransferase and that glycosylation of calcitonin by the transferase is inhibited by tunicamycin.	Tunicamycin	169-180	calcitonin related polypeptide alpha	Homo sapiens	123-133
2412675-8	1985	When prostatic tissue slices were incubated with tunicamycin, the unglycosylated arginine esterase obtained had a lower molecular weight than the in vitro translation product, suggesting that a signal peptide had been removed in the living cells.	Tunicamycin	49-60	arginine esterase	Canis lupus familiaris	81-98
2989336-9	1985	Tunicamycin-treated Hep G2 cells secreted five discrete forms of angiotensinogen, a predominant form of mol wt 46,200, with other forms (mol wt 46,800, 48,100, 49,200, and 49,600) representing 10% of secreted angiotensinogen.	Tunicamycin	0-11	angiotensinogen	Homo sapiens	65-80
2989336-9	1985	Tunicamycin-treated Hep G2 cells secreted five discrete forms of angiotensinogen, a predominant form of mol wt 46,200, with other forms (mol wt 46,800, 48,100, 49,200, and 49,600) representing 10% of secreted angiotensinogen.	Tunicamycin	0-11	angiotensinogen	Homo sapiens	209-224
2989336-12	1985	The other higher molecular weight forms of angiotensinogen secreted by tunicamycin-treated Hep G2 cells were shown to represent O-glycosylated angiotensinogen in that they were reduced to 46,200 mol wt by treatment with trifluoromethane sulfonic acid.	Tunicamycin	71-82	angiotensinogen	Homo sapiens	43-58
2989336-12	1985	The other higher molecular weight forms of angiotensinogen secreted by tunicamycin-treated Hep G2 cells were shown to represent O-glycosylated angiotensinogen in that they were reduced to 46,200 mol wt by treatment with trifluoromethane sulfonic acid.	Tunicamycin	71-82	angiotensinogen	Homo sapiens	143-158
3875019-11	1985	We have shown, however, that the peptide backbone of p43, as studied by both tunicamycin treatment of cells and endoglycosidase F digestion of immunoprecipitates, was identical in size to that of murine Qa-1.	Tunicamycin	77-88	aminoacyl tRNA synthetase complex-interacting multifunctional protein 1	Mus musculus	53-56
3886013-4	1985	Intact fibroblasts cultured in the presence of tunicamycin synthesized an Mr 20 000 form of tissue inhibitor of metalloproteinases, detectable intracellularly and extracellularly.	Tunicamycin	47-58	TIMP metallopeptidase inhibitor 1	Homo sapiens	92-130
3893560-0	1985	The effect of tunicamycin on transferrin synthesis and secretion in hormonally stimulated explants of rabbit mammary gland.	Tunicamycin	14-25	serotransferrin	Oryctolagus cuniculus	29-40
2983087-7	1985	Polypeptide p73 was immunodetected in the presence of tunicamycin and designated as a nascent recipient of N-linked sugars, whereas gp88 was considered to contain O-linked oligosaccharides because its synthesis was not affected by tunicamycin.	Tunicamycin	54-65	tumor protein p73	Homo sapiens	12-15
3888262-6	1985	In the presence of tunicamycin, both mnn9 and wild-type X2180 cells made a mannoprotein fraction with an average molecular weight of 140 000, whereas in the absence of the glycosylation inhibitor, the mnn9 mutant made material with a molecular weight of 180 000 and the mannoprotein made by wild-type cells was too large to penetrate the polyacrylamide gel.	Tunicamycin	19-30	mannosyltransferase complex subunit MNN9	Saccharomyces cerevisiae S288C	37-41
2580532-4	1985	For example, three glycoproteins are exported with rapid kinetics and secretion of only one, alpha 1-protease inhibitor, is inhibited by tunicamycin treatment.	Tunicamycin	137-148	serpin family A member 1	Homo sapiens	93-119
2580532-5	1985	In addition, three glycoproteins are secreted with intermediate kinetics and tunicamycin-treatment inhibits the secretion of two of these proteins, alpha 2-macroglobulin and ceruloplasmin but not the third, plasminogen.	Tunicamycin	77-88	alpha-2-macroglobulin	Homo sapiens	148-169
2580532-5	1985	In addition, three glycoproteins are secreted with intermediate kinetics and tunicamycin-treatment inhibits the secretion of two of these proteins, alpha 2-macroglobulin and ceruloplasmin but not the third, plasminogen.	Tunicamycin	77-88	ceruloplasmin	Homo sapiens	174-187
3871610-2	1985	Unglycosylated alpha 1-proteinase inhibitor was synthesized by hepatocytes in the presence of tunicamycin.	Tunicamycin	94-105	serpin family A member 1	Rattus norvegicus	15-43
3967652-5	1985	Tunicamycin treatment of cultures significantly delayed the secretion of hemopexin but not that of transferrin.	Tunicamycin	0-11	hemopexin	Rattus norvegicus	73-82
3965045-2	1985	Tissue factor activity was inducible by endotoxin, and its induction was inhibited by 1 microgram/mL of actinomycin D, 10 micrograms/mL of cycloheximide, and 0.2 micrograms/mL of tunicamycin.	Tunicamycin	179-190	coagulation factor III	Mus musculus	0-13
3902570-10	1985	Production of mature mouse IL-2 was inhibited by tunicamycin (TM), with precursor molecules accumulating in the cell extract.	Tunicamycin	49-60	interleukin 2	Mus musculus	27-31
2991546-3	1985	These decreased cellular responses are probably due to an underglycosylation of the NGF receptor, since the effects of tunicamycin are correlated with a decrease in 3H-fucose incorporation rather than a general decline in cellular metabolism as measured by viability and protein synthesis.	Tunicamycin	119-130	nerve growth factor receptor	Rattus norvegicus	84-96
2858069-10	1985	(3) Acetylcholinesterase release was also decreased by an inhibitor of protein glycosylation, tunicamycin.	Tunicamycin	94-105	acetylcholinesterase	Rattus norvegicus	4-24
2858069-14	1985	(3) Tunicamycin acts by decreasing the intracellular activity of acetylcholinesterase, possibly via enhanced proteolytic breakdown.	Tunicamycin	4-15	acetylcholinesterase	Rattus norvegicus	65-85
3931095-7	1985	Nearly all of the IRBP secreted by bovine retinas incubated with (3H)-leucine in the presence of tunicamycin was nonglycosylated and did not bind to concanavalin A.	Tunicamycin	97-108	retinol binding protein 3	Bos taurus	18-22
6092384-0	1984	Effect of tunicamycin and monensin on secretion of thyroxine-binding globulin by cultured human hepatoma (Hep G2) cells.	Tunicamycin	10-21	serpin family A member 7	Homo sapiens	51-77
6092384-10	1984	Tunicamycin, 5 micrograms/ml, completely blocked glycosylation and markedly affected TBG secretion, almost doubling the time required for the secretion of 50% of the protein.	Tunicamycin	0-11	serpin family A member 7	Homo sapiens	85-88
4046741-1	1985	Tunicamycin caused a dose and time dependent decrease in cytochrome P-450 in rat liver.	Tunicamycin	0-11	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	57-73
4046741-6	1985	A decrease in cytochrome P-450 was also observed in cultured rat hepatocytes treated with tunicamycin.	Tunicamycin	90-101	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	14-30
4046741-8	1985	This indicates that a decrease in protein synthesis may be responsible for the tunicamycin-induced decrease in cytochrome P-450 and drug metabolism.	Tunicamycin	79-90	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	111-127
6096695-7	1984	We identified a gene, ALG7, that is probably the structural gene for UDP-N-acetylglucosamine-1-P transferase, the enzyme inhibited by tunicamycin.	Tunicamycin	134-145	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Saccharomyces cerevisiae S288C	22-26
6237101-5	1984	The precursor of the IL 2 receptor isolated from tunicamycin-treated HUT102B2 or 12-O-tetradecanoyl phorbol 13-acetate-induced CCRF-CEM cells had the same Mr and isoelectric point.	Tunicamycin	49-60	interleukin 2	Homo sapiens	21-25
16593518-8	1984	Furthermore, the appearance of the mature polypeptide associated with carbonic anhydrase activity in the periplasmic space of C. reinhardtii is inhibited by tunicamycin, an antibiotic that prevents core glycosylation of polypeptides on the endoplasmic reticulum.	Tunicamycin	157-168	uncharacterized protein	Chlamydomonas reinhardtii	70-88
6432920-11	1984	These results suggest that maturation of tyrosinase may occur via T1" and T1"" as precursors of T3, or possibly T1 through the addition of N-glycosydically linked oligosaccharide moieties which can be interrupted by glucosamine and tunicamycin.	Tunicamycin	232-243	tyrosinase	Mus musculus	41-51
6088499-6	1984	In the presence of tunicamycin newly synthesized ASGP-R is a 34,000-Da nonglycosylated species which appears on the Hep G2 cell surface where it specifically binds 125I-ASOR.	Tunicamycin	19-30	asialoglycoprotein receptor 1	Homo sapiens	49-55
6088499-7	1984	There is no major effect on subsequent uptake and degradation of 125I-ASOR in cells whose ASGP-R was synthesized in the presence of tunicamycin.	Tunicamycin	132-143	asialoglycoprotein receptor 1	Homo sapiens	90-96
6088499-8	1984	The turnover of ASGP-R synthesized in the presence of either swainsonine or tunicamycin is not significantly altered from that found for the normal 46,000-Da species.	Tunicamycin	76-87	asialoglycoprotein receptor 1	Homo sapiens	16-22
6327813-5	1984	A study of surface iodination revealed that the former component was membrane-associated mature IL2R , and a pulse-chase study showed that the latter component was a precursor for IL2R that already possessed tunicamycin-sensitive N-linked sugar side chain(s).	Tunicamycin	208-219	interleukin 2 receptor subunit alpha	Homo sapiens	180-184
4092492-3	1985	Thus, treatment of 3T3-L1 adipocytes with tunicamycin causes the depletion of cellular insulin binding activity and the accumulation of an inactive aglyco proreceptor.	Tunicamycin	42-53	insulin	Homo sapiens	87-94
6205259-0	1984	Identification and partial characterization of the unglycosylated peptide of carcinoembryonic antigen synthesized by human tumor cell lines in the presence of tunicamycin.	Tunicamycin	159-170	CEA cell adhesion molecule 3	Homo sapiens	77-101
6205259-1	1984	Unglycosylated peptide backbones of carcinoembryonic antigen (CEA) synthesized by human tumor cell lines in the presence of tunicamycin were identified and analyzed by SDS-polyacrylamide gel electrophoresis.	Tunicamycin	124-135	CEA cell adhesion molecule 3	Homo sapiens	36-60
6205259-1	1984	Unglycosylated peptide backbones of carcinoembryonic antigen (CEA) synthesized by human tumor cell lines in the presence of tunicamycin were identified and analyzed by SDS-polyacrylamide gel electrophoresis.	Tunicamycin	124-135	CEA cell adhesion molecule 3	Homo sapiens	62-65
6205259-4	1984	In contrast, in the presence of tunicamycin, the native CEA molecules disappeared, and a new component that was precipitated with anti-CEA antibodies and labeled only with [3H]leucine but not with [14C]glucosamine was identified in each cell line.	Tunicamycin	32-43	CEA cell adhesion molecule 3	Homo sapiens	56-59
6375731-8	1984	Tunicamycin present during perfusion also induced a drop in lipoprotein lipase and tissue neutral lipase activity, indicating that glycosylation is necessary for secretion of lipoprotein lipase.	Tunicamycin	0-11	lipoprotein lipase	Rattus norvegicus	60-78
6375731-8	1984	Tunicamycin present during perfusion also induced a drop in lipoprotein lipase and tissue neutral lipase activity, indicating that glycosylation is necessary for secretion of lipoprotein lipase.	Tunicamycin	0-11	lipase G, endothelial type	Rattus norvegicus	72-78
6375731-8	1984	Tunicamycin present during perfusion also induced a drop in lipoprotein lipase and tissue neutral lipase activity, indicating that glycosylation is necessary for secretion of lipoprotein lipase.	Tunicamycin	0-11	lipoprotein lipase	Rattus norvegicus	175-193
6427217-15	1984	Neural retinas incubated with 3H-labeled leucine in the presence of tunicamycin secreted a form of IRBP that did not bind concanavalin A and had an Mr reduced by approximately 5,000.	Tunicamycin	68-79	retinol binding protein 3	Bos taurus	99-103
6323131-4	1984	To determine whether this loss of LH/hCG receptors was due to accelerated receptor degradation, turnover measurements were made using tunicamycin to inhibit LH/hCG receptor synthesis.	Tunicamycin	134-145	hypertrichosis 2 (generalised, congenital)	Homo sapiens	160-163
6725264-7	1984	Addition of tunicamycin (5 micrograms/ml) inhibited glycosylation of the initial form of haptoglobin detected, but subsequent proteolytic processing into alpha and beta chains still occurred.	Tunicamycin	12-23	haptoglobin	Oryctolagus cuniculus	89-100
6706977-5	1984	Purified liver parenchymal cells cultured in the presence of tunicamycin secrete fibrinogen polypeptides which lack carbohydrate moieties.	Tunicamycin	61-72	fibrinogen alpha chain S homeolog	Xenopus laevis	81-91
6200362-4	1984	In the presence of tunicamycin an unglycosylated form of M alpha 1-antitrypsin appears in the incubation medium but no corresponding unglycosylated version of the Z protein is secreted.	Tunicamycin	19-30	serpin family A member 1	Homo sapiens	59-78
6425062-10	1984	Exposure of the cells to tunicamycin, on the other hand, caused a prominent cytoplasmic accumulation of VIIIR:Ag and, within 96 h, led to the disappearance of most of the VIIIR:Ag-positive granules but did not affect the intracellular distribution of fibronectin.	Tunicamycin	25-36	fibronectin 1	Homo sapiens	251-262
6323296-3	1984	alpha 1-AT export to medium was delayed by tunicamycin, inhibited by cycloheximide but unaffected by colchicine.	Tunicamycin	43-54	serpin family A member 1	Homo sapiens	0-10
6697962-2	1984	Inhibition of glycosylation with tunicamycin permitted identification of the nonglycosylated form of secreted angiotensinogen.	Tunicamycin	33-44	angiotensinogen	Rattus norvegicus	110-125
6697962-3	1984	Whereas angiotensinogen secreted by hepatoma cells and hepatocytes showed electrophoretic heterogeneity (mol wt, 52-62 X 10(3], tunicamycin-treated cells secreted only a single angiotensinogen species [mol wt, 48.3 +/- 0.7 X 10(3) (mean +/- SD)], which could be cleaved by renin.	Tunicamycin	128-139	angiotensinogen	Rattus norvegicus	177-192
6697962-3	1984	Whereas angiotensinogen secreted by hepatoma cells and hepatocytes showed electrophoretic heterogeneity (mol wt, 52-62 X 10(3], tunicamycin-treated cells secreted only a single angiotensinogen species [mol wt, 48.3 +/- 0.7 X 10(3) (mean +/- SD)], which could be cleaved by renin.	Tunicamycin	128-139	renin	Rattus norvegicus	273-278
6697962-9	1984	4) The des-angiotensin I-angiotensinogen generated by renin treatment of the lysate had an electrophoretic mobility identical to that of des-AI-angiotensinogen produced by renin treatment of nonglycosylated angiotensinogen secreted by tunicamycin-treated hepatoma cells and hepatocytes.	Tunicamycin	235-246	angiotensinogen	Rattus norvegicus	25-40
6697962-9	1984	4) The des-angiotensin I-angiotensinogen generated by renin treatment of the lysate had an electrophoretic mobility identical to that of des-AI-angiotensinogen produced by renin treatment of nonglycosylated angiotensinogen secreted by tunicamycin-treated hepatoma cells and hepatocytes.	Tunicamycin	235-246	renin	Rattus norvegicus	54-59
6697962-9	1984	4) The des-angiotensin I-angiotensinogen generated by renin treatment of the lysate had an electrophoretic mobility identical to that of des-AI-angiotensinogen produced by renin treatment of nonglycosylated angiotensinogen secreted by tunicamycin-treated hepatoma cells and hepatocytes.	Tunicamycin	235-246	renin	Rattus norvegicus	172-177
6852052-6	1983	Acinar cells cultured in the presence of increasing concentrations of the N-glycosylation inhibitor tunicamycin synthesize 5-6 distinct precursor GP-2 species with apparent molecular weights decreasing from 73000-61000.	Tunicamycin	100-111	glycoprotein 2	Rattus norvegicus	146-150
6202280-1	1984	Synthesis of murine gamma interferon (MuIFN gamma) by phytohemagglutinin (PHA)-stimulated spleen cells was inhibited in a dose-dependent manner by graded concentrations of tunicamycin or 2-deoxy-glucose, both of which inhibit glycosylation.	Tunicamycin	172-183	interferon gamma	Mus musculus	20-49
6319010-5	1984	TGF-beta has little effect on the rate of overall protein synthesis, but the increase it induces in EGF binding can be completely inhibited by cycloheximide and tunicamycin.	Tunicamycin	161-172	epidermal growth factor like 1	Rattus norvegicus	100-103
6100257-7	1984	The protein glycosylation inhibitor tunicamycin was found to inhibit the ACTH produced increase in steroidogenesis and also to inhibit the synthesis of protein i under conditions which did not inhibit overall protein synthesis.	Tunicamycin	36-47	proopiomelanocortin	Homo sapiens	73-77
6373801-9	1984	Inhibition of N-linked glycosylation of apolipoprotein B with tunicamycin affects neither the assembly of glycerolipids into VLDL nor the secretion of the VLDL particle, indicating that aglyco -apolipoprotein B can serve as a functional component for VLDL assembly and secretion.	Tunicamycin	62-73	apolipoprotein B	Gallus gallus	40-56
6630229-1	1983	Tunicamycin, an inhibitor of asparagine-linked glycosylation of glycoprotein, has been used here to examine the role of N-linked oligosaccharides in secretion of ZP2 and ZP3, two of the three glycoproteins that constitute the mouse egg"s extracellular coat (zona pellucida).	Tunicamycin	0-11	zona pellucida glycoprotein 2	Mus musculus	162-165
6630229-1	1983	Tunicamycin, an inhibitor of asparagine-linked glycosylation of glycoprotein, has been used here to examine the role of N-linked oligosaccharides in secretion of ZP2 and ZP3, two of the three glycoproteins that constitute the mouse egg"s extracellular coat (zona pellucida).	Tunicamycin	0-11	zona pellucida glycoprotein 3	Mus musculus	170-173
6630229-11	1983	The apparent rates of synthesis of core-glycosylated ZP2 and ZP3 precursors synthesized in the absence of tunicamycin and of precursors synthesized in the presence of the drug are virtually identical.	Tunicamycin	106-117	zona pellucida glycoprotein 2	Mus musculus	53-56
6630229-11	1983	The apparent rates of synthesis of core-glycosylated ZP2 and ZP3 precursors synthesized in the absence of tunicamycin and of precursors synthesized in the presence of the drug are virtually identical.	Tunicamycin	106-117	zona pellucida glycoprotein 3	Mus musculus	61-64
6630229-12	1983	On the other hand, in the presence of tunicamycin, nascent ZP3 is incorporated into the zona pellucida as an extremely heterogeneous species (approximately equal to 51,000 Mr) at about three times the rate observed for mature ZP3 in the absence of tunicamycin.	Tunicamycin	38-49	zona pellucida glycoprotein 3	Mus musculus	59-62
6630229-12	1983	On the other hand, in the presence of tunicamycin, nascent ZP3 is incorporated into the zona pellucida as an extremely heterogeneous species (approximately equal to 51,000 Mr) at about three times the rate observed for mature ZP3 in the absence of tunicamycin.	Tunicamycin	38-49	zona pellucida glycoprotein 3	Mus musculus	226-229
6630229-12	1983	On the other hand, in the presence of tunicamycin, nascent ZP3 is incorporated into the zona pellucida as an extremely heterogeneous species (approximately equal to 51,000 Mr) at about three times the rate observed for mature ZP3 in the absence of tunicamycin.	Tunicamycin	248-259	zona pellucida glycoprotein 3	Mus musculus	59-62
6630229-13	1983	In the presence of tunicamycin, ZP2 is incorporated into the zona pellucida as 81,000 and 76,000 Mr species at about one-sixth the rate observed for mature ZP2 in the absence of the drug.	Tunicamycin	19-30	zona pellucida glycoprotein 2	Mus musculus	32-35
6630229-13	1983	In the presence of tunicamycin, ZP2 is incorporated into the zona pellucida as 81,000 and 76,000 Mr species at about one-sixth the rate observed for mature ZP2 in the absence of the drug.	Tunicamycin	19-30	zona pellucida glycoprotein 2	Mus musculus	156-159
6630229-15	1983	ZP2 synthesized in the presence of tunicamycin is relatively stable and accumulates intracellularly.	Tunicamycin	35-46	zona pellucida glycoprotein 2	Mus musculus	0-3
6675524-6	1983	Glycosylation-deficient CEA obtained from cells harvested from media supplemented with non-toxic levels of tunicamycin showed lower molecular weight and delayed filtration through Sephadex-G200.	Tunicamycin	107-118	CEA cell adhesion molecule 3	Homo sapiens	24-27
6628320-1	1983	Tunicamycin, an inhibitor of glycosylation, was incubated with ovine thyroid cells in culture to determine the role of glycosylation in the subsequent processing of thyroglobulin to form thyroid hormone.	Tunicamycin	0-11	thyroglobulin	Homo sapiens	165-178
6628320-5	1983	A low mol wt fragment of thyroglobulin was found after tunicamycin treatment, indicating increased susceptibility to or contact with proteases.	Tunicamycin	55-66	thyroglobulin	Homo sapiens	25-38
6316327-5	1983	Inhibition of protein glycosylation by tunicamycin generates smaller 125I-NGF-receptor complexes.	Tunicamycin	39-50	nerve growth factor	Rattus norvegicus	74-77
6864547-4	1983	Furthermore, 27,000 POMC comigrated with a previously characterized unglycosylated form of this prohormone produced by treatment of cells with tunicamycin.	Tunicamycin	143-154	pro-opiomelanocortin-alpha	Mus musculus	20-24
6349621-2	1983	Tunicamycin (1 microgram/ml) induced a steady decrease of insulin binding, which was decreased by 50% after 13 h. As the total number of binding sites per hepatocyte was 20000, the rate of the receptor degradation could not exceed 13 sites/min per hepatocyte.	Tunicamycin	0-11	insulin	Homo sapiens	58-65
6349621-7	1983	First, the rate of release of degraded insulin into the medium was 600 molecules/min per hepatocyte with 1 nM labelled hormone, and increased (preincubation with cycloheximide) or decreased (tunicamycin) as a function of the amount of cell-bound insulin.	Tunicamycin	191-202	insulin	Homo sapiens	39-46
6363129-2	1984	The effect of tunicamycin on synthesis and intracellular transport of pig small intestinal aminopeptidase N (EC 3.4.11.2), sucrase-isomaltase (EC 3.2.1.48-10) and maltase-glucoamylase (EC 3.2.1.20) was studied by labelling of mucosal explants with [35S]methionine.	Tunicamycin	14-25	alanyl aminopeptidase, membrane	Sus scrofa	91-107
6363129-5	1984	Treatment of aminopeptidase N and sucrase-isomaltase with endo F reduced the size of the high mannose forms approximately to those seen in the presence of tunicamycin.	Tunicamycin	155-166	alanyl aminopeptidase, membrane	Sus scrofa	13-29
6363129-5	1984	Treatment of aminopeptidase N and sucrase-isomaltase with endo F reduced the size of the high mannose forms approximately to those seen in the presence of tunicamycin.	Tunicamycin	155-166	sucrase-isomaltase	Sus scrofa	34-52
6605248-3	1983	Treatment of hepatocytes with tunicamycin led to the secretion of an unglycosylated alpha 1-proteinase inhibitor (Mr 41 000) which also formed a complex with elastase (Mr 66 000).	Tunicamycin	30-41	serpin family A member 1	Rattus norvegicus	84-112
6226284-10	1983	The transport of the precursors of cathepsin D into lysosomes is inhibited by tunicamycin.	Tunicamycin	78-89	cathepsin D	Homo sapiens	35-46
6351631-1	1983	We have examined the effect of insulin and tunicamycin, which cause decreases in cell surface insulin receptor numbers in peripheral tissues, on insulin receptors in neuron-enriched brain cell cultures.	Tunicamycin	43-54	insulin receptor	Rattus norvegicus	94-110
6874686-0	1983	Effect of tunicamycin on 3-hydroxy-3-methylglutaryl coenzyme A reductase in C-6 glial cells.	Tunicamycin	10-21	complement C6	Homo sapiens	76-79
6874686-9	1983	Second, incubation of C-6 cells with N-acetylglucosamine simultaneously with tunicamycin was accompanied by prevention of the drug"s effect on both HMG-CoA reductase and glycoprotein synthesis.	Tunicamycin	77-88	complement C6	Homo sapiens	22-25
6605298-0	1983	Expression of H-2 and viral antigens and resistance to the antitumor lysis of tunicamycin-treated MBL-2 lymphoma cells.	Tunicamycin	78-89	histocompatibility-2, MHC	Mus musculus	14-17
6605298-0	1983	Expression of H-2 and viral antigens and resistance to the antitumor lysis of tunicamycin-treated MBL-2 lymphoma cells.	Tunicamycin	78-89	mannose-binding lectin (protein C) 2	Mus musculus	98-103
6605298-2	1983	Treatment of the Moloney-virus-induced H-2b lymphoma target cells, MBL-2, with tunicamycin (TM), an inhibitor of the protein-N-linked glycosilation, was found to cause a loss of susceptibility to lysis by MSV-immune syngeneic effectors cells, while the same target cells remained fully sensitive to the lytic action of anti-H-2b-immune lymphocytes.	Tunicamycin	79-90	mannose-binding lectin (protein C) 2	Mus musculus	67-72
6602705-10	1983	Tunicamycin led to a marked reduction of the secretion of alpha 2-macroglobulin, alpha 1-acid glycoprotein and alpha 1-proteinase inhibitor, whereas the secretion of transferrin was less affected.	Tunicamycin	0-11	alpha-2-macroglobulin	Rattus norvegicus	58-79
6602705-10	1983	Tunicamycin led to a marked reduction of the secretion of alpha 2-macroglobulin, alpha 1-acid glycoprotein and alpha 1-proteinase inhibitor, whereas the secretion of transferrin was less affected.	Tunicamycin	0-11	serpin family A member 1	Rattus norvegicus	111-139
6190759-0	1983	Tunicamycin treatment inhibits the antiviral activity of interferon in mice.	Tunicamycin	0-11	interferon alpha 1	Homo sapiens	57-67
6190759-1	1983	Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes.	Tunicamycin	25-36	interferon alpha 1	Homo sapiens	121-131
6190759-1	1983	Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes.	Tunicamycin	25-36	interferon alpha 1	Homo sapiens	133-136
6190759-1	1983	Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes.	Tunicamycin	38-40	interferon alpha 1	Homo sapiens	121-131
6190759-1	1983	Earlier we reported that tunicamycin (TM) treatment of L cells in vitro significantly enhances the antiviral activity of interferon (IFN) against viruses (such as vesicular stomatitis, Sindbis, and herpes simplex) which bud from membranes.	Tunicamycin	38-40	interferon alpha 1	Homo sapiens	133-136
6344077-5	1983	Immunoprecipitation of N-CAM from 9-day brain cells treated with tunicamycin yielded corresponding components of Mr 130,000 and 160,000, suggesting that the differences between these two components of N-CAM are in the polypeptide rather than the carbohydrate portions of the molecules.	Tunicamycin	65-76	neural cell adhesion molecule 1	Homo sapiens	23-28
6304240-2	1983	In the presence of tunicamycin, they produced non-glycosylated, biologically active, IFN-beta with a molecular weight of 17000.	Tunicamycin	19-30	interferon beta 1	Homo sapiens	85-93
6854740-8	1983	Analysis by immunoprecipitation and sodium dodecyl sulfate-gel electrophoresis of intracellular [35S]methionine-labeled structural proteins synthesized in the presence and absence of tunicamycin supported the conclusion that E1 and E2 are glycoproteins.	Tunicamycin	183-194	small nucleolar RNA, H/ACA box 73A	Homo sapiens	225-234
6189826-7	1983	The in vitro synthesized polypeptides migrate on NaDodSO4-polyacrylamide gel electrophoresis slower than the respective unglycosylated laminin and entactin chains isolated from cells treated with tunicamycin.	Tunicamycin	196-207	nidogen 1	Mus musculus	147-155
6192804-6	1983	Tunicamycin reduced the incorporation of glucosamine into AFP with a concomitant decrease in molecular weight and microheterogeneity.	Tunicamycin	0-11	alpha fetoprotein	Mus musculus	58-61
6344077-5	1983	Immunoprecipitation of N-CAM from 9-day brain cells treated with tunicamycin yielded corresponding components of Mr 130,000 and 160,000, suggesting that the differences between these two components of N-CAM are in the polypeptide rather than the carbohydrate portions of the molecules.	Tunicamycin	65-76	neural cell adhesion molecule 1	Homo sapiens	201-206
6292303-8	1983	Release of the IgE isotype-specific helper factor was inhibited by cycloheximide and tunicamycin, and its activity was destroyed by treatment with trypsin and neuraminidase.	Tunicamycin	85-96	immunoglobulin heavy constant epsilon	Homo sapiens	15-18
6822533-0	1983	Effect of tunicamycin, an inhibitor of protein glycosylation, on the biological properties of acetylcholine receptor in cultured muscle cells.	Tunicamycin	10-21	cholinergic receptor nicotinic delta subunit	Gallus gallus	94-116
6822533-1	1983	We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells.	Tunicamycin	30-41	cholinergic receptor nicotinic delta subunit	Gallus gallus	141-163
6822533-1	1983	We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells.	Tunicamycin	30-41	cholinergic receptor nicotinic delta subunit	Gallus gallus	165-169
6822533-1	1983	We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells.	Tunicamycin	43-45	cholinergic receptor nicotinic delta subunit	Gallus gallus	141-163
6822533-1	1983	We have studied the effect of tunicamycin (TM), an antibiotic which inhibits the glycosylation of nascent proteins, on the properties of the acetylcholine receptor (AChR) at the surface of embryonic chick skeletal muscle cells.	Tunicamycin	43-45	cholinergic receptor nicotinic delta subunit	Gallus gallus	165-169
6829167-5	1983	The unglycosylated form of the altered PE2 synthesized in the presence of tunicamycin migrated at the same position as the unglycosylated PE2 obtained from tunicamycin-treated, parent strain-infected cells.	Tunicamycin	74-85	ETS2 repressor factor	Homo sapiens	39-42
6829167-5	1983	The unglycosylated form of the altered PE2 synthesized in the presence of tunicamycin migrated at the same position as the unglycosylated PE2 obtained from tunicamycin-treated, parent strain-infected cells.	Tunicamycin	156-167	ETS2 repressor factor	Homo sapiens	39-42
6829167-5	1983	The unglycosylated form of the altered PE2 synthesized in the presence of tunicamycin migrated at the same position as the unglycosylated PE2 obtained from tunicamycin-treated, parent strain-infected cells.	Tunicamycin	156-167	ETS2 repressor factor	Homo sapiens	138-141
11892795-3	1983	We have now used rabbit antisera that recognize ZP3 to immunoprecipitate [35S]methionine-labeled, intracellular precursors of this glycoprotein from growing oocytes cultured in vitro in the presence or absence of tunicamycin, a drug that prevents addition of N-linked oligosaccharides to nascent polypeptide chains.	Tunicamycin	213-224	zona pellucida glycoprotein 3	Mus musculus	48-51
6749836-3	1982	In the presence of tunicamycin, an inhibitor of the synthesis of protein-asparagine linked carbohydrate moieties, two smaller molecular forms each of precursor and mature proteinase A were synthesized, indicating that proteinase A contains N-linked carbohydrate which is apparently not required for processing.	Tunicamycin	19-30	proteinase A	Saccharomyces cerevisiae S288C	171-183
6820801-0	1982	Effect of tunicamycin on exo-1,3-beta-D-glucanase synthesis and secretion by cells and protoplasts of Saccharomyces cerevisiae.	Tunicamycin	10-21	Rad2 family nuclease EXO1	Saccharomyces cerevisiae S288C	25-30
6820801-1	1982	Addition of tunicamycin to the culture medium of growing Saccharomyces cerevisiae protoplasts or cells resulted in the formation of a modified exo-1,3-beta-D-glucanase which was detectable in both extracellular and intracellular fractions.	Tunicamycin	12-23	Rad2 family nuclease EXO1	Saccharomyces cerevisiae S288C	143-148
6820801-4	1982	Antibodies raised against the native protein readily precipitated the exo-1,3-beta-D-glucanase produced after tunicamycin treatment.	Tunicamycin	110-121	Rad2 family nuclease EXO1	Saccharomyces cerevisiae S288C	70-75
6816905-1	1982	Tunicamycin alters the biological properties of human interferon-alpha (HuIFN-alpha) produced in its presence by changing the mixture of IFN-alpha subtypes produced.	Tunicamycin	0-11	interferon alpha 1	Homo sapiens	74-83
6749836-3	1982	In the presence of tunicamycin, an inhibitor of the synthesis of protein-asparagine linked carbohydrate moieties, two smaller molecular forms each of precursor and mature proteinase A were synthesized, indicating that proteinase A contains N-linked carbohydrate which is apparently not required for processing.	Tunicamycin	19-30	proteinase A	Saccharomyces cerevisiae S288C	218-230
6749836-4	1982	Tunicamycin interferes also with the glycosylation of the proteinase B precursor, whereas no unglycosylated mature proteinase B could be detected.	Tunicamycin	0-11	proteinase B	Saccharomyces cerevisiae S288C	58-70
7117256-0	1982	Effect of tunicamycin on thyroglobulin secretion.	Tunicamycin	10-21	thyroglobulin	Rattus norvegicus	25-38
7045125-2	1982	Nonglycosylated fibronectin, from tunicamycin-treated chicken embryo fibroblasts, was degraded more rapidly to acid-soluble products than glycosylated fibronectin by pronase, thermolysin, trypsin, and chymotrypsin.	Tunicamycin	34-45	fibronectin 1	Gallus gallus	16-27
6286640-0	1982	Effect of tunicamycin on the synthesis, processing, and secretion of pro-opiomelanocortin peptides in mouse pituitary cells.	Tunicamycin	10-21	pro-opiomelanocortin-alpha	Mus musculus	69-89
6286640-2	1982	When glycosylation of POMC is inhibited in AtT-20 cells with the drug tunicamycin, a 26,000-dalton protein appears in place of the glycosylated 29,000- and 32,000-dalton forms of POMC.	Tunicamycin	70-81	pro-opiomelanocortin-alpha	Mus musculus	22-26
6286640-2	1982	When glycosylation of POMC is inhibited in AtT-20 cells with the drug tunicamycin, a 26,000-dalton protein appears in place of the glycosylated 29,000- and 32,000-dalton forms of POMC.	Tunicamycin	70-81	pro-opiomelanocortin-alpha	Mus musculus	179-183
6286640-3	1982	The 26,000-dalton form found in tunicamycin-treated cells has the same [35S]methionine tryptic peptides as 29,000- and 32,000-dalton POMC, indicating that the decrease in apparent mass is most likely due to loss of carbohydrate and not to changes in the peptide backbone.	Tunicamycin	32-43	pro-opiomelanocortin-alpha	Mus musculus	133-137
6286640-6	1982	Pulse-chase studies demonstrate that the 26,000-dalton unglycosylated POMC is the precursor of the smaller ACTH and endorphin molecules in tunicamycin-treated cells.	Tunicamycin	139-150	pro-opiomelanocortin-alpha	Mus musculus	70-74
6286640-6	1982	Pulse-chase studies demonstrate that the 26,000-dalton unglycosylated POMC is the precursor of the smaller ACTH and endorphin molecules in tunicamycin-treated cells.	Tunicamycin	139-150	pro-opiomelanocortin-alpha	Mus musculus	107-111
6286640-7	1982	Furthermore, all of the forms of ACTH and endorphin found in tunicamycin-treated cells are secreted.	Tunicamycin	61-72	pro-opiomelanocortin-alpha	Mus musculus	33-37
7117256-2	1982	When followed over periods of 4 h, the secretion of [14C]leucine-labeled thyroglobulin into the medium was reduced by 60-95% in the presence of 1 microgram/ml and 5 micrograms/ml of tunicamycin.	Tunicamycin	182-193	thyroglobulin	Rattus norvegicus	73-86
7117256-6	1982	It is concluded that tunicamycin suppresses thyroglobulin secretion and that this is not due to inhibited protein synthesis.	Tunicamycin	21-32	thyroglobulin	Rattus norvegicus	44-57
6802485-4	1982	Assay of tyrosinase of glucosamine- or tunicamycin-induced unpigmented melanoma cells has revealed a selective and marked decrease in the melanosome-rich large-granule fraction, but no substantial decrease in the total activity of remaining subcellular fractions.	Tunicamycin	39-50	tyrosinase	Homo sapiens	9-19
6922701-3	1982	Tunicamycin blocked glycosylation of pro-C4, C2 and factor B and inhibited secretion of the corresponding native complement proteins synthesized by guinea-pig peritoneal macrophages in tissue culture.	Tunicamycin	0-11	complement C2	Cavia porcellus	45-60
6972252-6	1981	The activity of the D-factor was slightly decreased by treating the L-cells with tunicamycin (0.5 microgram/ml) in the presence of 2% fetal calf serum, without any decrease in CSF activity.	Tunicamycin	81-92	leukemia inhibitory factor	Mus musculus	20-28
6116713-15	1981	The oligosaccharide moieties of procathepsin D and of the single chain and heavy chain forms of cathepsin D are cleaved by endoglycosidase H. Treatment of cells with tunicamycin arrests the biosynthetic pathway of cathepsin D at procathepsin D. The nonglycosylated procathepsin D is not proteolytically processed and its secretion is greatly inhibited.	Tunicamycin	166-177	cathepsin D	Canis lupus familiaris	35-46
6116713-15	1981	The oligosaccharide moieties of procathepsin D and of the single chain and heavy chain forms of cathepsin D are cleaved by endoglycosidase H. Treatment of cells with tunicamycin arrests the biosynthetic pathway of cathepsin D at procathepsin D. The nonglycosylated procathepsin D is not proteolytically processed and its secretion is greatly inhibited.	Tunicamycin	166-177	cathepsin D	Canis lupus familiaris	96-107
7336169-4	1981	On the other hand, treatment of melanoma cells with tunicamycin (final concentration, 1.0 microgram/ml) reduced the expression of MAA but did not affect susceptibility to ADCC.	Tunicamycin	52-63	MAA	Homo sapiens	130-133
7341241-6	1981	A, B1, B2 and C polypeptides are all glycosylated by an intracellular process involving the addition of tunicamycin and endo-beta-N-acetylglucosaminidase-H-sensitive N-linked oligosaccharide side chains.	Tunicamycin	104-115	B.burgdorferi-associated arthritis 2	Mus musculus	3-15
6171878-3	1981	Immunoprecipitation of HLA-A,B,C antigens from tunicamycin-treated cells with four monoclonal antibodies specific for the heavy chain and one specific for beta 2-microglobulin showed that the heavy-chain determinant detected by the antibody Q6/64 is absent from the non-glycosylated molecule.	Tunicamycin	47-58	major histocompatibility complex, class I, A	Homo sapiens	23-30
6171878-3	1981	Immunoprecipitation of HLA-A,B,C antigens from tunicamycin-treated cells with four monoclonal antibodies specific for the heavy chain and one specific for beta 2-microglobulin showed that the heavy-chain determinant detected by the antibody Q6/64 is absent from the non-glycosylated molecule.	Tunicamycin	47-58	beta-2-microglobulin	Homo sapiens	155-175
6802828-3	1982	We have found that secreted type heavy chains (mus) are rapidly degraded in these cells, with a half-life of 1.3 h. Some of the membrane type heavy chains (mum) are also rapidly catabolized but some are expressed in a stable form with a half-life of 13 h. Inhibiting the initial glycosylation of heavy chains with tunicamycin has differential effects on the catabolic rates of mus and mum chains.	Tunicamycin	314-325	latexin	Homo sapiens	156-159
6802828-4	1982	The turnover of mus chains is not affected by this inhibitor, but the degradation of mum chains is much more rapid after tunicamycin treatment.	Tunicamycin	121-132	latexin	Homo sapiens	85-88
6802828-6	1982	Tunicamycin treatment of Daudi cells thus seems to inhibit formation of stable mum protein, possibly by altering mu chain conformation and inhibiting its interaction with light chains.	Tunicamycin	0-11	latexin	Homo sapiens	79-82
6951191-2	1982	Loss of 40--60% of DNA polymerase alpha 2 activity was observed in tunicamycin-treated cells.	Tunicamycin	67-78	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	19-39
6951191-4	1982	However, DNA polymerase alpha 2 isolated from tunicamycin-treated cells was insensitive to ricin 1B.	Tunicamycin	46-57	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	9-29
6951191-5	1982	Heat treatment studies at 50 degrees C showed two completely different inactivation profiles for the DNA polymerase alpha 2 enzymes isolated from the tunicamycin-treated and untreated cells.	Tunicamycin	150-161	DNA polymerase alpha 1, catalytic subunit	Homo sapiens	101-121
6281457-2	1982	In vivo synthesis of this env precursor in the presence of the core glycosylation inhibitor tunicamycin yielded a precursor of approximately 61,000 daltons (P61env).	Tunicamycin	92-103	endogenous retrovirus group W member 1, envelope	Homo sapiens	26-29
7053388-6	1982	The antibiotic tunicamycin was shown to inhibit [3H] glucosamine incorporation into microsomal vitellogenin by 70%, without any significant effect on the synthesis of the protein backbone.	Tunicamycin	15-26	a1-a	Xenopus laevis	95-107
7028131-8	1981	These data indicate that the number of insulin binding sites in the cultured Chinese hamster kidney epithelial cells increased with high glucose concentrations in the culture medium, whereas tunicamycin, an inhibitor of protein glycosylation, lowered the number of insulin binding sites.	Tunicamycin	191-202	insulin	Cricetulus griseus	39-46
7028131-8	1981	These data indicate that the number of insulin binding sites in the cultured Chinese hamster kidney epithelial cells increased with high glucose concentrations in the culture medium, whereas tunicamycin, an inhibitor of protein glycosylation, lowered the number of insulin binding sites.	Tunicamycin	191-202	insulin	Cricetulus griseus	265-272
6975776-4	1981	Addition of tunicamycin (2 microgram/ml) or 2-deoxy-D-glucose (10 mM) to the culture neither decreased the yield of CSF relative to the cell number grown nor induced heterogeneity of the produced CSF.	Tunicamycin	12-23	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	116-119
6975776-4	1981	Addition of tunicamycin (2 microgram/ml) or 2-deoxy-D-glucose (10 mM) to the culture neither decreased the yield of CSF relative to the cell number grown nor induced heterogeneity of the produced CSF.	Tunicamycin	12-23	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	196-199
6975776-5	1981	However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal).	Tunicamycin	41-52	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	9-12
6975776-5	1981	However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal).	Tunicamycin	41-52	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	54-57
6975776-5	1981	However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal).	Tunicamycin	41-52	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	54-57
6975776-5	1981	However, CSF produced in the presence of tunicamycin (CSF-tm) was about 23 percent smaller in its molecular weight than normally produced CSF (CSF-normal).	Tunicamycin	41-52	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	54-57
6170312-2	1981	In RAJI cells the HLA-A, -B, and -C antigen heavy chains become core-glycosylated in the endoplasmic reticulum as evidenced by their sensitivity to endo-H digestion and tunicamycin treatment.	Tunicamycin	169-180	major histocompatibility complex, class I, A	Homo sapiens	18-35
6972252-9	1981	D-factor produced in the presence of tunicamycin had an apparent molecular weight of 25,000.	Tunicamycin	37-48	leukemia inhibitory factor	Mus musculus	0-8
6972252-10	1981	On the other hand, most of the CSF was eluted in the void volume, even when it was produced in the presence of tunicamycin.	Tunicamycin	111-122	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	31-34
6972252-11	1981	The D-factor produced in the presence of tunicamycin was more sensitive than normal D-factor was to trypsin or heat treatment at 70 degrees.	Tunicamycin	41-52	leukemia inhibitory factor	Mus musculus	4-12
6972252-12	1981	The CSF produced in the presence of tunicamycin was resistant to these treatments.	Tunicamycin	36-47	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	4-7
7228853-1	1981	Tunicamycin, which inhibits N-linked oligosaccharide chain addition to nascent polypeptides, interrupts glycosylation of the insulin receptor in 3T3-L1 adipocytes giving rise to inactive receptors.	Tunicamycin	0-11	insulin	Homo sapiens	125-132
7228853-2	1981	Chronic exposure of cells to low levels (100 ng/ml) of high performance liquid chromatography-purified tunicamycin causes a greater than or equal to 90% depletion of insulin binding to cell surface and Triton X-100-extractable receptors and a 93% inhibition of [3H]glucosamine incorporation into protein in alkali-stable form.	Tunicamycin	103-114	insulin	Homo sapiens	166-173
7228853-7	1981	This strongly suggests that inactive aglycoinsulin receptor accumulated post-translationally during chronic treatment with tunicamycin and then re-entered the glycosylation pathway when the inhibitor was removed giving rise to a functional insulin receptor.	Tunicamycin	123-134	insulin receptor	Homo sapiens	43-59
6783700-4	1981	In the presence of 5 microgram/ml tunicamycin (Tm), glycosylation of both membrane and secreted IgM is at least 90% inhibited, but total protein synthesis is equivalent in control and Tm-treated cells.	Tunicamycin	34-45	immunoglobulin heavy constant mu	Mus musculus	96-99
6173591-0	1981	Use of tunicamycin to prepare carbohydrate-deficient human immune interferon.	Tunicamycin	7-18	interferon gamma	Homo sapiens	59-76
6269546-0	1981	Glycosylation of cell surface receptors: tunicamycin treatment decreases insulin and growth hormone binding to different levels in cultured lymphocytes.	Tunicamycin	41-52	growth hormone 1	Homo sapiens	85-99
6457668-0	1981	[Tunicamycin inhibition of carbohydrate incorporation into thyroglobulin].	Tunicamycin	1-12	thyroglobulin	Rattus norvegicus	59-72
6457668-2	1981	Tg biosynthesis has been investigated by in vitro experiments, incubating rat thyroid glands with labeled amino-acid and carbohydrate in the presence of tunicamycin, a specific inhibitor of protein glycosylation.	Tunicamycin	153-164	thyroglobulin	Rattus norvegicus	0-2
6457668-3	1981	Tunicamycin inhibit Tg biosynthesis which is impaired in carbohydrate chains addition but slightly in the polypeptide synthesis, as shown by inhibition of 3H-glucosamine incorporation.	Tunicamycin	0-11	thyroglobulin	Rattus norvegicus	20-22
6457668-4	1981	Thus tunicamycin inhibits carbohydrate incorporation into Tg without affecting the polypeptide chain growth and decreases its secretion into the follicles.	Tunicamycin	5-16	thyroglobulin	Rattus norvegicus	58-60
6162638-4	1981	However, ovalbumin, which is transferred across the endoplasmic reticulum in the presence of tunicamycin and which is indistinguishable by immunoprecipitation, by two-dimensional gel electrophoresis and by concanavalin-A--Sepharose binding from the cytosolic form, is still secreted.	Tunicamycin	93-104	ovalbumin (SERPINB14)	Gallus gallus	9-18
7005335-1	1981	The effects of the inhibitor of N-linked glycosylation, tunicamycin, on the synthesis of HLA-A and -B antigens in the human lymphoblastoid cell line JY are described.	Tunicamycin	56-67	major histocompatibility complex, class I, A	Homo sapiens	89-101
7328676-4	1981	Tunicamycin-treated B16-F1 and B16-F10 cells lost their lung colonization abilities when injected intravenously into C57BL/6 mice, concomitant with lowered rates of adhesion to endothelial cell monolayers, endothelial extracellular matrix (basal lamina), and polyvinyl-immobilized fibronectin in vitro, suggesting that this drug inhibits experimental metastasis by modifying the surface glycoproteins involved in determining the adhesive properties of malignant cells.	Tunicamycin	0-11	fibronectin 1	Mus musculus	281-292
7396520-0	1980	Effect of tunicamycin on the glycosylation of rhodopsin.	Tunicamycin	10-21	rhodopsin	Homo sapiens	46-55
6992777-0	1980	Tunicamycin inhibits the differentiation of ST 13 fibroblasts to adipocytes with suppression of the insulin binding activity.	Tunicamycin	0-11	insulin	Homo sapiens	100-107
7354085-0	1980	Effect of tunicamycin on the biosynthesis of the major human red cell sialoglycoprotein, glycophorin A, in the leukemia cell line K562.	Tunicamycin	10-21	glycophorin A (MNS blood group)	Homo sapiens	89-102
7354085-4	1980	The synthesis of the N-glycosidic oligosaccharide of glycophorin A is inhibited by the antibiotic tunicamycin, while the O-glycosidic oligosaccharides are not affected.	Tunicamycin	98-109	glycophorin A (MNS blood group)	Homo sapiens	53-66
198786-6	1977	Analysis of biosynthetically labeled proteins showed that a high-molecular-weight protein, presumed to be related to fibronectin, is markedly reduced in the medium of cells cultured in the presence of tunicamycin.	Tunicamycin	201-212	fibronectin 1	Mus musculus	117-128
209036-3	1978	Tunicamycin inhibited glucosamine incorporation into rat liver transferrin and the apoprotein B chain of chick liver very low density lipoprotein (VLDL) by 75 to 90%.	Tunicamycin	0-11	transferrin	Rattus norvegicus	63-74
209036-3	1978	Tunicamycin inhibited glucosamine incorporation into rat liver transferrin and the apoprotein B chain of chick liver very low density lipoprotein (VLDL) by 75 to 90%.	Tunicamycin	0-11	very low density lipoprotein receptor	Gallus gallus	117-145
209036-3	1978	Tunicamycin inhibited glucosamine incorporation into rat liver transferrin and the apoprotein B chain of chick liver very low density lipoprotein (VLDL) by 75 to 90%.	Tunicamycin	0-11	very low density lipoprotein receptor	Gallus gallus	147-151
386885-4	1978	Loss of cell surface fibronectin as a result of viral transformation, or due to treatment of normal cells with tunicamycin, an inhibitor of protein glycosylation, may contribute to the reduced adhesion and altered morphology observed in these circumstances.	Tunicamycin	111-122	fibronectin 1	Homo sapiens	21-32
20487725-4	1980	The participation of the dolichol pathway in the glycosylation of rhodopsin was demonstrated by the inhibition of core-region glycosylation of this glycoprotein by the antibiotic, tunicamycin.	Tunicamycin	180-191	rhodopsin	Homo sapiens	66-75
118450-10	1979	Gel filtration in Nonidet P-40 of the cell lysates of tunicamycin-treated lymphocytes showed that the nonsecretory 8S IgM contains this second type of mu chains, whereas the IgM molecules of the secretory type contain plasma cell-like mu chains.	Tunicamycin	54-65	immunoglobulin heavy constant mu	Mus musculus	118-121
118450-10	1979	Gel filtration in Nonidet P-40 of the cell lysates of tunicamycin-treated lymphocytes showed that the nonsecretory 8S IgM contains this second type of mu chains, whereas the IgM molecules of the secretory type contain plasma cell-like mu chains.	Tunicamycin	54-65	immunoglobulin heavy constant mu	Mus musculus	174-177
486403-0	1979	N-Acetylglucosamine- 1 -phosphate transferase from hen oviduct: solubilization, characterization, and inhibition by tunicamycin.	Tunicamycin	116-127	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	0-45
448154-2	1979	Tunicamycin greatly inhibited the secretion of nonglycosylated MOPC 315 IgA in trypsin-treated cells.	Tunicamycin	0-11	immunoglobulin heavy constant alpha	Mus musculus	72-75
448154-5	1979	Sodium dodecyl sulfate polyacrylamide gel electrophoresis of 125I-labeled cell surface IgA re-expressed in the presence of tunicamycin revealed a protein with an apparent m.w.	Tunicamycin	123-134	immunoglobulin heavy constant alpha	Mus musculus	87-90
291008-1	1979	We have investigated the role of the carbohydrate moiety in the biological activity of fibronectin in vitro by using tunicamycin to inhibit the glycosylation of this glycoprotein.	Tunicamycin	117-128	fibronectin 1	Gallus gallus	87-98
291008-3	1979	Fibronectin synthesized in the presence of 0.5 microgram of tunicamycin per ml was not glycosylated, as determined by amino sugar analysis, lack of incorporation of [14C]glucosamine and [3H]mannose, and concanavalin A binding studies.	Tunicamycin	60-71	fibronectin 1	Gallus gallus	0-11
315316-4	1979	Furthermore, populations of cytolytic cells which had been pretreated with doses of tunicamycin sufficient to block the incorporation of mannose (or 2-DG) into glycoproteins were still fully susceptible to inhibition by 2-DG.	Tunicamycin	84-95	olfactory receptor family 7 subfamily E member 55 pseudogene	Homo sapiens	146-153
457783-0	1979	Tunicamycin-mediated depletion of insulin receptors in 3T3-L1 adipocytes.	Tunicamycin	0-11	insulin	Homo sapiens	34-41
457783-1	1979	Tunicamycin, an antibiotic that inhibits protein glycosylation, elicited a rapid depletion of insulin binding activity at the surface of 3T3-L1 adipocytes.	Tunicamycin	0-11	insulin	Homo sapiens	94-101
457783-2	1979	Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anti-insulin receptor antibody on hexose uptake and metabolism.	Tunicamycin	76-87	insulin	Homo sapiens	17-24
457783-2	1979	Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anti-insulin receptor antibody on hexose uptake and metabolism.	Tunicamycin	76-87	insulin	Homo sapiens	240-247
457783-2	1979	Disappearance of insulin receptors occurred more rapidly in the presence of tunicamycin than when protein synthesis was inhibited by cycloheximide and was accompanied by a diminution in sensitivity of the adipocytes to the acute effects of insulin and anti-insulin receptor antibody on hexose uptake and metabolism.	Tunicamycin	76-87	insulin	Homo sapiens	240-247
479287-6	1979	We have also examined the fate of PE2 and E1 in cells treated with tunicamycin, an inhibitor of glycosylation.	Tunicamycin	67-78	ETS2 repressor factor	Homo sapiens	34-37
32740777-5	2021	Here, we found that elevated sestrin2 is a protective process in neurons against chemical ER stress induced by tunicamycin (TM) or traumatic invasion, while treatment with PERK inhibitor or knockdown of ATF4 reduces sestrin2 expression upon ER stress.	Tunicamycin	111-122	sestrin 2	Homo sapiens	29-37
791099-7	1976	Tunicamycin also inhibits the apparent formation of proteinase A, whereas it does not affect the increase in the activities of a number of other enzymes.	Tunicamycin	0-11	proteinase A	Saccharomyces cerevisiae S288C	52-64
33964350-6	2021	We showed that tunicamycin (Tm)-activated sXBP1 bound to the TGTCAT domain and suppressed XRCC2 expression.	Tunicamycin	15-26	X-ray repair cross complementing 2	Homo sapiens	90-95
33964350-6	2021	We showed that tunicamycin (Tm)-activated sXBP1 bound to the TGTCAT domain and suppressed XRCC2 expression.	Tunicamycin	28-30	X-ray repair cross complementing 2	Homo sapiens	90-95
32740777-5	2021	Here, we found that elevated sestrin2 is a protective process in neurons against chemical ER stress induced by tunicamycin (TM) or traumatic invasion, while treatment with PERK inhibitor or knockdown of ATF4 reduces sestrin2 expression upon ER stress.	Tunicamycin	124-126	sestrin 2	Homo sapiens	29-37
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
33907834-0	2021	Attenuation of the upregulation of NF-kappaB and AP-1 DNA-binding activities induced by tunicamycin or hypoxia/reoxygenation in neonatal rat cardiomyocytes by SERCA2a overexpression.	Tunicamycin	88-99	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	49-53
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	X-box binding protein 1	Homo sapiens	112-116
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	X-box binding protein 1	Homo sapiens	198-202
33979382-10	2021	Furthermore, UPR upregulation by glucose-regulated protein 78 (GRP78) suppression or low dose tunicamycin alleviated IFNalpha mediated liver injury.	Tunicamycin	94-105	interferon alpha	Mus musculus	117-125
34015469-6	2021	Treatment with ER stressors thapsigargin, tunicamycin, and dithiolthreitol significantly increased PORCN gene expression, while treatment with thapsigargin and dithiolthreitol increased WLS gene expression.	Tunicamycin	42-53	porcupine O-acyltransferase	Homo sapiens	99-104
33738958-6	2021	Tunicamycin-(TM)-loaded transcytosis-targeting-peptide-(TTP)-decorated NPs (TM@TTP) are used to boost BBB transcytosis via inhibiting Mfsd2a.	Tunicamycin	0-11	major facilitator superfamily domain containing 2A	Homo sapiens	134-140
33939297-8	2021	Furthermore, nesfatin-1-mediated protection against H/R injury also vanished in the presence of tunicamycin (TM), an ER stress inducer.	Tunicamycin	96-107	nucleobindin 2	Rattus norvegicus	13-23
33939297-8	2021	Furthermore, nesfatin-1-mediated protection against H/R injury also vanished in the presence of tunicamycin (TM), an ER stress inducer.	Tunicamycin	109-111	nucleobindin 2	Rattus norvegicus	13-23
33840662-11	2021	At the same time, lipid accumulation was observed in the Sepp1 high expression cells induced by endoplasmic reticulum (ER) activator tunicamycin (Tm).	Tunicamycin	133-144	selenoprotein P	Homo sapiens	57-62
33666503-3	2021	Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively.	Tunicamycin	160-171	fatty acyl CoA reductase 1	Rattus norvegicus	53-79
33666503-3	2021	Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively.	Tunicamycin	160-171	fatty acyl CoA reductase 1	Rattus norvegicus	81-85
33666503-3	2021	Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively.	Tunicamycin	173-175	fatty acyl CoA reductase 1	Rattus norvegicus	53-79
33666503-3	2021	Surprisingly, we found that the peroxisomal protein, fatty acyl-CoA reductase 1 (FAR1), was upregulated by chemical and pathophysiological ER stress induced by tunicamycin (TM) and simulated ischemia/reperfusion (sI/R), respectively.	Tunicamycin	173-175	fatty acyl CoA reductase 1	Rattus norvegicus	81-85
33840662-11	2021	At the same time, lipid accumulation was observed in the Sepp1 high expression cells induced by endoplasmic reticulum (ER) activator tunicamycin (Tm).	Tunicamycin	146-148	selenoprotein P	Homo sapiens	57-62
33846370-5	2021	We modulated PERK expression using a plasmid, tunicamycin and siRNA against PERK, and then confirmed the target gene expression with real-time PCR and Northern blotting.	Tunicamycin	46-57	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	13-17
33908217-12	2021	T-6 cells transfected with miR-125b mimic and treated with Tunicamycin caused decrease in levels of cleaved caspase-3, sXBP1, CHOP, and LC3.	Tunicamycin	59-70	caspase 3	Rattus norvegicus	108-117
33908217-12	2021	T-6 cells transfected with miR-125b mimic and treated with Tunicamycin caused decrease in levels of cleaved caspase-3, sXBP1, CHOP, and LC3.	Tunicamycin	59-70	DNA-damage inducible transcript 3	Rattus norvegicus	126-130
33908217-12	2021	T-6 cells transfected with miR-125b mimic and treated with Tunicamycin caused decrease in levels of cleaved caspase-3, sXBP1, CHOP, and LC3.	Tunicamycin	59-70	annexin A3	Rattus norvegicus	136-139
33931075-16	2021	Importantly, both attenuation of glycosylation using tunicamycin and inhibition of TGFBR2 using LY2109761 differentially abrogated the stimulatory effect of ALG3 overexpression on cancer stemness and radioresistance.	Tunicamycin	53-64	ALG3 alpha-1,3- mannosyltransferase	Homo sapiens	157-161
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	solute carrier family 5 member 5	Rattus norvegicus	147-170
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	solute carrier family 5 member 5	Rattus norvegicus	172-175
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	thyroid peroxidase	Rattus norvegicus	198-201
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	thyroglobulin	Rattus norvegicus	207-220
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	thyroid stimulating hormone receptor	Rattus norvegicus	256-276
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	thyroid stimulating hormone receptor	Rattus norvegicus	278-282
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	transcription termination factor 1	Rattus norvegicus	317-322
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	transcription termination factor 2	Rattus norvegicus	357-362
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	paired box 8	Rattus norvegicus	368-385
33922129-1	2021	Recently, ER stress induced by tunicamycin (TM) was reported to inhibit the expression of key genes involved in thyroid hormone synthesis, such as sodium/iodide symporter (NIS), thyroid peroxidase (TPO) and thyroglobulin (TG), and their regulators such as thyrotropin receptor (TSHR), thyroid transcription factor-1 (TTF-1), thyroid transcription factor-2 (TTF-2) and paired box gene 8 (PAX-8), in FRTL-5 thyrocytes.	Tunicamycin	31-42	paired box 8	Rattus norvegicus	387-392
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	118-154
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	156-161
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	DNA-damage inducible transcript 3	Rattus norvegicus	167-200
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	DNA-damage inducible transcript 3	Rattus norvegicus	202-207
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	solute carrier family 5 member 5	Rattus norvegicus	223-226
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	thyroid peroxidase	Rattus norvegicus	228-231
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	thyroid stimulating hormone receptor	Rattus norvegicus	237-241
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	transcription termination factor 1	Rattus norvegicus	243-248
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	transcription termination factor 2	Rattus norvegicus	250-255
33922129-3	2021	While treatment of FRTL-5 cells with TM alone (0.1 microg/mL) for 48 h strongly induced the ER stress-sensitive genes heat shock protein family A member 5 (HSPA5) and DNA damage inducible transcript 3 (DDIT3) and repressed NIS, TPO, TG, TSHR, TTF-1, TTF-2 and PAX-8, combined treatment with TM (0.1 microg/mL) and RSV (10 microM) for 48 h attenuated this effect of TM.	Tunicamycin	37-39	paired box 8	Rattus norvegicus	260-265
33717236-6	2021	It was subsequently demonstrated that IL-1beta induced A549 cell autophagy, while tunicamycin-induced autophagy increased the IL-1beta expression level and weakened paclitaxel sensitivity.	Tunicamycin	82-93	interleukin 1 alpha	Homo sapiens	126-134
33392644-6	2021	Inhibition of the N-glycosylation with tunicamycin caused a significant increase of NaV1.5 channel current (INa) when applied for 24 h. Tunicamycin shifted the steady-state inactivation curve to the hyperpolarization direction, whereas the activation curve was unaffected.	Tunicamycin	39-50	sodium voltage-gated channel alpha subunit 5	Homo sapiens	84-90
33392644-6	2021	Inhibition of the N-glycosylation with tunicamycin caused a significant increase of NaV1.5 channel current (INa) when applied for 24 h. Tunicamycin shifted the steady-state inactivation curve to the hyperpolarization direction, whereas the activation curve was unaffected.	Tunicamycin	136-147	sodium voltage-gated channel alpha subunit 5	Homo sapiens	84-90
33916165-7	2021	Treatment with tunicamycin or thapsigargin, which induces ER stress, increases HTRA1 expression.	Tunicamycin	15-26	HtrA serine peptidase 1	Homo sapiens	79-84
33714955-6	2021	Furthermore, we found that ATF4 inhibition reduced tunicamycin-induced caspase-3 activation, ROS production, ELAM-1 expression, and HTMCs phagocytosis impairment.	Tunicamycin	51-62	activating transcription factor 4	Homo sapiens	27-31
33714955-6	2021	Furthermore, we found that ATF4 inhibition reduced tunicamycin-induced caspase-3 activation, ROS production, ELAM-1 expression, and HTMCs phagocytosis impairment.	Tunicamycin	51-62	caspase 3	Homo sapiens	71-80
33714955-6	2021	Furthermore, we found that ATF4 inhibition reduced tunicamycin-induced caspase-3 activation, ROS production, ELAM-1 expression, and HTMCs phagocytosis impairment.	Tunicamycin	51-62	selectin E	Homo sapiens	109-115
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	181-185
33609179-7	2021	Two common ERS stimulators, tunicamycin (Tm) and dithiothreitol (DTT) blocked the ameliorative effect of apelin on AHF.	Tunicamycin	28-39	APLN	Oryctolagus cuniculus	105-111
33609179-7	2021	Two common ERS stimulators, tunicamycin (Tm) and dithiothreitol (DTT) blocked the ameliorative effect of apelin on AHF.	Tunicamycin	41-43	APLN	Oryctolagus cuniculus	105-111
33603856-8	2021	TM injection significantly increased BiP expression and modified the topographic expression patterns of the UPR signaling proteins.	Tunicamycin	0-2	heat shock protein 5	Mus musculus	37-40
33603856-9	2021	In addition, immunohistochemical analysis of Beclin1 revealed an increased pericentral staining intensity following TM pretreatment.	Tunicamycin	116-118	beclin 1, autophagy related	Mus musculus	45-52
33507306-5	2021	We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs).	Tunicamycin	14-25	nuclear factor kappa B subunit 1	Homo sapiens	54-63
33507306-5	2021	We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs).	Tunicamycin	14-25	interleukin 6	Homo sapiens	106-110
33507306-5	2021	We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs).	Tunicamycin	14-25	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	115-119
33507306-5	2021	We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs).	Tunicamycin	14-25	tumor necrosis factor	Homo sapiens	135-144
33507306-5	2021	We found that tunicamycin-induced ER stress inhibited NF-kappaB activation and pro-inflammatory cytokine (IL-6 and COX2) production in TNF-alpha- or IL-1beta-treated normal endometrial stromal cells (NECSs).	Tunicamycin	14-25	interleukin 1 alpha	Homo sapiens	149-157
33507306-6	2021	Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta.	Tunicamycin	0-11	immunoglobulin kappa variable 1-27	Homo sapiens	40-43
33507306-6	2021	Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta.	Tunicamycin	0-11	CCAAT enhancer binding protein alpha	Homo sapiens	48-57
33507306-6	2021	Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta.	Tunicamycin	0-11	nuclear factor kappa B subunit 1	Homo sapiens	92-101
33507306-6	2021	Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta.	Tunicamycin	0-11	nuclear factor kappa B subunit 1	Homo sapiens	131-140
33507306-6	2021	Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta.	Tunicamycin	0-11	tumor necrosis factor	Homo sapiens	174-183
33507306-6	2021	Tunicamycin increased the expression of A20 and C/EBPbeta, which are negative regulators of NF-kappaB, and this increase inhibited NF-kappaB activity in NESCs incubated with TNF-alpha- or IL-1beta.	Tunicamycin	0-11	interleukin 1 alpha	Homo sapiens	188-196
33507306-9	2021	In contrast, upregulation of ER stress by tunicamycin significantly reduced IL-6 and COX2 production by inhibiting NF-kappaB activity in ECSCs.	Tunicamycin	42-53	interleukin 6	Homo sapiens	76-80
33507306-9	2021	In contrast, upregulation of ER stress by tunicamycin significantly reduced IL-6 and COX2 production by inhibiting NF-kappaB activity in ECSCs.	Tunicamycin	42-53	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	85-89
33507306-9	2021	In contrast, upregulation of ER stress by tunicamycin significantly reduced IL-6 and COX2 production by inhibiting NF-kappaB activity in ECSCs.	Tunicamycin	42-53	nuclear factor kappa B subunit 1	Homo sapiens	115-124
33655503-6	2021	Treatment with PNGase F and tunicamycin resulted in a reduction in both two-protein species, ~43 kDa and~85 kDa in size, by 2-4 kDa.	Tunicamycin	28-39	N-glycanase 1	Homo sapiens	15-21
33279504-8	2021	ERS stimulator (tunicamycin or DTT) blocked the beneficial effect of apelin.	Tunicamycin	16-27	apelin	Rattus norvegicus	69-75
33422538-3	2021	In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus.	Tunicamycin	22-33	mitogen activated protein kinase 3	Rattus norvegicus	198-204
33422538-3	2021	In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus.	Tunicamycin	22-33	cyclin-dependent kinase 5	Rattus norvegicus	210-235
33422538-3	2021	In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus.	Tunicamycin	22-33	cyclin-dependent kinase 5	Rattus norvegicus	237-241
33422538-3	2021	In the present study, tunicamycin-induced ER stress resulted in reactive astrogliosis-like events showing astroglial hypertrophy with the elevated extracellular signal-activated protein kinase 1/2 (ERK1/2) and cyclin-dependent kinase 5 (CDK5) phosphorylations in the CA1 region of the rat hippocampus.	Tunicamycin	22-33	carbonic anhydrase 1	Rattus norvegicus	267-270
33422538-4	2021	However, tunicamycin increased CDK5, but not ERK1/2, phosphorylation in the molecular layer of the dentate gyrus.	Tunicamycin	9-20	cyclin-dependent kinase 5	Rattus norvegicus	31-35
33422538-5	2021	Roscovitine (a CDK5 inhibitor) suppressed the effect of tunicamycin in the molecular layer of the dentate gyrus and the CA1 region, while U0126 (an ERK1/2 inhibitor) reversed it in the CA1 region.	Tunicamycin	56-67	cyclin-dependent kinase 5	Rattus norvegicus	15-19
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	eukaryotic translation initiation factor 2A	Homo sapiens	186-195
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	activating transcription factor 4	Homo sapiens	196-200
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
33413231-8	2021	Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment.	Tunicamycin	129-140	epiregulin	Homo sapiens	43-45
33127435-12	2021	In conclusion, TGF-beta1 partially protects CF apoptosis induced by sI/R or Tn, through a mechanism that would involve ER stress.	Tunicamycin	76-78	transforming growth factor, beta 1	Rattus norvegicus	15-24
33300079-13	2021	In addition, miR-6324 mimic partially reversed the effects of Dancr overexpression on Tm-induced apoptosis, ERS and autophagy.	Tunicamycin	86-88	microRNA 6324	Rattus norvegicus	13-21
33300079-13	2021	In addition, miR-6324 mimic partially reversed the effects of Dancr overexpression on Tm-induced apoptosis, ERS and autophagy.	Tunicamycin	86-88	differentiation antagonizing non-protein coding RNA	Rattus norvegicus	62-67
33413231-8	2021	Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment.	Tunicamycin	129-140	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	72-76
33413231-8	2021	Moreover, the data indicated that both the ER-resident and the secreted AGR2 enhance the survival capacity of PANC-1 cells after tunicamycin-induced ER stress and gemcitabine treatment.	Tunicamycin	129-140	epiregulin	Homo sapiens	149-151
33430288-5	2021	Tunicamycin-administered mice developed hyperinsulinemia, augmented lipolysis and increased circulating leptin and adiponectin.	Tunicamycin	0-11	leptin	Mus musculus	104-110
33430288-5	2021	Tunicamycin-administered mice developed hyperinsulinemia, augmented lipolysis and increased circulating leptin and adiponectin.	Tunicamycin	0-11	adiponectin, C1Q and collagen domain containing	Mus musculus	115-126
33430288-6	2021	Renal unfolded protein response (UPR) gene expression markers, the lipogenic transcription factor SREBP1 and the phosphorylation of eIF2alpha increased 8 h after tunicamycin administration.	Tunicamycin	162-173	sterol regulatory element binding transcription factor 1	Mus musculus	98-104
33430288-6	2021	Renal unfolded protein response (UPR) gene expression markers, the lipogenic transcription factor SREBP1 and the phosphorylation of eIF2alpha increased 8 h after tunicamycin administration.	Tunicamycin	162-173	eukaryotic translation initiation factor 2A	Mus musculus	132-141
33354279-9	2020	Notably, activating ER stress with tunicamycin (TM) reduced therapeutic effects of FGF10-PLGA microspheres in wound healing, whereas inhibition of ER stress with 4-phenyl butyric acid (4-PBA) improved the function of FGF10-PLGA microspheres.	Tunicamycin	35-46	fibroblast growth factor 10	Homo sapiens	83-88
33111200-9	2021	As a negative control, we have also analyzed the DEGs following treatment with an endoplasmic reticulum (ER) stress-inducing agent, tunicamycin, which was affected by BMAL1 deletion minimally.	Tunicamycin	132-143	aryl hydrocarbon receptor nuclear translocator like	Homo sapiens	167-172
33249722-10	2021	Further in vitro assays revealed that ATF4-OA-Exo promoted chondrocyte autophagy and inhibited chondrocyte apoptosis in the TNF-alpha- or tunicamycin-treated chondrocytes.	Tunicamycin	138-149	activating transcription factor 4	Mus musculus	38-42
33249722-10	2021	Further in vitro assays revealed that ATF4-OA-Exo promoted chondrocyte autophagy and inhibited chondrocyte apoptosis in the TNF-alpha- or tunicamycin-treated chondrocytes.	Tunicamycin	138-149	5'-3' exoribonuclease 1	Mus musculus	46-49
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
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	X-box binding protein 1	Homo sapiens	94-99
33296727-8	2021	Moreover, using an animal model of ER-stress-induced neurodegeneration, we demonstrated that MANF deficiency potentiated tunicamycin (TM)-induced ER stress and neurodegeneration.	Tunicamycin	121-132	mesencephalic astrocyte-derived neurotrophic factor	Mus musculus	93-97
33296727-8	2021	Moreover, using an animal model of ER-stress-induced neurodegeneration, we demonstrated that MANF deficiency potentiated tunicamycin (TM)-induced ER stress and neurodegeneration.	Tunicamycin	134-136	mesencephalic astrocyte-derived neurotrophic factor	Mus musculus	93-97
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	reticulon 4	Mus musculus	65-71
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	DNA-damage inducible transcript 3	Mus musculus	152-156
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	interleukin 6	Mus musculus	158-162
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	tumor necrosis factor	Mus musculus	167-176
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	reticulon 4	Mus musculus	65-69
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	DNA-damage inducible transcript 3	Mus musculus	249-253
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	interleukin 6	Mus musculus	255-259
33572505-10	2021	In addition, mice experiments data revealed that upregulation of Nogo-A in notexin- and tunicamycin-treated muscles was associated with upregulation of CHOP, IL-6 and TNF-alpha in WT group, while in Nogo-KO group resulted in low expression level of CHOP, IL-6 and TNF-alpha.	Tunicamycin	88-99	tumor necrosis factor	Mus musculus	264-273
33430442-7	2021	We also studied the replication of gt1 HEV in the ORF4-expressing tunicamycin-treated cell line.	Tunicamycin	66-77	cortactin binding protein 2	Homo sapiens	50-54
33272572-2	2021	In comparison to their normal counterparts, Optn-deficient mouse embryonic fibroblasts showed significantly higher cell death and caspase-3 activation upon treatment with tunicamycin and thapsigargin, inducers of ER stress.	Tunicamycin	171-182	caspase 3	Mus musculus	130-139
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	188-199	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	60-64
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	188-199	X-box binding protein 1	Mus musculus	65-69
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	188-199	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	74-78
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	188-199	activating transcription factor 4	Mus musculus	79-83
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	243-254	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	60-64
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	243-254	X-box binding protein 1	Mus musculus	65-69
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	243-254	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	74-78
33272572-3	2021	The transcript levels of some of the genes regulated by the IRE1-XBP1 and PERK-ATF4 pathways were upregulated in Optn-deficient cells, in comparison with normal cells, upon treatment with tunicamycin, and also in the brain cortex and liver of tunicamycin treated Optn-deficient mice.	Tunicamycin	243-254	activating transcription factor 4	Mus musculus	79-83
33354279-9	2020	Notably, activating ER stress with tunicamycin (TM) reduced therapeutic effects of FGF10-PLGA microspheres in wound healing, whereas inhibition of ER stress with 4-phenyl butyric acid (4-PBA) improved the function of FGF10-PLGA microspheres.	Tunicamycin	48-50	fibroblast growth factor 10	Homo sapiens	83-88
32888957-15	2020	Tunicamycin promoted OGD/R-induced decrease in cell viability and reversed NOD1 silencing-induced increase in cell viability.	Tunicamycin	0-11	nucleotide-binding oligomerization domain containing 1	Rattus norvegicus	75-79
32888957-16	2020	Tunicamycin also enhanced OGD/R-induced autophagy and reversed NOD1 silencing-induced inhibition in autophagy.	Tunicamycin	0-11	nucleotide-binding oligomerization domain containing 1	Rattus norvegicus	63-67
33045248-4	2020	We showed that deletion of MED2 leads to sensitivity to the ER stress inducer tunicamycin (TM) as well as a shortened replicative lifespan (RLS), accompanied by increased intracellular ROS levels and hyperpolarization of mitochondria.	Tunicamycin	78-89	Med2p	Saccharomyces cerevisiae S288C	27-31
32878739-11	2020	In CHO HcD6 cells treated with tunicamycin, the expression level of pdia4 was significantly increased.	Tunicamycin	31-42	protein disulfide-isomerase A4	Cricetulus griseus	68-73
33097029-2	2020	Our previous studies found that bleomycin and tunicamycin could induce ER stress and consequently trigger EMT accompanying with IL-32 overexpression.	Tunicamycin	46-57	interleukin 32	Homo sapiens	128-133
33164499-4	2020	The antibiotic compound tunicamycin is a natural product inhibitor of MraY that is also toxic to eukaryotes through its binding to GPT.	Tunicamycin	24-35	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	131-134
33298866-10	2020	In GECs incubated with tunicamycin, deletion of IRE1alpha attenuated upregulation of ER chaperones, LC3 lipidation, and LC3 transcription, compared with control GECs.	Tunicamycin	23-34	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	48-57
32996649-10	2020	Deglycosylation of CREBH induced by Tm could inhibit the proteolysis of CREBH induced by PA.	Tunicamycin	36-38	cAMP responsive element binding protein 3-like 3	Mus musculus	19-24
32996649-10	2020	Deglycosylation of CREBH induced by Tm could inhibit the proteolysis of CREBH induced by PA.	Tunicamycin	36-38	cAMP responsive element binding protein 3-like 3	Mus musculus	72-77
32996245-8	2020	Salubrinal restored the tunicamycin-induced decrease in the viability of primary calvarial osteoblasts and increased the expression of Runx2 and ALP, and decreased p-eIF2alpha/eIF2alpha in a dose-dependent manner.	Tunicamycin	24-35	RUNX family transcription factor 2	Rattus norvegicus	135-140
32996245-8	2020	Salubrinal restored the tunicamycin-induced decrease in the viability of primary calvarial osteoblasts and increased the expression of Runx2 and ALP, and decreased p-eIF2alpha/eIF2alpha in a dose-dependent manner.	Tunicamycin	24-35	eukaryotic translation initiation factor 2A	Rattus norvegicus	166-175
32996245-8	2020	Salubrinal restored the tunicamycin-induced decrease in the viability of primary calvarial osteoblasts and increased the expression of Runx2 and ALP, and decreased p-eIF2alpha/eIF2alpha in a dose-dependent manner.	Tunicamycin	24-35	eukaryotic translation initiation factor 2A	Rattus norvegicus	176-185
32607937-6	2020	We find that exposure of neural and endocrine cells to the cell stressors tunicamycin and thapsigargin increases cellular proSAAS mRNA and protein in Neuro2A cells.	Tunicamycin	74-85	proprotein convertase subtilisin/kexin type 1 inhibitor	Mus musculus	122-129
33050595-4	2020	Therefore, in this study, we aimed to explore the relationship between ER stress induced by tunicamycin and LXRalpha in hepatocytes and macrophages and clarify their possible mechanisms and roles in AS.	Tunicamycin	92-103	nuclear receptor subfamily 1 group H member 3	Homo sapiens	108-116
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	157-168	mitofusin 2	Homo sapiens	13-17
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	157-168	epiregulin	Homo sapiens	65-67
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	157-168	epiregulin	Homo sapiens	90-92
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	157-168	epiregulin	Homo sapiens	90-92
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	170-172	mitofusin 2	Homo sapiens	13-17
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	170-172	epiregulin	Homo sapiens	65-67
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	170-172	epiregulin	Homo sapiens	90-92
33149811-6	2020	Silencing of Mfn2 in HL-1 cells decreased the Ca2+ transfer from ER to mitochondria under ER stress conditions, which were induced by the ER stress agonist, tunicamycin (TM).	Tunicamycin	170-172	epiregulin	Homo sapiens	90-92
33149811-8	2020	Mfn2 silencing attenuated mitochondrial oxidative stress and Ca2+ overload, increased mitochondrial membrane potential and mitochondrial oxygen consumption, and protected cells from TM-induced apoptosis.	Tunicamycin	182-184	mitofusin 2	Homo sapiens	0-4
32981418-3	2021	We demonstrate that downregulation of RNF-5 decreased sensitivity to tunicamycin both in wild type and in an ire-1 mutant.	Tunicamycin	69-80	E3 ubiquitin ligase rnf-5;RING finger protein 5;RING-type domain-containing protein	Caenorhabditis elegans	38-43
32981418-3	2021	We demonstrate that downregulation of RNF-5 decreased sensitivity to tunicamycin both in wild type and in an ire-1 mutant.	Tunicamycin	69-80	Endoribonuclease;Serine/threonine-protein kinase	Caenorhabditis elegans	109-114
33050595-6	2020	Tunicamycin-induced ER stress caused liver injury; promoted the accumulation of cholesterol and triglycerides; inhibited the expression of LXRalpha, ABCA1 and ABCG1 in the livers of mice, thus reducing serum high-density lipoprotein (HDL)-C, low-density lipoprotein (LDL)-C, total cholesterol and triglyceride levels; however, LXR-623 could attenuate ER stress and reverse these changes.	Tunicamycin	0-11	nuclear receptor subfamily 1, group H, member 3	Mus musculus	139-147
33050595-6	2020	Tunicamycin-induced ER stress caused liver injury; promoted the accumulation of cholesterol and triglycerides; inhibited the expression of LXRalpha, ABCA1 and ABCG1 in the livers of mice, thus reducing serum high-density lipoprotein (HDL)-C, low-density lipoprotein (LDL)-C, total cholesterol and triglyceride levels; however, LXR-623 could attenuate ER stress and reverse these changes.	Tunicamycin	0-11	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	149-154
33050595-6	2020	Tunicamycin-induced ER stress caused liver injury; promoted the accumulation of cholesterol and triglycerides; inhibited the expression of LXRalpha, ABCA1 and ABCG1 in the livers of mice, thus reducing serum high-density lipoprotein (HDL)-C, low-density lipoprotein (LDL)-C, total cholesterol and triglyceride levels; however, LXR-623 could attenuate ER stress and reverse these changes.	Tunicamycin	0-11	ATP binding cassette subfamily G member 1	Mus musculus	159-164
33050595-8	2020	ER stress induced by tunicamycin could clearly be reversed by activating LXRalpha because it promoted cholesterol efflux by enhancing the expression of ABCA1 and ABCG1 in hepatocytes and macrophages, contributing to attenuation of the development of AS.	Tunicamycin	21-32	nuclear receptor subfamily 1 group H member 3	Homo sapiens	73-81
33050595-8	2020	ER stress induced by tunicamycin could clearly be reversed by activating LXRalpha because it promoted cholesterol efflux by enhancing the expression of ABCA1 and ABCG1 in hepatocytes and macrophages, contributing to attenuation of the development of AS.	Tunicamycin	21-32	ATP binding cassette subfamily A member 1	Homo sapiens	152-157
33050595-8	2020	ER stress induced by tunicamycin could clearly be reversed by activating LXRalpha because it promoted cholesterol efflux by enhancing the expression of ABCA1 and ABCG1 in hepatocytes and macrophages, contributing to attenuation of the development of AS.	Tunicamycin	21-32	ATP binding cassette subfamily G member 1	Homo sapiens	162-167
32039481-8	2020	The UPR activators dithiothreitol (DTT) and tunicamycin (TN) activated the UPR and reduced MYOCD along with SMC markers in vitro.	Tunicamycin	44-55	myocardin	Homo sapiens	91-96
33014334-0	2020	Tunicamycin promotes metastasis through upregulating endoplasmic reticulum stress induced GRP78 expression in thyroid carcinoma.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	90-95
33014334-8	2020	In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells.	Tunicamycin	13-24	heat shock protein family A (Hsp70) member 5	Homo sapiens	74-79
33014334-8	2020	In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells.	Tunicamycin	13-24	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	81-85
33014334-8	2020	In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells.	Tunicamycin	13-24	X-box binding protein 1	Homo sapiens	90-94
33014334-8	2020	In addition, tunicamycin-induced ER stress up-regulated the expression of GRP78, PERK and XBP1 as well as reversed the metastatic ability of GRP78 in ATC cells.	Tunicamycin	13-24	heat shock protein family A (Hsp70) member 5	Homo sapiens	141-146
32780887-3	2020	Here, we present data showing the b-ZIP transcription factor E4BP4 in both the hepatocytes and the mouse liver is potently induced by the chemical ER stress inducer tunicamycin or by high-fat, low-methionine, and choline-deficient (HFLMCD) diet.	Tunicamycin	165-176	nuclear factor, interleukin 3, regulated	Mus musculus	61-66
32780887-5	2020	Tunicamycin promotes the lipid droplet formation and alters lipid metabolic gene expression in primary mouse hepatocytes from E4bp4flox/flox but not E4bp4 liver-specific KO (E4bp4-LKO) mice.	Tunicamycin	0-11	nuclear factor, interleukin 3, regulated	Mus musculus	126-131
32673694-11	2020	Knockdown or chemical inhibition of CSNK2B and ACSL1 in Caco-2 cells reduced activity of the ATF6-dependent ERSE reporter gene, diminished transcription of the ATF6 target genes HSP90B1 and HSPA5 and reduced NF-kappaB reporter gene activation upon tunicamycin stimulation.	Tunicamycin	248-259	casein kinase 2 beta	Homo sapiens	36-42
32673694-11	2020	Knockdown or chemical inhibition of CSNK2B and ACSL1 in Caco-2 cells reduced activity of the ATF6-dependent ERSE reporter gene, diminished transcription of the ATF6 target genes HSP90B1 and HSPA5 and reduced NF-kappaB reporter gene activation upon tunicamycin stimulation.	Tunicamycin	248-259	acyl-CoA synthetase long chain family member 1	Homo sapiens	47-52
32673694-11	2020	Knockdown or chemical inhibition of CSNK2B and ACSL1 in Caco-2 cells reduced activity of the ATF6-dependent ERSE reporter gene, diminished transcription of the ATF6 target genes HSP90B1 and HSPA5 and reduced NF-kappaB reporter gene activation upon tunicamycin stimulation.	Tunicamycin	248-259	activating transcription factor 6	Homo sapiens	93-97
32673694-13	2020	Inhibitors of ACSL1 or CSNK2B prevented activation of ATF6 and reduced CXCL1 and TNF expression in these organoids upon induction of ER stress with tunicamycin.	Tunicamycin	148-159	acyl-CoA synthetase long chain family member 1	Homo sapiens	14-19
32673694-13	2020	Inhibitors of ACSL1 or CSNK2B prevented activation of ATF6 and reduced CXCL1 and TNF expression in these organoids upon induction of ER stress with tunicamycin.	Tunicamycin	148-159	casein kinase 2 beta	Homo sapiens	23-29
32673694-13	2020	Inhibitors of ACSL1 or CSNK2B prevented activation of ATF6 and reduced CXCL1 and TNF expression in these organoids upon induction of ER stress with tunicamycin.	Tunicamycin	148-159	activating transcription factor 6	Homo sapiens	54-58
32673694-14	2020	Injection of mice with inhibitors of ACSL1 or CSNK2B significantly reduced tunicamycin-mediated intestinal inflammation and IEC death and expression of CXCL1 and TNF in Atg16l1DeltaIEC mice.	Tunicamycin	75-86	acyl-CoA synthetase long-chain family member 1	Mus musculus	37-42
32673694-14	2020	Injection of mice with inhibitors of ACSL1 or CSNK2B significantly reduced tunicamycin-mediated intestinal inflammation and IEC death and expression of CXCL1 and TNF in Atg16l1DeltaIEC mice.	Tunicamycin	75-86	casein kinase 2, beta polypeptide	Mus musculus	46-52
32592208-9	2020	Our study revealed that the tunicamycin-induced persistent UPR expression led to apoptosis of chondrocytes and activation of autophagy incorporation with GRP78.	Tunicamycin	28-39	heat shock protein family A (Hsp70) member 5	Homo sapiens	154-159
32039481-8	2020	The UPR activators dithiothreitol (DTT) and tunicamycin (TN) activated the UPR and reduced MYOCD along with SMC markers in vitro.	Tunicamycin	57-59	myocardin	Homo sapiens	91-96
32039481-9	2020	The IRE1alpha inhibitor 4mu8C counteracted the effect of DTT and TN on SMC markers and MYOCD expression.	Tunicamycin	65-67	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	4-29
32039481-9	2020	The IRE1alpha inhibitor 4mu8C counteracted the effect of DTT and TN on SMC markers and MYOCD expression.	Tunicamycin	65-67	myocardin	Homo sapiens	87-92
32039481-11	2020	MRTFs also antagonized the UPR as indicated by reduced TN and DTT-mediated induction of CRELD2, MANF, PDIA4, and SDF2L1 following overexpression of MRTFs.	Tunicamycin	55-57	protein disulfide isomerase family A member 4	Homo sapiens	102-107
32039481-11	2020	MRTFs also antagonized the UPR as indicated by reduced TN and DTT-mediated induction of CRELD2, MANF, PDIA4, and SDF2L1 following overexpression of MRTFs.	Tunicamycin	55-57	stromal cell derived factor 2 like 1	Homo sapiens	113-119
32402213-6	2020	In contrast, structure-function experiments demonstrated that IL-13 binding to IL-13Ralpha2 was dependent on each of the four sites of N-glycosylation in IL-13Ralpha2, and experiments with tunicamycin and PNGase F demonstrated that IL-13-IL-13Ralpha2 binding was decreased when IL-13Ralpha2 N-glycosylation was diminished.	Tunicamycin	189-200	interleukin 13	Homo sapiens	62-67
32836022-7	2020	This stress up-regulated the expression of five glutamate decarboxylase (GAD) genes except GAD2 and GABA content of A. thaliana plants increased with an increasing concentration of tunicamycin (0.1 mug ml-1 and 0.25 mug ml-1).	Tunicamycin	181-192	glutamate decarboxylase	Arabidopsis thaliana	48-71
32836022-7	2020	This stress up-regulated the expression of five glutamate decarboxylase (GAD) genes except GAD2 and GABA content of A. thaliana plants increased with an increasing concentration of tunicamycin (0.1 mug ml-1 and 0.25 mug ml-1).	Tunicamycin	181-192	glutamate decarboxylase	Arabidopsis thaliana	73-76
32836022-7	2020	This stress up-regulated the expression of five glutamate decarboxylase (GAD) genes except GAD2 and GABA content of A. thaliana plants increased with an increasing concentration of tunicamycin (0.1 mug ml-1 and 0.25 mug ml-1).	Tunicamycin	181-192	glutamate decarboxylase 2	Arabidopsis thaliana	91-95
32962446-7	2021	Our findings suggest that short term TN treatment did not affect leukocyte movement to lymphoid compartments of the small intestine, but it altered villus architecture due to decreased PECAM-1 expression.	Tunicamycin	37-39	platelet and endothelial cell adhesion molecule 1	Homo sapiens	185-192
32910713-6	2021	When compared to wild-type CH12 cells, tfg KO CH12 cells were more sensitive towards ER stress induced by tunicamycin, monensin and proteasome inhibition or by expression of an ER-bound immunoglobulin (Ig) mu heavy (microH) chain.	Tunicamycin	106-117	Trk-fused gene	Mus musculus	39-42
32910713-9	2021	The GFP:RFP ratio of tandem-fluorescent-LC3 was higher in tunicamycin-treated CH12 tfg KO B cells, suggesting less autophagy flux during induced ER stress.	Tunicamycin	58-69	tripartite motif-containing 27	Mus musculus	8-11
32910713-9	2021	The GFP:RFP ratio of tandem-fluorescent-LC3 was higher in tunicamycin-treated CH12 tfg KO B cells, suggesting less autophagy flux during induced ER stress.	Tunicamycin	58-69	Trk-fused gene	Mus musculus	83-86
32973403-8	2020	Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha.	Tunicamycin	118-129	centromere protein F	Homo sapiens	9-14
32973403-8	2020	Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha.	Tunicamycin	118-129	centromere protein F	Homo sapiens	162-167
32973403-8	2020	Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha.	Tunicamycin	131-133	centromere protein F	Homo sapiens	9-14
32973403-8	2020	Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha.	Tunicamycin	131-133	centromere protein F	Homo sapiens	162-167
32973403-8	2020	Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha.	Tunicamycin	131-133	X-box binding protein 1	Homo sapiens	196-200
32973403-8	2020	Results: CENPF expression is dramatically reduced under ER stress induced by thapsigargin (TG), brefeldin A (BFA), or tunicamycin (TM) and this downregulation of CENPF expression was dependent on XBP1 and ATF6alpha.	Tunicamycin	131-133	activating transcription factor 6	Homo sapiens	205-214
32945983-13	2021	More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group.	Tunicamycin	54-65	family with sequence similarity 172 member A	Homo sapiens	33-40
32945983-13	2021	More importantly, the binding of FAM172A and eIF2a in tunicamycin-treated group increased significantly compared with the control group.	Tunicamycin	54-65	eukaryotic translation initiation factor 2 subunit alpha	Homo sapiens	45-50
33209200-4	2020	The results showed that tunicamycin (TM) induced downregulation of miR-637 in gastric cancer cells (AGS) and increase of apoptosis and ER stress.	Tunicamycin	24-35	microRNA 637	Homo sapiens	67-74
33209200-4	2020	The results showed that tunicamycin (TM) induced downregulation of miR-637 in gastric cancer cells (AGS) and increase of apoptosis and ER stress.	Tunicamycin	37-39	microRNA 637	Homo sapiens	67-74
33209200-7	2020	The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells.	Tunicamycin	138-140	microRNA 637	Homo sapiens	23-30
33209200-7	2020	The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells.	Tunicamycin	138-140	calreticulin	Homo sapiens	35-39
33209200-7	2020	The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells.	Tunicamycin	138-140	calreticulin	Homo sapiens	64-68
33209200-7	2020	The co-transfection of miR-637 and CALR in AGS cells show that, CALR overexpression could reverse the pro-apoptosis effects of miR-637 in TM-treated cells.	Tunicamycin	138-140	microRNA 637	Homo sapiens	127-134
32402213-6	2020	In contrast, structure-function experiments demonstrated that IL-13 binding to IL-13Ralpha2 was dependent on each of the four sites of N-glycosylation in IL-13Ralpha2, and experiments with tunicamycin and PNGase F demonstrated that IL-13-IL-13Ralpha2 binding was decreased when IL-13Ralpha2 N-glycosylation was diminished.	Tunicamycin	189-200	interleukin 13 receptor subunit alpha 2	Homo sapiens	79-91
32402213-6	2020	In contrast, structure-function experiments demonstrated that IL-13 binding to IL-13Ralpha2 was dependent on each of the four sites of N-glycosylation in IL-13Ralpha2, and experiments with tunicamycin and PNGase F demonstrated that IL-13-IL-13Ralpha2 binding was decreased when IL-13Ralpha2 N-glycosylation was diminished.	Tunicamycin	189-200	interleukin 13	Homo sapiens	79-84
32810137-8	2020	In contrast, tunicamycin induced (ER stress associated) apoptosis is further increased by ATM knockdown or inhibition, but not by P53 knockdown.	Tunicamycin	13-24	ATM serine/threonine kinase	Rattus norvegicus	90-93
32965004-5	2020	Different concentration of glucose was used to culture CHs for both 24 h and 72 h. Furthermore, Tunicamycin (TM) and 4-Phenylbutyric acid (4-PBA) were used to mediate ER stress of CHs, and human recombinant Skp2 protein was used to promote Skp2 expression.	Tunicamycin	109-111	S-phase kinase associated protein 2	Homo sapiens	207-211
32965004-5	2020	Different concentration of glucose was used to culture CHs for both 24 h and 72 h. Furthermore, Tunicamycin (TM) and 4-Phenylbutyric acid (4-PBA) were used to mediate ER stress of CHs, and human recombinant Skp2 protein was used to promote Skp2 expression.	Tunicamycin	109-111	S-phase kinase associated protein 2	Homo sapiens	240-244
32826849-9	2020	Furthermore, C57BL/6 mice was used to induce ER stress with TM intraperitoneal injection, PPARalpha and autophagy was upregulated in the mild-ER stress while downregulated in the serious ER stress, measured by qRT-PCR and immunoblotting, further confirmed the finding in vitro.	Tunicamycin	60-62	peroxisome proliferator activated receptor alpha	Mus musculus	90-99
32748834-5	2020	GRP78 and GRP94 expression was increased in cells treated with 3 nM thapsigargin or 0.1 mug/mL tunicamycin for 24 h, referred to as mild ER stress condition.	Tunicamycin	95-106	heat shock protein 5	Mus musculus	0-5
32748834-5	2020	GRP78 and GRP94 expression was increased in cells treated with 3 nM thapsigargin or 0.1 mug/mL tunicamycin for 24 h, referred to as mild ER stress condition.	Tunicamycin	95-106	heat shock protein 90, beta (Grp94), member 1	Mus musculus	10-15
32237184-8	2020	Also, induction of autophagy by tunicamycin resulted in apoptosis in diabetic PBMCs as observed by caspase 3 cleavage and reduced expression of Bcl2.	Tunicamycin	32-43	caspase 3	Homo sapiens	99-108
32237184-8	2020	Also, induction of autophagy by tunicamycin resulted in apoptosis in diabetic PBMCs as observed by caspase 3 cleavage and reduced expression of Bcl2.	Tunicamycin	32-43	BCL2 apoptosis regulator	Homo sapiens	144-148
32626998-7	2020	The ERS activator tunicamycin (TM) was used to counteract the ERO1alpha-induced reduction in ERS; however, the percentage of apoptotic cells and the level of mitochondrial damage did not change.	Tunicamycin	18-29	endoplasmic reticulum oxidoreductase 1 alpha	Homo sapiens	62-71
32626998-7	2020	The ERS activator tunicamycin (TM) was used to counteract the ERO1alpha-induced reduction in ERS; however, the percentage of apoptotic cells and the level of mitochondrial damage did not change.	Tunicamycin	31-33	endoplasmic reticulum oxidoreductase 1 alpha	Homo sapiens	62-71
32266019-5	2020	In the present study, RIPK1 was significantly downregulated in tunicamycin (TM)-induced ER stressed-human melanocytes.	Tunicamycin	63-74	receptor interacting serine/threonine kinase 1	Homo sapiens	22-27
32724824-4	2020	In the present study, we induced ER stress by tunicamycin (TM) treatment and showed that infection of MIN6 cells with Ad-DHCR24-myc rendered these cells resistant to caspase-3-mediated apoptosis induced by TM, while cells transfected with siRNAs targeting DHCR24 were more sensitive to TM.	Tunicamycin	46-57	24-dehydrocholesterol reductase	Mus musculus	121-127
32714930-7	2020	At the same time, staurosporine, nifedipine, and tunicamycin elicited an intermediate activation of caspase-3.	Tunicamycin	49-60	caspase 3	Homo sapiens	100-109
32332156-5	2020	We show that lactogens protect INS1 cells, primary rodent and human beta-cells in vitro against two distinct ER stressors, tunicamycin and thapsigargin, through activation of the JAK2/STAT5 pathway.	Tunicamycin	123-134	Janus kinase 2	Homo sapiens	179-183
32203149-6	2020	Urinary ERdj3 and MANF increased in rats injected with tunicamycin (in the absence of proteinuria).	Tunicamycin	55-66	DnaJ heat shock protein family (Hsp40) member B11	Rattus norvegicus	8-13
32203149-6	2020	Urinary ERdj3 and MANF increased in rats injected with tunicamycin (in the absence of proteinuria).	Tunicamycin	55-66	mesencephalic astrocyte-derived neurotrophic factor	Rattus norvegicus	18-22
31975462-3	2020	ch1 plants in low light exhibited a moderate activation of UPR genes, in particular bZIP60, and low concentrations of the UPR-inducer tunicamycin enhanced tolerance to photooxidative stress, together suggesting a role for UPR in plant acclimation to low 1 O2 levels.	Tunicamycin	134-145	Pheophorbide a oxygenase family protein with Rieske 2Fe-2S domain-containing protein	Arabidopsis thaliana	0-3
32031621-8	2020	Tunicamycin elicited time-dependent increase in GRP78 protein levels, direct interaction with latent TGF-beta1, and activated TGF-beta1 signaling.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	48-53
32031621-8	2020	Tunicamycin elicited time-dependent increase in GRP78 protein levels, direct interaction with latent TGF-beta1, and activated TGF-beta1 signaling.	Tunicamycin	0-11	transforming growth factor beta 1	Homo sapiens	101-110
32031621-8	2020	Tunicamycin elicited time-dependent increase in GRP78 protein levels, direct interaction with latent TGF-beta1, and activated TGF-beta1 signaling.	Tunicamycin	0-11	transforming growth factor beta 1	Homo sapiens	126-135
32205450-8	2020	SVB showed time-dependent induction after tunicamycin-induced ER stress, which depended on IRE1 and bZIP60 but not bZIP17 and bZIP28 in the unfolded protein response (UPR).	Tunicamycin	42-53	basic region/leucine zipper motif 60	Arabidopsis thaliana	100-106
32718038-8	2020	In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis.	Tunicamycin	68-79	DNA-damage inducible transcript 3	Mus musculus	169-193
32718038-8	2020	In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis.	Tunicamycin	68-79	DNA-damage inducible transcript 3	Mus musculus	195-199
32718038-8	2020	In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis.	Tunicamycin	81-83	DNA-damage inducible transcript 3	Mus musculus	169-193
32718038-8	2020	In a previous report we demonstrated that the pharmacological agent tunicamycin (TM) induced ER stress through altered protein glycosylation and induced high amounts of C/EBP-homologous protein (CHOP), resulting in hepatocyte apoptosis.	Tunicamycin	81-83	DNA-damage inducible transcript 3	Mus musculus	195-199
32718038-9	2020	We compared TM-induced ER stress in wild type, Lcn2-/-, and Chop null (Chop-/-) primary hepatocytes and found Chop-/- hepatocytes to attenuate ER stress responses and resist ER stress-induced hepatocyte apoptosis through canonical eIF2alpha/GADD34 signaling, inhibiting protein synthesis.	Tunicamycin	12-14	lipocalin 2	Mus musculus	47-51
32718038-9	2020	We compared TM-induced ER stress in wild type, Lcn2-/-, and Chop null (Chop-/-) primary hepatocytes and found Chop-/- hepatocytes to attenuate ER stress responses and resist ER stress-induced hepatocyte apoptosis through canonical eIF2alpha/GADD34 signaling, inhibiting protein synthesis.	Tunicamycin	12-14	eukaryotic translation initiation factor 2A	Mus musculus	231-240
32718038-9	2020	We compared TM-induced ER stress in wild type, Lcn2-/-, and Chop null (Chop-/-) primary hepatocytes and found Chop-/- hepatocytes to attenuate ER stress responses and resist ER stress-induced hepatocyte apoptosis through canonical eIF2alpha/GADD34 signaling, inhibiting protein synthesis.	Tunicamycin	12-14	protein phosphatase 1, regulatory subunit 15A	Mus musculus	241-247
32724824-4	2020	In the present study, we induced ER stress by tunicamycin (TM) treatment and showed that infection of MIN6 cells with Ad-DHCR24-myc rendered these cells resistant to caspase-3-mediated apoptosis induced by TM, while cells transfected with siRNAs targeting DHCR24 were more sensitive to TM.	Tunicamycin	59-61	24-dehydrocholesterol reductase	Mus musculus	121-127
32724824-4	2020	In the present study, we induced ER stress by tunicamycin (TM) treatment and showed that infection of MIN6 cells with Ad-DHCR24-myc rendered these cells resistant to caspase-3-mediated apoptosis induced by TM, while cells transfected with siRNAs targeting DHCR24 were more sensitive to TM.	Tunicamycin	59-61	myelocytomatosis oncogene	Mus musculus	52-55
32724824-6	2020	Cells infected with Ad-LacZ exhibited a rapid and strong activation of ATF6 and p38, peaking at 3 h after TM exposure.	Tunicamycin	106-108	activating transcription factor 6	Mus musculus	71-75
32724824-6	2020	Cells infected with Ad-LacZ exhibited a rapid and strong activation of ATF6 and p38, peaking at 3 h after TM exposure.	Tunicamycin	106-108	mitogen-activated protein kinase 14	Mus musculus	80-83
32407927-0	2020	Luteolin prevents liver from tunicamycin-induced endoplasmic reticulum stress via nuclear factor erythroid 2-related factor 2-dependent sestrin 2 induction.	Tunicamycin	29-40	NFE2 like bZIP transcription factor 2	Homo sapiens	82-125
32407927-0	2020	Luteolin prevents liver from tunicamycin-induced endoplasmic reticulum stress via nuclear factor erythroid 2-related factor 2-dependent sestrin 2 induction.	Tunicamycin	29-40	sestrin 2	Homo sapiens	136-145
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
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
32660483-4	2020	The purpose of this study is to investigate the effects of CaMKIV on ER stress, autophagic function and insulin signaling in tunicamycin-treated adipocytes.	Tunicamycin	125-136	calcium/calmodulin dependent protein kinase IV	Homo sapiens	59-65
32660483-4	2020	The purpose of this study is to investigate the effects of CaMKIV on ER stress, autophagic function and insulin signaling in tunicamycin-treated adipocytes.	Tunicamycin	125-136	insulin	Homo sapiens	104-111
32660483-6	2020	Tunicamycin-treated 3 T3-L1 adipocytes were treated with recombinant CaMKIV in the presence or absence of targeted-siRNA mediated down-regulation of CREB and mTOR.	Tunicamycin	0-11	calcium/calmodulin dependent protein kinase IV	Homo sapiens	69-75
32660483-6	2020	Tunicamycin-treated 3 T3-L1 adipocytes were treated with recombinant CaMKIV in the presence or absence of targeted-siRNA mediated down-regulation of CREB and mTOR.	Tunicamycin	0-11	cAMP responsive element binding protein 1	Homo sapiens	149-153
32660483-6	2020	Tunicamycin-treated 3 T3-L1 adipocytes were treated with recombinant CaMKIV in the presence or absence of targeted-siRNA mediated down-regulation of CREB and mTOR.	Tunicamycin	0-11	mechanistic target of rapamycin kinase	Homo sapiens	158-162
32660483-8	2020	RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II.	Tunicamycin	54-65	calcium/calmodulin dependent protein kinase IV	Homo sapiens	24-30
32660483-8	2020	RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II.	Tunicamycin	54-65	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	90-94
32660483-8	2020	RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II.	Tunicamycin	54-65	activating transcription factor 6	Homo sapiens	104-108
32660483-8	2020	RESULTS: Treatment with CaMKIV significantly reversed tunicamycin-induced expression of p-PERK, cleaved-ATF6, Atg7 and LC3II.	Tunicamycin	54-65	autophagy related 7	Homo sapiens	110-114
32660483-12	2020	However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes.	Tunicamycin	147-158	calcium/calmodulin dependent protein kinase IV	Homo sapiens	35-41
32660483-12	2020	However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes.	Tunicamycin	147-158	insulin	Homo sapiens	56-63
32660483-12	2020	However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes.	Tunicamycin	147-158	mechanistic target of rapamycin kinase	Homo sapiens	131-135
32660483-12	2020	However, the protective effects of CaMKIV on ER stress, insulin signaling, and autophagy function were nullified by suppression of mTOR or CREB in tunicamycin-treated adipocytes.	Tunicamycin	147-158	cAMP responsive element binding protein 1	Homo sapiens	139-143
32660483-13	2020	CONCLUSION: This study proves recombinant CaMKIV inhibits tunicamycin-induced ER stress and insulin resistance by regulating autophagy.	Tunicamycin	58-69	calcium/calmodulin dependent protein kinase IV	Homo sapiens	42-48
32664460-5	2020	Treatment with tunicamycin (Tm), the inhibitor of N-glycosylation of secreted glycoproteins, increased the transcript levels of SlBiP.	Tunicamycin	15-26	BEL1-like homeodomain protein 2	Solanum lycopersicum	128-133
32664460-5	2020	Treatment with tunicamycin (Tm), the inhibitor of N-glycosylation of secreted glycoproteins, increased the transcript levels of SlBiP.	Tunicamycin	28-30	BEL1-like homeodomain protein 2	Solanum lycopersicum	128-133
32378324-8	2020	Notably, chronic treatment of PCK rats with 4-PBA decreased liver weight, as well as both liver and cystic volumes, of animals under baseline conditions or after TM administration compared to controls.	Tunicamycin	162-164	phosphoenolpyruvate carboxykinase 1	Rattus norvegicus	30-33
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	60-65
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
32586376-8	2020	Further study indicated that ER stress agonist (tunicamycin) treatment in MSLC results in the translocation of XBP1, an ER stress sensor, into the nucleus to induce MCL-1 expression through direct binding to the - 313- to - 308-bp region of MCL-1 promoter.	Tunicamycin	48-59	X-box binding protein 1	Homo sapiens	111-115
32586376-8	2020	Further study indicated that ER stress agonist (tunicamycin) treatment in MSLC results in the translocation of XBP1, an ER stress sensor, into the nucleus to induce MCL-1 expression through direct binding to the - 313- to - 308-bp region of MCL-1 promoter.	Tunicamycin	48-59	myeloid cell leukemia sequence 1	Mus musculus	165-170
32586376-8	2020	Further study indicated that ER stress agonist (tunicamycin) treatment in MSLC results in the translocation of XBP1, an ER stress sensor, into the nucleus to induce MCL-1 expression through direct binding to the - 313- to - 308-bp region of MCL-1 promoter.	Tunicamycin	48-59	myeloid cell leukemia sequence 1	Mus musculus	241-246
32579556-3	2020	Overexpression of ISR1 is lethal and, at lower levels, causes sensitivity to tunicamycin and resistance to calcofluor white, implying impaired protein glycosylation and reduced chitin deposition.	Tunicamycin	77-88	putative protein kinase ISR1	Saccharomyces cerevisiae S288C	18-22
32522979-8	2020	Experiments with HCC xenograft models revealed that restoring SHQ1 levels enhanced the anti-tumor activity of the endoplasmic reticulum (ER) stress inducer tunicamycin (TM) and common chemotherapy drug paclitaxel (PTX).	Tunicamycin	156-167	SHQ1, H/ACA ribonucleoprotein assembly factor	Homo sapiens	62-66
32522979-8	2020	Experiments with HCC xenograft models revealed that restoring SHQ1 levels enhanced the anti-tumor activity of the endoplasmic reticulum (ER) stress inducer tunicamycin (TM) and common chemotherapy drug paclitaxel (PTX).	Tunicamycin	169-171	SHQ1, H/ACA ribonucleoprotein assembly factor	Homo sapiens	62-66
32504039-6	2020	FliI-KD cells treated with ER stress inducers, thapsigargin (TG), and tunicamycin exhibited activation of the unfolded protein response (UPR) and induction of UPR-related gene expression, which eventually triggered apoptosis.	Tunicamycin	70-81	flightless I actin binding protein	Mus musculus	0-4
32332695-3	2020	Here, we found that a pseudogene-derived lncRNA, Golgin A2 pseudogene 10 (GOLGA2P10), was frequently upregulated in HCC tissues and significantly elevated in hepatoma cells treated with ER stress inducers, such as tunicamycin and thapsigargin.	Tunicamycin	214-225	GOLGA2 pseudogene 10	Homo sapiens	49-72
32332695-3	2020	Here, we found that a pseudogene-derived lncRNA, Golgin A2 pseudogene 10 (GOLGA2P10), was frequently upregulated in HCC tissues and significantly elevated in hepatoma cells treated with ER stress inducers, such as tunicamycin and thapsigargin.	Tunicamycin	214-225	GOLGA2 pseudogene 10	Homo sapiens	74-83
32295457-11	2020	Subsequently, B7-33 (100 nmol/L) reduced tunicamycin (2.5 mug/mL) induced upregulation of GRP78 in an extracellular signal-regulated kinase 1/2-dependent manner.	Tunicamycin	41-52	heat shock protein 5	Mus musculus	90-95
32295457-11	2020	Subsequently, B7-33 (100 nmol/L) reduced tunicamycin (2.5 mug/mL) induced upregulation of GRP78 in an extracellular signal-regulated kinase 1/2-dependent manner.	Tunicamycin	41-52	mitogen-activated protein kinase 3	Mus musculus	102-143
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
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	heat shock protein family A (Hsp70) member 4	Homo sapiens	135-140
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	171-228
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	unc-51 like autophagy activating kinase 1	Homo sapiens	372-376
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	autophagy related 13	Homo sapiens	381-386
32035621-6	2020	Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin.	Tunicamycin	160-171	insulin	Homo sapiens	0-7
32035621-6	2020	Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin.	Tunicamycin	160-171	ribosomal protein S6 kinase B1	Homo sapiens	53-83
32035621-6	2020	Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin.	Tunicamycin	160-171	ribosomal protein S6 kinase B1	Homo sapiens	85-92
32035621-6	2020	Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin.	Tunicamycin	160-171	AKT serine/threonine kinase 1	Homo sapiens	98-127
32035621-6	2020	Insulin treatment upregulates the phosphorylation of ribosomal protein S6 kinase B1 (RPS6KB1) and AKT serine/threonine kinase 1 (AKT1), which was suppressed by tunicamycin.	Tunicamycin	160-171	AKT serine/threonine kinase 1	Homo sapiens	129-133
32035621-7	2020	Notably, ATG13 and ULK1 deficiency ameliorated tunicamycin-induced insulin resistance, with enhanced RPS6KB1 and AKT1 phosphorylation in KO cells compared to WT cells.	Tunicamycin	47-58	autophagy related 13	Homo sapiens	9-14
32035621-7	2020	Notably, ATG13 and ULK1 deficiency ameliorated tunicamycin-induced insulin resistance, with enhanced RPS6KB1 and AKT1 phosphorylation in KO cells compared to WT cells.	Tunicamycin	47-58	unc-51 like autophagy activating kinase 1	Homo sapiens	19-23
32035621-7	2020	Notably, ATG13 and ULK1 deficiency ameliorated tunicamycin-induced insulin resistance, with enhanced RPS6KB1 and AKT1 phosphorylation in KO cells compared to WT cells.	Tunicamycin	47-58	insulin	Homo sapiens	67-74
32035621-8	2020	Although ULK1 and ATG13 are necessary for autophagy induction after tunicamycin-induced ER stress, autophagy does not seem to directly affect tunicamycin-induced cell death, ER stress, or insulin resistance.	Tunicamycin	68-79	unc-51 like autophagy activating kinase 1	Homo sapiens	9-13
32035621-8	2020	Although ULK1 and ATG13 are necessary for autophagy induction after tunicamycin-induced ER stress, autophagy does not seem to directly affect tunicamycin-induced cell death, ER stress, or insulin resistance.	Tunicamycin	68-79	autophagy related 13	Homo sapiens	18-23
32268491-0	2020	Overexpression of GRP78/BiP in P-Glycoprotein-Positive L1210 Cells is Responsible for Altered Response of Cells to Tunicamycin as a Stressor of the Endoplasmic Reticulum.	Tunicamycin	115-126	heat shock protein 5	Mus musculus	18-23
32268491-0	2020	Overexpression of GRP78/BiP in P-Glycoprotein-Positive L1210 Cells is Responsible for Altered Response of Cells to Tunicamycin as a Stressor of the Endoplasmic Reticulum.	Tunicamycin	115-126	heat shock protein 5	Mus musculus	24-27
32268491-2	2020	However, we found previously that P-gp-positive sublines of L1210 murine leukemia cells (R and T) but not parental P-gp-negative parental cells (S) are resistant to the endoplasmic reticulum (ER) stressor tunicamycin (an N-glycosylation inhibitor).	Tunicamycin	205-216	phosphoglycolate phosphatase	Mus musculus	34-38
32268491-3	2020	Here, we elucidated the mechanism of tunicamycin resistance in P-gp-positive cells.	Tunicamycin	37-48	phosphoglycolate phosphatase	Mus musculus	63-67
32268491-4	2020	We found that tunicamycin at a sublethal concentration of 0.1 microM induced retention of the cells in the G1 phase of the cell cycle only in the P-gp negative variant of L1210 cells.	Tunicamycin	14-25	phosphoglycolate phosphatase	Mus musculus	146-150
32268491-5	2020	P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein).	Tunicamycin	143-154	phosphoglycolate phosphatase	Mus musculus	0-4
32268491-5	2020	P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein).	Tunicamycin	143-154	heat shock protein 5	Mus musculus	83-88
32268491-5	2020	P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein).	Tunicamycin	143-154	heat shock protein 5	Mus musculus	89-92
32268491-5	2020	P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein).	Tunicamycin	143-154	phosphoglycolate phosphatase	Mus musculus	113-117
32268491-5	2020	P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein).	Tunicamycin	143-154	DNA-damage inducible transcript 3	Mus musculus	186-190
32268491-5	2020	P-gp-positive L1210 cell variants had higher expression of the ER stress chaperone GRP78/BiP compared to that of P-gp-negative cells, in which tunicamycin induced larger upregulation of CHOP (C/EBP homologous protein).	Tunicamycin	143-154	DNA-damage inducible transcript 3	Mus musculus	192-216
32268491-6	2020	Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle.	Tunicamycin	97-108	phosphoglycolate phosphatase	Mus musculus	30-34
32268491-6	2020	Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle.	Tunicamycin	97-108	heat shock protein 5	Mus musculus	75-80
32268491-6	2020	Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle.	Tunicamycin	97-108	heat shock protein 5	Mus musculus	81-84
32268491-6	2020	Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle.	Tunicamycin	97-108	DNA-damage inducible transcript 3	Mus musculus	117-121
32268491-6	2020	Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle.	Tunicamycin	145-156	phosphoglycolate phosphatase	Mus musculus	30-34
32268491-6	2020	Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle.	Tunicamycin	145-156	heat shock protein 5	Mus musculus	75-80
32268491-6	2020	Transfection of the sensitive P-gp-negative cells with plasmids containing GRP78/BiP antagonized tunicamycin-induced CHOP expression and reduced tunicamycin-induced arrest of cells in the G1 phase of the cell cycle.	Tunicamycin	145-156	heat shock protein 5	Mus musculus	81-84
32268491-7	2020	Taken together, these data suggest that the resistance of P-gp-positive cells to tunicamycin is due to increased levels of GRP78/BiP, which is overexpressed in both resistant variants of L1210 cells.	Tunicamycin	81-92	phosphoglycolate phosphatase	Mus musculus	58-62
32268491-7	2020	Taken together, these data suggest that the resistance of P-gp-positive cells to tunicamycin is due to increased levels of GRP78/BiP, which is overexpressed in both resistant variants of L1210 cells.	Tunicamycin	81-92	heat shock protein 5	Mus musculus	123-128
32268491-7	2020	Taken together, these data suggest that the resistance of P-gp-positive cells to tunicamycin is due to increased levels of GRP78/BiP, which is overexpressed in both resistant variants of L1210 cells.	Tunicamycin	81-92	heat shock protein 5	Mus musculus	129-132
32266019-5	2020	In the present study, RIPK1 was significantly downregulated in tunicamycin (TM)-induced ER stressed-human melanocytes.	Tunicamycin	76-78	receptor interacting serine/threonine kinase 1	Homo sapiens	22-27
32266019-9	2020	Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes.	Tunicamycin	141-143	BCL2 associated X, apoptosis regulator	Homo sapiens	58-61
32266019-9	2020	Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes.	Tunicamycin	141-143	caspase 3	Homo sapiens	66-75
32266019-9	2020	Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes.	Tunicamycin	141-143	BCL2 apoptosis regulator	Homo sapiens	114-119
32256145-6	2020	Our results demonstrate that PKR inhibition suppresses tunicamycin-mediated ER stress without altering the insulin production capacity of the cells.	Tunicamycin	55-66	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	29-32
31940218-6	2020	Exposure of hASM to tunicamycin was used as a positive control.	Tunicamycin	20-31	H19 imprinted maternally expressed transcript	Homo sapiens	12-16
31940218-9	2020	We found that exposure of hASM cells to tunicamycin activated all three ER stress pathways.	Tunicamycin	40-51	H19 imprinted maternally expressed transcript	Homo sapiens	26-30
31630283-8	2020	In addition, FFAs induced phosphorylation of the p65 subunit of NF-kappaB was largely inhibited by pretreatment with tunicamycin in 3T3-L1 adipocytes.	Tunicamycin	117-128	RELA proto-oncogene, NF-kB subunit	Homo sapiens	49-73
32086320-9	2020	GRP78 autoantigen expression was upregulated among human aortic endothelial cells (HAECs) stressed by incubation with tunicamycin (an unfolded protein response inducer) or exposure to culture media flow disturbances.	Tunicamycin	118-129	heat shock protein family A (Hsp70) member 5	Homo sapiens	0-5
32059483-6	2020	In response to TN- or isoproterenol-induced ER stress, mice deficient for SIRT1 exhibited suppressed autophagy along with exacerbated cardiac dysfunction.	Tunicamycin	15-17	sirtuin 1	Mus musculus	74-79
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	169-202
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	204-208
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	heat shock protein family A (Hsp70) member 4	Homo sapiens	240-245
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	257-262
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	activating transcription factor 4	Homo sapiens	298-302
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	activating transcription factor 6	Homo sapiens	305-309
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	71-82	X-box binding protein 1	Homo sapiens	365-388
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	vitamin D receptor	Homo sapiens	453-471
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	vitamin D receptor	Homo sapiens	473-476
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	169-202
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	204-208
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	heat shock protein family A (Hsp70) member 4	Homo sapiens	240-245
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	257-262
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	activating transcription factor 4	Homo sapiens	298-302
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	activating transcription factor 6	Homo sapiens	305-309
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
32040528-4	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	X-box binding protein 1	Homo sapiens	365-388
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	vitamin D receptor	Homo sapiens	453-471
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	vitamin D receptor	Homo sapiens	473-476
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	activating transcription factor 4	Homo sapiens	109-113
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	activating transcription factor 6	Homo sapiens	115-119
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
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	131-136
32040528-6	2020	In addition, 1,25D3 (100 nM) antagonized the effect of TG (10 nM) and TM (1 mug/mL) on mRNA and protein levels of VDR and mRNA levels of genes involved in production and degradation of 1,25D3 in MCF-7 cells (P &lt; 0.05).	Tunicamycin	70-72	vitamin D receptor	Homo sapiens	114-117
31894252-7	2020	Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94).	Tunicamycin	89-100	activating transcription factor 6	Homo sapiens	173-206
31894252-7	2020	Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94).	Tunicamycin	89-100	X-box binding protein 1	Homo sapiens	252-275
31894252-7	2020	Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94).	Tunicamycin	89-100	gastrin releasing peptide	Homo sapiens	350-353
31894252-7	2020	Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94).	Tunicamycin	89-100	eukaryotic translation initiation factor 2A	Homo sapiens	380-423
31894252-7	2020	Subsequent to experimentally inducing ER stress in AGR2vH-overexpressing CCA cells using tunicamycin, the UPR pathway was activated by the upregulation of UPR marker genes (activating transcription factor 6, eukaryotic initiation factor 2a and spliced X-box binding protein 1), UPR proteins [binding immunoglobulin protein/glucose-regulated protein (GRP)78 kDa and phosphorylated eukaryotic translation initiation factor 2a] and UPR downstream targets (GRP94).	Tunicamycin	89-100	heat shock protein 90 beta family member 1	Homo sapiens	453-458
31837328-3	2020	The present study focuses on exploring the effects of CTCF on tunicamycin (TM)-induced endoplasmic reticulum (ER) stress, and investigating the underlying mechanisms.	Tunicamycin	62-73	CCCTC-binding factor	Homo sapiens	54-58
31837328-3	2020	The present study focuses on exploring the effects of CTCF on tunicamycin (TM)-induced endoplasmic reticulum (ER) stress, and investigating the underlying mechanisms.	Tunicamycin	75-77	CCCTC-binding factor	Homo sapiens	54-58
31834612-4	2020	IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays.	Tunicamycin	122-133	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	0-9
31834612-4	2020	IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays.	Tunicamycin	122-133	X-box binding protein 1	Mus musculus	50-54
31834612-4	2020	IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays.	Tunicamycin	122-133	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	0-4
31834612-4	2020	IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays.	Tunicamycin	135-137	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	0-9
31834612-4	2020	IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays.	Tunicamycin	135-137	X-box binding protein 1	Mus musculus	50-54
31834612-4	2020	IRE1alpha deficiency prevented almost all spliced XBP1 (sXBP1) protein expression by treatment with thapsigargin (Tg) and tunicamycin (Tm); these phenomena paralleled the values measured by our two Nanoluciferase-based IRE1 assays.	Tunicamycin	135-137	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	0-4
31834612-5	2020	However, cell viability and protein expression of other ER stress-responsive factors in the IRE1alpha-deficient cells were comparable to those in the parental wild-type cells with or without Tm treatment.	Tunicamycin	191-193	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	92-101
31834612-10	2020	Co-treatment with KIRA6 and Tm induced LC3 II, cleaved caspase-9, and cleaved caspase-3; however, IRE1alpha-deficiency did not abolish the expression of these two cleaved caspases.	Tunicamycin	28-30	caspase 9	Mus musculus	55-64
31834612-10	2020	Co-treatment with KIRA6 and Tm induced LC3 II, cleaved caspase-9, and cleaved caspase-3; however, IRE1alpha-deficiency did not abolish the expression of these two cleaved caspases.	Tunicamycin	28-30	caspase 9	Mus musculus	171-179
31834612-11	2020	On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells.	Tunicamycin	36-38	activating transcription factor 4	Mus musculus	47-51
31834612-11	2020	On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells.	Tunicamycin	36-38	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	68-72
31834612-11	2020	On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells.	Tunicamycin	36-38	activating transcription factor 4	Mus musculus	185-189
31834612-11	2020	On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells.	Tunicamycin	130-132	caspase 9	Mus musculus	169-177
31834612-11	2020	On the other hand, KIRA6 prohibited Tm-induced ATF4 induction in an IRE1-independent manner; however, co-treatment with KIRA6 and Tm also induced LC3 II and two cleaved caspases in the ATF4-deficient Neuro2a cells.	Tunicamycin	130-132	activating transcription factor 4	Mus musculus	185-189
31919559-8	2020	The concomitant inflammation/metabolism TRN occurred similarly after acute LPS and tunicamycin challenges, in chronic mouse models and also in human liver diseases.	Tunicamycin	83-94	transportin 1	Mus musculus	40-43
31746423-10	2020	Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin.	Tunicamycin	15-17	activating transcription factor 6	Homo sapiens	189-194
31746423-10	2020	Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin.	Tunicamycin	15-17	activating transcription factor 4	Homo sapiens	196-200
31746423-10	2020	Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin.	Tunicamycin	15-17	fibronectin 1	Homo sapiens	259-270
31746423-10	2020	Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin.	Tunicamycin	15-17	vimentin	Homo sapiens	272-280
31746423-10	2020	Treatment with TM or TG increased the expression of the ER stress markers glucose-regulated protein 78, phosphorylated eukaryotic initiation factor 2alpha, activating transcription factor (ATF)6, ATF4 and inositol-requiring protein 1alpha and the EMT markers fibronectin, vimentin, alpha-smooth muscle actin and neural cadherin.	Tunicamycin	15-17	cadherin 2	Homo sapiens	312-327
31904504-9	2020	Moreover, more than one-third of the cobalt-sensitive mutants were also sensitive to tunicamycin, and cobalt stress might induce the unfolded protein response (UPR) through serine/threonine kinase and endoribonuclease Ire1.	Tunicamycin	85-96	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	218-222
32057287-9	2020	The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner.	Tunicamycin	27-38	heat shock protein 5	Mus musculus	53-58
32057287-9	2020	The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner.	Tunicamycin	27-38	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	63-67
32057287-9	2020	The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner.	Tunicamycin	40-42	heat shock protein 5	Mus musculus	53-58
32057287-9	2020	The results indicated that tunicamycin (TM) elevated GRP78 and PERK expression of AMs in ALI mice in a dose-dependent manner.	Tunicamycin	40-42	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	63-67
32057287-10	2020	Low dosage of TM abated LC3I expression, increased LC3II and Beclin1 expression, triggered ER stress and AM autophagy, and alleviated pathological changes of AMs in ALI mice.	Tunicamycin	14-16	beclin 1, autophagy related	Mus musculus	61-68
32057287-11	2020	Also, in ALI mice, low dosage of TM attenuated goblet cell proliferation of tracheal wall, and declined LW/BW ratio, ELGV, total cells and neutrophils, protein concentrations in BALF, and IL-6 and TNF-alpha expression in lung tissues and BALF.	Tunicamycin	33-35	interleukin 6	Mus musculus	188-192
32057287-11	2020	Also, in ALI mice, low dosage of TM attenuated goblet cell proliferation of tracheal wall, and declined LW/BW ratio, ELGV, total cells and neutrophils, protein concentrations in BALF, and IL-6 and TNF-alpha expression in lung tissues and BALF.	Tunicamycin	33-35	tumor necrosis factor	Mus musculus	197-206
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	29-40	LOW QUALITY PROTEIN: X-box-binding protein 1	Larimichthys crocea	101-105
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	29-40	tumor necrosis factor b (TNF superfamily, member 2)	Larimichthys crocea	187-214
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	29-40	tumor necrosis factor b (TNF superfamily, member 2)	Larimichthys crocea	216-224
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	29-40	interleukin-1 beta	Larimichthys crocea	252-269
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	42-44	LOW QUALITY PROTEIN: X-box-binding protein 1	Larimichthys crocea	101-105
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	42-44	tumor necrosis factor b (TNF superfamily, member 2)	Larimichthys crocea	187-214
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	42-44	tumor necrosis factor b (TNF superfamily, member 2)	Larimichthys crocea	216-224
31904542-9	2020	The ER stress-inducing agent tunicamycin (Tm) and PA treatment significantly activated the IRE1alpha-XBP1s signaling pathway and increased the pro-inflammatory genes expression including tumor necrosis factor alpha (tnfalpha), interleukin 6 (il-6) and interleukin 1beta (il-1beta) (P &lt; 0.05).	Tunicamycin	42-44	interleukin-1 beta	Larimichthys crocea	252-269
31904542-10	2020	When KIRA6, the IRE1alpha kinase inhibitor, was used to block the IRE1alpha-XBP1s signaling pathway, the Tm and PA-induced pro-inflammatory genes expression was significantly suppressed (P &lt; 0.05).	Tunicamycin	105-107	LOW QUALITY PROTEIN: X-box-binding protein 1	Larimichthys crocea	76-80
31965068-11	2020	UCP1 mRNA expression in differentiated human white adipocytes was significantly reduced after incubation with thapsigargin, tunicamycin, homocysteine, TNF-alpha, or IL-beta, and significantly increased after incubation with exendin 4, dapagliflozin, and telmisartan.	Tunicamycin	124-135	uncoupling protein 1	Homo sapiens	0-4
31926341-4	2020	PLK4 expression was dramatically reduced under ER stress induced by brefeldin A (BFA), tunicamycin (TM), or thapsigargin (TG) and down regulation of PLK4 expression was dependent on activating transcription factor 6 (ATF6) and CCAAT/enhancer-binding proteinbeta (C/EBPbeta).	Tunicamycin	87-98	polo like kinase 4	Homo sapiens	0-4
31926341-4	2020	PLK4 expression was dramatically reduced under ER stress induced by brefeldin A (BFA), tunicamycin (TM), or thapsigargin (TG) and down regulation of PLK4 expression was dependent on activating transcription factor 6 (ATF6) and CCAAT/enhancer-binding proteinbeta (C/EBPbeta).	Tunicamycin	100-102	polo like kinase 4	Homo sapiens	0-4
31563460-5	2020	Furthermore, CCL5 attenuated tunicamycin-induced endoplasmic reticulum (ER) stress signaling, and lipopolysaccharides-triggered inflammatory responses in pLE and pTr cells.	Tunicamycin	29-40	C-C motif chemokine 5	Sus scrofa	13-17
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	121-173
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	175-179
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	eukaryotic translation initiation factor 2A	Homo sapiens	243-252
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	121-173
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	175-179
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	eukaryotic translation initiation factor 2A	Homo sapiens	243-252
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
31974624-7	2020	Reverse transcription-quantitative PCR analysis demonstrated that TM promoted miR-421 expression in human melanocytes.	Tunicamycin	66-68	microRNA 421	Homo sapiens	78-85
31974624-9	2020	RIPK1 expression was significantly downregulated in TM-induced human melanocytes.	Tunicamycin	52-54	receptor interacting serine/threonine kinase 1	Homo sapiens	0-5
31974624-12	2020	In addition, the miR-421 inhibitor increased viability and reduced apoptosis in TM-treated melanocytes.	Tunicamycin	80-82	microRNA 421	Homo sapiens	17-24
31974624-13	2020	Furthermore, all these effects of the miR-421 inhibitor on TM-induced human melanocytes were reversed by RIPK1-shRNA.	Tunicamycin	59-61	microRNA 421	Homo sapiens	38-45
31974624-13	2020	Furthermore, all these effects of the miR-421 inhibitor on TM-induced human melanocytes were reversed by RIPK1-shRNA.	Tunicamycin	59-61	receptor interacting serine/threonine kinase 1	Homo sapiens	105-110
31974624-14	2020	Further analyses revealed that the miR-421 inhibitor activated the phosphoinositide 3 kinase/protein kinase B/mammalian target of rapamycin signaling pathway in TM-induced human melanocytes.	Tunicamycin	161-163	microRNA 421	Homo sapiens	35-42
31978676-7	2020	RESULTS: Induction of ER stress in TM treated groups were confirmed by significantly increased mRNA and protein levels of GRP78.	Tunicamycin	35-37	heat shock protein family A (Hsp70) member 5	Homo sapiens	122-127
31978676-10	2020	A significant increase was observed in C22-C24 CERs, C1P, caspase-3, caspase-12, NFkappaB1 mRNA and NF-kappaB p65 protein levels in cells treated with TM compared to controls.	Tunicamycin	151-153	caspase 3	Homo sapiens	58-67
31978676-10	2020	A significant increase was observed in C22-C24 CERs, C1P, caspase-3, caspase-12, NFkappaB1 mRNA and NF-kappaB p65 protein levels in cells treated with TM compared to controls.	Tunicamycin	151-153	nuclear factor kappa B subunit 1	Homo sapiens	81-90
31978676-10	2020	A significant increase was observed in C22-C24 CERs, C1P, caspase-3, caspase-12, NFkappaB1 mRNA and NF-kappaB p65 protein levels in cells treated with TM compared to controls.	Tunicamycin	151-153	RELA proto-oncogene, NF-kB subunit	Homo sapiens	100-113
32259048-5	2020	Pharmacologic induction of UPR with tunicamycin (Tm)-stimulated RANKL expression in cultures of primary osteoblastic cells and in osteoblast and osteocyte cell lines.	Tunicamycin	36-47	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	64-69
32259048-5	2020	Pharmacologic induction of UPR with tunicamycin (Tm)-stimulated RANKL expression in cultures of primary osteoblastic cells and in osteoblast and osteocyte cell lines.	Tunicamycin	49-51	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	64-69
32259048-6	2020	Pharmacologic inhibition of the UPR blunted Tm-induced RANKL production.	Tunicamycin	44-46	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	55-60
31940720-9	2020	p-AMPK and FTO induced mild ER stress; however, tunicamycin-induced severe ER stress suppressed FTO expression and AMPK activation.	Tunicamycin	48-59	fat mass and obesity associated	Mus musculus	96-99
31548168-7	2020	RESULTS: Tunicamycin or d-galactosamine significantly induced ER stress and necroptosis, as well as eIF2alpha phosphorylation, in mice and LO2 cells (p&lt;0.05).	Tunicamycin	9-20	eukaryotic translation initiation factor 2A	Mus musculus	100-109
31548168-11	2020	TNFR1 expression was reduced in d-galactosamine-treated mice (p&lt;0.05) and cells incubated with tunicamycin for 12 and 24h (p&lt;0.05).	Tunicamycin	98-109	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	0-5
31689235-8	2020	We further demonstrated that tunicamycin-induced ER stress in HepG2 cells led to increased p66Shc protein abundance, suggesting that ER stress may underlie the programmed effects observed in vivo.	Tunicamycin	29-40	SHC adaptor protein 1	Rattus norvegicus	91-97
31566068-1	2020	Tunicamycins, which are nucleoside natural products, inhibit both bacterial phospho-N-acetylmuraminic acid (MurNAc)-pentapeptide translocase (MraY) and human UDP-N-acetylglucosamine (GlcNAc): polyprenol phosphate translocase (GPT).	Tunicamycin	0-12	glutamic--pyruvic transaminase	Homo sapiens	226-229
31689455-9	2020	Furthermore, ER stress-mediated apoptosis, determined by the protein levels of CCAAT/enhancer-binding protein-homologous protein and cleaved caspase 12, was increased in tunicamycin or calcification media-treated VSMCs, but the increased effect was reversed in EPO-treated groups.	Tunicamycin	170-181	DNA-damage inducible transcript 3	Rattus norvegicus	79-128
31689455-9	2020	Furthermore, ER stress-mediated apoptosis, determined by the protein levels of CCAAT/enhancer-binding protein-homologous protein and cleaved caspase 12, was increased in tunicamycin or calcification media-treated VSMCs, but the increased effect was reversed in EPO-treated groups.	Tunicamycin	170-181	caspase 12	Rattus norvegicus	141-151
31689455-9	2020	Furthermore, ER stress-mediated apoptosis, determined by the protein levels of CCAAT/enhancer-binding protein-homologous protein and cleaved caspase 12, was increased in tunicamycin or calcification media-treated VSMCs, but the increased effect was reversed in EPO-treated groups.	Tunicamycin	170-181	erythropoietin	Rattus norvegicus	261-264
31888113-6	2019	Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells.	Tunicamycin	44-55	prostaglandin-endoperoxide synthase 2	Homo sapiens	95-111
31888113-6	2019	Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells.	Tunicamycin	44-55	prostaglandin-endoperoxide synthase 2	Homo sapiens	113-118
31888113-6	2019	Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells.	Tunicamycin	44-55	heat shock protein family A (Hsp70) member 5	Homo sapiens	151-156
31888113-6	2019	Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells.	Tunicamycin	44-55	mitogen-activated protein kinase 14	Homo sapiens	193-196
31888113-6	2019	Simultaneously, induction of ER stress with tunicamycin resulted in an increased expression of Cyclooxygenase 2 (COX-2) and Glucose-regulated protein (GRP78) concomitant with the activation of p38 MAPK/PI3K/Akt in HepG2 cells.	Tunicamycin	44-55	AKT serine/threonine kinase 1	Homo sapiens	207-210
31888113-8	2019	Consistent with the inhibition of COX-2 or p38 MAPK, copretreatment with TM and MLPE drastically recovered cytotoxicity and caspase-3 activation in the presence of DOX.	Tunicamycin	73-75	prostaglandin-endoperoxide synthase 2	Homo sapiens	34-39
31888113-8	2019	Consistent with the inhibition of COX-2 or p38 MAPK, copretreatment with TM and MLPE drastically recovered cytotoxicity and caspase-3 activation in the presence of DOX.	Tunicamycin	73-75	mitogen-activated protein kinase 14	Homo sapiens	43-46
31888113-8	2019	Consistent with the inhibition of COX-2 or p38 MAPK, copretreatment with TM and MLPE drastically recovered cytotoxicity and caspase-3 activation in the presence of DOX.	Tunicamycin	73-75	caspase 3	Homo sapiens	124-133
31834935-3	2019	Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor.	Tunicamycin	119-130	lysine methyltransferase 2A	Homo sapiens	283-286
31834935-3	2019	Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor.	Tunicamycin	119-130	fms related receptor tyrosine kinase 3	Homo sapiens	336-340
31834935-3	2019	Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor.	Tunicamycin	132-134	lysine methyltransferase 2A	Homo sapiens	283-286
31834935-3	2019	Here, we show that the triple combination of the differentiating agent retinoic acid (RA), the ER stress-inducing drug tunicamycin (Tm), and arsenic trioxide (ATO), able to generate oxidative stress, leads to the death of AML cell lines expressing fusion proteins involving the gene MLL and the internal tandem duplication (ITD) in the FLT3 tyrosine kinase receptor.	Tunicamycin	132-134	fms related receptor tyrosine kinase 3	Homo sapiens	336-340
31861550-0	2019	Unification of Opposites between Two Antioxidant Transcription Factors Nrf1 and Nrf2 in Mediating Distinct Cellular Responses to the Endoplasmic Reticulum Stressor Tunicamycin.	Tunicamycin	164-175	nuclear respiratory factor 1	Homo sapiens	71-75
31861550-0	2019	Unification of Opposites between Two Antioxidant Transcription Factors Nrf1 and Nrf2 in Mediating Distinct Cellular Responses to the Endoplasmic Reticulum Stressor Tunicamycin.	Tunicamycin	164-175	NFE2 like bZIP transcription factor 2	Homo sapiens	80-84
31861550-3	2019	Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU).	Tunicamycin	170-181	nuclear respiratory factor 1	Homo sapiens	92-96
31861550-3	2019	Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU).	Tunicamycin	170-181	NFE2 like bZIP transcription factor 2	Homo sapiens	101-105
31861550-3	2019	Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU).	Tunicamycin	183-185	nuclear respiratory factor 1	Homo sapiens	92-96
31861550-3	2019	Herein, we report a unity of opposites between these two antioxidant transcription factors, Nrf1 and Nrf2, in coordinating distinct cellular responses to the ER stressor tunicamycin (TU).	Tunicamycin	183-185	NFE2 like bZIP transcription factor 2	Homo sapiens	101-105
31861550-4	2019	The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks.	Tunicamycin	4-6	nuclear respiratory factor 1	Homo sapiens	34-38
31861550-4	2019	The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks.	Tunicamycin	4-6	NFE2 like bZIP transcription factor 2	Homo sapiens	43-47
31861550-4	2019	The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks.	Tunicamycin	4-6	glutamate-cysteine ligase modifier subunit	Homo sapiens	60-64
31861550-4	2019	The TU-inducible transcription of Nrf1 and Nrf2, as well as GCLM (glutamate cysteine ligase modifier subunit) and HO-1 (heme oxygenase 1), was accompanied by activation of ER stress signaling networks.	Tunicamycin	4-6	heme oxygenase 1	Homo sapiens	66-136
31861550-7	2019	Interestingly, Nrf1 glycosylation and its trans-activity to mediate the transcriptional expression of the 26S proteasomal subunits, were repressed by TU.	Tunicamycin	150-152	nuclear respiratory factor 1	Homo sapiens	15-19
31861550-9	2019	Furthermore,&amp;nbsp;caNrf2DeltaN also enhanced induction of PERK and IRE1 by TU, but reduced expression of ATF4 and HO-1.	Tunicamycin	79-81	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	62-66
31861550-9	2019	Furthermore,&amp;nbsp;caNrf2DeltaN also enhanced induction of PERK and IRE1 by TU, but reduced expression of ATF4 and HO-1.	Tunicamycin	79-81	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	71-75
31861550-9	2019	Furthermore,&amp;nbsp;caNrf2DeltaN also enhanced induction of PERK and IRE1 by TU, but reduced expression of ATF4 and HO-1.	Tunicamycin	79-81	heme oxygenase 1	Homo sapiens	118-122
31861550-10	2019	Thus, it is inferred that such distinct roles of Nrf1 and Nrf2 are unified to maintain cell homeostasis by a series of coordinated ER-to-nuclear signaling responses to TU.	Tunicamycin	168-170	nuclear respiratory factor 1	Homo sapiens	49-53
31861550-10	2019	Thus, it is inferred that such distinct roles of Nrf1 and Nrf2 are unified to maintain cell homeostasis by a series of coordinated ER-to-nuclear signaling responses to TU.	Tunicamycin	168-170	NFE2 like bZIP transcription factor 2	Homo sapiens	58-62
31861550-13	2019	Interestingly, Nrf1 is more potent than Nrf2 at mediating the cytoprotective responses against the cytotoxicity of TU alone plus tBHQ (tert-butylhydroquinone).	Tunicamycin	115-117	nuclear respiratory factor 1	Homo sapiens	15-19
31861550-13	2019	Interestingly, Nrf1 is more potent than Nrf2 at mediating the cytoprotective responses against the cytotoxicity of TU alone plus tBHQ (tert-butylhydroquinone).	Tunicamycin	115-117	NFE2 like bZIP transcription factor 2	Homo sapiens	40-44
31713417-6	2019	Additionally, using ERNB we evaluated CES2 regulation in DL-dithiothreitol (DTT) and tunicamycin-induced ER stress.	Tunicamycin	85-96	carboxylesterase 2	Homo sapiens	38-42
31619316-5	2019	NOD2 deficiency increased ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) in VSMCs in the presence of tunicamycin (TM), an ER stress inducer.	Tunicamycin	162-173	nucleotide-binding oligomerization domain containing 2	Mus musculus	0-4
32046379-10	2020	Overexpression of IRS1 significantly ameliorated palmitate- or tunicamycin-induced impairment of aromatase expression and estradiol generation.	Tunicamycin	63-74	insulin receptor substrate 1	Mus musculus	18-22
31604108-9	2019	KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells.	Tunicamycin	19-21	calreticulin	Rattus norvegicus	76-79
31604108-9	2019	KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells.	Tunicamycin	19-21	NFE2 like bZIP transcription factor 2	Rattus norvegicus	114-118
31604108-9	2019	KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells.	Tunicamycin	19-21	activating transcription factor 4	Rattus norvegicus	160-164
31604108-9	2019	KEY FINDING: TG or TM induced H9c2 cell injury and ER-phagy and upregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation, and expression of ATF4, Beclin 1, and LC3B-II compared with control cells.	Tunicamycin	19-21	beclin 1	Rattus norvegicus	166-174
31604108-10	2019	Treatment with ERS inhibitors decreased TG- or TM-induced ER-phagy, downregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation and the expression of ATF4, Beclin 1 and LC3B-II.	Tunicamycin	47-49	activating transcription factor 4	Rattus norvegicus	169-173
31604108-10	2019	Treatment with ERS inhibitors decreased TG- or TM-induced ER-phagy, downregulated CRT expression, PERK phosphorylation, Nrf2 nuclear translocation and the expression of ATF4, Beclin 1 and LC3B-II.	Tunicamycin	47-49	beclin 1	Rattus norvegicus	175-183
31604108-11	2019	Moreover, a Nrf2 inhibitor downregulated the expression of ATF4, Beclin 1 and LC3B-II and alleviated TG- or TM-induced ER-phagy and H9c2 cell injury.	Tunicamycin	108-110	NFE2 like bZIP transcription factor 2	Rattus norvegicus	12-16
31604108-11	2019	Moreover, a Nrf2 inhibitor downregulated the expression of ATF4, Beclin 1 and LC3B-II and alleviated TG- or TM-induced ER-phagy and H9c2 cell injury.	Tunicamycin	108-110	activating transcription factor 4	Rattus norvegicus	59-63
31787756-5	2019	The inhibition of PRMT1 augments tunicamycin (TN)-triggered ER stress response in cardiomyocytes while PRMT1 overexpression attenuates it.	Tunicamycin	33-44	protein arginine methyltransferase 1	Homo sapiens	18-23
31787756-5	2019	The inhibition of PRMT1 augments tunicamycin (TN)-triggered ER stress response in cardiomyocytes while PRMT1 overexpression attenuates it.	Tunicamycin	46-48	protein arginine methyltransferase 1	Homo sapiens	18-23
31138438-0	2019	MANF deletion abrogates early larval Caenorhabditis elegans stress response to tunicamycin and Pseudomonas aeruginosa.	Tunicamycin	79-90	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	0-4
31138438-6	2019	Surprisingly, larval growth arrest observed in wild-type nematodes reared on tunicamycin is completely prevented in the manf-1 (tm3603) mutant.	Tunicamycin	77-88	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	120-124
31138438-7	2019	Transcriptional microarray analysis revealed that manf-1 mutant L1 larvae exhibit a novel modulation of innate immunity genes in response to tunicamycin.	Tunicamycin	141-152	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	50-54
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	fms related receptor tyrosine kinase 3	Homo sapiens	23-27
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	fms related receptor tyrosine kinase 3	Homo sapiens	124-128
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	fms related receptor tyrosine kinase 3	Homo sapiens	124-128
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	226-231
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	281-286
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	fms related receptor tyrosine kinase 3	Homo sapiens	124-128
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	heat shock protein 90 alpha family class A member 1	Homo sapiens	311-316
31533545-5	2019	Results: Inhibition of FLT3 mutant cells by drugs reported in recent literatures involves the influence of glycosylation of FLT3: 2-deoxy-D-glucose, Tunicamycin and Fluvastatin are reported to inhibit N-glycosylation of FLT3; Pim-1 inhibitors are proved to block the inhibition of Pim-1 on FLT3 Oglycosylation; HSP90 inhibitors and Tyrosine Kinase Inhibitors are shown to increase fully glycosylated form of FLT3.	Tunicamycin	149-160	fms related receptor tyrosine kinase 3	Homo sapiens	124-128
31619316-5	2019	NOD2 deficiency increased ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) in VSMCs in the presence of tunicamycin (TM), an ER stress inducer.	Tunicamycin	175-177	nucleotide-binding oligomerization domain containing 2	Mus musculus	0-4
31619316-5	2019	NOD2 deficiency increased ER stress-induced cell death and expression levels of apoptosis mediators (cleaved caspase-3, Bax, and Bak) in VSMCs in the presence of tunicamycin (TM), an ER stress inducer.	Tunicamycin	175-177	BCL2-antagonist/killer 1	Mus musculus	129-132
31619316-9	2019	Taken together, these data suggest that the induction of ER stress through NOD2 expression can protect against TM-induced cell death in VSMCs.	Tunicamycin	111-113	nucleotide-binding oligomerization domain containing 2	Mus musculus	75-79
31721015-5	2019	Notably, UFL1 expression in BMECs was increased by endoplasmic reticulum (ER) stress induced by treatment with tunicamycin (TM).	Tunicamycin	111-122	UFM1 specific ligase 1	Bos taurus	9-13
31721015-5	2019	Notably, UFL1 expression in BMECs was increased by endoplasmic reticulum (ER) stress induced by treatment with tunicamycin (TM).	Tunicamycin	124-126	UFM1 specific ligase 1	Bos taurus	9-13
31721015-6	2019	ER stress-related gene expression was further increased in UFL1 knockdown cells upon TM treatment.	Tunicamycin	85-87	UFM1 specific ligase 1	Bos taurus	59-63
31504391-5	2019	Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3.	Tunicamycin	27-38	proprotein convertase subtilisin/kexin type 2	Mus musculus	80-83
31504391-5	2019	Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3.	Tunicamycin	27-38	proprotein convertase subtilisin/kexin type 1	Mus musculus	112-117
31504391-5	2019	Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3.	Tunicamycin	27-38	proprotein convertase subtilisin/kexin type 1	Homo sapiens	146-151
31504391-5	2019	Enhanced susceptibility to tunicamycin-induced ER stress was observed in AtT-20/PC2 cell clones in which murine PC1/3 was replaced by human N221D PC1/3, as compared to wild-type human PC1/3.	Tunicamycin	27-38	proprotein convertase subtilisin/kexin type 1	Homo sapiens	146-151
31534165-7	2019	Tg and Tunicamycin strongly reduced neurosphere forming ability of GSCs that was linked with potent PERK-dependent downregulation of SOX2 protein.	Tunicamycin	7-18	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	100-104
31889041-7	2019	Levels of cleaved caspase-12 were significantly decreased in the thapsigargin- or tunicamycin-4-PBA combination treatments.	Tunicamycin	82-93	caspase 12	Rattus norvegicus	18-28
31889041-8	2019	Therefore, whether melatonin regulates the amylin expression/oligomerization in thapsigargin- or tunicamycin-combined with Bafilomycin A1 (autophagy inhibitor) or MG132 (proteasome inhibitor) treatments were investigated.	Tunicamycin	97-108	islet amyloid polypeptide	Rattus norvegicus	43-49
31889041-9	2019	Amylin expression/oligomerization with melatonin treatment was significantly decreased in the thapsigargin- or tunicamycin-combined Bafilomycin A1 or MG132 treatments.	Tunicamycin	111-122	islet amyloid polypeptide	Rattus norvegicus	0-6
31315072-11	2019	A further in vivo analysis showed that Suhuang-driven pharmacological inactivation of NLRP3 inflammasome and amelioration of pulmonary dysfunction were reversed by an ER stress inducer tunicamycin, well confirming the beneficial effects of Suhuang on pulmonary function by regulation of ER stress.	Tunicamycin	185-196	NLR family pyrin domain containing 3	Homo sapiens	86-91
31291699-3	2019	Full-length CREB3 detected under resting conditions disappeared following treatment with tunicamycin, brefeldin A and nigericin.	Tunicamycin	89-100	cAMP responsive element binding protein 3	Homo sapiens	12-17
31534165-7	2019	Tg and Tunicamycin strongly reduced neurosphere forming ability of GSCs that was linked with potent PERK-dependent downregulation of SOX2 protein.	Tunicamycin	7-18	SRY-box transcription factor 2	Homo sapiens	133-137
31336877-0	2019	Tunicamycin Sensitivity-Suppression by High Gene Dosage Reveals New Functions of the Yeast Hog1 MAP Kinase.	Tunicamycin	0-11	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	91-95
31108175-12	2019	It indicated that the rIL-6 can significantly alleviate autophagy induced by Tm.	Tunicamycin	77-79	interleukin 6	Rattus norvegicus	22-27
31001857-4	2019	Through systematic screening of FAD mutants, we found that a mutant of FAD2 resulted in a hypersensitive response to tunicamycin, a chemical inducer of ER stress.	Tunicamycin	117-128	fatty acid desaturase 2	Arabidopsis thaliana	71-75
31001857-7	2019	Moreover, glycerolipid profiling of both mutants and overexpressors of FAD2 under tunicamycin-induced ER stress conditions, along with phenotypic screening of the mutants of the FAD family, suggested that the ratio of monounsaturated fatty acids to polyunsaturated fatty acids, particularly 18:1 to 18:2 species, may be an important factor in allowing the ER membrane to cope with ER stress.	Tunicamycin	82-93	fatty acid desaturase 2	Arabidopsis thaliana	71-75
31167779-6	2019	In this study, we show that the ER stress inducers tunicamycin and thapsigargin lead to the activation of PKD1 in human prostate cancer PC-3 cells and in hepatoma HepG2 cells through a PKCdelta-dependent mechanism.	Tunicamycin	51-62	protein kinase D1	Homo sapiens	106-110
31521187-4	2019	RESULTS: We found that hyl1 mutant plants are more sensitive to tunicamycin, an inhibitor of N-linked glycosylation that causes ER stress than wild-type plants.	Tunicamycin	64-75	dsRNA-binding domain-like superfamily protein	Arabidopsis thaliana	23-27
31430074-0	2019	Renal response to tunicamycin-induced endoplasmic reticulum stress in BDNF heterozygous mice.	Tunicamycin	18-29	brain derived neurotrophic factor	Mus musculus	70-74
31430074-2	2019	OBJECTIVES: The aim of this study was to determine whether endogenously produced BDNF protects the kidneys against tunicamycin-induced (Tm) ER stress.	Tunicamycin	115-126	brain derived neurotrophic factor	Mus musculus	81-85
30861618-7	2019	Based on the docking calculations, top hit compounds were identified to disrupt both Keap1a and Keap1b interaction with Nrf2 which include quercetin 3,4"-diglucoside, flavin adenine dinucleotide disodium salt hydrate, salvianolic acid A, tunicamycin and esculin.	Tunicamycin	238-249	kelch-like ECH-associated protein 1a	Danio rerio	85-91
30861618-7	2019	Based on the docking calculations, top hit compounds were identified to disrupt both Keap1a and Keap1b interaction with Nrf2 which include quercetin 3,4"-diglucoside, flavin adenine dinucleotide disodium salt hydrate, salvianolic acid A, tunicamycin and esculin.	Tunicamycin	238-249	kelch-like ECH-associated protein 1b	Danio rerio	96-102
30861618-7	2019	Based on the docking calculations, top hit compounds were identified to disrupt both Keap1a and Keap1b interaction with Nrf2 which include quercetin 3,4"-diglucoside, flavin adenine dinucleotide disodium salt hydrate, salvianolic acid A, tunicamycin and esculin.	Tunicamycin	238-249	nfe2 like bZIP transcription factor 2a	Danio rerio	120-124
30280512-4	2019	The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes.	Tunicamycin	74-85	vesicle-associated membrane protein 721	Arabidopsis thaliana	33-40
30280512-4	2019	The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes.	Tunicamycin	74-85	vesicle-associated membrane protein 721	Arabidopsis thaliana	192-199
30280512-4	2019	The greater growth inhibition in VAMP721/722-deficient plants, induced by tunicamycin, suggests that plants under ER stress maintain physiological homeostasis, at least in part, by regulating VAMP721/722 levels, as VAMP721/722 are known to participate in various biological processes.	Tunicamycin	74-85	vesicle-associated membrane protein 721	Arabidopsis thaliana	192-199
31109102-7	2019	Selenate and tunicamycin (Tm) treatment were used to induce SELENOF up-regulation.	Tunicamycin	13-24	selenoprotein F	Homo sapiens	60-67
31183612-5	2019	In cells treated with tunicamycin, resveratrol increased the expression of clusterin mRNA and protein and the secreted clusterin protein level in conditioned medium.	Tunicamycin	22-33	clusterin	Homo sapiens	75-84
31183612-5	2019	In cells treated with tunicamycin, resveratrol increased the expression of clusterin mRNA and protein and the secreted clusterin protein level in conditioned medium.	Tunicamycin	22-33	clusterin	Homo sapiens	119-128
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.	Tunicamycin	195-206	SEL1L adaptor subunit of ERAD E3 ubiquitin ligase	Homo sapiens	176-181
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.	Tunicamycin	195-206	synoviolin 1	Homo sapiens	186-190
30912977-6	2019	SSC-linked NRG1 clusters were severely disrupted in acutely stressed MNs and after tunicamycin-induced ER stress.	Tunicamycin	83-94	neuregulin 1	Mus musculus	11-15
30653687-7	2019	mGPDH deletion exacerbated tunicamycin (ER stress inducer)-induced hepatic steatosis, whereas tauroursodeoxycholic acid (ER stress inhibitor) rescued mGPDH depletion-induced steatosis on an HFD.	Tunicamycin	27-38	glycerol phosphate dehydrogenase 2, mitochondrial	Mus musculus	0-5
30664704-7	2019	Infusion of ER stress inducer (tunicamycin, Tun) in control mice induced ER stress in MRA and reduced phosphorylation of AMPK, eNOS synthase phosphorylation, and EDR in MRA without affecting systolic blood pressure (SBP).	Tunicamycin	31-42	nitric oxide synthase 3, endothelial cell	Mus musculus	127-131
30854665-6	2019	High-throughput sequencing analysis identified miR-23a-3p as one of the most abundant microRNAs in exosomes derived from tunicamycin (TM)-treated HCC cells (Exo-TMs).	Tunicamycin	121-132	microRNA 23a	Homo sapiens	47-54
30977402-6	2019	Tunicamycin increased the expression of PERK, leading to Nrf2 nuclear import, and tauroursodeoxycholate suppressed Nrf2 activation through PERK during ER stress, indicating that PERK activation is required for Nrf2 nuclear entry.	Tunicamycin	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	40-44
30977402-6	2019	Tunicamycin increased the expression of PERK, leading to Nrf2 nuclear import, and tauroursodeoxycholate suppressed Nrf2 activation through PERK during ER stress, indicating that PERK activation is required for Nrf2 nuclear entry.	Tunicamycin	0-11	nuclear factor, erythroid derived 2, like 2	Mus musculus	57-61
30417358-4	2019	Thus, in the present study, we aimed to investigate the effects of A2aR activation in MIN6 beta cells undergoing tunicamycin (TM)-mediated ER stress.	Tunicamycin	113-124	adenosine A2a receptor	Mus musculus	67-71
30417358-4	2019	Thus, in the present study, we aimed to investigate the effects of A2aR activation in MIN6 beta cells undergoing tunicamycin (TM)-mediated ER stress.	Tunicamycin	126-128	adenosine A2a receptor	Mus musculus	67-71
30417358-13	2019	Altogether, the present study revealed that A2aR signaling through PKA/Akt/CREB mediators alleviated TM cytotoxicity effects in MIN6 beta cells.	Tunicamycin	101-103	adenosine A2a receptor	Mus musculus	44-48
30417358-13	2019	Altogether, the present study revealed that A2aR signaling through PKA/Akt/CREB mediators alleviated TM cytotoxicity effects in MIN6 beta cells.	Tunicamycin	101-103	thymoma viral proto-oncogene 1	Mus musculus	71-74
30417358-13	2019	Altogether, the present study revealed that A2aR signaling through PKA/Akt/CREB mediators alleviated TM cytotoxicity effects in MIN6 beta cells.	Tunicamycin	101-103	cAMP responsive element binding protein 1	Mus musculus	75-79
31243264-6	2019	We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis.	Tunicamycin	101-112	heat shock protein family A (Hsp70) member 5	Homo sapiens	38-43
31243264-6	2019	We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis.	Tunicamycin	101-112	secreted protein acidic and cysteine rich	Homo sapiens	48-53
31243264-6	2019	We found that the interaction between GRP78 and SPARC increased during exposure to 5-FU, CPT-11, and tunicamycin, resulting in an attenuation of GRP78"s inhibition of apoptosis.	Tunicamycin	101-112	heat shock protein family A (Hsp70) member 5	Homo sapiens	145-150
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	0-11	colony stimulating factor 1 (macrophage)	Mus musculus	83-88
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	0-11	interleukin 12b	Mus musculus	216-223
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	0-11	interleukin 12a	Mus musculus	228-235
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	0-11	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	267-273
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	13-15	colony stimulating factor 1 (macrophage)	Mus musculus	83-88
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	13-15	interleukin 12b	Mus musculus	216-223
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	13-15	interleukin 12a	Mus musculus	228-235
31293572-3	2019	Tunicamycin (Tm) treatment of bone marrow derived macrophages (BMDM) cultured with M-CSF cultured bone marrow derived macrophages (M-BMDM) had markedly amplified M1-like responses to LPS, exhibiting higher levels of IL12p40 and IL12p35 mRNAs while BMDM cultured with GM-CSF, which normally express high IL12 subunit production in response to LPS, were relatively unaltered.	Tunicamycin	13-15	colony stimulating factor 2 (granulocyte-macrophage)	Mus musculus	267-273
30926605-0	2019	The kinase PERK and the transcription factor ATF4 play distinct and essential roles in autophagy resulting from tunicamycin-induced ER stress.	Tunicamycin	112-123	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	11-15
30926605-0	2019	The kinase PERK and the transcription factor ATF4 play distinct and essential roles in autophagy resulting from tunicamycin-induced ER stress.	Tunicamycin	112-123	activating transcription factor 4	Homo sapiens	45-49
30926605-4	2019	By analyzing the flux of LC3 through the autophagic pathway, as well as the sequestration and degradation of autophagic cargo, we here conclusively show that the classical ER stressor tunicamycin (TM) enhances autophagic activity in mammalian cells.	Tunicamycin	184-195	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	25-28
30926605-4	2019	By analyzing the flux of LC3 through the autophagic pathway, as well as the sequestration and degradation of autophagic cargo, we here conclusively show that the classical ER stressor tunicamycin (TM) enhances autophagic activity in mammalian cells.	Tunicamycin	197-199	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	25-28
31275960-6	2019	In addition, our findings demonstrated that IRE1 and HAC1 (two upstream modulators of the UPR) are required for the survival of gas1Delta yeast cells under the tunicamycin stress.	Tunicamycin	160-171	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	44-48
31275960-6	2019	In addition, our findings demonstrated that IRE1 and HAC1 (two upstream modulators of the UPR) are required for the survival of gas1Delta yeast cells under the tunicamycin stress.	Tunicamycin	160-171	transcription factor HAC1	Saccharomyces cerevisiae S288C	53-57
31275960-7	2019	On the other hand, we provided evidence that the GAS1 overexpression caused an obvious sensitivity to the low-tunicamycin-concentration (0.25 mug/mL).	Tunicamycin	110-121	1,3-beta-glucanosyltransferase GAS1	Saccharomyces cerevisiae S288C	49-53
31281585-6	2019	In vitro, ZYZ-803 ameliorates ERS-related necroptosis induced by tunicamycin, and such effect has been depending on the receptor-interacting protein 3- (RIP3-) Ca2+-calmodulin-dependent protein kinase (CaMKII) signaling pathway.	Tunicamycin	65-76	receptor interacting serine/threonine kinase 3	Homo sapiens	120-200
30154447-9	2019	Importantly, these drugs also included ER stress-inducing agents, such as thapsigargin and tunicamycin, a form of cell death for which a critical pro-apoptotic function of caspase-12 has previously been reported.	Tunicamycin	91-102	caspase 12	Mus musculus	172-182
31109102-7	2019	Selenate and tunicamycin (Tm) treatment were used to induce SELENOF up-regulation.	Tunicamycin	26-28	selenoprotein F	Homo sapiens	60-67
31071981-6	2019	Inducing ER stress with tunicamycin activated the Wnt/beta-catenin pathway, whereas reducing ER stress with 4-phenylbutyric acid inhibited it.	Tunicamycin	24-35	catenin beta 1	Homo sapiens	54-66
30703445-5	2019	The ER stress activators thapsigargin (Tg) and tunicamycin (Tm) markedly reduced Bmal1-Luc oscillation amplitudes and induced phase delay shifts in NIH3T3 cells.	Tunicamycin	47-58	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	81-86
30703445-5	2019	The ER stress activators thapsigargin (Tg) and tunicamycin (Tm) markedly reduced Bmal1-Luc oscillation amplitudes and induced phase delay shifts in NIH3T3 cells.	Tunicamycin	60-62	aryl hydrocarbon receptor nuclear translocator-like	Mus musculus	81-86
30336657-3	2019	METHODS: In primary human nasal epithelial cells, the effect of tunicamycin (an ER stress inducer) and 4-phenylbutyric acid (4-PBA, ER stress inhibitor) on the expression of MUC5AC and MUC5B was investigated by reverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and immunoblot analysis.	Tunicamycin	64-75	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	174-180
30336657-3	2019	METHODS: In primary human nasal epithelial cells, the effect of tunicamycin (an ER stress inducer) and 4-phenylbutyric acid (4-PBA, ER stress inhibitor) on the expression of MUC5AC and MUC5B was investigated by reverse transcriptase-polymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and immunoblot analysis.	Tunicamycin	64-75	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	185-190
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	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	50-56
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	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	61-66
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	X-box binding protein 1	Homo sapiens	152-175
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	X-box binding protein 1	Homo sapiens	177-182
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
30336657-5	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	activating transcription factor 6	Homo sapiens	268-272
30336657-6	2019	In addition, 4-PBA attenuated the tunicamycin-induced expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules.	Tunicamycin	34-45	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	69-75
30336657-6	2019	In addition, 4-PBA attenuated the tunicamycin-induced expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules.	Tunicamycin	34-45	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	80-85
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	X-box binding protein 1	Homo sapiens	33-38
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
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	activating transcription factor 6	Homo sapiens	50-54
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	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	136-142
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	mucin 5B, oligomeric mucus/gel-forming	Homo sapiens	147-152
30711450-6	2019	Recombinant CCL21 improved pTr and pLE cell proliferation through activation of the PI3K and MAPK pathways and suppression of tunicamycin-induced endoplasmic reticulum (ER) stress or LPS-induced inflammation.	Tunicamycin	126-137	C-C motif chemokine ligand 21	Sus scrofa	12-17
30824472-0	2019	Sphingolipid/Pkh1/2-TORC1/Sch9 Signaling Regulates Ribosome Biogenesis in Tunicamycin-Induced Stress Response in Yeast.	Tunicamycin	74-85	serine/threonine protein kinase PKH1	Saccharomyces cerevisiae S288C	13-19
30824472-0	2019	Sphingolipid/Pkh1/2-TORC1/Sch9 Signaling Regulates Ribosome Biogenesis in Tunicamycin-Induced Stress Response in Yeast.	Tunicamycin	74-85	serine/threonine protein kinase SCH9	Saccharomyces cerevisiae S288C	26-30
30824472-3	2019	Here, we describe a novel regulatory model, in which tunicamycin-mediated stress induces the accumulation of long-chain sphingoid bases and subsequent activation of Pkh1/2 signaling, which leads to decreased expression of ribosomal protein genes via the downstream effectors Pkc1 and Sch9.	Tunicamycin	53-64	serine/threonine protein kinase PKH1	Saccharomyces cerevisiae S288C	165-171
30824472-3	2019	Here, we describe a novel regulatory model, in which tunicamycin-mediated stress induces the accumulation of long-chain sphingoid bases and subsequent activation of Pkh1/2 signaling, which leads to decreased expression of ribosomal protein genes via the downstream effectors Pkc1 and Sch9.	Tunicamycin	53-64	protein kinase C	Saccharomyces cerevisiae S288C	275-279
30824472-3	2019	Here, we describe a novel regulatory model, in which tunicamycin-mediated stress induces the accumulation of long-chain sphingoid bases and subsequent activation of Pkh1/2 signaling, which leads to decreased expression of ribosomal protein genes via the downstream effectors Pkc1 and Sch9.	Tunicamycin	53-64	serine/threonine protein kinase SCH9	Saccharomyces cerevisiae S288C	284-288
30824472-6	2019	Our results suggest that sphingolipid/Pkh1/2-TORC1/Sch9 signaling is an important determinant for adaptation to tunicamycin-induced stress.	Tunicamycin	112-123	serine/threonine protein kinase PKH1	Saccharomyces cerevisiae S288C	38-44
30979007-5	2019	Significant changes in gene and protein expression were found upon tunicamycin treatment for CB1 and CB2, as well as for GPR55 receptors, but not for transient receptor potential vanilloid 1 (TRPV1).	Tunicamycin	67-78	cannabinoid receptor 1	Homo sapiens	93-96
30824472-6	2019	Our results suggest that sphingolipid/Pkh1/2-TORC1/Sch9 signaling is an important determinant for adaptation to tunicamycin-induced stress.	Tunicamycin	112-123	serine/threonine protein kinase SCH9	Saccharomyces cerevisiae S288C	51-55
30894460-3	2019	Treatment with the ER stress inducer tunicamycin resulted in the splicing of a 32-nucleotide fragment of a basic leucine zipper 1 (bZIP1) transcription factor (CrbZIP1) mRNA by CrIRE1 that, in turn, resulted in the loss of the transmembrane domain in CrbZIP1, and the translocation of CrbZIP1 from the ER to the nucleus.	Tunicamycin	37-48	uncharacterized protein	Chlamydomonas reinhardtii	177-183
30753838-3	2019	Here we report that ZBTB7A functions as an important prosurvival factor in osteosarcoma cells undergoing pharmacological ER stress-induced by tunicamycin (TM) or thapsigargin (TG).	Tunicamycin	142-153	zinc finger and BTB domain containing 7A	Homo sapiens	20-26
30753838-3	2019	Here we report that ZBTB7A functions as an important prosurvival factor in osteosarcoma cells undergoing pharmacological ER stress-induced by tunicamycin (TM) or thapsigargin (TG).	Tunicamycin	155-157	zinc finger and BTB domain containing 7A	Homo sapiens	20-26
30979007-5	2019	Significant changes in gene and protein expression were found upon tunicamycin treatment for CB1 and CB2, as well as for GPR55 receptors, but not for transient receptor potential vanilloid 1 (TRPV1).	Tunicamycin	67-78	cannabinoid receptor 2	Homo sapiens	101-104
30979007-6	2019	Deglycosylation experiments with N-glycosidase-F and immunoblot of cell membranes derived from SH-SY5Y cells confirmed the presence of one glycosylated form in CB1 (70 kDa), that was reduced by tunicamycin.	Tunicamycin	194-205	cannabinoid receptor 1	Homo sapiens	160-163
30979007-7	2019	Morphological studies demonstrated the co-localization of CB1 with GlcNAc residues, and showed that tunicamycin reduced CB1 membrane expression with a marked nuclear localization, as confirmed by immunoblotting.	Tunicamycin	100-111	cannabinoid receptor 1	Homo sapiens	120-123
30953513-5	2019	In vitro, tunicamycin treatment and genetic tools were used to produce non-glycosylated and lowly glycosylated CD147.	Tunicamycin	10-21	basigin (Ok blood group)	Homo sapiens	111-116
31508171-3	2019	In our study, 3T3-L1 adipocytes were pre-treated with ERS inhibitors tauroursodeoxycholic acid (TUDCA), Ex-4 and an ERS inducer tunicamycin (TM) then induced insulin resistance.	Tunicamycin	128-139	insulin	Homo sapiens	158-165
31508171-3	2019	In our study, 3T3-L1 adipocytes were pre-treated with ERS inhibitors tauroursodeoxycholic acid (TUDCA), Ex-4 and an ERS inducer tunicamycin (TM) then induced insulin resistance.	Tunicamycin	141-143	insulin	Homo sapiens	158-165
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	143-148
30238980-8	2019	Furthermore, tunicamycin-induced endoplasmic reticulum (ER) stress was inactivated by ephrin A1 treatment of BEND cells.	Tunicamycin	13-24	ephrin A1	Bos taurus	86-95
30914711-5	2019	Moreover, PSP/reg expression is induced by the canonical chemical inducers of ER stress, tunicamycin and thapsigargin.	Tunicamycin	89-100	regenerating family member 1 alpha	Homo sapiens	14-17
30680482-0	2019	NF-kappaB contributes to Smac mimetic-conferred protection from tunicamycin-induced apoptosis.	Tunicamycin	64-75	nuclear factor kappa B subunit 1	Homo sapiens	0-9
30680482-0	2019	NF-kappaB contributes to Smac mimetic-conferred protection from tunicamycin-induced apoptosis.	Tunicamycin	64-75	diablo IAP-binding mitochondrial protein	Homo sapiens	25-29
30680482-2	2019	Here, we report that Smac mimetic-mediated activation of NF-kappaB contributes to the rescue of cancer cells from tunicamycin (TM)-triggered apoptosis.	Tunicamycin	114-125	diablo IAP-binding mitochondrial protein	Homo sapiens	21-25
30680482-2	2019	Here, we report that Smac mimetic-mediated activation of NF-kappaB contributes to the rescue of cancer cells from tunicamycin (TM)-triggered apoptosis.	Tunicamycin	114-125	nuclear factor kappa B subunit 1	Homo sapiens	57-66
30784934-4	2019	Morin downregulated the expression of GRP78, central regulator of ER stress response, induced by ER stress inducer tunicamycin.	Tunicamycin	115-126	heat shock protein family A (Hsp70) member 5	Homo sapiens	38-43
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
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	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	161-165
30930751-5	2019	In addition, mitochondrial protection of Homer1a was blocked by the ER stress activator Tunicamycin (TM) with a re-escalated ROS level, increasing ATP and MMP loss.	Tunicamycin	88-99	homer scaffold protein 1	Homo sapiens	41-48
30930751-5	2019	In addition, mitochondrial protection of Homer1a was blocked by the ER stress activator Tunicamycin (TM) with a re-escalated ROS level, increasing ATP and MMP loss.	Tunicamycin	101-103	homer scaffold protein 1	Homo sapiens	41-48
30615971-4	2019	Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt.	Tunicamycin	71-82	lipocalin 2	Mus musculus	19-23
30615971-4	2019	Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt.	Tunicamycin	71-82	lipocalin 2	Mus musculus	122-126
30615971-4	2019	Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt.	Tunicamycin	84-86	lipocalin 2	Mus musculus	19-23
30615971-4	2019	Upon incubation of Lcn2-/- and wild type (wt) primary hepatocytes with tunicamycin (TM) or thapsigargin (TG) we found the Lcn2-/- hepatocytes to react with strong UPR to the ER stress, as evidenced by significantly increased levels of Grp94, Bip and Chop mRNA and protein compared to the wt.	Tunicamycin	84-86	lipocalin 2	Mus musculus	122-126
30600443-5	2019	N-linked glycosylation synthesis inhibitor tunicamycin causes a reduction of CaV3.1-T-type Ca2+ channel current (CaV3.1-ICa.T) when applied for 12 h or longer.	Tunicamycin	43-54	calcium voltage-gated channel subunit alpha1 G	Homo sapiens	77-83
30620686-6	2019	We found that Pak2 cardiac deleted mice (Pak2-CKO) under tunicamycin stress or pressure overload manifested a defective ER response, cardiac dysfunction, and profound cell death.	Tunicamycin	57-68	p21 (RAC1) activated kinase 2	Mus musculus	14-18
30620686-6	2019	We found that Pak2 cardiac deleted mice (Pak2-CKO) under tunicamycin stress or pressure overload manifested a defective ER response, cardiac dysfunction, and profound cell death.	Tunicamycin	57-68	p21 (RAC1) activated kinase 2	Mus musculus	41-45
30452882-10	2019	Although the endoplasmic reticulum stressors thapsigargin and tunicamycin induced markedly and sustained expression of ATF4 and XBP-1, they did not induce RAGE shedding to the same level as TNF-alpha, suggesting that ATF4 is necessary but not sufficient alone for TNF-alpha-mediated RAGE shedding.	Tunicamycin	62-73	activating transcription factor 4	Homo sapiens	119-123
30452882-10	2019	Although the endoplasmic reticulum stressors thapsigargin and tunicamycin induced markedly and sustained expression of ATF4 and XBP-1, they did not induce RAGE shedding to the same level as TNF-alpha, suggesting that ATF4 is necessary but not sufficient alone for TNF-alpha-mediated RAGE shedding.	Tunicamycin	62-73	X-box binding protein 1	Homo sapiens	128-133
30600443-5	2019	N-linked glycosylation synthesis inhibitor tunicamycin causes a reduction of CaV3.1-T-type Ca2+ channel current (CaV3.1-ICa.T) when applied for 12 h or longer.	Tunicamycin	43-54	calcium voltage-gated channel subunit alpha1 G	Homo sapiens	113-119
30600443-7	2019	Use-dependent inactivation of CaV3.1-ICa.T was accelerated, and recovery from inactivation was prolonged by tunicamycin (24 h).	Tunicamycin	108-119	calcium voltage-gated channel subunit alpha1 G	Homo sapiens	30-36
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	31-36
30820153-0	2019	Involvement of Orai1 in tunicamycin-induced endothelial dysfunction.	Tunicamycin	24-35	ORAI calcium release-activated calcium modulator 1	Homo sapiens	15-20
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	100-103
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
30820153-8	2019	Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.	Tunicamycin	14-25	ORAI calcium release-activated calcium modulator 1	Homo sapiens	47-52
30820153-8	2019	Regulation of tunicamycin-induced ER stress by Orai1 indicates that modification of Orai1 activity may have therapeutic value for conditions with ER stress-induced endothelial dysfunction.	Tunicamycin	14-25	ORAI calcium release-activated calcium modulator 1	Homo sapiens	84-89
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
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	tribbles pseudokinase 3	Homo sapiens	72-77
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	mechanistic target of rapamycin kinase	Homo sapiens	214-218
30483742-0	2019	Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-kappaB signaling pathway.	Tunicamycin	0-11	pentraxin 3	Homo sapiens	88-92
30770792-0	2019	Smac mimetic suppresses tunicamycin-induced apoptosis via resolution of ER stress.	Tunicamycin	24-35	diablo IAP-binding mitochondrial protein	Homo sapiens	0-4
30770792-2	2019	Here, we discover that Smac mimetic suppresses tunicamycin (TM)-induced apoptosis via resolution of the unfolded protein response (UPR) and ER stress.	Tunicamycin	47-58	diablo IAP-binding mitochondrial protein	Homo sapiens	23-27
30770792-2	2019	Here, we discover that Smac mimetic suppresses tunicamycin (TM)-induced apoptosis via resolution of the unfolded protein response (UPR) and ER stress.	Tunicamycin	60-62	diablo IAP-binding mitochondrial protein	Homo sapiens	23-27
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	83-111
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	113-118
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
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	168-201
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	203-207
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	X-box binding protein 1	Homo sapiens	229-252
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	X-box binding protein 1	Homo sapiens	254-258
30770792-9	2019	Thus, our study is the first to show that Smac mimetic protects from TM-triggered apoptosis by resolving the UPR and ER stress.	Tunicamycin	69-71	diablo IAP-binding mitochondrial protein	Homo sapiens	42-46
30566828-6	2019	When N-linked glycosylation was inhibited by tunicamycin or abolished by the N39Q, N39A, or T41A mutation, CTRP12 cleavage was enhanced.	Tunicamycin	45-56	C1q and TNF related 12	Homo sapiens	107-113
30448406-7	2019	Treating EVT-like JEG-3 and HTR8/SVneo cells with ER stress inducers (tunicamycin and thapsigargin) suppressed MMP2 mRNA and protein expression, secretion, and activity and reduced their invasiveness.	Tunicamycin	70-81	matrix metallopeptidase 2	Homo sapiens	111-115
30539651-5	2019	Concomitant treatment of tunicamycin and transfection of cells with MIOX-pcDNA led to a marked generation of ROS, which was reduced by MIOX-siRNA.	Tunicamycin	25-36	myo-inositol oxygenase	Mus musculus	68-72
30539651-5	2019	Concomitant treatment of tunicamycin and transfection of cells with MIOX-pcDNA led to a marked generation of ROS, which was reduced by MIOX-siRNA.	Tunicamycin	25-36	myo-inositol oxygenase	Mus musculus	135-139
30539651-11	2019	Also, their tunicamycin-induced accentuated expression in tubular cells was notably reduced with MIOX-siRNA.	Tunicamycin	12-23	myo-inositol oxygenase	Mus musculus	97-101
30483742-0	2019	Tunicamycin enhances the suppressive effects of cisplatin on lung cancer growth through PTX3 glycosylation via AKT/NF-kappaB signaling pathway.	Tunicamycin	0-11	AKT serine/threonine kinase 1	Homo sapiens	111-114
30483742-7	2019	Furthermore, we found that deglycosylated PTX3 (dePTX3) by tunicamycin (TM), which is N-glycan precursor biosynthesis blocker, and PNGase F significantly reduced the survival and migration of lung cancer cells.	Tunicamycin	59-70	pentraxin 3	Homo sapiens	42-46
30483742-7	2019	Furthermore, we found that deglycosylated PTX3 (dePTX3) by tunicamycin (TM), which is N-glycan precursor biosynthesis blocker, and PNGase F significantly reduced the survival and migration of lung cancer cells.	Tunicamycin	72-74	pentraxin 3	Homo sapiens	42-46
30475171-0	2019	Both thapsigargin- and tunicamycin-induced endoplasmic reticulum stress increases expression of Hrd1 in IRE1-dependent fashion.	Tunicamycin	23-34	synoviolin 1	Homo sapiens	96-100
30475171-0	2019	Both thapsigargin- and tunicamycin-induced endoplasmic reticulum stress increases expression of Hrd1 in IRE1-dependent fashion.	Tunicamycin	23-34	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	104-108
30475171-3	2019	RESULTS: We demonstrate that ER stress, induced by thapsigargin or tunicamycin, correlates with the increased expression of Hrd1 in both SH-SY5Y and SK-N-SH cells.	Tunicamycin	67-78	synoviolin 1	Homo sapiens	124-128
30475171-6	2019	Inhibition of IRE1 associated with the inhibition of XBP1 splicing does not affect the survival of SH-SY5Y cells treated with either thapsigargin or tunicamycin but results in the complete suppression of both the thapsigargin- and tunicamycin-induced expression of Hrd1.	Tunicamycin	231-242	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	14-18
31111119-4	2019	We provide further evidence that ER stress inducing agents (Tunicamycin and Brefeldin A) disrupts Ca2+ homeostasis by directly inhibiting TRPC1-mediated Ca2+ entry, which led to ER stress in salivary gland cells.	Tunicamycin	60-71	transient receptor potential cation channel, subfamily C, member 1	Mus musculus	138-143
31216950-6	2019	Since VAMP721/722 amounts were reported not to be increased by an ER stress inducer, tunicamycin in crt1/2 plants, our results suggest that ER stress and immune signalings distinctly control cellular abundance of VAMP721/722.	Tunicamycin	85-96	compromized recognition of TCV 1	Arabidopsis thaliana	100-106
30692541-4	2019	Oleic acid with or without tunicamycin significantly increases the formation of nucleoplasmic LDs, to which CDP-choline diacylglycerol phosphotransferase alpha (CCTalpha) is recruited, resulting in activation of phosphatidylcholine (PC) synthesis.	Tunicamycin	27-38	phosphate cytidylyltransferase 1A, choline	Homo sapiens	161-169
30429217-6	2019	Interestingly, calreticulin was sufficient for attenuating ER stress in tunicamycin- or thapsigargin-treated HeLa cells, whereas lentivirus-mediated shRNA calreticulin knockdown exacerbated ER stress.	Tunicamycin	72-83	calreticulin	Homo sapiens	15-27
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	caspase 3	Homo sapiens	148-157
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
30641938-5	2019	Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo.	Tunicamycin	158-169	uncoupling protein 1 (mitochondrial, proton carrier)	Mus musculus	37-57
30641938-5	2019	Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo.	Tunicamycin	158-169	uncoupling protein 1 (mitochondrial, proton carrier)	Mus musculus	59-63
30420428-7	2019	However, RyR blockade distinctly prevented beta-cell death, propagation of the unfolded protein response (UPR), and dysfunctional glucose-induced Ca2+ oscillations in tunicamycin-treated INS-1 beta cells and mouse islets and Akita islets.	Tunicamycin	167-178	ryanodine receptor 2	Rattus norvegicus	9-12
30475171-6	2019	Inhibition of IRE1 associated with the inhibition of XBP1 splicing does not affect the survival of SH-SY5Y cells treated with either thapsigargin or tunicamycin but results in the complete suppression of both the thapsigargin- and tunicamycin-induced expression of Hrd1.	Tunicamycin	231-242	X-box binding protein 1	Homo sapiens	53-57
30133247-5	2018	However, degradation of cytidylate kinase (CMK), which catalyzes reactions involved in the synthesis of both ribonucleotides and deoxyribonucleotides, blocks both DNA replication and wall teichoic acid biosynthesis, producing cytological effects identical to those created by simultaneously inhibiting both processes with the antibiotics ciprofloxacin and tunicamycin.	Tunicamycin	356-367	cytidine/uridine monophosphate kinase 1	Homo sapiens	24-41
30133247-5	2018	However, degradation of cytidylate kinase (CMK), which catalyzes reactions involved in the synthesis of both ribonucleotides and deoxyribonucleotides, blocks both DNA replication and wall teichoic acid biosynthesis, producing cytological effects identical to those created by simultaneously inhibiting both processes with the antibiotics ciprofloxacin and tunicamycin.	Tunicamycin	356-367	cytidine/uridine monophosphate kinase 1	Homo sapiens	43-46
30619478-10	2018	Moreover, induction of ER stress by tunicamycin and thapsigargin markedly increases Nrf2 expression, which is abolished in cells pretreated with XBP1 splicing inhibitors 4mu8C and quinotrierixin.	Tunicamycin	36-47	NFE2 like bZIP transcription factor 2	Homo sapiens	84-88
30619478-10	2018	Moreover, induction of ER stress by tunicamycin and thapsigargin markedly increases Nrf2 expression, which is abolished in cells pretreated with XBP1 splicing inhibitors 4mu8C and quinotrierixin.	Tunicamycin	36-47	X-box binding protein 1	Homo sapiens	145-149
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
30567393-3	2018	Tunicamycin (TM) treatment significantly increased mRNA levels of CHOP and GRP78, and induced lipid accumulation in the liver.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	75-80
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
30567393-3	2018	Tunicamycin (TM) treatment significantly increased mRNA levels of CHOP and GRP78, and induced lipid accumulation in the liver.	Tunicamycin	13-15	heat shock protein family A (Hsp70) member 5	Homo sapiens	75-80
30588337-7	2018	Our screens confirmed that MFSD2A and ARF4, which were identified in previous screens, are necessary for tunicamycin- and brefeldin A-induced cytotoxicity, respectively.	Tunicamycin	105-116	major facilitator superfamily domain containing 2A	Homo sapiens	27-33
30588337-7	2018	Our screens confirmed that MFSD2A and ARF4, which were identified in previous screens, are necessary for tunicamycin- and brefeldin A-induced cytotoxicity, respectively.	Tunicamycin	105-116	ADP ribosylation factor 4	Homo sapiens	38-42
30556167-4	2018	We found that 17-AAG (tanespimycin), an HSP90 (heat shock protein 90) inhibitor often used to kill cancer cells, could potently inhibit tunicamycin-induced ERS and the downstream nuclear factor kappa B activity in neonatal rat cardiomyocytes, leading to diminished apoptotic signaling and thus enhanced cell survival.	Tunicamycin	136-147	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	40-45
30556167-4	2018	We found that 17-AAG (tanespimycin), an HSP90 (heat shock protein 90) inhibitor often used to kill cancer cells, could potently inhibit tunicamycin-induced ERS and the downstream nuclear factor kappa B activity in neonatal rat cardiomyocytes, leading to diminished apoptotic signaling and thus enhanced cell survival.	Tunicamycin	136-147	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	47-68
30063946-3	2018	Because obesity promotes endoplasmic reticulum (ER) stress, we sought to determine how tunicamycin-induced ER stress affected Gnrh1 gene expression in the mouse hypothalamic cell line GT1-7.	Tunicamycin	87-98	gonadotropin releasing hormone 1	Mus musculus	126-131
30063946-4	2018	Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos.	Tunicamycin	0-11	gonadotropin releasing hormone 1	Mus musculus	36-41
30063946-4	2018	Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos.	Tunicamycin	0-11	mitogen-activated protein kinase 8	Mus musculus	56-59
30063946-4	2018	Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos.	Tunicamycin	0-11	gonadotropin releasing hormone 1	Mus musculus	119-124
30063946-4	2018	Tunicamycin repressed expression of Gnrh1 in a PKC- and JNK-dependent manner, while upregulating expression of a known Gnrh1 repressor, Fos.	Tunicamycin	0-11	FBJ osteosarcoma oncogene	Mus musculus	136-139
30063946-7	2018	Using a small molecule inhibitor, we determined that AP-1 was required for Gnrh1 repression by high-dose palmitate or tunicamycin-induced ER stress.	Tunicamycin	118-129	jun proto-oncogene	Mus musculus	53-57
30063946-7	2018	Using a small molecule inhibitor, we determined that AP-1 was required for Gnrh1 repression by high-dose palmitate or tunicamycin-induced ER stress.	Tunicamycin	118-129	gonadotropin releasing hormone 1	Mus musculus	75-80
30647729-4	2018	ER stress induced by tunicamycin administration increased TG2 protein levels in the mouse prefrontal cortex (PFC).	Tunicamycin	21-32	transglutaminase 2, C polypeptide	Mus musculus	58-61
30173922-6	2018	We showed that disruption of ER homeostasis by treating adult rat cardiomyocytes in culture with tunicamycin leads to contractile dysfunction through JNK signaling pathway.	Tunicamycin	97-108	mitogen-activated protein kinase 8	Rattus norvegicus	150-153
30253173-7	2018	In particular, EX-4 treatment restored HFD- and tunicamycin-induced Nrf2 nuclear translocation to control levels.	Tunicamycin	48-59	nuclear factor, erythroid derived 2, like 2	Mus musculus	68-72
30417434-19	2018	Taken together, adenosine upregulated Bcl-2 and GADD34 to protect PBCs against Tu-induced apoptosis and increase Insulin secretion.	Tunicamycin	79-81	B cell leukemia/lymphoma 2	Mus musculus	38-43
30417434-19	2018	Taken together, adenosine upregulated Bcl-2 and GADD34 to protect PBCs against Tu-induced apoptosis and increase Insulin secretion.	Tunicamycin	79-81	protein phosphatase 1, regulatory subunit 15A	Mus musculus	48-54
30533198-14	2018	Tunicamycin upregulated p62 and protected synovial fibroblasts from BAY 11-7085-induced cell death.	Tunicamycin	0-11	sequestosome 1	Homo sapiens	24-27
30533221-9	2018	Stimulation with IL-1beta or tunicamycin induced hepatic GDF15 expression in hepatocytes.	Tunicamycin	29-40	growth differentiation factor 15	Homo sapiens	57-62
30017234-7	2018	ER stress inducer, tunicamycin (200 ng/mL) significantly increased the level of autophagy and reduced expression of fibronectin in HCFs, both of which were reversed by 4 Phenylbutyric acid.	Tunicamycin	19-30	fibronectin 1	Homo sapiens	116-127
30017234-9	2018	LC3 co-localized with fibronectin when stimulated HCFs with tunicamycin.	Tunicamycin	60-71	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	0-3
30017234-9	2018	LC3 co-localized with fibronectin when stimulated HCFs with tunicamycin.	Tunicamycin	60-71	fibronectin 1	Homo sapiens	22-33
30056252-10	2018	Subsequently, incubation with either MCR antagonists significantly augmented NO2/NO3 levels (stable NO metabolites) and this was attenuated by silencing of MCR or tunicamycin.	Tunicamycin	163-174	nuclear receptor subfamily 3 group C member 2	Homo sapiens	37-40
30360492-5	2018	In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant.	Tunicamycin	13-24	transcription factor HAC1	Saccharomyces cerevisiae S288C	38-42
30360492-5	2018	In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant.	Tunicamycin	13-24	Elongator subunit ELP3	Saccharomyces cerevisiae S288C	80-84
30360492-5	2018	In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant.	Tunicamycin	13-24	pseudouridine synthase DEG1	Saccharomyces cerevisiae S288C	85-89
30360492-5	2018	In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant.	Tunicamycin	26-28	transcription factor HAC1	Saccharomyces cerevisiae S288C	38-42
30360492-5	2018	In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant.	Tunicamycin	26-28	Elongator subunit ELP3	Saccharomyces cerevisiae S288C	80-84
30360492-5	2018	In addition, tunicamycin (TM) induced HAC1 splicing is strongly impaired in the elp3 deg1 mutant.	Tunicamycin	26-28	pseudouridine synthase DEG1	Saccharomyces cerevisiae S288C	85-89
30287474-4	2018	Further characterization of FKH-9 suggests that loss of FKH-9 enhances resistance to the ER toxin tunicamycin and results in enhanced ER-associated degradation (ERAD).	Tunicamycin	98-109	Fork-head domain-containing protein	Caenorhabditis elegans	28-33
30287474-4	2018	Further characterization of FKH-9 suggests that loss of FKH-9 enhances resistance to the ER toxin tunicamycin and results in enhanced ER-associated degradation (ERAD).	Tunicamycin	98-109	Fork-head domain-containing protein	Caenorhabditis elegans	56-61
30291216-8	2018	Desmogleins (Dsgs) 1 and 3, which constitute the core structure of desmosomes, were well transported to the cell-cell borders, but the amount decreased and showed an aberrant distribution at the cell borders in tunicamycin-treated keratinocytes.	Tunicamycin	211-222	desmoglein 1	Homo sapiens	0-26
30451898-5	2018	Indeed, in ER stressors-treated cells with thapsigargin, brefeldin A or tunicamycin, a greater increase in necrosis and decrease of ATP content was observed in NUPR1-defficent cells.	Tunicamycin	72-83	nuclear protein transcription regulator 1	Mus musculus	160-165
30096296-6	2018	Then we identified compound 20(S)-25-methoxyl-dammarane-3beta,12beta,20-triol (25-OCH3-PPD) could inhibit the promoter activity of SelS, further results showed that 25-OCH3-PPD effectively inhibited tunicamycin (TM) induced up-regulation of SelS expression in both mRNA and protein levels.	Tunicamycin	199-210	selenoprotein S	Homo sapiens	131-135
30096296-7	2018	Moreover, 25-OCH3-PPD significantly inhibited glucose-regulated protein 78 (GRP78; the major ER stress marker) expression in TM-induced ER stress in HepG2 and HEK293T cells, suggesting that 25-OCH3-PPD could attenuate ER stress in these cells.	Tunicamycin	125-127	heat shock protein family A (Hsp70) member 5	Homo sapiens	46-74
30096296-7	2018	Moreover, 25-OCH3-PPD significantly inhibited glucose-regulated protein 78 (GRP78; the major ER stress marker) expression in TM-induced ER stress in HepG2 and HEK293T cells, suggesting that 25-OCH3-PPD could attenuate ER stress in these cells.	Tunicamycin	125-127	heat shock protein family A (Hsp70) member 5	Homo sapiens	76-81
30245625-5	2018	In vitro, p58IPK-deficient RGCs show reduced viability and are more susceptible to cell death induced by the ER stress inducer tunicamycin (TM).	Tunicamycin	127-138	DnaJ heat shock protein family (Hsp40) member C3	Mus musculus	10-16
30063110-6	2018	In addition, we demonstrated that tunicamycin-induced ER stress in vitro upregulated ATF6 and CIP2A.	Tunicamycin	34-45	activating transcription factor 6	Homo sapiens	85-89
30063110-6	2018	In addition, we demonstrated that tunicamycin-induced ER stress in vitro upregulated ATF6 and CIP2A.	Tunicamycin	34-45	cellular inhibitor of PP2A	Homo sapiens	94-99
29894845-4	2018	Induction of ERS (Tunicamycin) in vivo in mice or ex vivo in mouse arteries led to severe arterial endothelial dysfunction (i.e. reduced flow-dependent, NO mediated dilatation in isolated small mesenteric arteries), and this was prevented by the PTP1B inhibitor trodusquemine and absent in PTP1B-/- mice.	Tunicamycin	18-29	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	246-251
29894845-4	2018	Induction of ERS (Tunicamycin) in vivo in mice or ex vivo in mouse arteries led to severe arterial endothelial dysfunction (i.e. reduced flow-dependent, NO mediated dilatation in isolated small mesenteric arteries), and this was prevented by the PTP1B inhibitor trodusquemine and absent in PTP1B-/- mice.	Tunicamycin	18-29	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	290-295
29894845-5	2018	Trodusquemine also prevented the Tunicamycin -induced increased arterial levels of the molecular ERS actors 78 kDa glucose-regulated protein (GRP78) and Activating Transcription Factor 6 (ATF6alpha).	Tunicamycin	33-44	heat shock protein 5	Mus musculus	142-147
29894845-5	2018	Trodusquemine also prevented the Tunicamycin -induced increased arterial levels of the molecular ERS actors 78 kDa glucose-regulated protein (GRP78) and Activating Transcription Factor 6 (ATF6alpha).	Tunicamycin	33-44	activating transcription factor 6	Mus musculus	188-197
29894845-6	2018	Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay).	Tunicamycin	0-11	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	51-56
29894845-6	2018	Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay).	Tunicamycin	0-11	heat shock protein 5	Mus musculus	62-67
29894845-6	2018	Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay).	Tunicamycin	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	95-147
29894845-6	2018	Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay).	Tunicamycin	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	149-153
29894845-6	2018	Tunicamycin strongly increased the interactions of PTP1B with GRP78 and the activated forms of protein kinase RNA-like endoplasmic reticulum kinase (PERK) and IRE1alpha (proximity Ligation Assay).	Tunicamycin	0-11	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	159-168
30107908-5	2018	We demonstrated here that oxicam-NSAIDs suppressed the activation of caspase-3 and cell death caused by MPP+ or ER stress-inducer, tunicamycin, in SH-SY5Y cells.	Tunicamycin	131-142	caspase 3	Homo sapiens	69-78
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
30185560-6	2018	Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype.	Tunicamycin	147-158	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Saccharomyces cerevisiae S288C	78-82
30185560-6	2018	Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype.	Tunicamycin	147-158	proteasome core particle subunit beta 6	Saccharomyces cerevisiae S288C	118-122
30185560-6	2018	Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype.	Tunicamycin	250-261	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Saccharomyces cerevisiae S288C	78-82
30185560-6	2018	Among these genes, overexpression of UDP-N-acetylglucosamine-1-P transferase (ALG7), a subunit of the 20S proteasome (PRE7), and YBR085C-A induced tunicamycin resistance in wild-type cells, whereas deletion of all three genes completely reversed the tunicamycin-resistance phenotype.	Tunicamycin	250-261	proteasome core particle subunit beta 6	Saccharomyces cerevisiae S288C	118-122
30209265-5	2018	Reduction in GRP78 expression during tunicamycin-induced endoplasmic reticulum stress also suppressed MTII-mediated internalization of MC4R and cAMP-mediated transcriptional activity.	Tunicamycin	37-48	heat shock protein 5	Mus musculus	13-18
30209265-5	2018	Reduction in GRP78 expression during tunicamycin-induced endoplasmic reticulum stress also suppressed MTII-mediated internalization of MC4R and cAMP-mediated transcriptional activity.	Tunicamycin	37-48	metallothionein 2	Mus musculus	102-106
30209265-5	2018	Reduction in GRP78 expression during tunicamycin-induced endoplasmic reticulum stress also suppressed MTII-mediated internalization of MC4R and cAMP-mediated transcriptional activity.	Tunicamycin	37-48	melanocortin 4 receptor	Mus musculus	135-139
30206979-5	2018	Furthermore, tunicamycin treatment downregulated GPR177 expression in a dose-dependent manner.	Tunicamycin	13-24	Wnt ligand secretion mediator	Homo sapiens	49-55
30206979-8	2018	Small interfering RNA-mediated knockdown of GPR177 leads to sensitization to ER stress and induces apoptosis of cancer cells along with tunicamycin treatment.	Tunicamycin	136-147	Wnt ligand secretion mediator	Homo sapiens	44-50
30206979-11	2018	Efficacy of tunicamycin chemotherapy treatments depended on GPR177 expression in gastric cancer cell lines.	Tunicamycin	12-23	Wnt ligand secretion mediator	Homo sapiens	60-66
30245625-5	2018	In vitro, p58IPK-deficient RGCs show reduced viability and are more susceptible to cell death induced by the ER stress inducer tunicamycin (TM).	Tunicamycin	140-142	DnaJ heat shock protein family (Hsp40) member C3	Mus musculus	10-16
29430617-5	2018	In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment.	Tunicamycin	30-41	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	153-157
29430617-5	2018	In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment.	Tunicamycin	30-41	X-box binding protein 1	Mus musculus	173-196
29430617-5	2018	In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment.	Tunicamycin	30-41	X-box binding protein 1	Mus musculus	198-202
29430617-5	2018	In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment.	Tunicamycin	30-41	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	267-271
29430617-5	2018	In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment.	Tunicamycin	30-41	X-box binding protein 1	Mus musculus	272-276
29430617-5	2018	In this study, treatment with tunicamycin, an ER stress inducer, enhanced the phosphorylation level of inositol-requiring ER-to-nucleus signal kinase 1 (IRE1) and increased X-box-binding protein 1 (XBP1) mRNA splicing activity in the mouse PFC, whereas inhibition of IRE1/XBP1 pathway in PFC by a viral particle approach attenuated social behavioral deficits caused by tunicamycin treatment.	Tunicamycin	369-380	X-box binding protein 1	Mus musculus	198-202
29430617-6	2018	Reduced estrogen receptor beta (ERbeta) protein levels were found in the PFC of male mice following tunicamycin treatment.	Tunicamycin	100-111	estrogen receptor 2 (beta)	Mus musculus	8-30
29430617-6	2018	Reduced estrogen receptor beta (ERbeta) protein levels were found in the PFC of male mice following tunicamycin treatment.	Tunicamycin	100-111	estrogen receptor 2 (beta)	Mus musculus	32-38
29430617-7	2018	Pretreatment with an ERbeta specific agonist, ERB-041 significantly attenuated tunicamycin-induced deficits in social behavior, and activation of IRE1/XBP1 pathway in mouse PFC.	Tunicamycin	79-90	estrogen receptor 2 (beta)	Mus musculus	21-27
29430617-7	2018	Pretreatment with an ERbeta specific agonist, ERB-041 significantly attenuated tunicamycin-induced deficits in social behavior, and activation of IRE1/XBP1 pathway in mouse PFC.	Tunicamycin	79-90	estrogen receptor 2 (beta)	Mus musculus	46-49
29430617-8	2018	Moreover, ERB-041 inhibited tunicamycin-induced increases in functional connectivity between PFC and hippocampus in male mice.	Tunicamycin	28-39	estrogen receptor 2 (beta)	Mus musculus	10-13
29936187-10	2018	mRNA and protein ratios of apoptotic modulators (Bax/Bcl2) are higher in 158JP oligodendrocytes which are also more vulnerable than 158N cells to tunicamycin-induced ER-stress.	Tunicamycin	146-157	BCL2 associated X, apoptosis regulator	Homo sapiens	49-52
29936187-10	2018	mRNA and protein ratios of apoptotic modulators (Bax/Bcl2) are higher in 158JP oligodendrocytes which are also more vulnerable than 158N cells to tunicamycin-induced ER-stress.	Tunicamycin	146-157	BCL2 apoptosis regulator	Homo sapiens	53-57
30127865-6	2018	Results demonstrated that tunicamycin administration promoted apoptosis of glioblastoma cells through the upregulation of poly(ADP-ribose) polymerase and caspase-9.	Tunicamycin	26-37	poly(ADP-ribose) polymerase 1	Homo sapiens	122-149
30127865-0	2018	MEG-3-mediated Wnt/beta-catenin signaling pathway controls the inhibition of tunicamycin-mediated viability in glioblastoma.	Tunicamycin	77-88	maternally expressed 3	Homo sapiens	0-5
30127865-0	2018	MEG-3-mediated Wnt/beta-catenin signaling pathway controls the inhibition of tunicamycin-mediated viability in glioblastoma.	Tunicamycin	77-88	catenin beta 1	Homo sapiens	19-31
30147026-4	2018	Increased expression of ER stress markers, inflammation and apoptosis of alveolar epithelial cells were observed in Atg4b-deficient mice compared to WT mice, when treated with the ER stress inducer tunicamycin.	Tunicamycin	198-209	autophagy related 4B, cysteine peptidase	Mus musculus	116-121
30147026-5	2018	After tunicamycin treatment, Atg4b null lungs showed accumulation of its substrate LC3-I, demonstrating that these mice failed to induce autophagy despite the ER stress conditions.	Tunicamycin	6-17	autophagy related 4B, cysteine peptidase	Mus musculus	29-34
30147026-6	2018	We also showed that compromised autophagy in lungs from Atg4b null mice is associated with exacerbated lung damage, epithelial apoptosis and the development of lung fibrosis at 21 days after tunicamycin treatment.	Tunicamycin	191-202	autophagy related 4B, cysteine peptidase	Mus musculus	56-61
30147026-7	2018	Our findings indicate that ATG4B protein and autophagy are essential to mitigate ER stress and to prevent tunicamycin-induced epithelial apoptosis and lung fibrosis.	Tunicamycin	106-117	autophagy related 4B, cysteine peptidase	Mus musculus	27-32
30127865-6	2018	Results demonstrated that tunicamycin administration promoted apoptosis of glioblastoma cells through the upregulation of poly(ADP-ribose) polymerase and caspase-9.	Tunicamycin	26-37	caspase 9	Homo sapiens	154-163
30127865-8	2018	Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/beta-catenin in glioblastoma cells.	Tunicamycin	14-25	maternally expressed 3	Homo sapiens	54-81
30127865-8	2018	Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/beta-catenin in glioblastoma cells.	Tunicamycin	14-25	maternally expressed 3	Homo sapiens	83-88
30127865-8	2018	Additionally, tunicamycin increased the expression of maternally expressed gene-3 (MEG-3) and wingless/integrated (Wnt)/beta-catenin in glioblastoma cells.	Tunicamycin	14-25	catenin beta 1	Homo sapiens	120-132
30127865-9	2018	Results also indicated that tunicamycin administration promoted the Wnt/beta-catenin signaling pathway in glioblastoma cells.	Tunicamycin	28-39	catenin beta 1	Homo sapiens	72-84
30127865-10	2018	Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma.	Tunicamycin	29-40	maternally expressed 3	Homo sapiens	13-18
30127865-10	2018	Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma.	Tunicamycin	29-40	catenin beta 1	Homo sapiens	76-88
30127865-10	2018	Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma.	Tunicamycin	139-150	maternally expressed 3	Homo sapiens	13-18
30127865-10	2018	Knockdown of MEG-3 inhibited tunicamycin-mediated downregulation of the Wnt/beta-catenin signaling pathway, which was inhibited further by tunicamycin-mediated inhibition of viability and aggressiveness in glioblastoma.	Tunicamycin	139-150	catenin beta 1	Homo sapiens	76-88
30127865-12	2018	In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy.	Tunicamycin	43-54	maternally expressed 3	Homo sapiens	114-119
30127865-12	2018	In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy.	Tunicamycin	43-54	catenin beta 1	Homo sapiens	133-145
30127865-12	2018	In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy.	Tunicamycin	173-184	maternally expressed 3	Homo sapiens	114-119
30127865-12	2018	In conclusion, these results indicate that tunicamycin may inhibit the viability and aggressiveness by regulating MEG-3-mediated Wnt/beta-catenin signaling, suggesting that tunicamycin may be a potential anticancer agent for glioblastoma therapy.	Tunicamycin	173-184	catenin beta 1	Homo sapiens	133-145
30111858-5	2018	CRELD2 expression in Neuro2a cells was induced at the late phase after treatment with tunicamycin (Tm) compared with rapid induction of growth arrest and DNA damage inducible gene 153 (GADD153).	Tunicamycin	86-97	cysteine-rich with EGF-like domains 2	Mus musculus	0-6
30081561-0	2018	Induction of Liver Steatosis in BAP31-Deficient Mice Burdened with Tunicamycin-Induced Endoplasmic Reticulum Stress.	Tunicamycin	67-78	B cell receptor associated protein 31	Mus musculus	32-37
30081561-4	2018	In this study, wild-type and liver-specific BAP31-depleted mice were administrated with ER stress activator of Tunicamycin, the markers of ER stress, liver steatosis, and the underlying molecular mechanisms were determined.	Tunicamycin	111-122	B cell receptor associated protein 31	Mus musculus	44-49
30081561-5	2018	BAP31 deficiency increased Tunicamycin-induced hepatic lipid accumulation, aggravated liver dysfunction, and increased the mRNA levels of ER stress markers, including glucose-regulated protein 78 (GRP78), X-box binding protein 1 (XBP1), inositol-requiring protein-1alpha (IRE1alpha) and C/EBP homologous protein (CHOP), thus promoting ER stress in vivo and in vitro.	Tunicamycin	27-38	B cell receptor associated protein 31	Mus musculus	0-5
30081561-8	2018	Finally, BAP31 deficiency increased Tunicamycin-induced hepatic inflammatory response.	Tunicamycin	36-47	B cell receptor associated protein 31	Mus musculus	9-14
30081561-9	2018	These results demonstrate that BAP31 deficiency increased Tunicamycin-induced ER stress, impaired VLDL secretion and exogenous lipid clearance, and reduced fatty acid beta-oxidation, which eventually resulted in liver steatosis.	Tunicamycin	58-69	B cell receptor associated protein 31	Mus musculus	31-36
29871846-1	2018	A series of compounds was discovered that induce the production of VGF mRNA in SH-SY5Y cells and exhibit cytoprotection under tunicamycin induced endoplasmic reticulum (ER) stress.	Tunicamycin	126-137	VGF nerve growth factor inducible	Homo sapiens	67-70
29800817-3	2018	Werner (WRN) mutant cell lines AG11395, AG05229 and normal aged fibroblast AG13129 display a deficient response to tunicamycin mediated endoplasmic reticulum (ER) stress induced autophagy compared to clinically unaffected GM00637 and normal young fibroblast GM03440.	Tunicamycin	115-126	WRN RecQ like helicase	Homo sapiens	8-11
29553832-7	2018	Tunicamycin-induced deglycosylation inhibited TRPV4 activity and compromised [Ca2+]i signaling in NHK cells.	Tunicamycin	0-11	transient receptor potential cation channel subfamily V member 4	Homo sapiens	46-51
29575057-6	2018	Mice subjected to acute ER stress by pioglitazone administration and a low-dose tunicamycin injection presented a maladaptive UPR activation in SAT along with reduced adiponectin synthesis and secretion and increased lipolysis with respect to VAT, associated with lipid accumulation in skeletal muscle and liver.	Tunicamycin	80-91	adiponectin, C1Q and collagen domain containing	Mus musculus	167-178
29845243-4	2018	Notably, tunicamycin treatment, an endoplasmic reticulum (ER) stress inducer, induced the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha), but decreased ATF4 protein levels in the mouse liver.	Tunicamycin	9-20	eukaryotic translation initiation factor 2A	Mus musculus	109-156
29845243-4	2018	Notably, tunicamycin treatment, an endoplasmic reticulum (ER) stress inducer, induced the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha), but decreased ATF4 protein levels in the mouse liver.	Tunicamycin	9-20	eukaryotic translation initiation factor 2A	Mus musculus	158-167
29845243-4	2018	Notably, tunicamycin treatment, an endoplasmic reticulum (ER) stress inducer, induced the phosphorylation of eukaryotic translation initiation factor 2alpha (eIF2alpha), but decreased ATF4 protein levels in the mouse liver.	Tunicamycin	9-20	activating transcription factor 4	Mus musculus	184-188
29876740-5	2018	MANF-deficient N2a significantly elevated OS-9 protein after tunicamycin treatment; however, no specific differences in intra- and extracellular status of NHK protein were observed between wild-type and MANF-deficient cells.	Tunicamycin	61-72	mesencephalic astrocyte-derived neurotrophic factor	Mus musculus	0-4
29728739-11	2018	In the cultured renal arteries, tunicamycin and thapsigargin increased the expression of binding immunoglobulin protein (BiP), an ER stress marker.	Tunicamycin	32-43	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	89-119
29728739-11	2018	In the cultured renal arteries, tunicamycin and thapsigargin increased the expression of binding immunoglobulin protein (BiP), an ER stress marker.	Tunicamycin	32-43	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	121-124
29684334-4	2018	We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I.	Tunicamycin	51-62	mitogen-activated protein kinase 8	Mus musculus	101-104
29684334-4	2018	We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I.	Tunicamycin	51-62	mitogen-activated protein kinase kinase 7	Mus musculus	109-113
29684334-4	2018	We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I.	Tunicamycin	64-66	mitogen-activated protein kinase 8	Mus musculus	101-104
29684334-4	2018	We found that treatment with the ER stress inducer tunicamycin (TM) increased the phosphorylation of JNK and MKK7 in HT22 cells, which was nullified by GADD45beta-I.	Tunicamycin	64-66	mitogen-activated protein kinase kinase 7	Mus musculus	109-113
29684334-5	2018	GADD45beta-I significantly attenuated TM-induced toxicity via inhibiting apoptotic cell death, as evidenced by decreased number of TUNEL-positive cells and reduced caspase-3 activity.	Tunicamycin	38-40	caspase 3	Mus musculus	164-173
30034224-16	2018	In vitro, emodin treatment was further found to decrease the GRP78 level induced by high glucose or tunicamycin (TM).	Tunicamycin	100-111	heat shock protein 5	Mus musculus	61-66
30034224-16	2018	In vitro, emodin treatment was further found to decrease the GRP78 level induced by high glucose or tunicamycin (TM).	Tunicamycin	113-115	heat shock protein 5	Mus musculus	61-66
29988028-7	2018	Pharmacological activation of AMPK by metformin significantly abrogated the loss of RUNX2-S118 phosphorylation and protected from tunicamycin-induced endoplasmic reticulum stress, high glucose-induced in vitro adipogenesis and streptozotocin-induced in vivo bone adiposity and bone phenotype.	Tunicamycin	130-141	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	30-34
30034372-8	2018	Tunicamycin-treated bacteria or the bacterial WTA preparation suppressed NF-kappaB and inflammatory cytokine production (TNFalpha, and IL-6) from murine macrophage cell line (RAW 264.7) indicating the reduced WTA level possibly attenuates an inflammatory response.	Tunicamycin	0-11	tumor necrosis factor	Mus musculus	121-129
30034372-8	2018	Tunicamycin-treated bacteria or the bacterial WTA preparation suppressed NF-kappaB and inflammatory cytokine production (TNFalpha, and IL-6) from murine macrophage cell line (RAW 264.7) indicating the reduced WTA level possibly attenuates an inflammatory response.	Tunicamycin	0-11	interleukin 6	Mus musculus	135-139
29758225-6	2018	Indeed, we found that ER stress induced by thapsigargin and tunicamycin led to increased expression of TRPV6 via ATF6alpha signaling branch.	Tunicamycin	60-71	transient receptor potential cation channel subfamily V member 6	Homo sapiens	103-108
29675957-2	2018	Here, we injected tunicamycin (TM), a recognized ER stress inducer, into the brain ventricle of Sprague-Dawley (SD) rats to induce the unfolded protein response (UPR), demonstrated by the enhanced phosphorylation of pancreatic ER kinase (PERK), inositol-requiring enzyme-1 (IRE-1) and activating transcription factor-6 (ATF-6).	Tunicamycin	18-29	activating transcription factor 6	Rattus norvegicus	320-325
29675957-5	2018	Simultaneous inhibition of GSK-3beta by hippocampal infusion of SB216763 (SB) attenuated TM-induced UPR and spatial memory impairment with restoration of pS129-CREB and synaptic plasticity.	Tunicamycin	89-91	glycogen synthase kinase 3 alpha	Rattus norvegicus	27-36
29675957-2	2018	Here, we injected tunicamycin (TM), a recognized ER stress inducer, into the brain ventricle of Sprague-Dawley (SD) rats to induce the unfolded protein response (UPR), demonstrated by the enhanced phosphorylation of pancreatic ER kinase (PERK), inositol-requiring enzyme-1 (IRE-1) and activating transcription factor-6 (ATF-6).	Tunicamycin	18-29	activating transcription factor 6	Rattus norvegicus	285-318
29758225-6	2018	Indeed, we found that ER stress induced by thapsigargin and tunicamycin led to increased expression of TRPV6 via ATF6alpha signaling branch.	Tunicamycin	60-71	activating transcription factor 6	Homo sapiens	113-122
29891966-7	2018	The inhibition of N-glycosylation by tunicamycin or glucose starvation markedly reduced proIGF-1Ea and mature IGF-1 production.	Tunicamycin	37-48	insulin like growth factor 1	Homo sapiens	91-96
29650257-5	2018	An ER stress-inducing chemical, tunicamycin, increased the activities of caspase-3 and -4, whereas pretreatment with NPY decreased caspase-3 and -4 activities during the ER stress response.	Tunicamycin	32-43	caspase 3	Homo sapiens	73-89
29879176-3	2018	METHOD: ERS in INS-1-3 cells was induced by exposure cells to thapsigargin (TG), tunicamycin (TM) or palmitic acid (PA) +high glucose (HG).	Tunicamycin	81-92	forkhead box M1	Homo sapiens	15-20
29879176-3	2018	METHOD: ERS in INS-1-3 cells was induced by exposure cells to thapsigargin (TG), tunicamycin (TM) or palmitic acid (PA) +high glucose (HG).	Tunicamycin	94-96	forkhead box M1	Homo sapiens	15-20
29650257-6	2018	In addition, NPY suppressed the activation of three major ER stress sensors during the tunicamycin-induced ER stress response.	Tunicamycin	87-98	neuropeptide Y	Homo sapiens	13-16
29649564-4	2018	Both overexpression of XBP1s and tunicamycin treatment were able to enhance MANF transcription.	Tunicamycin	33-44	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	76-80
29688606-7	2018	Interestingly, although the degree of endogenous BiP3 protein accumulation in the ssi2 mutant was comparable to that in wild-type plants treated with the ER stress inducer tunicamycin, much less BiP3 transcripts were detected in the ssi2 mutant compared to tunicamycin-treated wild-type plants.	Tunicamycin	172-183	Plant stearoyl-acyl-carrier-protein desaturase family protein	Arabidopsis thaliana	82-86
28444413-4	2018	MATERIAL AND METHODS: Initially, the expression of CDNF was tested by treating H9c2 cells with various concentrations of tunicamycin (TM) and performing reverse-transcriptase polymerase chain reaction and Western blotting.	Tunicamycin	121-132	cerebral dopamine neurotrophic factor	Rattus norvegicus	51-55
29620275-7	2018	Compared with in cells prior to treatment, human leukemia cells treated with tunicamycin exhibited increased expression of p-PERK, p-eIF2alpha and GRP78 after 72 h (P&lt;0.05).	Tunicamycin	77-88	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	125-129
29620275-7	2018	Compared with in cells prior to treatment, human leukemia cells treated with tunicamycin exhibited increased expression of p-PERK, p-eIF2alpha and GRP78 after 72 h (P&lt;0.05).	Tunicamycin	77-88	eukaryotic translation initiation factor 2A	Homo sapiens	133-142
29620275-7	2018	Compared with in cells prior to treatment, human leukemia cells treated with tunicamycin exhibited increased expression of p-PERK, p-eIF2alpha and GRP78 after 72 h (P&lt;0.05).	Tunicamycin	77-88	heat shock protein family A (Hsp70) member 5	Homo sapiens	147-152
29744053-3	2018	Results: In the present study, we showed that intestinal epithelial cells (IEC-6) incubated with tunicamycin led to caspase-3-dependent apoptotic cell death.	Tunicamycin	97-108	caspase 3	Homo sapiens	116-125
29764928-6	2018	Our results show that ER stress maker GRP78 expression was increased in human endometrial Ishikawa and endometrial stromal cells (ESCs) treated with tunicamycin.	Tunicamycin	149-160	heat shock protein family A (Hsp70) member 5	Homo sapiens	38-43
29764928-7	2018	Addition of estrogen decreased tunicamycin-induced GRP78 expression.	Tunicamycin	31-42	heat shock protein family A (Hsp70) member 5	Homo sapiens	51-56
29626480-5	2018	TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice.	Tunicamycin	18-29	insulin receptor	Mus musculus	46-62
29626480-5	2018	TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice.	Tunicamycin	18-29	insulin receptor	Mus musculus	64-66
29626480-5	2018	TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice.	Tunicamycin	18-29	activating transcription factor 6	Mus musculus	92-101
29626480-5	2018	TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice.	Tunicamycin	31-33	insulin receptor	Mus musculus	46-62
29626480-5	2018	TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice.	Tunicamycin	31-33	insulin receptor	Mus musculus	64-66
29626480-5	2018	TSPA restored the tunicamycin (TM)-stimulated insulin receptor (IR) desensitization through ATF6alpha activation, inhibited gluconeogenesis and efficiently improved glucose homeostasis on db/db mice.	Tunicamycin	31-33	activating transcription factor 6	Mus musculus	92-101
29545069-6	2018	We defined that the post-acute response was dependent on SVCT2 located in early secretory compartments, and its trafficking was abolished with Tunicamycin and Brefeldin A treatment.	Tunicamycin	143-154	solute carrier family 23 member 2	Homo sapiens	57-62
29784903-7	2018	L-NAME, tunicamycin, and Genipin attenuated vasodilation in WT, WT-EX and ApoE KO-EX, but not in ApoE KO.	Tunicamycin	8-19	apolipoprotein E	Mus musculus	74-78
29744053-5	2018	Further study demonstrated that tunicamycin-induced cell death was enhanced by rapamycin, a specific inhibitor of mTORC1.	Tunicamycin	32-43	CREB regulated transcription coactivator 1	Mus musculus	114-120
29744053-7	2018	These effects of tunicamycin were exacerbated by mTORC1 inhibitor.	Tunicamycin	17-28	CREB regulated transcription coactivator 1	Mus musculus	49-55
29555819-3	2018	Here we show that the Grb10 gene could be reactivated in adult mouse liver by acute endoplasmic reticulum stress (ER stress) such as tunicamycin or a short-term high-fat diet (HFD) challenge, concurrently with increased unfolded protein response (UPR) and hepatosteatosis.	Tunicamycin	133-144	growth factor receptor bound protein 10	Mus musculus	22-27
29717117-5	2018	We found that tunicamycin (TU), but no other ER stress inducers, sensitized mouse fibroblasts and hippocampal neuronal cells to TRAIL-induced apoptosis.	Tunicamycin	14-25	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	128-133
29717117-5	2018	We found that tunicamycin (TU), but no other ER stress inducers, sensitized mouse fibroblasts and hippocampal neuronal cells to TRAIL-induced apoptosis.	Tunicamycin	27-29	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	128-133
29454702-6	2018	The CCL2 in MAC-T cells attenuates endoplasmic reticulum stress induced by tunicamycin, suggesting that CCL2 regulates intracellular synthesis of proteins and lipids and prevents activation of apoptotic pathways initiated in response to endoplasmic reticulum stress.	Tunicamycin	75-86	C-C motif chemokine 2	Bos taurus	4-8
29454702-6	2018	The CCL2 in MAC-T cells attenuates endoplasmic reticulum stress induced by tunicamycin, suggesting that CCL2 regulates intracellular synthesis of proteins and lipids and prevents activation of apoptotic pathways initiated in response to endoplasmic reticulum stress.	Tunicamycin	75-86	C-C motif chemokine 2	Bos taurus	104-108
29488603-8	2018	Flow cytometry assays indicated that miR-124 transfection attenuated apoptosis resistance of osteosarcoma to tunicamycin, potentially via the downregulation of P53 and Bcl-2 apoptosis regulator expression.	Tunicamycin	109-120	tumor protein p53	Homo sapiens	160-163
29385296-6	2018	Both allelic ire1 knock-down mutants ire1-1 and ire1-2 were much more sensitive than their parental strain CC-4533 to the ER stress inducers tunicamycin, dithiothreitol and brefeldin A.	Tunicamycin	141-152	uncharacterized protein	Chlamydomonas reinhardtii	13-17
29385296-6	2018	Both allelic ire1 knock-down mutants ire1-1 and ire1-2 were much more sensitive than their parental strain CC-4533 to the ER stress inducers tunicamycin, dithiothreitol and brefeldin A.	Tunicamycin	141-152	uncharacterized protein	Chlamydomonas reinhardtii	37-43
29385296-6	2018	Both allelic ire1 knock-down mutants ire1-1 and ire1-2 were much more sensitive than their parental strain CC-4533 to the ER stress inducers tunicamycin, dithiothreitol and brefeldin A.	Tunicamycin	141-152	uncharacterized protein	Chlamydomonas reinhardtii	37-41
29385296-7	2018	Treatment with a low concentration of tunicamycin resulted in growth arrest and cytolysis in ire1 mutants, but not in CC-4533 cells.	Tunicamycin	38-49	uncharacterized protein	Chlamydomonas reinhardtii	93-97
29385296-9	2018	The survival of ire1 mutants treated with tunicamycin improved in the presence of the ROS scavenger glutathione, suggesting that ire1 mutants failed to maintain ROS levels under ER stress.	Tunicamycin	42-53	uncharacterized protein	Chlamydomonas reinhardtii	16-20
29385296-9	2018	The survival of ire1 mutants treated with tunicamycin improved in the presence of the ROS scavenger glutathione, suggesting that ire1 mutants failed to maintain ROS levels under ER stress.	Tunicamycin	42-53	uncharacterized protein	Chlamydomonas reinhardtii	129-133
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	X-box binding protein 1	Homo sapiens	90-113
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	activating transcription factor 4	Homo sapiens	122-155
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	activating transcription factor 4	Homo sapiens	156-160
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	192-197
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
29805584-0	2018	Tunicamycin inhibits progression of glioma cells through downregulation of the MEG-3-regulated wnt/beta-catenin signaling pathway.	Tunicamycin	0-11	maternally expressed 3	Homo sapiens	79-84
29805584-0	2018	Tunicamycin inhibits progression of glioma cells through downregulation of the MEG-3-regulated wnt/beta-catenin signaling pathway.	Tunicamycin	0-11	catenin beta 1	Homo sapiens	99-111
29634759-6	2018	The aim of this study is to investigate how tunicamycin treatment, that induces eIF2 phosphorylation, affects mRNA translation in erythroblasts.	Tunicamycin	44-55	eukaryotic translation initiation factor 2 subunit beta	Homo sapiens	80-84
29634759-8	2018	Treatment of erythroblasts with Tunicamycin (Tm) increased phosphorylation of eIF2 2-fold.	Tunicamycin	32-43	eukaryotic translation initiation factor 2 subunit beta	Homo sapiens	78-82
28847729-5	2018	Administration of chemical ER stressor tunicamycin to activate the UPR pathway resulted in robust increase of hepatic and circulating GDF15 levels.	Tunicamycin	39-50	growth differentiation factor 15	Mus musculus	134-139
29343429-6	2018	The endoplasmic reticulum (ER) stress condition and the related unfolded protein response (UPR), triggered by treatment with thapsigargin and tunicamycin, cause an increase of the cap-independent translation of ACC1 mRNA in HepG2 cells, despite the overall reduction in global protein synthesis.	Tunicamycin	142-153	acetyl-CoA carboxylase alpha	Homo sapiens	211-215
29377347-0	2018	Tunicamycin inhibits cell proliferation and migration in hepatocellular carcinoma through suppression of CD44s and the ERK1/2 pathway.	Tunicamycin	0-11	CD44 molecule (Indian blood group)	Homo sapiens	105-109
29377347-0	2018	Tunicamycin inhibits cell proliferation and migration in hepatocellular carcinoma through suppression of CD44s and the ERK1/2 pathway.	Tunicamycin	0-11	mitogen-activated protein kinase 3	Homo sapiens	119-125
29291402-4	2018	Tunicamycin (Tm) was employed to excite CHOP expression, and two CHOP small interfering RNAs (siRNAs) were used to inhibit CHOP expression.	Tunicamycin	0-11	DNA-damage inducible transcript 3	Rattus norvegicus	40-44
28885691-8	2018	Consistent with this result, the stimulated unfolded protein response (UPR) regulatory proteins induced by tunicamycin were down-regulated by FGF2.	Tunicamycin	107-118	fibroblast growth factor 2	Bos taurus	142-146
29541178-7	2018	Mechanism analysis demonstrated that Tunicamycin inhibited the protein kinase B (Akt) and nuclear factor-kappaB (NF-kappaB) signaling pathways, whilst Akt overexpression significantly cancelled out the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells, as compared with control cells.	Tunicamycin	37-48	thymoma viral proto-oncogene 1	Mus musculus	81-84
29541178-7	2018	Mechanism analysis demonstrated that Tunicamycin inhibited the protein kinase B (Akt) and nuclear factor-kappaB (NF-kappaB) signaling pathways, whilst Akt overexpression significantly cancelled out the Tunicamycin-inhibited growth and aggressiveness of breast cancer cells, as compared with control cells.	Tunicamycin	202-213	thymoma viral proto-oncogene 1	Mus musculus	151-154
29541178-9	2018	In conclusion, these results indicate that Tunicamycin may inhibit the growth and aggressiveness of breast cancer cells via regulation of the Akt/NF-kappaB signaling pathway.	Tunicamycin	43-54	thymoma viral proto-oncogene 1	Mus musculus	142-145
28822264-8	2018	RESULT: Tunicamycin greatly increased protein levels of GRP94.	Tunicamycin	8-19	heat shock protein 90, beta (Grp94), member 1	Mus musculus	56-61
29273683-6	2018	Inhibiting glycosylation by tunicamycin also markedly reduced human and rat CBG steroid-binding activities.	Tunicamycin	28-39	serpin family A member 6	Rattus norvegicus	76-79
29323465-3	2018	Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response.	Tunicamycin	42-53	sequestosome-1	Cricetulus griseus	103-109
29323465-3	2018	Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response.	Tunicamycin	42-53	endoplasmic reticulum chaperone BiP	Cricetulus griseus	111-116
29323465-3	2018	Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response.	Tunicamycin	42-53	homocysteine-responsive endoplasmic reticulum-resident ubiquitin-like domain member 1 protein	Cricetulus griseus	122-129
29323465-3	2018	Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response.	Tunicamycin	42-53	cyclic AMP-dependent transcription factor ATF-5	Cricetulus griseus	204-208
29323465-3	2018	Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response.	Tunicamycin	42-53	teneurin-4	Cricetulus griseus	210-214
29323465-3	2018	Time course induction of ER stress, using tunicamycin (TM), shows a group of genes such as Chop, Trb3, Sqstm1, Grp78, and Herpud1 respond rapidly to TM inhibition of N-glycosylation, while others such as Atf5, Odz4, and Birc5 exhibits a delayed response.	Tunicamycin	42-53	survivin	Cricetulus griseus	220-225
29707686-5	2018	Before commencing SCNT, somatic cells treated with tunicamycin (TM), an ER stress inducer, confirmed the splicing of Xbp1 mRNA and increased expressions of ER stress-associated genes.	Tunicamycin	51-62	X-box binding protein 1	Homo sapiens	117-121
28825160-5	2018	Next, we established Neuro2a cells with edited GADD34 and ATF4/GADD34 genes and found that ATF4 acts as a proapoptotic factor, but GADD34 depletion did not attenuate the expression of cleaved caspase-3 induced by tunicamycin treatment.	Tunicamycin	213-224	activating transcription factor 4	Mus musculus	91-95
29344654-0	2018	Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway.	Tunicamycin	0-11	mitogen-activated protein kinase 1	Homo sapiens	85-88
29344654-0	2018	Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway.	Tunicamycin	0-11	mitogen-activated protein kinase 8	Homo sapiens	89-92
29344654-0	2018	Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway.	Tunicamycin	0-11	AKT serine/threonine kinase 1	Homo sapiens	102-105
29344654-0	2018	Tunicamycin inhibits colon carcinoma growth and aggressiveness via modulation of the ERK-JNK-mediated AKT/mTOR signaling pathway.	Tunicamycin	0-11	mechanistic target of rapamycin kinase	Homo sapiens	106-110
29344654-4	2018	Western blotting, immunohistochemistry, apoptotic assays and immunofluorescence were used to analyze the therapeutic effects of tunicamycin on apoptosis, growth, aggressiveness and cell cycle of colon tumor cells, by downregulation of fibronectin, vimentin and E-cadherin expression levels.	Tunicamycin	128-139	fibronectin 1	Homo sapiens	235-246
29344654-4	2018	Western blotting, immunohistochemistry, apoptotic assays and immunofluorescence were used to analyze the therapeutic effects of tunicamycin on apoptosis, growth, aggressiveness and cell cycle of colon tumor cells, by downregulation of fibronectin, vimentin and E-cadherin expression levels.	Tunicamycin	128-139	vimentin	Homo sapiens	248-256
29344654-4	2018	Western blotting, immunohistochemistry, apoptotic assays and immunofluorescence were used to analyze the therapeutic effects of tunicamycin on apoptosis, growth, aggressiveness and cell cycle of colon tumor cells, by downregulation of fibronectin, vimentin and E-cadherin expression levels.	Tunicamycin	128-139	cadherin 1	Homo sapiens	261-271
29344654-6	2018	In addition, tunicamycin administration promoted apoptosis of colon carcinoma cells via upregulation of apoptotic protease activating factor 1 and cytochrome c expression levels, which are proteins that have a role in mitochondrial apoptosis signaling.	Tunicamycin	13-24	apoptotic peptidase activating factor 1	Homo sapiens	104-142
29344654-6	2018	In addition, tunicamycin administration promoted apoptosis of colon carcinoma cells via upregulation of apoptotic protease activating factor 1 and cytochrome c expression levels, which are proteins that have a role in mitochondrial apoptosis signaling.	Tunicamycin	13-24	cytochrome c, somatic	Homo sapiens	147-159
29344654-8	2018	Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells.	Tunicamycin	39-50	mitogen-activated protein kinase 1	Homo sapiens	100-137
29344654-8	2018	Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells.	Tunicamycin	39-50	mitogen-activated protein kinase 1	Homo sapiens	139-142
29344654-8	2018	Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells.	Tunicamycin	39-50	mitogen-activated protein kinase 8	Homo sapiens	145-174
29344654-8	2018	Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells.	Tunicamycin	39-50	AKT serine/threonine kinase 1	Homo sapiens	197-200
29344654-8	2018	Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells.	Tunicamycin	39-50	mechanistic target of rapamycin kinase	Homo sapiens	217-246
29344654-8	2018	Mechanistic analysis demonstrated that tunicamycin reduced expression and phosphorylation levels of extracellular signal-regulated kinase (ERK), c-JUN N-terminal kinase (JNK) and protein kinase B (AKT), and inhibited mammalian target of rapamycin (mTOR) expression levels in colon carcinoma cells.	Tunicamycin	39-50	mechanistic target of rapamycin kinase	Homo sapiens	248-252
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	43-54	mitogen-activated protein kinase 1	Homo sapiens	29-32
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	43-54	mitogen-activated protein kinase 8	Homo sapiens	82-85
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	43-54	AKT serine/threonine kinase 1	Homo sapiens	87-90
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	43-54	mechanistic target of rapamycin kinase	Homo sapiens	95-99
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	134-145	mitogen-activated protein kinase 1	Homo sapiens	29-32
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	134-145	mitogen-activated protein kinase 8	Homo sapiens	82-85
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	134-145	AKT serine/threonine kinase 1	Homo sapiens	87-90
29344654-9	2018	Endogenous overexpression of ERK inhibited tunicamycin-mediated downregulation of JNK, AKT and mTOR expression, which further blocked tunicamycin-mediated inhibition of growth and aggressiveness of colon carcinoma.	Tunicamycin	134-145	mechanistic target of rapamycin kinase	Homo sapiens	95-99
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	44-55	mitogen-activated protein kinase 1	Homo sapiens	118-121
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	44-55	mitogen-activated protein kinase 8	Homo sapiens	122-125
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	44-55	AKT serine/threonine kinase 1	Homo sapiens	135-138
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	44-55	mechanistic target of rapamycin kinase	Homo sapiens	139-143
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	182-193	mitogen-activated protein kinase 1	Homo sapiens	118-121
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	182-193	mitogen-activated protein kinase 8	Homo sapiens	122-125
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	182-193	AKT serine/threonine kinase 1	Homo sapiens	135-138
29344654-11	2018	In conclusion, these results suggested that tunicamycin may inhibit growth and aggressiveness of colon cancer via the ERK-JNK-mediated AKT/mTOR signaling pathway, and suggested that tunicamycin may be a potential anti-cancer agent for colon carcinoma therapy.	Tunicamycin	182-193	mechanistic target of rapamycin kinase	Homo sapiens	139-143
29459785-2	2018	The enzyme UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosaminephosphotransferase (GlcNAc-1-P-transferase or GPT) catalyzes the first and committed step of N-linked glycosylation in the endoplasmic reticulum membrane, and it is the target of the natural product tunicamycin.	Tunicamycin	272-283	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	11-91
29459785-2	2018	The enzyme UDP-N-acetylglucosamine:dolichyl-phosphate N-acetylglucosaminephosphotransferase (GlcNAc-1-P-transferase or GPT) catalyzes the first and committed step of N-linked glycosylation in the endoplasmic reticulum membrane, and it is the target of the natural product tunicamycin.	Tunicamycin	272-283	glutamic--pyruvic transaminase	Homo sapiens	119-122
29459785-3	2018	Tunicamycin has potent antibacterial activity, inhibiting the bacterial cell wall synthesis enzyme MraY, but its usefulness as an antibiotic is limited by off-target inhibition of human GPT.	Tunicamycin	0-11	glutamic--pyruvic transaminase	Homo sapiens	186-189
29459785-5	2018	Here we present crystal structures of human GPT in complex with tunicamycin.	Tunicamycin	64-75	glutamic--pyruvic transaminase	Homo sapiens	44-47
29459785-6	2018	Structural and functional analyses reveal the difference between GPT and MraY in their mechanisms of inhibition by tunicamycin.	Tunicamycin	115-126	glutamic--pyruvic transaminase	Homo sapiens	65-68
29275936-3	2018	This study investigated the effect of Akt2 knockdown on tunicamycin (TM)-induced cytotoxicity in cardiomyocytes and the underlying mechanisms with a focus on the JNK-Wnt pathway.	Tunicamycin	56-67	AKT serine/threonine kinase 2	Homo sapiens	38-42
29275936-3	2018	This study investigated the effect of Akt2 knockdown on tunicamycin (TM)-induced cytotoxicity in cardiomyocytes and the underlying mechanisms with a focus on the JNK-Wnt pathway.	Tunicamycin	69-71	AKT serine/threonine kinase 2	Homo sapiens	38-42
29212664-8	2018	Failure to induce the unfolded protein response in trl1Delta cells grown with tunicamycin is lethal owing to their inability to ligate HAC1 after its cleavage by Ire1.	Tunicamycin	78-89	transcription factor HAC1	Saccharomyces cerevisiae S288C	135-139
29212664-8	2018	Failure to induce the unfolded protein response in trl1Delta cells grown with tunicamycin is lethal owing to their inability to ligate HAC1 after its cleavage by Ire1.	Tunicamycin	78-89	bifunctional endoribonuclease/protein kinase IRE1	Saccharomyces cerevisiae S288C	162-166
29495436-5	2018	In the present study, tunicamycin, an N-glycosyltransferase inhibitor, was employed to treat CHO cells (CHO-CRT) stably expressing full-length recombinant mouse CRT in secreted form for preparation of aberrantly glycosylated eCRT (tun-eCRT).	Tunicamycin	22-33	calreticulin	Homo sapiens	108-111
29495436-5	2018	In the present study, tunicamycin, an N-glycosyltransferase inhibitor, was employed to treat CHO cells (CHO-CRT) stably expressing full-length recombinant mouse CRT in secreted form for preparation of aberrantly glycosylated eCRT (tun-eCRT).	Tunicamycin	22-33	calreticulin	Mus musculus	161-164
29206917-3	2018	Paraffin sections from N-glycosylation inhibitor tunicamycin treated ER-/PR-/HER2+ (double negative) breast tumor in athymic nude mice exhibited reduced N-glycan but increased GRP78 expression.	Tunicamycin	49-60	erb-b2 receptor tyrosine kinase 2	Homo sapiens	77-81
29206917-3	2018	Paraffin sections from N-glycosylation inhibitor tunicamycin treated ER-/PR-/HER2+ (double negative) breast tumor in athymic nude mice exhibited reduced N-glycan but increased GRP78 expression.	Tunicamycin	49-60	heat shock protein 5	Mus musculus	176-181
29206917-4	2018	We have evaluated the effect of tunicamycin on cellular localization of GRP78 in metastatic human breast cancer cells MDA-MB-231 (ER-/PR-/HER2-).	Tunicamycin	32-43	heat shock protein family A (Hsp70) member 5	Homo sapiens	72-77
29206917-7	2018	GRP78 expression (protein and mRNA) was higher in tunicamycin (1.0 mug/mL) treated MCF-7 and MDA-MB-231 cells.	Tunicamycin	50-61	heat shock protein family A (Hsp70) member 5	Homo sapiens	0-5
29206917-12	2018	The conclusion, GRP78 is expressed neither on the outer-leaflet of the (ER-/PR-/HER2-) human breast cancer cells nor it is secreted into the culture media during tunicamycin-induced ER stress.	Tunicamycin	162-173	heat shock protein family A (Hsp70) member 5	Homo sapiens	16-21
29307512-11	2018	ER stress was readily induced by Tunicamycin and resulted in a reduction of insulin mRNA.	Tunicamycin	33-44	insulin	Homo sapiens	76-83
29079428-0	2018	Globular adiponectin protects hepatocytes from tunicamycin-induced cell death via modulation of the inflammasome and heme oxygenase-1 induction.	Tunicamycin	47-58	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	9-20
29079428-0	2018	Globular adiponectin protects hepatocytes from tunicamycin-induced cell death via modulation of the inflammasome and heme oxygenase-1 induction.	Tunicamycin	47-58	heme oxygenase 1	Rattus norvegicus	117-133
29079428-5	2018	In the present study, we examined the protective effect of globular adiponectin (gAcrp) on tunicamycin-induced cell death and further investigated its potential underlying mechanisms in rat hepatocytes.	Tunicamycin	91-102	adiponectin, C1Q and collagen domain containing	Rattus norvegicus	68-79
29079428-7	2018	Interestingly, gAcrp prevented the tunicamycin-induced activation of the inflammasome, a key platform involved in the production of inflammatory cytokines that induces pyroptosis, determined by suppression of interleukin-1beta (IL-1beta) maturation, apoptosis-associated speck-like protein containing a carboxy-terminal CARD (ASC) speck formation, and caspase-1 activation.	Tunicamycin	35-46	interleukin 1 beta	Rattus norvegicus	209-226
29079428-7	2018	Interestingly, gAcrp prevented the tunicamycin-induced activation of the inflammasome, a key platform involved in the production of inflammatory cytokines that induces pyroptosis, determined by suppression of interleukin-1beta (IL-1beta) maturation, apoptosis-associated speck-like protein containing a carboxy-terminal CARD (ASC) speck formation, and caspase-1 activation.	Tunicamycin	35-46	interleukin 1 beta	Rattus norvegicus	228-236
29079428-7	2018	Interestingly, gAcrp prevented the tunicamycin-induced activation of the inflammasome, a key platform involved in the production of inflammatory cytokines that induces pyroptosis, determined by suppression of interleukin-1beta (IL-1beta) maturation, apoptosis-associated speck-like protein containing a carboxy-terminal CARD (ASC) speck formation, and caspase-1 activation.	Tunicamycin	35-46	caspase 1	Rattus norvegicus	352-361
29079428-9	2018	In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells.	Tunicamycin	221-232	heme oxygenase 1	Rattus norvegicus	27-43
29079428-9	2018	In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells.	Tunicamycin	221-232	heme oxygenase 1	Rattus norvegicus	45-49
29079428-9	2018	In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells.	Tunicamycin	418-429	heme oxygenase 1	Rattus norvegicus	27-43
29079428-9	2018	In addition, inhibition of heme oxygenase-1 (HO-1) signaling by pretreatment with SnPP, a pharmacological inhibitor of HO-1, or transfection with an siRNA targeting HO-1, abrogated the protective effects of gAcrp against tunicamycin-induced cell death and abolished the suppressive effect on the inflammasome activation, demonstrating that HO-1 signaling plays a crucial role in the protective effect of gAcrp against tunicamycin-induced damage in liver cells.	Tunicamycin	418-429	heme oxygenase 1	Rattus norvegicus	45-49
29382365-12	2018	Tunicamycin induced apoptosis of MZB1+ cells in target organs, resulting in decreased serum anti-dsDNA antibody levels.	Tunicamycin	0-11	marginal zone B and B1 cell specific protein	Homo sapiens	33-37
29531800-3	2018	To this end, we investigated the effects of a subcytotoxic concentration of Tunicamycin in IRE1alpha-proficient and in IRE1alpha-deficient cells, by pharmacological inhibition with 4mu8 C or down-regulation by specific siRNA.	Tunicamycin	76-87	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	91-100
28987725-12	2017	RESULTS: Tunicamycin, 20% mechanical forces and hypoxia (1% O2) all significantly increased chondrocytes apoptosis rates and expression of ERS markers (GRP78, GRP94 and Caspase 12).	Tunicamycin	9-20	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	152-157
29705800-7	2018	RESULTS: A549 cells switched from a cobblestone-like appearance to an elongated fibroblast like appearance after exposure to tunicamycin or bleomycin, accompanied by increased expression of N-cadherin, alpha-SMA and Collagen I.	Tunicamycin	125-136	cadherin 2	Homo sapiens	190-200
29705800-8	2018	Meanwhile, GRP78 was upregulated in A549 cells exposed to tunicamycin or bleomycin.	Tunicamycin	58-69	heat shock protein family A (Hsp70) member 5	Homo sapiens	11-16
29705800-10	2018	Moreover, tunicamycin and bleomycin promoted the expression of HDAC2 and HDAC6, and HDACs inhibitor SAHA abrogated the morphological and biochemical changes in A549 cells.	Tunicamycin	10-21	histone deacetylase 2	Homo sapiens	63-68
29705800-10	2018	Moreover, tunicamycin and bleomycin promoted the expression of HDAC2 and HDAC6, and HDACs inhibitor SAHA abrogated the morphological and biochemical changes in A549 cells.	Tunicamycin	10-21	histone deacetylase 6	Homo sapiens	73-78
29105510-10	2018	In vitro, T6 cells exposed to tunicamycin by increasing abundances of CHOP, sXBP1, cleaved caspase-3, and LC3BII were diminished in the cell cultures transfected with the miR-29a mimic.	Tunicamycin	30-41	DNA-damage inducible transcript 3	Mus musculus	70-74
29105510-10	2018	In vitro, T6 cells exposed to tunicamycin by increasing abundances of CHOP, sXBP1, cleaved caspase-3, and LC3BII were diminished in the cell cultures transfected with the miR-29a mimic.	Tunicamycin	30-41	microRNA 29a	Mus musculus	171-178
29962431-6	2018	In mice, postprandial and tunicamycin-induced ER stress was significantly reduced by overexpression of FGF21 using a recombinant adenovirus.	Tunicamycin	26-37	fibroblast growth factor 21	Mus musculus	103-108
29154199-6	2018	Importantly, UVB treatment perturbs the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and LC3-II turnover in response to treatment with MTOR inhibitors (Torin 1 and pp242), as well as endoplasmic reticular stress (A23187 and tunicamycin), inositol pathway (L690,330) and autophagy inducers (resveratrol and STF62247).	Tunicamycin	258-269	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	102-105
29154199-6	2018	Importantly, UVB treatment perturbs the conversion of microtubule-associated protein 1 light chain 3 (LC3)-I to LC3-II and LC3-II turnover in response to treatment with MTOR inhibitors (Torin 1 and pp242), as well as endoplasmic reticular stress (A23187 and tunicamycin), inositol pathway (L690,330) and autophagy inducers (resveratrol and STF62247).	Tunicamycin	258-269	mechanistic target of rapamycin kinase	Homo sapiens	169-173
29234100-5	2017	The total number of ER-mitochondria associations detected by this approach increases in response to tunicamycin-induced ER stress, serum deprivation or reduced levels of mitofusin 2 (MFN2).	Tunicamycin	100-111	mitofusin 2	Homo sapiens	170-181
29234100-5	2017	The total number of ER-mitochondria associations detected by this approach increases in response to tunicamycin-induced ER stress, serum deprivation or reduced levels of mitofusin 2 (MFN2).	Tunicamycin	100-111	mitofusin 2	Homo sapiens	183-187
29212948-4	2017	For the first time to our knowledge, we demonstrate that CRELD2 can serve as a sensitive urinary biomarker for detecting ER stress in podocytes or renal tubular cells in murine models of podocyte ER stress-induced nephrotic syndrome and tunicamycin- or ischemia-reperfusion-induced acute kidney injury (AKI), respectively.	Tunicamycin	237-248	cysteine-rich with EGF-like domains 2	Mus musculus	57-63
29303997-7	2018	A role for glycosylation in cell-surface tetherin expression is supported by tunicamycin treatment, which inhibits the first step of N-linked glycosylation and impairs both cell-surface expression and antiviral activity.	Tunicamycin	77-88	bone marrow stromal cell antigen 2	Homo sapiens	41-49
30637701-12	2018	Inhibition of GPT with tunicamycin downregulates the DPMS catalytic activity quantitatively.	Tunicamycin	23-34	glutamic--pyruvic transaminase	Homo sapiens	14-17
30637701-12	2018	Inhibition of GPT with tunicamycin downregulates the DPMS catalytic activity quantitatively.	Tunicamycin	23-34	dolichyl-phosphate mannosyltransferase subunit 1, catalytic	Bos taurus	53-57
30637701-14	2018	Interestingly, nano-formulated tunicamycin is three times more potent in inhibiting the cell cycle progression than the native tunicamycin and is supported by downregulation of the ratio of phospho-p53 to total-p53 as well as phospho-Rb to total Rb.	Tunicamycin	31-42	tumor protein p53	Homo sapiens	198-201
30637701-14	2018	Interestingly, nano-formulated tunicamycin is three times more potent in inhibiting the cell cycle progression than the native tunicamycin and is supported by downregulation of the ratio of phospho-p53 to total-p53 as well as phospho-Rb to total Rb.	Tunicamycin	31-42	tumor protein p53	Homo sapiens	211-214
28987725-12	2017	RESULTS: Tunicamycin, 20% mechanical forces and hypoxia (1% O2) all significantly increased chondrocytes apoptosis rates and expression of ERS markers (GRP78, GRP94 and Caspase 12).	Tunicamycin	9-20	heat shock protein 90 beta family member 1	Rattus norvegicus	159-164
28987725-12	2017	RESULTS: Tunicamycin, 20% mechanical forces and hypoxia (1% O2) all significantly increased chondrocytes apoptosis rates and expression of ERS markers (GRP78, GRP94 and Caspase 12).	Tunicamycin	9-20	caspase 12	Rattus norvegicus	169-179
28941626-4	2017	WT and PTP1B knockout mice were subjected to the ER stress inducer tunicamycin (1mg/kg).	Tunicamycin	67-78	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	7-12
28941626-8	2017	Levels of serine phosphorylation of IRS-1, TRIB3, Atg5/7, LC3B and the autophagy adaptor p62 were significantly upregulated while IRS-1 tyrosine phosphorylation was reduced by tunicamycin, the effect of which were obliterated by PTP1B ablation.	Tunicamycin	176-187	insulin receptor substrate 1	Mus musculus	36-41
28063235-11	2017	In addition, adiponectin inhibited tunicamycin-induced endoplasmic reticulum (ER)-stress through effects on ER stress regulated proteins in pLE cells.	Tunicamycin	35-46	adiponectin, C1Q and collagen domain containing	Homo sapiens	13-24
29293771-9	2017	Furthermore, adiponectin reduced tunicamycin-induced expression and activation of endoplasmic reticulum stress-related proteins in MAC-T cells and attenuated the repressive effect of tunicamycin on proliferation of MAC-T cells.	Tunicamycin	33-44	adiponectin, C1Q and collagen domain containing	Bos taurus	13-24
29293771-9	2017	Furthermore, adiponectin reduced tunicamycin-induced expression and activation of endoplasmic reticulum stress-related proteins in MAC-T cells and attenuated the repressive effect of tunicamycin on proliferation of MAC-T cells.	Tunicamycin	183-194	adiponectin, C1Q and collagen domain containing	Bos taurus	13-24
28150859-8	2017	In addition, cell death resulting from tunicamycin-induced ER stress was prevented when pLE cells were treated with the combination of tunicamycin and BDNF which also decreased cells in the Sub-G1 phase of the cell cycle.	Tunicamycin	39-50	brain derived neurotrophic factor	Sus scrofa	151-155
29066182-8	2017	Exposure of PCECs to the chemical ER stress inducer tunicamycin also increased sEH expression.	Tunicamycin	52-63	epoxide hydrolase 2	Homo sapiens	79-82
29066182-10	2017	The impairment of endothelium-dependent vasorelaxation induced by Ang-II or tunicamycin was ameliorated by inhibitors of ER stress or sEH.	Tunicamycin	76-87	epoxide hydrolase 2	Homo sapiens	134-137
29226084-4	2017	The N-glycosylation inhibitor tunicamycin reduced the apparent molecular weight of immunoreactivity associated with myc-tagged GPR61 by 1-2 kDa, which was comparable to the evident molecular weight of the myc-tagged N12S GPR61 mutant with disrupted consensus N-glycosylation site.	Tunicamycin	30-41	G protein-coupled receptor 61	Homo sapiens	127-132
29226084-4	2017	The N-glycosylation inhibitor tunicamycin reduced the apparent molecular weight of immunoreactivity associated with myc-tagged GPR61 by 1-2 kDa, which was comparable to the evident molecular weight of the myc-tagged N12S GPR61 mutant with disrupted consensus N-glycosylation site.	Tunicamycin	30-41	G protein-coupled receptor 61	Homo sapiens	221-226
29226084-5	2017	Analysis of GPR61 expression demonstrated that tunicamycin treatment reduced considerably heterologous expression of GPR61 in the cell membrane despite the N12S GPR61 mutant being readily expressed at the cell surface.	Tunicamycin	47-58	G protein-coupled receptor 61	Homo sapiens	12-17
29226084-5	2017	Analysis of GPR61 expression demonstrated that tunicamycin treatment reduced considerably heterologous expression of GPR61 in the cell membrane despite the N12S GPR61 mutant being readily expressed at the cell surface.	Tunicamycin	47-58	G protein-coupled receptor 61	Homo sapiens	117-122
29226084-5	2017	Analysis of GPR61 expression demonstrated that tunicamycin treatment reduced considerably heterologous expression of GPR61 in the cell membrane despite the N12S GPR61 mutant being readily expressed at the cell surface.	Tunicamycin	47-58	G protein-coupled receptor 61	Homo sapiens	117-122
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	caspase 3	Homo sapiens	78-87
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
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
28951205-5	2017	YAP1 protein expression was downregulated by tunicamycin and the phosphorylation of YAP1 at the Ser127 site was significantly increased by tunicamycin.	Tunicamycin	45-56	Yes1 associated transcriptional regulator	Homo sapiens	0-4
28951205-5	2017	YAP1 protein expression was downregulated by tunicamycin and the phosphorylation of YAP1 at the Ser127 site was significantly increased by tunicamycin.	Tunicamycin	139-150	Yes1 associated transcriptional regulator	Homo sapiens	0-4
28951205-5	2017	YAP1 protein expression was downregulated by tunicamycin and the phosphorylation of YAP1 at the Ser127 site was significantly increased by tunicamycin.	Tunicamycin	139-150	Yes1 associated transcriptional regulator	Homo sapiens	84-88
28951205-6	2017	Tunicamycin further decreased cell viability followed by an increase in caspase-3 processing in the absence of YAP1 when compared with treatment only with tunicamycin or siYAP1.	Tunicamycin	0-11	caspase 3	Homo sapiens	72-81
28951205-7	2017	On the other hand, overexpression of a constitutively active YAP1 (YAP1-5SA), which lacks five serine phosphorylation sites, significantly prevented the caspase-3 processing and restored the decrease in cell viability induced by tunicamycin.	Tunicamycin	229-240	Yes1 associated transcriptional regulator	Homo sapiens	61-65
28951205-7	2017	On the other hand, overexpression of a constitutively active YAP1 (YAP1-5SA), which lacks five serine phosphorylation sites, significantly prevented the caspase-3 processing and restored the decrease in cell viability induced by tunicamycin.	Tunicamycin	229-240	Yes1 associated transcriptional regulator	Homo sapiens	67-75
28951205-8	2017	Overexpression of YAP1-5SA significantly inhibited tunicamycin-induced caspase-8 processing without affecting phosphorylation of p-38 and Akt.	Tunicamycin	51-62	Yes1 associated transcriptional regulator	Homo sapiens	18-26
28951205-8	2017	Overexpression of YAP1-5SA significantly inhibited tunicamycin-induced caspase-8 processing without affecting phosphorylation of p-38 and Akt.	Tunicamycin	51-62	caspase 8	Homo sapiens	71-80
28951205-9	2017	Furthermore, the overexpression of YAP1-5SA significantly restored the decrease in ANKRD1 expression induced by tunicamycin.	Tunicamycin	112-123	Yes1 associated transcriptional regulator	Homo sapiens	35-43
28951205-9	2017	Furthermore, the overexpression of YAP1-5SA significantly restored the decrease in ANKRD1 expression induced by tunicamycin.	Tunicamycin	112-123	ankyrin repeat domain 1	Homo sapiens	83-89
28951205-10	2017	The inhibition of tunicamycin-induced caspase-3 cleavage by YAP1-5SA was markedly attenuated in ANKRD1-knockdown cells.	Tunicamycin	18-29	caspase 3	Homo sapiens	38-47
28951205-10	2017	The inhibition of tunicamycin-induced caspase-3 cleavage by YAP1-5SA was markedly attenuated in ANKRD1-knockdown cells.	Tunicamycin	18-29	Yes1 associated transcriptional regulator	Homo sapiens	60-68
28951205-10	2017	The inhibition of tunicamycin-induced caspase-3 cleavage by YAP1-5SA was markedly attenuated in ANKRD1-knockdown cells.	Tunicamycin	18-29	ankyrin repeat domain 1	Homo sapiens	96-102
29095946-4	2017	Treatment of FRTL-5 thyrocytes with the ER stress inducer tunicamycin (TM) dose-dependently increased the mRNA and/or protein levels of known UPR target genes, stimulated phosphorylation of the ER stress sensor protein kinase RNA-like ER kinase (PERK) and of the PERK target protein eukaryotic initiation factor 2alpha (eIF2alpha) and caused splicing of the ER stress-sensitive transcription factor X-box binding protein (XBP-1) (P &lt; 0.05).	Tunicamycin	58-69	eukaryotic translation initiation factor 2A	Rattus norvegicus	320-329
29095946-4	2017	Treatment of FRTL-5 thyrocytes with the ER stress inducer tunicamycin (TM) dose-dependently increased the mRNA and/or protein levels of known UPR target genes, stimulated phosphorylation of the ER stress sensor protein kinase RNA-like ER kinase (PERK) and of the PERK target protein eukaryotic initiation factor 2alpha (eIF2alpha) and caused splicing of the ER stress-sensitive transcription factor X-box binding protein (XBP-1) (P &lt; 0.05).	Tunicamycin	58-69	X-box binding protein 1	Rattus norvegicus	422-427
28880013-5	2017	Pretreatment with the N-linked glycosylation inhibitor tunicamycin, osimertinib clearly decreased the production of new PD-L1 protein probably due to a reduction in mRNA.	Tunicamycin	55-66	CD274 molecule	Homo sapiens	120-125
28634818-7	2017	In cells treated with the ER stressors thapsigargin and tunicamycin, expression of SG2NA was increased at both mRNA and protein levels.	Tunicamycin	56-67	striatin, calmodulin binding protein 3	Mus musculus	83-88
28383761-9	2017	Meanwhile, in mouse liver phosphorylation of eIF2alpha, a factor that regulates NMD, was increased by both tunicamycin and nutritional interventions.	Tunicamycin	107-118	eukaryotic translation initiation factor 2A	Mus musculus	45-54
28383761-10	2017	Hepatic expression of GRP78, a central chaperone in ER stress responses, was increased by tunicamycin but not by the nutritional interventions.	Tunicamycin	90-101	heat shock protein 5	Mus musculus	22-27
28597972-5	2017	We then found that overexpression of SERP1 could rescue GLP-1R glycosylation after application of tunicamycin to block N-linked glycosylation.	Tunicamycin	98-109	stress associated endoplasmic reticulum protein 1	Homo sapiens	37-42
28597972-8	2017	Moreover, as a GLP-1R interactor, SERP1 could also partly reverse the accumulation of tunicamycin-induced ER stress.	Tunicamycin	86-97	glucagon like peptide 1 receptor	Homo sapiens	15-21
28597972-8	2017	Moreover, as a GLP-1R interactor, SERP1 could also partly reverse the accumulation of tunicamycin-induced ER stress.	Tunicamycin	86-97	stress associated endoplasmic reticulum protein 1	Homo sapiens	34-39
28597972-9	2017	Taken together, our findings identify a group of proteins that interact with GLP-1R and show that one specific interacting protein, SERP1, has an important role in facilitating the glycosylation of GLP-1R and rescuing its activities after ER stress induced by tunicamycin.	Tunicamycin	260-271	glucagon like peptide 1 receptor	Homo sapiens	77-83
28597972-9	2017	Taken together, our findings identify a group of proteins that interact with GLP-1R and show that one specific interacting protein, SERP1, has an important role in facilitating the glycosylation of GLP-1R and rescuing its activities after ER stress induced by tunicamycin.	Tunicamycin	260-271	stress associated endoplasmic reticulum protein 1	Homo sapiens	132-137
28597972-9	2017	Taken together, our findings identify a group of proteins that interact with GLP-1R and show that one specific interacting protein, SERP1, has an important role in facilitating the glycosylation of GLP-1R and rescuing its activities after ER stress induced by tunicamycin.	Tunicamycin	260-271	glucagon like peptide 1 receptor	Homo sapiens	198-204
29285262-8	2017	Treatment of MV4-11 cells with receptor trafficking inhibitors, tunicamycin and brefeldin A, resulted in deglycosylation of NOX4 and NOX4D.	Tunicamycin	64-75	NADPH oxidase 4	Homo sapiens	124-128
28949374-4	2017	In the present study, it was demonstrated that mild ER stress resulted in upregulated expression levels of FGF21 and its main receptors, as a response to cell compensation, at the induction of &lt;=5 microM tunicamycin (TM).	Tunicamycin	207-218	fibroblast growth factor 21	Rattus norvegicus	107-112
28949374-4	2017	In the present study, it was demonstrated that mild ER stress resulted in upregulated expression levels of FGF21 and its main receptors, as a response to cell compensation, at the induction of &lt;=5 microM tunicamycin (TM).	Tunicamycin	220-222	fibroblast growth factor 21	Rattus norvegicus	107-112
28841673-2	2017	We demonstrated the induction of ER stress in response to tunicamycin stimulation, as evidenced by increased expression of chaperone proteins Grp78, Grp94, and enhanced eukaryotic initiation factor 2 subunit 1 (eIF2alpha) phosphorylation in hepatocellular carcinoma cells.	Tunicamycin	58-69	heat shock protein family A (Hsp70) member 5	Homo sapiens	142-147
28935975-10	2017	TSG-6 also blocked both tunicamycin- and palmitate-induced apoptosis of hepatocytes and increased their viability by inducing autophagy formation in these cells.	Tunicamycin	24-35	tumor necrosis factor alpha induced protein 6	Mus musculus	0-5
28904368-7	2017	Our TUNEL experiments using tunicamycin, an apoptosis inducer, and GADD34, an inhibitor of eIF2alpha phosphorylation, demonstrated that PC1-5TMC inhibits apoptosis of HEK293T cells in a PKR-eIF2alpha-dependent manner, with concurrent up- and down-regulation of Bcl-2 and Bax, respectively, revealed by Western blotting.	Tunicamycin	28-39	polycystin 1, transient receptor potential channel interacting	Homo sapiens	136-139
28688763-7	2017	Interestingly, the level of SLC30A10 mRNA was significantly increased by tunicamycin as an ER stressor, suggesting that the induction of SLC30A10 by MPP+ was caused via ER stress.	Tunicamycin	73-84	solute carrier family 30 member 10	Homo sapiens	28-36
28688763-7	2017	Interestingly, the level of SLC30A10 mRNA was significantly increased by tunicamycin as an ER stressor, suggesting that the induction of SLC30A10 by MPP+ was caused via ER stress.	Tunicamycin	73-84	solute carrier family 30 member 10	Homo sapiens	137-145
28779263-0	2017	Tunicamycin potentiates paclitaxel-induced apoptosis through inhibition of PI3K/AKT and MAPK pathways in breast cancer.	Tunicamycin	0-11	thymoma viral proto-oncogene 1	Mus musculus	80-83
28779263-2	2017	However, tunicamycin has the ability to downregulate AKT and MAPK pathways.	Tunicamycin	9-20	thymoma viral proto-oncogene 1	Mus musculus	53-56
28779263-11	2017	Both annexin V-FITC/propidium iodide assay and TUNEL assay indicated that the combination of tunicamycin with paclitaxel resulted in significant increased cell apoptosis as compared with individual treatment in vitro and in vivo.	Tunicamycin	93-104	annexin A5	Mus musculus	5-14
28779263-13	2017	Western blotting analysis confirmed that tunicamycin decreased paclitaxel-induced upregulation of survival signal pathways such as AKT and MAPK.	Tunicamycin	41-52	thymoma viral proto-oncogene 1	Mus musculus	131-134
28779263-14	2017	CONCLUSION: These results revealed that tunicamycin synergistically enhanced the antitumor effects of paclitaxel through potentiating apoptosis via inhibiting paclitaxel-induced elevation of AKT and MAPK pathways.	Tunicamycin	40-51	thymoma viral proto-oncogene 1	Mus musculus	191-194
28580641-4	2017	Melatonin significantly inhibited GCD2 corneal cell death, caspase-3 activation, and poly (ADP-ribose) polymerase 1 cleavage caused by the ER stress inducer, tunicamycin.	Tunicamycin	158-169	poly(ADP-ribose) polymerase 1	Homo sapiens	59-115
28580641-9	2017	Interestingly, melatonin treatments enhanced SEL1L levels and suppressed the inhibition of SEL1L N-glycosylation caused by tunicamycin.	Tunicamycin	123-134	SEL1L adaptor subunit of ERAD E3 ubiquitin ligase	Homo sapiens	91-96
27660269-0	2017	ER Stress Induced by Tunicamycin Triggers alpha-Synuclein Oligomerization, Dopaminergic Neurons Death and Locomotor Impairment: a New Model of Parkinson"s Disease.	Tunicamycin	21-32	synuclein alpha	Rattus norvegicus	42-57
27660269-8	2017	In addition, we observed an extensive alpha-synuclein oligomerization in SNpc of Tm-injected animals when compared with DMSO-injected controls.	Tunicamycin	81-83	synuclein alpha	Rattus norvegicus	38-53
28753226-9	2017	Disruption of endoplasmic reticulum (ER)-to-Golgi transport by co-expression of Sar1(H74L) trapped tunicamycin-released AtFucTc-GFP in the ER, however, without NE localization.	Tunicamycin	99-110	synaptobrevin-related protein 1	Arabidopsis thaliana	80-84
28980921-7	2017	The glycosylation inhibitor tunicamycin inhibited the recovery of both CD71 and GPA, and BADGP inhibited the recovery of GPA.	Tunicamycin	28-39	transferrin receptor	Homo sapiens	71-75
28980921-7	2017	The glycosylation inhibitor tunicamycin inhibited the recovery of both CD71 and GPA, and BADGP inhibited the recovery of GPA.	Tunicamycin	28-39	glycophorin A (MNS blood group)	Homo sapiens	80-83
28841673-2	2017	We demonstrated the induction of ER stress in response to tunicamycin stimulation, as evidenced by increased expression of chaperone proteins Grp78, Grp94, and enhanced eukaryotic initiation factor 2 subunit 1 (eIF2alpha) phosphorylation in hepatocellular carcinoma cells.	Tunicamycin	58-69	heat shock protein 90 beta family member 1	Homo sapiens	149-154
28841673-2	2017	We demonstrated the induction of ER stress in response to tunicamycin stimulation, as evidenced by increased expression of chaperone proteins Grp78, Grp94, and enhanced eukaryotic initiation factor 2 subunit 1 (eIF2alpha) phosphorylation in hepatocellular carcinoma cells.	Tunicamycin	58-69	eukaryotic translation initiation factor 2A	Homo sapiens	211-220
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
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
28839162-4	2017	Pharmacologic ER stress induced by tunicamycin upregulates miR-204 and downregulates Sirt1 in the vascular wall/endothelium in vivo and in endothelial cells in vitro.	Tunicamycin	35-46	microRNA 204	Mus musculus	59-66
28839162-4	2017	Pharmacologic ER stress induced by tunicamycin upregulates miR-204 and downregulates Sirt1 in the vascular wall/endothelium in vivo and in endothelial cells in vitro.	Tunicamycin	35-46	sirtuin 1	Mus musculus	85-90
28839162-5	2017	Inhibition of miR-204 protects against tunicamycin-induced vascular/endothelial ER stress, associated impairment of endothelium-dependent vasorelaxation, and preserves endothelial Sirt1.	Tunicamycin	39-50	microRNA 204	Mus musculus	14-21
28839162-5	2017	Inhibition of miR-204 protects against tunicamycin-induced vascular/endothelial ER stress, associated impairment of endothelium-dependent vasorelaxation, and preserves endothelial Sirt1.	Tunicamycin	39-50	sirtuin 1	Mus musculus	180-185
28955790-6	2017	Using a selected clone, we observed that the expression of HiBiT-tagged ATF4 in the selected cells varied in response to treatment with protein synthesis inhibitors or proteasome inhibitors and tunicamycin.	Tunicamycin	194-205	activating transcription factor 4	Mus musculus	72-76
28777337-7	2017	Besides, tunicamycin remarkably increased hepatic triglyceride content and suppressed the expression of apolipoprotein B100.	Tunicamycin	9-20	apolipoprotein B	Mus musculus	104-123
28777337-8	2017	In addition, tunicamycin-treated mice had lower serum levels of triglyceride, apolipoprotein B, low-density lipoprotein cholesterol and high-density lipoprotein cholesterol.	Tunicamycin	13-24	apolipoprotein B	Mus musculus	78-94
28777337-9	2017	Gene expression of peroxisome proliferator-activated receptor alpha was decreased by tunicamycin, but the protein level was increased.	Tunicamycin	85-96	peroxisome proliferator activated receptor alpha	Mus musculus	19-67
28495589-3	2017	ER stress was induced in brain-derived mouse bEnd5 endothelial cells by thapsigargin or tunicamycin and caused apoptotic cell death over a 72h period.	Tunicamycin	88-99	BEN domain containing 5	Mus musculus	45-50
28453460-1	2017	OBJECTIVE: The study is to explore the role of tunicamycin-induced endoplasmic reticulum stress (ERS) in human ovarian cancer (OC) SKOV3 cells proliferation, migration and invasion by modulating the activity of PI3K/AKT/mTOR pathway.	Tunicamycin	47-58	AKT serine/threonine kinase 1	Homo sapiens	216-219
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	111-122	polo like kinase 2	Homo sapiens	0-4
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	polo like kinase 2	Homo sapiens	0-4
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	polo like kinase 2	Homo sapiens	157-161
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	activating transcription factor 4	Homo sapiens	190-223
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	activating transcription factor 4	Homo sapiens	225-229
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
28624282-4	2017	Treatment of MDBK cells with 2 different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), strongly induced ER stress as evident from induction of ER stress target genes, increased phosphorylation of PKR-like ER kinase, and enhanced splicing of X-box binding protein 1.	Tunicamycin	83-94	X-box binding protein 1	Bos taurus	255-278
28624282-4	2017	Treatment of MDBK cells with 2 different ER stress inducers, thapsigargin (TG) and tunicamycin (TM), strongly induced ER stress as evident from induction of ER stress target genes, increased phosphorylation of PKR-like ER kinase, and enhanced splicing of X-box binding protein 1.	Tunicamycin	96-98	X-box binding protein 1	Bos taurus	255-278
28407373-5	2017	We demonstrated that wild-type and s1p mutant plants produce the active, nuclear form of bZIP28 in response to the ER stress inducer tunicamycin.	Tunicamycin	133-144	SITE-1 protease	Arabidopsis thaliana	35-38
28407373-5	2017	We demonstrated that wild-type and s1p mutant plants produce the active, nuclear form of bZIP28 in response to the ER stress inducer tunicamycin.	Tunicamycin	133-144	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	89-95
28596490-6	2017	We discovered that interfering with N-linked glycosylation of GPER, either by mutation of the predicted glycosylation sites or pharmacologically with tunicamycin, drives GPER into the nucleus.	Tunicamycin	150-161	G protein-coupled estrogen receptor 1	Homo sapiens	62-66
28596490-6	2017	We discovered that interfering with N-linked glycosylation of GPER, either by mutation of the predicted glycosylation sites or pharmacologically with tunicamycin, drives GPER into the nucleus.	Tunicamycin	150-161	G protein-coupled estrogen receptor 1	Homo sapiens	170-174
28067406-7	2017	Ninj1 N-glycosylation was characterized by treatment of tunicamycin and substitution of Asn to Gln or Ala.	Tunicamycin	56-67	ninjurin 1	Homo sapiens	0-5
28482072-9	2017	In response to the ER stress inducer tunicamycin, PGC-1alpha expression was decreased, whereas the ER stress inhibitor 4-phenylbutyric acid blocked high glucose-suppressed PGC-1alpha expression.	Tunicamycin	37-48	PPARG coactivator 1 alpha	Homo sapiens	50-60
28482072-9	2017	In response to the ER stress inducer tunicamycin, PGC-1alpha expression was decreased, whereas the ER stress inhibitor 4-phenylbutyric acid blocked high glucose-suppressed PGC-1alpha expression.	Tunicamycin	37-48	PPARG coactivator 1 alpha	Homo sapiens	172-182
28537902-3	2017	Increasing concentrations of tunicamycin and CDDP activated ERS in SKOV3 cells, reduced cell viability and proliferation, increased apoptosis and autophagy, enhanced expression of ERS-related proteins, and inhibited expression of PI3K/AKT/mTOR pathway-related proteins.	Tunicamycin	29-40	AKT serine/threonine kinase 1	Homo sapiens	235-238
28537902-3	2017	Increasing concentrations of tunicamycin and CDDP activated ERS in SKOV3 cells, reduced cell viability and proliferation, increased apoptosis and autophagy, enhanced expression of ERS-related proteins, and inhibited expression of PI3K/AKT/mTOR pathway-related proteins.	Tunicamycin	29-40	mechanistic target of rapamycin kinase	Homo sapiens	239-243
28720827-9	2017	In the SH-SY5Y human cells, tunicamycin (TM), a PERK activator, promoted transcription of hsp27; and necrosis induced by glutamate could be rescued by TM, associated with reduced p53 accumulation.	Tunicamycin	28-39	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	48-52
28720827-9	2017	In the SH-SY5Y human cells, tunicamycin (TM), a PERK activator, promoted transcription of hsp27; and necrosis induced by glutamate could be rescued by TM, associated with reduced p53 accumulation.	Tunicamycin	28-39	heat shock protein family B (small) member 1	Homo sapiens	90-95
28720827-9	2017	In the SH-SY5Y human cells, tunicamycin (TM), a PERK activator, promoted transcription of hsp27; and necrosis induced by glutamate could be rescued by TM, associated with reduced p53 accumulation.	Tunicamycin	28-39	tumor protein p53	Homo sapiens	179-182
28453460-1	2017	OBJECTIVE: The study is to explore the role of tunicamycin-induced endoplasmic reticulum stress (ERS) in human ovarian cancer (OC) SKOV3 cells proliferation, migration and invasion by modulating the activity of PI3K/AKT/mTOR pathway.	Tunicamycin	47-58	mechanistic target of rapamycin kinase	Homo sapiens	220-224
28453460-11	2017	CONCLUSION: The study provides strong evidence that tunicamycin-induced ERS induces the apoptosis of human OC SKOV3 cells through inhibiting PI3K/AKT/mTOR signaling pathway.	Tunicamycin	52-63	AKT serine/threonine kinase 1	Homo sapiens	146-149
28453460-11	2017	CONCLUSION: The study provides strong evidence that tunicamycin-induced ERS induces the apoptosis of human OC SKOV3 cells through inhibiting PI3K/AKT/mTOR signaling pathway.	Tunicamycin	52-63	mechanistic target of rapamycin kinase	Homo sapiens	150-154
28433684-4	2017	Treatment with tunicamycin (Tm) increased SESN2 protein and mRNA levels and reporter gene activity.	Tunicamycin	15-26	sestrin 2	Homo sapiens	42-47
28671633-2	2017	Here, we show that the overexpression of P-gp in L1210 cells leads to resistance to tunicamycin and benzyl 2-acetamido-2-deoxy-alpha-d-galactopyranoside (GalNAc-alpha-O-benzyl).	Tunicamycin	84-95	phosphoglycolate phosphatase	Mus musculus	41-45
28671633-3	2017	Tunicamycin induces both glycosylation depression and ubiquitination improvement of P-gp.	Tunicamycin	0-11	phosphoglycolate phosphatase	Mus musculus	84-88
28671633-8	2017	Elevation of protein ubiquitination after tunicamycin treatment in these cells leads to protein folding rather than protein degradation, resulting at least in the partial lack of cell sensitivity to tunicamycin in L1210 cells after P-gp expression.	Tunicamycin	42-53	phosphoglycolate phosphatase	Mus musculus	232-236
28487369-5	2017	In N-glycosylation inhibition experiments, we find that treatment with tunicamycin and siRNA-mediated knockdown of the Golgi N-acetylglucosaminyltransferase I gene (MGAT1) induce partial loss of both total and cell-surface levels of the largest mucin, MUC16, and a concomitant reduction in glycocalyx barrier function.	Tunicamycin	71-82	alpha-1,3-mannosyl-glycoprotein 2-beta-N-acetylglucosaminyltransferase	Homo sapiens	165-170
28418178-6	2017	In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance.	Tunicamycin	116-127	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	71-79
28418178-6	2017	In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance.	Tunicamycin	116-127	basic region/leucine zipper motif 60	Arabidopsis thaliana	94-102
28418178-6	2017	In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance.	Tunicamycin	129-131	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	71-79
28418178-6	2017	In this study, we discovered that UPR-associated transcription factors AtbZIP17, AtbZIP28 and AtbZIP60 responded to tunicamycin (TM) and NaCl induced ER stress and subsequently enhanced Arabidopsis thaliana abiotic stress tolerance.	Tunicamycin	129-131	basic region/leucine zipper motif 60	Arabidopsis thaliana	94-102
28487369-5	2017	In N-glycosylation inhibition experiments, we find that treatment with tunicamycin and siRNA-mediated knockdown of the Golgi N-acetylglucosaminyltransferase I gene (MGAT1) induce partial loss of both total and cell-surface levels of the largest mucin, MUC16, and a concomitant reduction in glycocalyx barrier function.	Tunicamycin	71-82	LOC100508689	Homo sapiens	245-250
28487369-5	2017	In N-glycosylation inhibition experiments, we find that treatment with tunicamycin and siRNA-mediated knockdown of the Golgi N-acetylglucosaminyltransferase I gene (MGAT1) induce partial loss of both total and cell-surface levels of the largest mucin, MUC16, and a concomitant reduction in glycocalyx barrier function.	Tunicamycin	71-82	mucin 16, cell surface associated	Homo sapiens	252-257
28667325-3	2017	The present study reported ER stress induction by tunicamycin treatment that resulted in IRE1alpha-mediated XBP1 mRNA splicing and autophagy.	Tunicamycin	50-61	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	89-98
28667325-3	2017	The present study reported ER stress induction by tunicamycin treatment that resulted in IRE1alpha-mediated XBP1 mRNA splicing and autophagy.	Tunicamycin	50-61	X-box binding protein 1	Homo sapiens	108-112
28662078-8	2017	Even so, the fibroblasts of patients with DPAGT1-CDG seemed to be more sensitive to the stressor tunicamycin.	Tunicamycin	97-108	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	42-48
28978049-4	2017	We showed GRP78/BiP translocation to PC3 cell surface in the presence of tunicamycin, an ER stress inductor, and demonstrated the existence of a GRP78/BiP-dependent non-canonical Nrf2 activation, responsible for increased resistance to ER-stress induced apoptosis.	Tunicamycin	73-84	heat shock protein family A (Hsp70) member 5	Homo sapiens	10-15
28978049-4	2017	We showed GRP78/BiP translocation to PC3 cell surface in the presence of tunicamycin, an ER stress inductor, and demonstrated the existence of a GRP78/BiP-dependent non-canonical Nrf2 activation, responsible for increased resistance to ER-stress induced apoptosis.	Tunicamycin	73-84	heat shock protein family A (Hsp70) member 5	Homo sapiens	16-19
28978049-5	2017	We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment.	Tunicamycin	54-65	NFE2 like bZIP transcription factor 2	Homo sapiens	73-77
28978049-5	2017	We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment.	Tunicamycin	54-65	AKT serine/threonine kinase 1	Homo sapiens	104-107
28978049-5	2017	We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment.	Tunicamycin	54-65	heat shock protein family A (Hsp70) member 5	Homo sapiens	142-147
28978049-5	2017	We found that, even in the absence of ROS production, tunicamycin causes Nrf2 activation, and activates Akt signaling, events bulnted by anti-GRP78/BiP antibody treatment.	Tunicamycin	54-65	heat shock protein family A (Hsp70) member 5	Homo sapiens	148-151
28562344-5	2017	We showed PHB accumulated at different levels in melanoma cell lines under stressing stimuli, such as (i) treatment with temozolomide (TMZ), dacarbazine (DTIC) and cisplatin; (ii) serum deprivation; (iii) tunicamycin, an UPR inducer.	Tunicamycin	205-216	prohibitin 1	Homo sapiens	10-13
28562344-6	2017	Prohibitin accumulated in the mitochondria of melanoma cells after cisplatin and tunicamycin treatment and its de novo accumulation led to chemoresistance melanoma cell lines.	Tunicamycin	81-92	prohibitin 1	Homo sapiens	0-10
28562344-7	2017	In contrast, PHB knock-down sensitized melanoma cells to cisplatin and tunicamycin treatment.	Tunicamycin	71-82	prohibitin 1	Homo sapiens	13-16
28630443-6	2017	Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP.	Tunicamycin	25-36	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	45-49
28630443-6	2017	Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP.	Tunicamycin	25-36	eukaryotic translation initiation factor 2A	Homo sapiens	50-59
28630443-6	2017	Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP.	Tunicamycin	25-36	activating transcription factor 4	Homo sapiens	60-64
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
28630443-6	2017	Both chaperones mitigate tunicamycin induced PERK-eIF2alpha-ATF4-CHOP arm of UPR and expression of BiP.	Tunicamycin	25-36	growth differentiation factor 10	Homo sapiens	99-102
28674530-7	2017	Additional ER stressors such as tunicamycin and thapsigargin also promoted IL-23 expression by PAMP-stimulated DCs.	Tunicamycin	32-43	interleukin 23 subunit alpha	Homo sapiens	75-80
28674530-7	2017	Additional ER stressors such as tunicamycin and thapsigargin also promoted IL-23 expression by PAMP-stimulated DCs.	Tunicamycin	32-43	YME1 like 1 ATPase	Homo sapiens	95-99
28522733-9	2017	Similarly, administration of either GSK2656157 or overexpression of PERK-K618A in primary neurons rescues the loss of dendritic outgrowth and number of synapses after treatment with a PERK activator, tunicamycin.	Tunicamycin	200-211	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	68-72
28577569-5	2017	METHODS: Human apoA-I was overexpressed in HepG2 hepatocytes, which were then treated with 2 mug/mL tunicamycin or 500 muM palmitic acid.	Tunicamycin	100-111	apolipoprotein A1	Homo sapiens	15-21
28978108-0	2017	Tunicamycin induced endoplasmic reticulum stress promotes apoptosis of prostate cancer cells by activating mTORC1.	Tunicamycin	0-11	CREB regulated transcription coactivator 1	Mus musculus	107-113
28978108-3	2017	To delineate the role of candidate genes in the apoptotic process under ER stress and to search for new therapeutic strategies to treat metastatic castration resistant prostate cancer, we performed whole genome expression microarray analysis in tunicamycin treated metastatic androgen-insensitive prostate cancer cells, PC-3.	Tunicamycin	245-256	proprotein convertase subtilisin/kexin type 1	Homo sapiens	320-324
28978108-8	2017	Overall, our data demonstrate that tunicamycin induced ER stress promotes prostate cancer cell death by activating mTORC1 through eNOS-RagC pathway.	Tunicamycin	35-46	CREB regulated transcription coactivator 1	Mus musculus	115-121
28978108-8	2017	Overall, our data demonstrate that tunicamycin induced ER stress promotes prostate cancer cell death by activating mTORC1 through eNOS-RagC pathway.	Tunicamycin	35-46	nitric oxide synthase 3	Homo sapiens	130-134
28978108-8	2017	Overall, our data demonstrate that tunicamycin induced ER stress promotes prostate cancer cell death by activating mTORC1 through eNOS-RagC pathway.	Tunicamycin	35-46	Ras related GTP binding C	Homo sapiens	135-139
27941872-7	2017	In vitro, AGR2 expression was stimulated by tunicamycin-induced endoplasmic reticulum (ER) stress in both KRAS wild-type normal pancreas cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeostasis.	Tunicamycin	44-55	anterior gradient 2, protein disulphide isomerase family member	Homo sapiens	10-14
27941872-7	2017	In vitro, AGR2 expression was stimulated by tunicamycin-induced endoplasmic reticulum (ER) stress in both KRAS wild-type normal pancreas cells, as well as in KRAS mutated pancreatic cancer cells and was essential for ER homoeostasis.	Tunicamycin	44-55	KRAS proto-oncogene, GTPase	Homo sapiens	106-110
28811964-8	2017	Suppression of glycosylation with tunicamycin caused a shift in molecular weight and significant decrease in the expression of PD-L2 protein.	Tunicamycin	34-45	programmed cell death 1 ligand 2	Homo sapiens	127-132
28631572-7	2017	Tunicamycin led to increased expression of GRP78.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	43-48
28631572-8	2017	With tunicamycin treatment, phosphorylation of PERK and eIF2alpha and CHOP expression increased.	Tunicamycin	5-16	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	47-51
28631572-8	2017	With tunicamycin treatment, phosphorylation of PERK and eIF2alpha and CHOP expression increased.	Tunicamycin	5-16	eukaryotic translation initiation factor 2A	Homo sapiens	56-65
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
28631572-10	2017	With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins.	Tunicamycin	19-30	BCL2 associated X, apoptosis regulator	Homo sapiens	82-85
28631572-10	2017	With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins.	Tunicamycin	19-30	BCL2 apoptosis regulator	Homo sapiens	133-138
28631572-10	2017	With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins.	Tunicamycin	19-30	AKT serine/threonine kinase 1	Homo sapiens	174-177
28631572-10	2017	With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins.	Tunicamycin	19-30	mechanistic target of rapamycin kinase	Homo sapiens	178-182
28397086-8	2017	Our findings indicate that exposure to tunicamycin (0.5 mug/mL) for 2 h induces the expression of GRP78 and CHOP, and apoptotic markers (caspase-3 and caspase-12) and causes a significant reduction in renal cell viability.	Tunicamycin	39-50	caspase 12	Rattus norvegicus	151-161
28336294-9	2017	Interestingly, we found that ER stress induced by either palmitate, tunicamycin, or thapsigargin led to the degradation of Plin2, an important lipid droplet binding protein.	Tunicamycin	68-79	perilipin 2	Rattus norvegicus	123-128
28521463-11	2017	ERp46 overexpression led to reduced sensitivity to ER stress as indicated by higher half maximal inhibitory concentrations for tunicamycin and thapsigargin in ERp46+ cells.	Tunicamycin	127-138	thioredoxin domain containing 5	Homo sapiens	0-5
28521463-11	2017	ERp46 overexpression led to reduced sensitivity to ER stress as indicated by higher half maximal inhibitory concentrations for tunicamycin and thapsigargin in ERp46+ cells.	Tunicamycin	127-138	thioredoxin domain containing 5	Homo sapiens	159-164
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	eukaryotic translation initiation factor 2 subunit gamma	Homo sapiens	91-95
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
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	AKT serine/threonine kinase 1	Homo sapiens	146-149
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	mechanistic target of rapamycin kinase	Homo sapiens	157-161
28459209-14	2017	Our study provide evidence that endoplasmic reticulum stress activated by tunicamycin could promote breast cancer cell autophagy and apoptosis and enhance chemosensitivity of MCF-7 cells by inhibiting the PI3K/AKT/mTOR signaling pathway.	Tunicamycin	74-85	AKT serine/threonine kinase 1	Homo sapiens	210-213
28459209-14	2017	Our study provide evidence that endoplasmic reticulum stress activated by tunicamycin could promote breast cancer cell autophagy and apoptosis and enhance chemosensitivity of MCF-7 cells by inhibiting the PI3K/AKT/mTOR signaling pathway.	Tunicamycin	74-85	mechanistic target of rapamycin kinase	Homo sapiens	214-218
28351617-6	2017	Molecular size of FAM5C was reduced by treatment with N-glycosidase F and in FAM5C-expressing cells cultured in the presence of the N-glycosylation inhibitor tunicamycin.	Tunicamycin	158-169	BMP/retinoic acid inducible neural specific 3	Homo sapiens	18-23
28351617-6	2017	Molecular size of FAM5C was reduced by treatment with N-glycosidase F and in FAM5C-expressing cells cultured in the presence of the N-glycosylation inhibitor tunicamycin.	Tunicamycin	158-169	BMP/retinoic acid inducible neural specific 3	Homo sapiens	77-82
28351617-7	2017	FAM5C was secreted by the cells and the secretion of FAM5C was blocked by tunicamycin.	Tunicamycin	74-85	BMP/retinoic acid inducible neural specific 3	Homo sapiens	0-5
28351617-7	2017	FAM5C was secreted by the cells and the secretion of FAM5C was blocked by tunicamycin.	Tunicamycin	74-85	BMP/retinoic acid inducible neural specific 3	Homo sapiens	53-58
28397086-8	2017	Our findings indicate that exposure to tunicamycin (0.5 mug/mL) for 2 h induces the expression of GRP78 and CHOP, and apoptotic markers (caspase-3 and caspase-12) and causes a significant reduction in renal cell viability.	Tunicamycin	39-50	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	98-103
28397086-8	2017	Our findings indicate that exposure to tunicamycin (0.5 mug/mL) for 2 h induces the expression of GRP78 and CHOP, and apoptotic markers (caspase-3 and caspase-12) and causes a significant reduction in renal cell viability.	Tunicamycin	39-50	DNA-damage inducible transcript 3	Rattus norvegicus	108-112
28397086-8	2017	Our findings indicate that exposure to tunicamycin (0.5 mug/mL) for 2 h induces the expression of GRP78 and CHOP, and apoptotic markers (caspase-3 and caspase-12) and causes a significant reduction in renal cell viability.	Tunicamycin	39-50	caspase 3	Rattus norvegicus	137-146
28460451-3	2017	In this study we show that abrogation of FLT3ITD glycoprotein maturation using low doses of the N-glycosylation inhibitor tunicamycin has anti-proliferative and pro-apoptotic effects on FLT3ITD-expressing human and murine cell lines.	Tunicamycin	122-133	fms related receptor tyrosine kinase 3	Homo sapiens	41-45
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	110-162
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	164-168
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
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
28202509-6	2017	Accordingly, SCNN1B sensitized gastric cancer cells to the UPR-inducing drug tunicamycin.	Tunicamycin	77-88	sodium channel epithelial 1 subunit beta	Homo sapiens	13-19
28399139-0	2017	Ibutilide treatment protects against ER stress induced apoptosis by regulating calumenin expression in tunicamycin treated cardiomyocytes.	Tunicamycin	103-114	calumenin	Rattus norvegicus	79-88
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	117-122
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	heat shock protein 90 beta family member 1	Rattus norvegicus	124-129
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	calumenin	Rattus norvegicus	134-143
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	caspase 3	Rattus norvegicus	217-226
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	DNA-damage inducible transcript 3	Rattus norvegicus	233-237
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	activating transcription factor 6	Rattus norvegicus	239-243
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	X-box binding protein 1	Rattus norvegicus	261-266
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	BCL2 associated X, apoptosis regulator	Rattus norvegicus	281-284
28399139-5	2017	RNC were treated with tunicamycin and the degree of ER stress was assessed by quantifying mRNA and protein levels of GRP78, GRP94 and calumenin, and examined the extent of apoptosis by assessing the protein levels of caspase-3/9/12, CHOP, ATF6, p-PERK, spliced XBP-1, the ratio of Bax/Bcl-2 and the percentage of deoxynucleotidyl-transferase- mediated dUTP nick end labeling (TUNEL) positive cells.	Tunicamycin	22-33	BCL2, apoptosis regulator	Rattus norvegicus	285-290
28399139-6	2017	RESULTS: We demonstrate ibutilide attenuated the up-regulation of ER stress markers GRP78 and GRP94 and rescued the decline in calumenin mRNA and protein levels in tunicamycin treated cardiomyocytes.	Tunicamycin	164-175	calumenin	Rattus norvegicus	127-136
28397086-9	2017	Pre-treatment of cells with piperine and its cyclohexylamino analog decreased the tunicamycin-induced upregulation of GRP78 and CHOP and cell death.	Tunicamycin	82-93	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	118-123
28397086-9	2017	Pre-treatment of cells with piperine and its cyclohexylamino analog decreased the tunicamycin-induced upregulation of GRP78 and CHOP and cell death.	Tunicamycin	82-93	DNA-damage inducible transcript 3	Rattus norvegicus	128-132
27932512-9	2017	Catalase was induced by the canonical ER stressor, tunicamycin, and by I/R in cardiac myocytes from wild-type but not in cardiac myocytes from ATF6 knockout mice.	Tunicamycin	51-62	catalase	Mus musculus	0-8
28331281-9	2017	Exposure to blue LED light in combination with ER stress inducers (tunicamycin and dithiothreitol) induced the aggregation of S-opsin.	Tunicamycin	67-78	opsin 1 (cone pigments), short-wave-sensitive (color blindness, tritan)	Mus musculus	126-133
28131804-5	2017	IFN-lambda1 could also inhibit HCV-induced or tunicamycin (a known inducer of autophagy with similar mechanism to HCV infection) -induced LC3B-II expression and autophagosome formation.	Tunicamycin	46-57	interferon alpha 1	Homo sapiens	0-3
28131804-5	2017	IFN-lambda1 could also inhibit HCV-induced or tunicamycin (a known inducer of autophagy with similar mechanism to HCV infection) -induced LC3B-II expression and autophagosome formation.	Tunicamycin	46-57	microtubule associated protein 1 light chain 3 beta	Homo sapiens	138-142
27885588-0	2017	A mouse model reveals that Mfsd2a is critical for unfolded protein response upon exposure to tunicamycin.	Tunicamycin	93-104	major facilitator superfamily domain containing 2A	Mus musculus	27-33
27885588-2	2017	Mfsd2a functions as a transporter for docosahexaenoic acid and also plays a role in the unfolded protein response (UPR) upon tunicamycin (TM) exposure.	Tunicamycin	125-136	major facilitator superfamily domain containing 2A	Mus musculus	0-6
27885588-2	2017	Mfsd2a functions as a transporter for docosahexaenoic acid and also plays a role in the unfolded protein response (UPR) upon tunicamycin (TM) exposure.	Tunicamycin	138-140	major facilitator superfamily domain containing 2A	Mus musculus	0-6
27341688-3	2017	We aimed to investigate whether ERS induced by oxLDL or tunicamycin (TM) in human macrophages is associated with the stimulation of MMP-9 expression and secretion.	Tunicamycin	56-67	matrix metallopeptidase 9	Homo sapiens	132-137
27341688-6	2017	Treatment of oxLDL or TM-incubated cells with ERS inhibitor, sodium phenylbutyrate decreased MMP-9 gene expression, secretion, and activity.	Tunicamycin	22-24	matrix metallopeptidase 9	Homo sapiens	93-98
27862269-3	2017	In this study, we demonstrated that the Arp2/3 complex was required for reduction of ribosome protein gene expression in response to defective secretion by addition of tunicamycin.	Tunicamycin	168-179	actin-related protein 2	Saccharomyces cerevisiae S288C	40-44
28275095-6	2017	In line with this, Bap1 KO mice are more sensitive to tunicamycin-induced renal damage.	Tunicamycin	54-65	Brca1 associated protein 1	Mus musculus	19-23
28246389-9	2017	Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM.	Tunicamycin	110-121	bone gamma-carboxyglutamate protein	Homo sapiens	149-160
28303141-4	2017	FKBP13 expression was induced largely in the lumen of ER in response to treatment with an ER stressor tunicamycin or overexpression of an adaptive unfolded protein response (UPR) protein X-box binding protein 1 (XBP1).	Tunicamycin	102-113	FK506 binding protein 2	Mus musculus	0-6
28100484-12	2017	But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased.	Tunicamycin	25-36	hyaluronan synthase 2	Mus musculus	52-56
28100484-12	2017	But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased.	Tunicamycin	25-36	prostaglandin-endoperoxide synthase 2	Mus musculus	58-63
28100484-12	2017	But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased.	Tunicamycin	25-36	prostaglandin F receptor	Mus musculus	69-74
28100484-12	2017	But, after treating with tunicamycin, the levels of Has2, Ptgs2, and Ptgfr increased relatively, whereas Igfbp4 expression decreased.	Tunicamycin	25-36	insulin-like growth factor binding protein 4	Mus musculus	105-111
27915415-0	2017	Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway.	Tunicamycin	31-42	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	80-85
28246389-6	2017	In in vitro experiments, insulin resistance was induced by applying tunicamycin to HUVECs.	Tunicamycin	68-79	insulin	Homo sapiens	25-32
28246389-9	2017	Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM.	Tunicamycin	110-121	bone gamma-carboxyglutamate protein	Homo sapiens	15-26
28246389-9	2017	Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM.	Tunicamycin	110-121	insulin	Homo sapiens	46-53
28246389-9	2017	Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM.	Tunicamycin	110-121	AKT serine/threonine kinase 1	Homo sapiens	83-86
28246389-9	2017	Uncarboxylated osteocalcin partially improves insulin signal transduction via PI3K/Akt/NF-kappaB signaling in tunicamycin-induced HUVECs, suggesting osteocalcin as a potential treatment for the vascular complications of T2DM.	Tunicamycin	110-121	nuclear factor kappa B subunit 1	Homo sapiens	87-96
27915415-0	2017	Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway.	Tunicamycin	31-42	mitogen-activated protein kinase 8	Homo sapiens	86-89
27915415-0	2017	Exendin-4 protects HUVECs from tunicamycin-induced apoptosis via inhibiting the IRE1a/JNK/caspase-3 pathway.	Tunicamycin	31-42	caspase 3	Homo sapiens	90-99
27915415-8	2017	Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4.	Tunicamycin	109-120	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	26-35
27915415-8	2017	Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4.	Tunicamycin	109-120	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	36-45
27915415-8	2017	Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4.	Tunicamycin	109-120	mitogen-activated protein kinase 8	Homo sapiens	49-52
27915415-8	2017	Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4.	Tunicamycin	109-120	mitogen-activated protein kinase 8	Homo sapiens	53-56
27915415-8	2017	Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4.	Tunicamycin	109-120	caspase 3	Homo sapiens	68-77
27915415-8	2017	Similarly, the ratio of p-IRE1alpha/IRE1alpha, p-JNK/JNK and active caspase-3/procaspase-3 were increased by tunicamycin (10 mug/ml); an effect that was counteracted by Exendin-4.	Tunicamycin	109-120	caspase 3	Homo sapiens	78-90
28298914-3	2017	Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response.	Tunicamycin	20-31	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	123-155
28298914-3	2017	Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response.	Tunicamycin	20-31	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	157-161
28298914-3	2017	Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response.	Tunicamycin	33-35	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	123-155
28298914-3	2017	Here, we report the tunicamycin (TM) -induced ER stress response in Arabidopsis roots by monitoring expression patterns of immunoglobulin-binding protein 3 (BiP3), a representative marker for the response.	Tunicamycin	33-35	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	157-161
27488499-3	2017	In this study, we firstly treated fetal rat spinal cord neuron cells (SCN) and PC12 cells with ER stress activator thapsigargin (TG) or tunicamycin (TM) and then detected the expression pattern of SCIRR69 in response to ER stress at mRNA and protein levels using real-time PCR assay and immunoblotting.	Tunicamycin	136-147	cAMP responsive element binding protein 3-like 2	Rattus norvegicus	197-204
27383524-0	2017	Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma.	Tunicamycin	0-11	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	80-84
27383524-0	2017	Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma.	Tunicamycin	0-11	activating transcription factor 4	Mus musculus	85-89
27383524-0	2017	Tunicamycin aggravates endoplasmic reticulum stress and airway inflammation via PERK-ATF4-CHOP signaling in a murine model of neutrophilic asthma.	Tunicamycin	0-11	DNA-damage inducible transcript 3	Mus musculus	90-94
27383524-4	2017	RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling.	Tunicamycin	9-20	interleukin 6	Mus musculus	150-154
27383524-4	2017	RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling.	Tunicamycin	9-20	chemokine (C-X-C motif) ligand 15	Mus musculus	156-160
27383524-4	2017	RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling.	Tunicamycin	9-20	tumor necrosis factor	Mus musculus	166-175
27383524-4	2017	RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling.	Tunicamycin	9-20	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	180-184
27383524-4	2017	RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling.	Tunicamycin	9-20	activating transcription factor 4	Mus musculus	185-189
27383524-4	2017	RESULTS: Tunicamycin not only induced ER stress in mouse bronchial epithelial cells, but also increased expression of inflammation indicators such as IL-6, IL-8, and TNF-alpha via PERK-ATF4-CHOP signaling.	Tunicamycin	9-20	DNA-damage inducible transcript 3	Mus musculus	190-194
27383524-6	2017	Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVALPS-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma.	Tunicamycin	14-25	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	204-208
27383524-6	2017	Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVALPS-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma.	Tunicamycin	14-25	activating transcription factor 4	Mus musculus	209-213
27383524-6	2017	Administering tunicamycin further increased protein expression levels of ER stress indicators and inflammatory cytokines, and resulted in more severe asthma phenotypes in OVALPS-OVA mice, suggesting that PERK-ATF4-CHOP signaling is associated with airway inflammation in neutrophil-dominant asthma.	Tunicamycin	14-25	DNA-damage inducible transcript 3	Mus musculus	214-218
28223691-5	2017	Maintenance of SKBR-3 cells in tunicamycin (an inhibitor of N-linked glycosylation) resulted in an increase in sensitivity to DXR (0.1 muM DXR P &lt; 0.001) and a decrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P &lt; 0.001).	Tunicamycin	31-42	insulin like growth factor 1	Homo sapiens	190-195
28230089-3	2017	These studies aimed to determine whether the ET-1 system promotes renal ER stress development in response to tunicamycin.	Tunicamycin	109-120	endothelin 1	Rattus norvegicus	45-49
28230089-5	2017	Tunicamycin treatment similarly increased cortical ER stress markers in both rat genotypes; however, only ETB def rats showed a 14-24 fold increase from baseline for medullary GRP78, sXBP-1, and CHOP.	Tunicamycin	0-11	DNA-damage inducible transcript 3	Rattus norvegicus	195-199
28230089-6	2017	Pre-treatment of TG-con rats with the ETA blocker ABT-627 for 1 week prior to tunicamycin injection significantly reduced the ER stress response in cortex and medulla, and also inhibited renal apoptosis.	Tunicamycin	78-89	endothelin receptor type A	Rattus norvegicus	38-41
28230089-8	2017	In conclusion, the ET-1 system is important for the development of tunicamycin-induced renal ER stress and apoptosis.	Tunicamycin	67-78	endothelin 1	Rattus norvegicus	19-23
28223691-5	2017	Maintenance of SKBR-3 cells in tunicamycin (an inhibitor of N-linked glycosylation) resulted in an increase in sensitivity to DXR (0.1 muM DXR P &lt; 0.001) and a decrease in sensitivity to IGF-1 alone and to IGF-1 supplemented with EGF (P &lt; 0.001).	Tunicamycin	31-42	insulin like growth factor 1	Homo sapiens	209-214
26838680-6	2017	Moreover, Gstp1/p2-/- cells were significantly more sensitive to the cytotoxic effects of the ER-stress inducing drugs, thapsigargin (7-fold) and tunicamycin (2-fold).	Tunicamycin	146-157	glutathione S-transferase, pi 1	Mus musculus	10-15
28246472-7	2017	Dramatically increased CCAAT-enhancer-binding protein homologous protein level, suppressed COX-2 and decreased Bcl-2/Bax ratio by melatonin or ATF-6 siRNA contributed the enhanced HepG2 cell apoptosis under tunicamycin (an ER stress inducer) stimulation.	Tunicamycin	207-218	BCL2 apoptosis regulator	Homo sapiens	111-116
28246472-7	2017	Dramatically increased CCAAT-enhancer-binding protein homologous protein level, suppressed COX-2 and decreased Bcl-2/Bax ratio by melatonin or ATF-6 siRNA contributed the enhanced HepG2 cell apoptosis under tunicamycin (an ER stress inducer) stimulation.	Tunicamycin	207-218	activating transcription factor 6	Homo sapiens	143-148
28007835-4	2017	Among mutants harboring a single native or chimeric RPL7 allele, expression from the RPL7A locus exceeded that from the RPL7B locus, and more Rpl7a was expressed from either locus than Rpl7b Phenotypic differences in tunicamycin sensitivity, ASH1 mRNA localization, and mobility of the Ty1 retrotransposon were strongly correlated with Rpl7 and ribosome levels, but not with the Rpl7 or snoRNA isoform expressed.	Tunicamycin	217-228	Rlp7p	Saccharomyces cerevisiae S288C	52-56
28030827-8	2017	Furthermore, Sirt1 attenuated tunicamycin-induced cold intolerance and elevating thermogenesis by inhibiting ER stress and apoptosis in iBAT.	Tunicamycin	30-41	sirtuin 1	Mus musculus	13-18
28181559-9	2017	Moreover, pharmacologic induction of ER stress with tunicamycin downregulated endothelial Cav1 and impaired endothelium-dependent vasorelaxation that was rescued by overexpressing Cav1.	Tunicamycin	52-63	caveolin 1	Homo sapiens	90-94
28181559-9	2017	Moreover, pharmacologic induction of ER stress with tunicamycin downregulated endothelial Cav1 and impaired endothelium-dependent vasorelaxation that was rescued by overexpressing Cav1.	Tunicamycin	52-63	caveolin 1	Homo sapiens	180-184
28024901-6	2017	The ER stress inducer, tunicamycin, also up-regulated the kinase activity and protein expression of Cdk5 in podocytes accompanied with the increasing of GRP78.	Tunicamycin	23-34	cyclin dependent kinase 5	Homo sapiens	100-104
28024901-6	2017	The ER stress inducer, tunicamycin, also up-regulated the kinase activity and protein expression of Cdk5 in podocytes accompanied with the increasing of GRP78.	Tunicamycin	23-34	heat shock protein family A (Hsp70) member 5	Homo sapiens	153-158
28024901-7	2017	On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation.	Tunicamycin	58-69	cyclin dependent kinase 5	Homo sapiens	19-23
28024901-7	2017	On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation.	Tunicamycin	58-69	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	39-44
28024901-7	2017	On the other hand, Cdk5 phosphorylates MEKK1 at Ser280 in tunicamycin treated podocytes, and together, they increase the JNK phosphorylation.	Tunicamycin	58-69	mitogen-activated protein kinase 8	Homo sapiens	121-124
27693501-7	2017	In cultured human chondrocytes Sesn1, 2 and 3 were expressed and increased by tunicamycin, an endoplasmic reticulum (ER) stress response inducer and 2-deoxyglucose (2DG), a metabolic stress inducer.	Tunicamycin	78-89	sestrin 1	Homo sapiens	31-45
27278863-3	2017	Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription.	Tunicamycin	203-214	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	230-234
27993557-3	2017	In vitro, NRG-1 directly inhibited the upregulation of ER stress markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein and cleaved caspase-12 induced by the ER stress inducers tunicamycin or dithiothreitol in both neonatal and adult ventricular myocytes.	Tunicamycin	218-229	neuregulin 1	Rattus norvegicus	10-15
27993557-3	2017	In vitro, NRG-1 directly inhibited the upregulation of ER stress markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein and cleaved caspase-12 induced by the ER stress inducers tunicamycin or dithiothreitol in both neonatal and adult ventricular myocytes.	Tunicamycin	218-229	caspase 12	Rattus norvegicus	173-183
27909053-5	2017	In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice.	Tunicamycin	129-140	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
27909053-5	2017	In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice.	Tunicamycin	129-140	MIR7-3 host gene	Homo sapiens	154-158
27909053-5	2017	In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice.	Tunicamycin	142-144	proprotein convertase subtilisin/kexin type 9	Homo sapiens	61-66
27909053-5	2017	In contrast, a significant reduction in the secreted form of PCSK9 protein was observed in the media from both thapsigargin- and tunicamycin (TM)-treated HuH7 cells, mouse primary hepatocytes, and in the plasma of TM-treated C57BL/6 mice.	Tunicamycin	142-144	MIR7-3 host gene	Homo sapiens	154-158
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	TNF superfamily member 10	Homo sapiens	49-54
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	mitogen-activated protein kinase 8	Homo sapiens	76-79
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
27603596-0	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	TNF receptor superfamily member 10b	Homo sapiens	94-97
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	epidermal growth factor receptor	Homo sapiens	137-141
27603596-2	2017	This paper reports that the combination of tunicamycin plus TRAIL produced a strong synergistic effect in TRAIL-sensitive human colon cancer HCT116 cells and TRAIL-resistant HT-29 cells.	Tunicamycin	43-54	TNF superfamily member 10	Homo sapiens	106-111
27603596-2	2017	This paper reports that the combination of tunicamycin plus TRAIL produced a strong synergistic effect in TRAIL-sensitive human colon cancer HCT116 cells and TRAIL-resistant HT-29 cells.	Tunicamycin	43-54	TNF superfamily member 10	Homo sapiens	106-111
27603596-3	2017	On a cellular mechanistic level, tunicamycin-enhanced TRAIL-induced apoptosis by death receptor (DR) 5 upregulation and DR4 deglycosylation.	Tunicamycin	33-44	TNF superfamily member 10	Homo sapiens	54-59
27603596-3	2017	On a cellular mechanistic level, tunicamycin-enhanced TRAIL-induced apoptosis by death receptor (DR) 5 upregulation and DR4 deglycosylation.	Tunicamycin	33-44	TNF receptor superfamily member 10a	Homo sapiens	120-123
27603596-4	2017	Knockdown of DR5 but not DR4 expression by specific shRNAs or siRNAs significantly increased tunicamycin-mediated and TRAIL-mediated cell viability.	Tunicamycin	93-104	TNF receptor superfamily member 10b	Homo sapiens	13-16
27603596-6	2017	In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin.	Tunicamycin	13-24	epidermal growth factor receptor	Homo sapiens	35-67
27603596-6	2017	In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin.	Tunicamycin	13-24	AKT serine/threonine kinase 1	Homo sapiens	121-124
27603596-6	2017	In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin.	Tunicamycin	13-24	TNF superfamily member 10	Homo sapiens	213-218
27603596-6	2017	In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin.	Tunicamycin	236-247	epidermal growth factor receptor	Homo sapiens	35-67
27603596-6	2017	In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin.	Tunicamycin	236-247	AKT serine/threonine kinase 1	Homo sapiens	121-124
27603596-6	2017	In addition, tunicamycin inhibited epidermal growth factor receptor glycosylation and the downstream signaling pathways, Akt and extracellular signal-regulated kinases activation, which might also be required for TRAIL sensitization by tunicamycin.	Tunicamycin	236-247	TNF superfamily member 10	Homo sapiens	213-218
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	TNF superfamily member 10	Homo sapiens	45-50
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	mitogen-activated protein kinase 8	Homo sapiens	83-86
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
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	TNF receptor superfamily member 10b	Homo sapiens	101-104
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	epidermal growth factor receptor	Homo sapiens	144-176
27856453-4	2017	APPROACH AND RESULTS: In endothelial cells, we found that ER stress induced by tunicamycin activates the NADPH (nicotinamide adenine dinucleotide phosphate) oxidase Nox4 focally on the ER surface but not on the plasma membrane.	Tunicamycin	79-90	NADPH oxidase 4	Homo sapiens	165-169
27717825-7	2017	Tunicamycin (TM) or thapsigargin (Tg) induced ER stress blunted leptin sensitivity and inhibited preadipocyte proliferation.	Tunicamycin	0-11	leptin	Mus musculus	64-70
27717825-7	2017	Tunicamycin (TM) or thapsigargin (Tg) induced ER stress blunted leptin sensitivity and inhibited preadipocyte proliferation.	Tunicamycin	13-15	leptin	Mus musculus	64-70
27803246-8	2017	Furthermore, the sensitivity of cells to tunicamycin without ER-PM contact was considerably elevated by the deletion of RIM21.	Tunicamycin	41-52	Rim21p	Saccharomyces cerevisiae S288C	120-125
28349059-11	2017	Pretreatment by IRE1 agonist tunicamycin or JNK agonist anisomycin attenuated the effect of psoralen on osteoporotic osteoblasts.	Tunicamycin	29-40	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	16-20
27740623-7	2017	Some of the effects of TM7SF3 silencing are evident both under basal conditions, in otherwise untreated cells, as well as under different stress conditions induced by thapsigargin, tunicamycin or a mixture of pro-inflammatory cytokines (tumor necrosis factor alpha, interleukin-1 beta and interferon gamma).	Tunicamycin	181-192	transmembrane 7 superfamily member 3	Homo sapiens	23-29
27796797-10	2017	We also found that sublethal ER stress caused by tunicamycin treatment induced the synthesis of PYCR1 in murine fibroblasts.	Tunicamycin	49-60	pyrroline-5-carboxylate reductase 1	Mus musculus	96-101
29130967-6	2017	The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR.	Tunicamycin	44-55	tumor protein p53	Homo sapiens	11-14
29130967-6	2017	The mutant p53 cell lines were treated with tunicamycin to induce ERS and rapamycin in order to inhibit mTOR.	Tunicamycin	44-55	mechanistic target of rapamycin kinase	Homo sapiens	104-108
27886513-4	2017	Pretreatment with an ER stress inducer, tunicamycin or thapsigargin, inhibited human chorionic gonadotropin (hCG)-stimulated progesterone production in cultured human GLCs.	Tunicamycin	40-51	chorionic gonadotropin subunit beta 5	Homo sapiens	109-112
27886513-5	2017	Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction.	Tunicamycin	32-43	chorionic gonadotropin subunit beta 5	Homo sapiens	54-57
27886513-5	2017	Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction.	Tunicamycin	32-43	steroidogenic acute regulatory protein	Homo sapiens	83-121
27886513-5	2017	Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction.	Tunicamycin	32-43	steroidogenic acute regulatory protein	Homo sapiens	123-127
27886513-5	2017	Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction.	Tunicamycin	32-43	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	133-167
27886513-5	2017	Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction.	Tunicamycin	32-43	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	169-178
27886513-5	2017	Pretreatment of human GLCs with tunicamycin inhibited hCG-stimulated expression of steroidogenic acute regulatory protein (StAR) and 3beta-hydroxysteroid dehydrogenase (3beta-HSD) messenger RNAs (mRNAs) without affecting expression of cytochrome P450 cholesterol side-chain cleavage enzyme (P450scc), as determined by real-time quantitative polymerase chain reaction.	Tunicamycin	32-43	cytochrome P450 family 11 subfamily A member 1	Homo sapiens	291-298
27886513-6	2017	Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation.	Tunicamycin	18-29	chorionic gonadotropin subunit beta 5	Homo sapiens	45-48
27886513-6	2017	Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation.	Tunicamycin	18-29	steroidogenic acute regulatory protein	Homo sapiens	74-78
27886513-6	2017	Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation.	Tunicamycin	18-29	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	91-100
27886513-6	2017	Pretreatment with tunicamycin also inhibited hCG-stimulated expression of StAR protein and 3beta-HSD enzyme activity in cultured human GLCs, as determined by Western blot analysis and an enzyme immunoassay, respectively, but did not affect hCG-induced intracellular 3",5"-cyclic adenosine monophosphate accumulation.	Tunicamycin	18-29	chorionic gonadotropin subunit beta 5	Homo sapiens	240-243
27886513-7	2017	Furthermore, tunicamycin attenuated hCG-induced protein kinase A and extracellular signal-regulated kinase activation, as determined by Western blot analysis.	Tunicamycin	13-24	chorionic gonadotropin subunit beta 5	Homo sapiens	36-39
27886513-8	2017	In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea.	Tunicamycin	26-37	chorionic gonadotropin subunit beta 5	Homo sapiens	105-108
27886513-8	2017	In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea.	Tunicamycin	26-37	chorionic gonadotropin subunit beta 5	Homo sapiens	133-136
27886513-8	2017	In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea.	Tunicamycin	26-37	chorionic gonadotropin subunit beta 5	Homo sapiens	133-136
27886513-8	2017	In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea.	Tunicamycin	26-37	steroidogenic acute regulatory protein	Homo sapiens	216-220
27886513-8	2017	In vivo administration of tunicamycin to pregnant mare serum gonadotropin-treated immature mice prior to hCG treatment inhibited the hCG-stimulated increase in serum progesterone levels and hCG-induced expression of StAR and 3beta-HSD mRNA in the ovary without affecting serum estradiol levels or the number of corpora lutea.	Tunicamycin	26-37	hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase 1	Homo sapiens	225-234
27278863-3	2017	Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription.	Tunicamycin	203-214	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	235-240
27278863-3	2017	Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription.	Tunicamycin	203-214	activating transcription factor 4	Homo sapiens	244-248
27278863-3	2017	Here, we show that oxidative stress, induced by stimulation of the cells with the oxidant arsenite, strongly activated gene transcription via the stress-responsive element (StRE), while phorbol ester or tunicamycin, activators of AP-1/c-Jun or ATF4, respectively, activated AP-1 or nutrient-sensing response element-mediated transcription.	Tunicamycin	203-214	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	274-278
27870947-5	2017	Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS.	Tunicamycin	33-44	fms related receptor tyrosine kinase 3	Homo sapiens	84-88
27870947-5	2017	Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS.	Tunicamycin	33-44	NADPH oxidase 4	Homo sapiens	143-147
27870947-5	2017	Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS.	Tunicamycin	33-44	cytochrome b-245 alpha chain	Homo sapiens	172-179
27870947-5	2017	Receptor trafficking inhibitors; Tunicamycin and Brefeldin A induce ER retention of FLT3-ITD, resulting in a decrease in protein expression of NOX4 and its partner protein p22phox, thus demonstrating the critical importance of FLT3-ITD localization for the generation of pro-survival ROS.	Tunicamycin	33-44	fms related receptor tyrosine kinase 3	Homo sapiens	227-231
27616576-2	2016	In this study, we investigated whether treatment with tunicamycin, an endoplasmic reticulum (ER) stress inducer, led to the accumulation of alpha-syn in PC12 cells, and where alpha-syn protein was accumulated, and finally, whether bibenzyl compound 20c, a novel compound isolated from Gastrodia elata (Tian ma), could alleviate the accumulation of alpha-syn and ER stress activation in tunicamycin-treated PC12 cells.	Tunicamycin	54-65	synuclein alpha	Rattus norvegicus	140-149
27996033-3	2016	XBP1 induction accompanied both culture-based HSC activation and ER stress induced by tunicamycin.	Tunicamycin	86-97	X-box binding protein 1	Homo sapiens	0-4
27616576-10	2016	CONCLUSION: Tunicamycin treatment caused accumulation of alpha-syn monomer and oligomer in PC12 cells.	Tunicamycin	12-23	synuclein alpha	Rattus norvegicus	57-66
27882945-3	2016	In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue.	Tunicamycin	29-40	heat shock protein 5	Mus musculus	157-162
27882945-3	2016	In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue.	Tunicamycin	29-40	DNA-damage inducible transcript 3	Mus musculus	164-168
27882945-3	2016	In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue.	Tunicamycin	29-40	activating transcription factor 2	Mus musculus	170-174
27882945-3	2016	In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue.	Tunicamycin	29-40	caspase 3	Mus musculus	179-188
27882945-3	2016	In this study, we found that tunicamycin-induced ER stress increased serum free fatty acid (FFA) and impaired glucose tolerance, elevated the mRNA levels of GRP78, Chop, ATF2 and caspase 3, but reduced adiponectin mRNA level in white adipose tissue.	Tunicamycin	29-40	adiponectin, C1Q and collagen domain containing	Mus musculus	202-213
27496643-8	2016	The functional consequences of ER stress- GR signaling crosstalk were assessed and demonstrated that long time exposure (24-48 h) of A549 cells to dexamethasone (10(-6) M) reversed the Tunicamycin-induced cell death, a phenomenon associated with parallel increases in GR protein content, increases in cell survival parameters and decreases in cell apoptosis-related parameters.	Tunicamycin	185-196	nuclear receptor subfamily 3 group C member 1	Homo sapiens	42-44
27496643-8	2016	The functional consequences of ER stress- GR signaling crosstalk were assessed and demonstrated that long time exposure (24-48 h) of A549 cells to dexamethasone (10(-6) M) reversed the Tunicamycin-induced cell death, a phenomenon associated with parallel increases in GR protein content, increases in cell survival parameters and decreases in cell apoptosis-related parameters.	Tunicamycin	185-196	nuclear receptor subfamily 3 group C member 1	Homo sapiens	268-270
28104755-6	2017	Tunicamycin (TM) treatment resulted in expression of non-glycosylated SMPDL3A that was not secreted, and was largely degraded by the proteasome.	Tunicamycin	0-11	sphingomyelin phosphodiesterase acid like 3A	Homo sapiens	70-77
27612916-6	2016	This amino acid change was predicted to create a putative N-glycosylation motif NX(S/T) subsequently validated upon endoglycosidase H treatment of microsomal fractions and inhibition of N-glycosylation of endogenously produced UGT2B7 with tunicamycin in human embryonic kidney (HEK293) cells.	Tunicamycin	239-250	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	227-233
27980366-0	2016	Tunicamycin-induced Endoplasmic Reticulum Stress Upregulates the Expression of Pentraxin 3 in Human Retinal Pigment Epithelial Cells.	Tunicamycin	0-11	pentraxin 3	Homo sapiens	79-90
27980366-1	2016	PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19.	Tunicamycin	81-92	pentraxin 3	Homo sapiens	47-58
27980366-1	2016	PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19.	Tunicamycin	81-92	pentraxin 3	Homo sapiens	60-64
27980366-1	2016	PURPOSE: To investigate the production of long pentraxin 3 (PTX3) in response to tunicamycin-induced endoplasmic reticulum (ER) stress and its role in ER stress-associated cell death, PTX3 expression was evaluated in the human retinal pigment epithelial cell line, ARPE-19.	Tunicamycin	81-92	pentraxin 3	Homo sapiens	184-188
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
27980366-5	2016	RESULTS: The protein and mRNA levels of PTX3 were found to be significantly increased by tunicamycin treatment.	Tunicamycin	89-100	pentraxin 3	Homo sapiens	40-44
27980366-7	2016	Furthermore, pretreatment with the NF-kappaB inhibitor abolished tunicamycin-induced PTX3 production.	Tunicamycin	65-76	pentraxin 3	Homo sapiens	85-89
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
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	pentraxin 3	Homo sapiens	128-132
27980366-9	2016	CONCLUSIONS: These results suggest that PTX3 production increased in the presence of tunicamycin-induced ER stress.	Tunicamycin	85-96	pentraxin 3	Homo sapiens	40-44
27616576-7	2016	RESULTS: Treatment of PC12 cells with tunicamycin (0.5-10 mug/mL) dose-dependently increased the accumulation of alpha-syn monomer (19 kDa) and oligomer (55 kDa), and decreased the cell viability.	Tunicamycin	38-49	synuclein alpha	Rattus norvegicus	113-122
27582391-5	2016	Removing N-glycosylation from the CD16 protein core by tunicamycin also increases the ligand binding affinity.	Tunicamycin	55-66	Fc gamma receptor IIIa	Homo sapiens	34-38
27808250-4	2016	Here we observed that rapamycin, which inhibits the nutrient-sensing complex mTORC1, increased ER-mitochondria coupling in HeLa cells to a similar extent as did tunicamycin.	Tunicamycin	161-172	CREB regulated transcription coactivator 1	Mus musculus	77-83
27654581-7	2016	Moreover, overexpression of Hax1 protected from apoptotic events triggered by Tunicamycin-induced ER stress.	Tunicamycin	78-89	HCLS1 associated protein X-1	Homo sapiens	28-32
27654581-8	2016	Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death.	Tunicamycin	20-31	HCLS1 associated protein X-1	Homo sapiens	33-37
27654581-8	2016	Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death.	Tunicamycin	20-31	mitofusin 1	Homo sapiens	94-112
27654581-8	2016	Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death.	Tunicamycin	20-31	mitofusin 1	Homo sapiens	114-118
27654581-8	2016	Upon treatment with Tunicamycin, Hax1 protected from mitochondrial fission, downregulation of mitofusins 1 and 2 (MFN1 and MFN2), loss of mitochondrial membrane potential ( Psim), production of reactive oxygen species (ROS) and apoptotic cell death.	Tunicamycin	20-31	mitofusin 2	Homo sapiens	123-127
27565667-5	2016	Inhibition of N-glycosylation by tunicamycin indicated that N-glycosylation of S2-expressed hFIX had occurred to a similar extent as in the CHO-produced hFIX.	Tunicamycin	33-44	coagulation factor IX	Homo sapiens	92-96
27599897-8	2016	Furthermore, the SiHa cells were exposed to tunicamycin (TM), an endoplasmic reticulum (ER) stress inducer that inactivates STAT3, with or without TRAIL.	Tunicamycin	44-55	signal transducer and activator of transcription 3	Homo sapiens	124-129
27599897-8	2016	Furthermore, the SiHa cells were exposed to tunicamycin (TM), an endoplasmic reticulum (ER) stress inducer that inactivates STAT3, with or without TRAIL.	Tunicamycin	57-59	signal transducer and activator of transcription 3	Homo sapiens	124-129
27678294-6	2016	The level of SLC30A3 mRNA was significantly increased by tunicamycin treatment in human neuroblastoma cell line (SH-SY5Y) and human embryonic kidney cell line (HEK293).	Tunicamycin	57-68	solute carrier family 30 member 3	Homo sapiens	13-20
27678294-7	2016	Cell viability under tunicamycin treatment was significantly decreased in SLC30A3 knockdown cells by siRNA in comparison with negative control (NC) cells.	Tunicamycin	21-32	solute carrier family 30 (zinc transporter), member 3	Mus musculus	74-81
27678294-11	2016	The level of ERK1/2 phosphorylation was significantly increased by tunicamycin treatment in NC cells, not in SLC30A3 knockdown cells.	Tunicamycin	67-78	mitogen-activated protein kinase 3	Mus musculus	13-19
27611865-9	2016	This expression was distinct from the UPR induced by well-studied ER stress inducer, tunicamycin, which robustly activated CHOP, PDIA4 and Dnajb9.	Tunicamycin	85-96	DNA damage-inducible transcript 3 protein	Oryzias latipes	123-127
27611865-9	2016	This expression was distinct from the UPR induced by well-studied ER stress inducer, tunicamycin, which robustly activated CHOP, PDIA4 and Dnajb9.	Tunicamycin	85-96	protein disulfide-isomerase A4	Oryzias latipes	129-134
27611865-9	2016	This expression was distinct from the UPR induced by well-studied ER stress inducer, tunicamycin, which robustly activated CHOP, PDIA4 and Dnajb9.	Tunicamycin	85-96	dnaJ homolog subfamily B member 9	Oryzias latipes	139-145
27486236-7	2016	Enhanced Fgf21 expression attenuated tunicamycin-induced endoplasmic reticulum stress, as demonstrated by using a neutralizing antibody against FGF21.	Tunicamycin	37-48	fibroblast growth factor 21	Mus musculus	9-14
27486236-7	2016	Enhanced Fgf21 expression attenuated tunicamycin-induced endoplasmic reticulum stress, as demonstrated by using a neutralizing antibody against FGF21.	Tunicamycin	37-48	fibroblast growth factor 21	Mus musculus	144-149
27489309-7	2016	In contrast, SERCA2 activation with a small molecule allosteric activator increased ER Ca(2+) storage and rescued tunicamycin-induced beta-cell death.	Tunicamycin	114-125	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	13-19
27763330-0	2016	The expression of P-gp in leukemia cells is associated with cross-resistance to protein N-glycosylation inhibitor tunicamycin.	Tunicamycin	114-125	phosphoglycolate phosphatase	Homo sapiens	18-22
27763330-1	2016	In P-gp-positive cell variants obtained from L1210 cells either by selection with vincristine (L1210/R) or by transfection with the human gene encoding P-gp (L1210/T), we have previously described cross-resistance to tunicamycin (TNM), a protein N-glycosylation inhibitor.	Tunicamycin	217-228	phosphoglycolate phosphatase	Mus musculus	3-7
27763330-1	2016	In P-gp-positive cell variants obtained from L1210 cells either by selection with vincristine (L1210/R) or by transfection with the human gene encoding P-gp (L1210/T), we have previously described cross-resistance to tunicamycin (TNM), a protein N-glycosylation inhibitor.	Tunicamycin	217-228	phosphoglycolate phosphatase	Homo sapiens	152-156
28011957-11	2016	Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP.	Tunicamycin	0-11	heat shock protein 90 beta family member 1	Homo sapiens	64-69
28011957-11	2016	Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP.	Tunicamycin	0-11	peptidyl arginine deiminase 1	Homo sapiens	71-74
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
28011957-11	2016	Tunicamycin treatment, as expected, increased the expression of Grp94, PDI, CHOP and inactivated PARP.	Tunicamycin	0-11	poly(ADP-ribose) polymerase 1	Homo sapiens	97-101
26957214-8	2016	Whereas autophagy induced by rapamycin or low serum levels caused a preferential loss of the mature p80 proteolytic cleavage product, infection with herpes simplex virus-1 and induction of cell stress with tunicamycin caused preferential loss of full-length Toll-like receptor-9, which is localized to the endoplasmic reticulum.	Tunicamycin	206-217	toll like receptor 9	Homo sapiens	258-278
27416758-4	2016	Whereas the glucocorticoid, dexamethasone, protects from tunicamycin-induced cell death, silencing endogeneous GILZ in dexamethasone-treated cancer cells alter the capacity of glucocorticoids to protect from tunicamycin-mediated apoptosis.	Tunicamycin	208-219	TSC22 domain family member 3	Homo sapiens	111-115
27328454-7	2016	Mutagenesis of the putative ATF4-response element prevented the induction of luciferase activity in response to ATF4 overproduction, as well as in response to mitochondrial electron transfer chain inhibition by piericidin A and ER stress induction by tunicamycin and brefeldin A.	Tunicamycin	251-262	activating transcription factor 4	Homo sapiens	28-32
27449753-7	2016	Elevated ER stress markers, oxidative stress and reduction of NO bioavailability induced by tunicamycin in HUVECs, C57BJ/6J and PPARdelta WT mouse aortas were reversed by paeonol treatment.	Tunicamycin	92-103	peroxisome proliferator activator receptor delta	Mus musculus	128-137
27449753-10	2016	The present study delineates that paeonol protects against tunicamycin-induced vascular endothelial dysfunction by inhibition of ER stress and oxidative stress, thus elevating NO bioavailability via the AMPK/PPARdelta signaling pathway.	Tunicamycin	59-70	peroxisome proliferator activator receptor delta	Mus musculus	208-217
27667108-8	2016	The in vitro experiment of tunicamycin-induced hepatocyte apoptosis showed that inhibition of GSK3beta activity increased the cell survival rate.	Tunicamycin	27-38	glycogen synthase kinase 3 beta	Mus musculus	94-102
27667109-1	2016	Objective: To profile the gene expression changes associated with endoplasmic reticulum stress in INS-1-3 cells induced by thapsigargin (TG) and tunicamycin (TM).	Tunicamycin	145-156	forkhead box M1	Homo sapiens	98-103
27667109-1	2016	Objective: To profile the gene expression changes associated with endoplasmic reticulum stress in INS-1-3 cells induced by thapsigargin (TG) and tunicamycin (TM).	Tunicamycin	158-160	forkhead box M1	Homo sapiens	98-103
27321910-4	2016	We show that the EP2 receptor agonist butaprost protects TM cell death mediated by the ER stress inducer tunicamycin through a cyclic AMP (cAMP)-dependent mechanism, but independent of the classical cAMP sensors, protein kinase A and exchange proteins activated by cAMP.	Tunicamycin	105-116	prostaglandin E receptor 2	Homo sapiens	17-20
27562249-6	2016	Furthermore, AICAR inhibited macrophage ER stress responses triggered by ER-stressors thapsigargin or tunicamycin.	Tunicamycin	102-113	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	13-18
27350212-0	2016	Tunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24- phenotype breast cancer stem cells.	Tunicamycin	0-11	CD44 molecule (Indian blood group)	Homo sapiens	96-100
27322083-4	2016	Biochemical assays demonstrated that sphere-forming cells were shifted to pro-survival signaling through the inactivation of IRE1 (XBP-1 splicing) and activation of PERK (elF2alpha phosphorylation) branches under tunicamycin-induced ER stress conditions.	Tunicamycin	213-224	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	125-129
27322083-4	2016	Biochemical assays demonstrated that sphere-forming cells were shifted to pro-survival signaling through the inactivation of IRE1 (XBP-1 splicing) and activation of PERK (elF2alpha phosphorylation) branches under tunicamycin-induced ER stress conditions.	Tunicamycin	213-224	X-box binding protein 1	Homo sapiens	131-136
27322083-4	2016	Biochemical assays demonstrated that sphere-forming cells were shifted to pro-survival signaling through the inactivation of IRE1 (XBP-1 splicing) and activation of PERK (elF2alpha phosphorylation) branches under tunicamycin-induced ER stress conditions.	Tunicamycin	213-224	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	165-169
27322083-5	2016	The proportion of apoptotic cells among sphere-forming cells was markedly increased by the tunicamycin+PERK inhibitor (PERKi) treatment, indicating that PERKi sensitized sphere-forming cells to tunicamycin-induced apoptosis.	Tunicamycin	194-205	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	103-107
27350212-0	2016	Tunicamycin-induced endoplasmic reticulum stress reduces in vitro subpopulation and invasion of CD44+/CD24- phenotype breast cancer stem cells.	Tunicamycin	0-11	CD24 molecule	Homo sapiens	102-106
27350212-4	2016	In this study we show effect of tunicamycin on subpopulation and invasion of CD44+/CD24- MCF7 breast cancer stem cells.	Tunicamycin	32-43	CD44 molecule (Indian blood group)	Homo sapiens	77-81
27350212-4	2016	In this study we show effect of tunicamycin on subpopulation and invasion of CD44+/CD24- MCF7 breast cancer stem cells.	Tunicamycin	32-43	CD24 molecule	Homo sapiens	83-87
27350212-5	2016	CD44+/CD24- cells were isolated from MCF7 cell line by fluorescence activated cell sorting (FACS) and treated with tunicamycin.	Tunicamycin	115-126	CD44 molecule (Indian blood group)	Homo sapiens	0-4
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	X-box binding protein 1	Homo sapiens	27-32
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	activating transcription factor 6	Homo sapiens	34-38
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
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	CD44 molecule (Indian blood group)	Homo sapiens	106-110
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	CD24 molecule	Homo sapiens	112-116
27350212-10	2016	Also, a significant decline in CD44+/CD24- cell subpopulation was determined in the cells treated with tunicamycin.	Tunicamycin	103-114	CD44 molecule (Indian blood group)	Homo sapiens	31-35
27350212-10	2016	Also, a significant decline in CD44+/CD24- cell subpopulation was determined in the cells treated with tunicamycin.	Tunicamycin	103-114	CD24 molecule	Homo sapiens	37-41
27350212-11	2016	The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin.	Tunicamycin	188-199	CD44 molecule (Indian blood group)	Homo sapiens	120-124
27350212-11	2016	The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin.	Tunicamycin	188-199	CD24 molecule	Homo sapiens	126-130
27350212-11	2016	The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin.	Tunicamycin	188-199	CD44 molecule (Indian blood group)	Homo sapiens	136-140
27350212-11	2016	The results also showed inhibited invasion, increased cell death, suppressed proliferation and reduced migration in the CD44+/CD24- and CD44+/CD24- rich MCF7 cell culture, under effect of tunicamycin.	Tunicamycin	188-199	CD24 molecule	Homo sapiens	142-146
27350212-12	2016	Our results indicate that CD44+/CD24- phenotype MCF7 cells are susceptible to tunicamycin.	Tunicamycin	78-89	CD44 molecule (Indian blood group)	Homo sapiens	26-30
27350212-12	2016	Our results indicate that CD44+/CD24- phenotype MCF7 cells are susceptible to tunicamycin.	Tunicamycin	78-89	CD24 molecule	Homo sapiens	32-36
27350212-13	2016	The results showed that tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation and in vitro invasion and accelerates tumorosphore formation.	Tunicamycin	24-35	CD44 molecule (Indian blood group)	Homo sapiens	65-69
27350212-13	2016	The results showed that tunicamycin-induced ER stress suppresses CD44+/CD24- phenotype cell subpopulation and in vitro invasion and accelerates tumorosphore formation.	Tunicamycin	24-35	CD24 molecule	Homo sapiens	71-75
25966993-8	2016	Treatment of mice with tunicamycin (Tm) (an ER stress inducer) increased PHLDA3 expression in the liver.	Tunicamycin	23-34	pleckstrin homology like domain, family A, member 3	Mus musculus	73-79
27350212-14	2016	These results suggest that tunicamycin-induced ER stress inhibits CD44+/CD24- phenotype MCF7 breast cancer stem cells.	Tunicamycin	27-38	CD44 molecule (Indian blood group)	Homo sapiens	66-70
25966993-8	2016	Treatment of mice with tunicamycin (Tm) (an ER stress inducer) increased PHLDA3 expression in the liver.	Tunicamycin	36-38	pleckstrin homology like domain, family A, member 3	Mus musculus	73-79
27350212-14	2016	These results suggest that tunicamycin-induced ER stress inhibits CD44+/CD24- phenotype MCF7 breast cancer stem cells.	Tunicamycin	27-38	CD24 molecule	Homo sapiens	72-76
26586570-3	2016	We show here that SK2 channels are present in ER membranes of neuronal HT-22 cells, and that positive pharmacological modulation of SK2 channels with CyPPA protects against cell death induced by the ER stressors brefeldin A and tunicamycin.	Tunicamycin	228-239	skin antigen 2	Mus musculus	18-21
27779479-4	2016	Moreover, since diabetes induces endoplasmic reticulum (ER) stress, we compared the role of TRPA1 in diabetes and ER stress by assessing whether tunicamycin-induced ER stress, without diabetes, produces TRPA1-mediated pain hypersensitivity and by assessing whether ER stress and diabetes have similar modulatory effects on MG-induced hypersensitivity.	Tunicamycin	145-156	transient receptor potential cation channel subfamily A member 1	Homo sapiens	203-208
27779479-5	2016	In vitro patch clamp recording was performed to assess whether tunicamycin is a TRPA1 agonist.	Tunicamycin	63-74	transient receptor potential cation channel subfamily A member 1	Homo sapiens	80-85
27779479-9	2016	In vitro patch clamp recording indicated that tunicamycin itself (30 muM) is not a TRPA1 agonist.	Tunicamycin	46-57	latexin	Homo sapiens	69-72
27468698-4	2016	In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion.	Tunicamycin	82-93	nicotinamide phosphoribosyltransferase	Homo sapiens	135-143
27468698-4	2016	In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion.	Tunicamycin	82-93	resistin	Homo sapiens	148-156
27468698-4	2016	In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion.	Tunicamycin	95-97	nicotinamide phosphoribosyltransferase	Homo sapiens	135-143
27468698-4	2016	In vitro, like ERS inhibitor 4-phenylbutyric acid (PBA), HDL inhibited ox-LDL- or tunicamycin (TM, an ERS inducer)-induced increase in visfatin and resistin secretion.	Tunicamycin	95-97	resistin	Homo sapiens	148-156
27344174-7	2016	Pharmacological inhibition of LAT1 increased the growth inhibitory effects and the inactivation of the mTOR pathway resulting from glycosylation defects, an effect further emphasized during the regrowth period post-treatment with tunicamycin.	Tunicamycin	230-241	solute carrier family 7 member 5	Homo sapiens	30-34
27344174-7	2016	Pharmacological inhibition of LAT1 increased the growth inhibitory effects and the inactivation of the mTOR pathway resulting from glycosylation defects, an effect further emphasized during the regrowth period post-treatment with tunicamycin.	Tunicamycin	230-241	mechanistic target of rapamycin kinase	Homo sapiens	103-107
27321923-3	2016	ER stress, induced by tunicamycin or SOD1(G93A), activates HIPK2 by phosphorylating highly conserved serine and threonine residues (S359/T360) within the activation loop of the HIPK2 kinase domain.	Tunicamycin	22-33	homeodomain interacting protein kinase 2	Mus musculus	59-64
27321923-3	2016	ER stress, induced by tunicamycin or SOD1(G93A), activates HIPK2 by phosphorylating highly conserved serine and threonine residues (S359/T360) within the activation loop of the HIPK2 kinase domain.	Tunicamycin	22-33	homeodomain interacting protein kinase 2	Mus musculus	177-182
27109260-7	2016	From this, paclitaxel (PTX) was identified to efficiently inhibit the promoter activity of the SelS gene, and further results revealed that PTX significantly inhibited the tunicamycin-induced upregulation of SelS at the mRNA and protein levels in HepG2 and HEK293T cells.	Tunicamycin	172-183	selenoprotein S	Homo sapiens	95-99
27109260-7	2016	From this, paclitaxel (PTX) was identified to efficiently inhibit the promoter activity of the SelS gene, and further results revealed that PTX significantly inhibited the tunicamycin-induced upregulation of SelS at the mRNA and protein levels in HepG2 and HEK293T cells.	Tunicamycin	172-183	selenoprotein S	Homo sapiens	208-212
27214655-8	2016	DIO suppressed uroguanylin through ER stress, an effect mimicked by tunicamycin and blocked by TUDCA.	Tunicamycin	68-79	guanylate cyclase activator 2b (retina)	Mus musculus	15-26
27177927-5	2016	Furthermore, mutant CALR protein stability and secretion were examined using brefeldin A, MG132, spautin-1, and tunicamycin treatment.	Tunicamycin	112-123	calreticulin	Mus musculus	20-24
27032713-4	2016	The ER stress inducer tunicamycin increased human chorionic gonadotropin-induced VEGFA production in human granulosa cells through the induction of XBP1(S), and pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) abrogated the effect of tunicamycin.	Tunicamycin	22-33	vascular endothelial growth factor A	Homo sapiens	81-86
27032713-4	2016	The ER stress inducer tunicamycin increased human chorionic gonadotropin-induced VEGFA production in human granulosa cells through the induction of XBP1(S), and pretreatment with the ER stress inhibitor tauroursodeoxycholic acid (TUDCA) abrogated the effect of tunicamycin.	Tunicamycin	22-33	X-box binding protein 1	Homo sapiens	148-152
27119230-0	2016	ER stress inducer tunicamycin suppresses the self-renewal of glioma-initiating cell partly through inhibiting Sox2 translation.	Tunicamycin	18-29	SRY-box transcription factor 2	Homo sapiens	110-114
27119230-6	2016	Indeed, tunicamycin reduces the expression of self-renewal regulator Sox2 at translation level.	Tunicamycin	8-19	SRY-box transcription factor 2	Homo sapiens	69-73
27119230-7	2016	Overexpression of Sox2 obviously abrogates the reduction in glioma-initiating cell self-renewal induced by tunicamycin.	Tunicamycin	107-118	SRY-box transcription factor 2	Homo sapiens	18-22
27119230-8	2016	Taken together, tunicamycin suppresses the self-renewal and tumorigenic potential of glioma-initiating cell partly through reducing Sox2 translation.	Tunicamycin	16-27	SRY-box transcription factor 2	Homo sapiens	132-136
27281343-6	2016	When the N-linked glycosylation in ABCC11-expressing cells was chemically inhibited by tunicamycin treatment, the maturation of ABCC11 was suppressed and its protein level was significantly decreased.	Tunicamycin	87-98	ATP binding cassette subfamily C member 11	Homo sapiens	35-41
27281343-6	2016	When the N-linked glycosylation in ABCC11-expressing cells was chemically inhibited by tunicamycin treatment, the maturation of ABCC11 was suppressed and its protein level was significantly decreased.	Tunicamycin	87-98	ATP binding cassette subfamily C member 11	Homo sapiens	128-134
27169842-3	2016	Furthermore, it successfully demonstrated that the ER membrane is rapidly reorganized in the perinuclear region by an ER stress inducer, tunicamycin.	Tunicamycin	137-148	ETS transcription factor ELK3	Homo sapiens	51-53
27169842-3	2016	Furthermore, it successfully demonstrated that the ER membrane is rapidly reorganized in the perinuclear region by an ER stress inducer, tunicamycin.	Tunicamycin	137-148	ETS transcription factor ELK3	Homo sapiens	118-120
27151646-3	2016	METHODS: Gene and protein expression of ICAM-1 in primary BRECs cultured in medium containing increasing concentrations of mannose or glucose in the presence or absence of tunicamycin were studied with reverse transcription-polymerase chain reaction and Western blot analysis, and the expression level of ICAM-1 at the surface of BRECs was examined with an immunofluorescence analysis.	Tunicamycin	172-183	intercellular adhesion molecule 1	Bos taurus	40-46
27151646-6	2016	Consistent with these results, a dramatic increase in the N-glycosylation of ICAM-1 in BRECs cultured with a high concentration of glucose was observed, which could be partially attenuated by tunicamycin treatment.	Tunicamycin	192-203	intercellular adhesion molecule 1	Bos taurus	77-83
26586570-3	2016	We show here that SK2 channels are present in ER membranes of neuronal HT-22 cells, and that positive pharmacological modulation of SK2 channels with CyPPA protects against cell death induced by the ER stressors brefeldin A and tunicamycin.	Tunicamycin	228-239	skin antigen 2	Mus musculus	132-135
26740123-5	2016	In accordance with these findings in vivo, osteocalcin treatment also displayed a protective impact on adipocytes and myocytes against tunicamycin- or palmitate-induced ER stress and autophagy dysfunction in an XBP-1-independent manner, with these effects of osteocalcin being reversed by inhibition of mammalian target of rapamycin (mTOR) or nuclear factor-kappaB (NF-kappaB).	Tunicamycin	135-146	bone gamma-carboxyglutamate protein	Homo sapiens	43-54
27330716-0	2016	Endoplasmic reticulum stress induced by tunicamycin increases resistin messenger ribonucleic acid through the pancreatic endoplasmic reticulum eukaryotic initiation factor 2alpha kinase-activating transcription factor 4-CAAT/enhancer binding protein-alpha homologous protein pathway in THP-1 human monocytes.	Tunicamycin	40-51	resistin	Homo sapiens	62-70
27330716-0	2016	Endoplasmic reticulum stress induced by tunicamycin increases resistin messenger ribonucleic acid through the pancreatic endoplasmic reticulum eukaryotic initiation factor 2alpha kinase-activating transcription factor 4-CAAT/enhancer binding protein-alpha homologous protein pathway in THP-1 human monocytes.	Tunicamycin	40-51	activating transcription factor 4	Homo sapiens	186-219
27330716-3	2016	Tunicamycin is known to induce endoplasmic reticulum (ER) stress, and reduce resistin gene expression in 3T3-L1 mouse adipocytes.	Tunicamycin	0-11	resistin	Mus musculus	77-85
27330716-6	2016	The effect of endotoxin/lipopolysaccharides or tunicamycin on resistin gene expression was analyzed in THP-1 human monocytes.	Tunicamycin	47-58	resistin	Homo sapiens	62-70
27330716-10	2016	Tunicamycin also increased resistin mRNA.	Tunicamycin	0-11	resistin	Mus musculus	27-35
27330716-12	2016	Tunicamycin-induced resistin mRNA was inhibited by chemical chaperone, 4-phenylbutyric acid.	Tunicamycin	0-11	resistin	Mus musculus	20-28
27330716-13	2016	The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA.	Tunicamycin	87-98	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	24-28
27330716-13	2016	The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA.	Tunicamycin	87-98	activating transcription factor 4	Homo sapiens	30-63
27330716-13	2016	The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA.	Tunicamycin	87-98	activating transcription factor 4	Homo sapiens	65-69
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
27330716-13	2016	The knockdown of either PERK, activating transcription factor 4 (ATF4) or CHOP reduced tunicamycin-induced resistin mRNA.	Tunicamycin	87-98	resistin	Mus musculus	107-115
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	resistin	Mus musculus	75-83
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	101-105
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	activating transcription factor 4	Homo sapiens	106-110
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
27123103-5	2016	Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1.	Tunicamycin	80-91	R-spondin 1	Homo sapiens	41-46
27123103-5	2016	Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1.	Tunicamycin	80-91	R-spondin 1	Homo sapiens	193-198
27123103-5	2016	Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1.	Tunicamycin	93-95	R-spondin 1	Homo sapiens	41-46
27123103-5	2016	Furthermore, treatment of wild-type (wt) RSPO1-overexpressing HT1080 cells with tunicamycin (TM), which inhibits N-glycosylation, resulted in a significant reduction in the molecular weight of RSPO1.	Tunicamycin	93-95	R-spondin 1	Homo sapiens	193-198
27073326-3	2016	In this study, we have demonstrated for the first time that the expression level of miR-663 was significantly upregulated in HCC cells co-incubated with tunicamycin, an ER stress inducer, as measured by a microRNA-chromatin immunoprecipitation microarray and quantitative real-time polymerase chain reaction; however, the effect of miR-663 on HCC cell apoptosis remains unknown.	Tunicamycin	153-164	microRNA 663a	Homo sapiens	84-91
26828122-4	2016	Using several approaches including inhibiting de novo N-glycosylation in human colonic epithelial NCM460 cells with tunicamycin as well as enzymatic de-glycosylation, we show that the hTPPT protein is, indeed, a glycoprotein.	Tunicamycin	116-127	solute carrier family 44 member 4	Homo sapiens	184-189
26711306-3	2016	The hepatic I/R injury, demonstrated by serum aminotransferase level and the ultra-structure of the liver, was alleviated by administration of tunicamycin, which induced ER stress in rat liver by activating inositol-requiring enzyme 1 (IRE1) and upregulating 78 kDa glucose-regulated protein (GRP78).	Tunicamycin	143-154	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	236-240
26711306-3	2016	The hepatic I/R injury, demonstrated by serum aminotransferase level and the ultra-structure of the liver, was alleviated by administration of tunicamycin, which induced ER stress in rat liver by activating inositol-requiring enzyme 1 (IRE1) and upregulating 78 kDa glucose-regulated protein (GRP78).	Tunicamycin	143-154	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	293-298
26796921-4	2016	Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM.	Tunicamycin	0-11	mitogen-activated protein kinase 1	Homo sapiens	103-107
26796921-4	2016	Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM.	Tunicamycin	0-11	mitogen-activated protein kinase 1	Homo sapiens	148-151
26796921-4	2016	Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM.	Tunicamycin	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	159-162
26796921-4	2016	Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM.	Tunicamycin	0-11	mitogen-activated protein kinase 1	Homo sapiens	164-167
26796921-4	2016	Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	214-219
26796921-4	2016	Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM.	Tunicamycin	0-11	mitogen-activated protein kinase kinase 7	Homo sapiens	255-258
26796921-4	2016	Tunicamycin (TM), an ER stress inducer, constitutively activates the mitogen-activated protein kinase (MAPK)/extracellular signal regulated kinase (ERK), and (MEK)/ERK pathway which plays a role in upregulation of GRP78 by ER stress in that inhibition of MEK by U0126 reduces the levels of GRP78 and blocks its upregulation by TM.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	290-295
26796921-5	2016	Inhibition of the MEK/ERK pathway by U0126 sensitizes breast cancer cells to TM-induced apoptosis.	Tunicamycin	77-79	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
26796921-5	2016	Inhibition of the MEK/ERK pathway by U0126 sensitizes breast cancer cells to TM-induced apoptosis.	Tunicamycin	77-79	mitogen-activated protein kinase 1	Homo sapiens	22-25
26796921-7	2016	This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4.	Tunicamycin	45-47	mitogen-activated protein kinase kinase 7	Homo sapiens	83-86
26796921-7	2016	This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4.	Tunicamycin	45-47	mitogen-activated protein kinase 1	Homo sapiens	87-90
26796921-7	2016	This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4.	Tunicamycin	45-47	heat shock protein family A (Hsp70) member 5	Homo sapiens	95-100
26796921-7	2016	This sensitization of breast cancer cells to TM-induced apoptosis by inhibition of MEK/ERK and GRP78 is caspase-dependent, at least in part, by activation of caspase-4.	Tunicamycin	45-47	caspase 4	Homo sapiens	158-167
27011164-8	2016	Additionally, ER stress inducer tunicamycin significantly increased the expression level of C/EBP beta in hPDLCs.	Tunicamycin	32-43	CCAAT enhancer binding protein beta	Homo sapiens	92-102
27011164-9	2016	Blocking of C/EBP beta by siRNA resulted in a significant decrease in the secretion of IL-6 and IL-8 and expression of MMP-8 and MMP-9 induced by tunicamycin treatment in hPDLCs.	Tunicamycin	146-157	CCAAT enhancer binding protein beta	Homo sapiens	12-22
27011164-9	2016	Blocking of C/EBP beta by siRNA resulted in a significant decrease in the secretion of IL-6 and IL-8 and expression of MMP-8 and MMP-9 induced by tunicamycin treatment in hPDLCs.	Tunicamycin	146-157	matrix metallopeptidase 8	Homo sapiens	119-124
27011164-9	2016	Blocking of C/EBP beta by siRNA resulted in a significant decrease in the secretion of IL-6 and IL-8 and expression of MMP-8 and MMP-9 induced by tunicamycin treatment in hPDLCs.	Tunicamycin	146-157	matrix metallopeptidase 9	Homo sapiens	129-134
26521941-4	2016	Cardiomyocyte ERS-triggered apoptosis induced by 100 ng/ml tunicamycin (TM) or 1 muM thapsigargin (TG), ERS inducers, was significantly reduced by miR-185 overexpression.	Tunicamycin	59-70	microRNA 185	Homo sapiens	147-154
26966233-7	2016	Consistent with these findings, the induction of UPR by tunicamycin treatment increases phosphorylation of Syt1p, resulting in Arl1p activation.	Tunicamycin	56-67	Arf family guanine nucleotide exchange factor SYT1	Saccharomyces cerevisiae S288C	107-112
27073326-3	2016	In this study, we have demonstrated for the first time that the expression level of miR-663 was significantly upregulated in HCC cells co-incubated with tunicamycin, an ER stress inducer, as measured by a microRNA-chromatin immunoprecipitation microarray and quantitative real-time polymerase chain reaction; however, the effect of miR-663 on HCC cell apoptosis remains unknown.	Tunicamycin	153-164	microRNA 663a	Homo sapiens	332-339
26747710-12	2016	This protection was stimulus-independent as nCDase(-/-) cells were also protected from endoplasmic reticulum (ER) stressors [tunicamycin (TN) or thapsigargin (TG)].	Tunicamycin	125-136	N-acylsphingosine amidohydrolase 2	Mus musculus	44-50
25160872-5	2016	Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress.	Tunicamycin	56-67	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	105-114
26966233-7	2016	Consistent with these findings, the induction of UPR by tunicamycin treatment increases phosphorylation of Syt1p, resulting in Arl1p activation.	Tunicamycin	56-67	Arf family GTPase ARL1	Saccharomyces cerevisiae S288C	127-132
26718307-7	2016	PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes.	Tunicamycin	84-95	6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3	Homo sapiens	0-6
26718307-7	2016	PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes.	Tunicamycin	84-95	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	41-45
26718307-7	2016	PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes.	Tunicamycin	84-95	activating transcription factor 3	Homo sapiens	47-51
26718307-7	2016	PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes.	Tunicamycin	84-95	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	53-57
26718307-7	2016	PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes.	Tunicamycin	84-95	eukaryotic translation initiation factor 2A	Homo sapiens	61-70
26718307-7	2016	PFKFB3 also modulated the expressions of PERK, ATF3, IRE1, p-eIF2alpha and MMP13 in tunicamycin-exposed chondrocytes.	Tunicamycin	84-95	matrix metallopeptidase 13	Homo sapiens	75-80
26750440-6	2016	Inhibition of miR-29a expression using sequence-specific antagomirs or the overexpression of Mcl-1 decreased cell death following tunicamycin treatment, while gene silencing of Mcl-1 increased cell death.	Tunicamycin	130-141	microRNA 29a	Homo sapiens	14-21
26750440-6	2016	Inhibition of miR-29a expression using sequence-specific antagomirs or the overexpression of Mcl-1 decreased cell death following tunicamycin treatment, while gene silencing of Mcl-1 increased cell death.	Tunicamycin	130-141	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	93-98
26888485-9	2016	NGR1 inhibits Tunicamycin-induced cell death and cardiac dysfunction.	Tunicamycin	14-25	reticulon 4 receptor	Rattus norvegicus	0-4
26851027-3	2016	Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene.	Tunicamycin	109-120	ATM serine/threonine kinase	Homo sapiens	358-387
26851027-3	2016	Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene.	Tunicamycin	109-120	ATM serine/threonine kinase	Homo sapiens	389-392
26851027-3	2016	Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene.	Tunicamycin	109-120	mitogen-activated protein kinase 8	Homo sapiens	403-426
26851027-3	2016	Small interfering RNA-mediated suppression of protein kinase RNA-like endoplasmic reticulum kinase inhibited tunicamycin-induced induction of 78 kDa glucose-regulated protein, C/EBP homologous protein, pro-caspase-12 cleavage, cytosolic Ca(++) increase and apoptosis, but did not attenuate the increase in cytosolic Ca(++) level and apoptosis induced by GA. Ataxia telangiectasia mutated (ATM)-mediated c-Jun N-terminal kinase (JNK) phosphorylation and apoptosis by GA was blocked by dantrolene.	Tunicamycin	109-120	mitogen-activated protein kinase 8	Homo sapiens	428-431
26939760-3	2016	The ER stress inductor tunicamycin (TM) significantly decreased the expression of FAM3A at both mRNA and protein levels, which was shown to be dependent on the induction of reactive oxygen species (ROS).	Tunicamycin	23-34	FAM3 metabolism regulating signaling molecule A	Mus musculus	82-87
26939760-3	2016	The ER stress inductor tunicamycin (TM) significantly decreased the expression of FAM3A at both mRNA and protein levels, which was shown to be dependent on the induction of reactive oxygen species (ROS).	Tunicamycin	36-38	FAM3 metabolism regulating signaling molecule A	Mus musculus	82-87
25160872-5	2016	Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress.	Tunicamycin	56-67	activating transcription factor 6	Homo sapiens	116-120
25160872-5	2016	Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress.	Tunicamycin	56-67	eukaryotic translation initiation factor 2A	Homo sapiens	125-134
25160872-5	2016	Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress.	Tunicamycin	69-71	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	105-114
26472337-4	2016	Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin.	Tunicamycin	272-283	RNA binding motif protein 3	Homo sapiens	18-22
25160872-5	2016	Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress.	Tunicamycin	69-71	activating transcription factor 6	Homo sapiens	116-120
26472337-4	2016	Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin.	Tunicamycin	272-283	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	137-141
26472337-4	2016	Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin.	Tunicamycin	272-283	RNA binding motif protein 3	Homo sapiens	183-187
25160872-5	2016	Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1alpha, ATF6 and eIF2alpha) of ER stress.	Tunicamycin	69-71	eukaryotic translation initiation factor 2A	Homo sapiens	125-134
26472337-4	2016	Further, blocking RBM3 expression in human embryonic kidney HEK293 cells by specific small interfering RNAs increased phosphorylation of PERK and eIF2alpha, whereas overexpression of RBM3 prevented PERK-eIF2alpha-CHOP signaling during ER stress induced by thapsigargin or tunicamycin.	Tunicamycin	272-283	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	198-202
26616221-4	2016	In this work, ApoE(-/-) mice underwent perivascular carotid collar placement surgeries or sham operations were given higher (3.0mg/kg) and lower (0.3mg/kg) doses of tunicamycin (TM), and plaque stability was evaluated.	Tunicamycin	165-176	apolipoprotein E	Mus musculus	14-18
26893680-6	2016	Treatment of A549 cells with tunicamycin followed by cisplatin resulted in elevated BAG1 levels.	Tunicamycin	29-40	BAG cochaperone 1	Homo sapiens	84-88
26058460-8	2016	Furthermore, SelS silence enhanced endoplasmic reticulum (ER) stress induced by hydrogen peroxide or tunicamycin, as showed by the increased protein levels of ER chaperone 78 kDa glucose-regulated protein (GRP78), ER stress transducer phosphorylated protein kinase RNA like ER kinase (PERK), and the proapoptotic transcription factor C/EBP homologous protein (CHOP).	Tunicamycin	101-112	selenoprotein S	Homo sapiens	13-17
26551463-8	2015	Pre-incubation with ER stress inducer tunicamycin before leucine stimulation increased S6K1 phosphorylation beyond the level reached by leucine alone.	Tunicamycin	38-49	ribosomal protein S6 kinase, polypeptide 1	Mus musculus	87-91
26577412-6	2015	Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation.	Tunicamycin	25-36	X-box binding protein 1	Homo sapiens	90-94
26577412-6	2015	Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation.	Tunicamycin	25-36	activating transcription factor 4	Homo sapiens	96-100
26577412-6	2015	Carbenoxolone attenuated tunicamycin induced ER stress-mediated molecules such as spliced XBP1, ATF4, ATF6, CHOP, and ROS generation.	Tunicamycin	25-36	activating transcription factor 6	Homo sapiens	102-106
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
26603934-5	2015	Biochemical characterisation of transiently expressed human CPX-1 revealed that CPX-1 was secreted in an N-glycosylation-dependent manner as treatment with the N-glycosylation inhibitor tunicamycin inhibited secretion concomitant with a reduction in CPX-1 mobility on Western blot.	Tunicamycin	186-197	carboxypeptidase X, M14 family member 1	Homo sapiens	60-65
26603934-5	2015	Biochemical characterisation of transiently expressed human CPX-1 revealed that CPX-1 was secreted in an N-glycosylation-dependent manner as treatment with the N-glycosylation inhibitor tunicamycin inhibited secretion concomitant with a reduction in CPX-1 mobility on Western blot.	Tunicamycin	186-197	carboxypeptidase X, M14 family member 1	Homo sapiens	80-85
26603934-5	2015	Biochemical characterisation of transiently expressed human CPX-1 revealed that CPX-1 was secreted in an N-glycosylation-dependent manner as treatment with the N-glycosylation inhibitor tunicamycin inhibited secretion concomitant with a reduction in CPX-1 mobility on Western blot.	Tunicamycin	186-197	carboxypeptidase X, M14 family member 1	Homo sapiens	80-85
26709511-7	2015	In addition, Ang 1-7 decreased the levels of ER stress markers and augmented NO production in HUVECs treated with ER stress inducer, tunicamycin.	Tunicamycin	133-144	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	13-18
26782403-6	2015	The reverse transcription quantitative polymerase chain reaction results showed that knockdown Herp inhibited the expression of ER stress-related genes during exposure to tunicamycin or thapsigargin.	Tunicamycin	171-182	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	95-99
26782403-7	2015	In RAW 264.7 macrophages, knockdown Herp markedly attenuated the expression of inflammatory cytokines when exposed to tunicamycin; however, it strongly enhanced the expression of inflammatory cytokines when exposed to thapsigargin.	Tunicamycin	118-129	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	36-40
26782403-8	2015	We concluded that Herp lentiviral shRNA vectors had been successfully constructed; knockdown Herp inhibited ER stress and had a different effect on inflammatory responses in RAW 264.7 macrophages depending on whether they were exposed to tunicamycin or thapsigargin.	Tunicamycin	238-249	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	18-22
26782403-8	2015	We concluded that Herp lentiviral shRNA vectors had been successfully constructed; knockdown Herp inhibited ER stress and had a different effect on inflammatory responses in RAW 264.7 macrophages depending on whether they were exposed to tunicamycin or thapsigargin.	Tunicamycin	238-249	homocysteine inducible ER protein with ubiquitin like domain 1	Homo sapiens	93-97
28955827-4	2016	Moreover, in cultured brown adipocytes exposed to tunicamycin and hydrogen peroxide, at concentrations not affecting cellular viability, GDF1 expression was significantly downregulated.	Tunicamycin	50-61	growth differentiation factor 1	Mus musculus	137-141
26680341-7	2015	The most remarkable effect was that of tunicamycin, an inhibitor of the first step of N-glycosylation, which resulted in significantly reduced KIR3DL1-Fc binding despite sustained expression of HLA-B*57:01 on 721.221 cells.	Tunicamycin	39-50	killer cell immunoglobulin like receptor, three Ig domains and long cytoplasmic tail 1	Homo sapiens	143-150
26680341-7	2015	The most remarkable effect was that of tunicamycin, an inhibitor of the first step of N-glycosylation, which resulted in significantly reduced KIR3DL1-Fc binding despite sustained expression of HLA-B*57:01 on 721.221 cells.	Tunicamycin	39-50	major histocompatibility complex, class I, B	Homo sapiens	194-199
26680341-8	2015	This effect was paralleled by decreased activation of KIR3DL1zeta+ Jurkat reporter cells, as well as increased degranulation of primary human KIR3DL1+ NK cell clones when encountering HLA-B*57:01-expressing 721.221 cells that were pre-treated with tunicamycin.	Tunicamycin	248-259	major histocompatibility complex, class I, B	Homo sapiens	184-189
26419929-4	2015	Treating HepG2 cells with human recombinant CTRP9 significantly ameliorated palmitate- or tunicamycin-induced dysregulation of lipid metabolism, caspase 3 activity and chromatin condensation, which lead to reduction of hepatic triglyceride (TG) accumulation.	Tunicamycin	90-101	C1q and TNF related 9	Homo sapiens	44-49
26419929-4	2015	Treating HepG2 cells with human recombinant CTRP9 significantly ameliorated palmitate- or tunicamycin-induced dysregulation of lipid metabolism, caspase 3 activity and chromatin condensation, which lead to reduction of hepatic triglyceride (TG) accumulation.	Tunicamycin	90-101	caspase 3	Homo sapiens	145-154
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	C1q and TNF related 9	Homo sapiens	13-18
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	eukaryotic translation initiation factor 2A	Homo sapiens	90-99
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
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	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	110-115
26740650-5	2016	We evoked mild endoplasmic reticulum (ER) stress with tunicamycin (Tu), producing modest increases in the level of nuclear ATF6, phosphorylated eukaryotic initiation factor 2alpha, nuclear XBP1, and the downstream proapoptotic effector nuclear C/EBP homologous protein.	Tunicamycin	54-65	activating transcription factor 6	Mus musculus	123-127
26740650-5	2016	We evoked mild endoplasmic reticulum (ER) stress with tunicamycin (Tu), producing modest increases in the level of nuclear ATF6, phosphorylated eukaryotic initiation factor 2alpha, nuclear XBP1, and the downstream proapoptotic effector nuclear C/EBP homologous protein.	Tunicamycin	67-69	activating transcription factor 6	Mus musculus	123-127
26740650-5	2016	We evoked mild endoplasmic reticulum (ER) stress with tunicamycin (Tu), producing modest increases in the level of nuclear ATF6, phosphorylated eukaryotic initiation factor 2alpha, nuclear XBP1, and the downstream proapoptotic effector nuclear C/EBP homologous protein.	Tunicamycin	67-69	X-box binding protein 1	Mus musculus	189-193
27582328-6	2016	Tunicamycin increased the expression of BiP in organ-cultured arteries.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	40-43
26021843-7	2016	Cardiac cell pretreatment with tunicamycin, an inducer of trib3, also protected them against H2O2-induced cell death.	Tunicamycin	31-42	tribbles pseudokinase 3	Rattus norvegicus	58-63
26058460-6	2016	SelS gene silence by small interference RNA (siRNA) rendered VSMCs more sensitive to hydrogen peroxide- or tunicamycin- induced injury and apoptosis, as determined by MTT assay, Hoechst staining, and annexin V/propidium iodide staining.	Tunicamycin	107-118	selenoprotein S	Homo sapiens	0-4
26567221-5	2016	Inhibition of N-glycosylation with tunicamycin resulted in a molecular shift of HMGB1 as assessed by gel electrophoresis.	Tunicamycin	35-46	high mobility group box 1	Homo sapiens	80-85
26497741-9	2015	The apoptotic rate and the loss of mitochondrial membrane potential (DeltaPsim) of the TM-stimulated chondrocytes treated with BZD was markedly decreased compared with those of chondrocytes not treated with BZD, as shown by 4",6-diamidino-2-phenylindole (DAPI) staining, Annexin V-FITC binding assay and JC-1 assay.	Tunicamycin	87-89	annexin A5	Rattus norvegicus	271-280
26531105-0	2015	Knockdown of 15-kDa selenoprotein (Sep15) increases hLE cells" susceptibility to tunicamycin-induced apoptosis.	Tunicamycin	81-92	selenoprotein F	Homo sapiens	13-33
26531105-0	2015	Knockdown of 15-kDa selenoprotein (Sep15) increases hLE cells" susceptibility to tunicamycin-induced apoptosis.	Tunicamycin	81-92	selenoprotein F	Homo sapiens	35-40
26531105-2	2015	The results showed that sole knockdown of Sep15 by RNA interference did not result in apoptosis; however, reduction of Sep15 expression aggravated tunicamycin (Tm)-induced cell apoptosis and caspases activation.	Tunicamycin	147-158	selenoprotein F	Homo sapiens	119-124
26531105-2	2015	The results showed that sole knockdown of Sep15 by RNA interference did not result in apoptosis; however, reduction of Sep15 expression aggravated tunicamycin (Tm)-induced cell apoptosis and caspases activation.	Tunicamycin	160-162	selenoprotein F	Homo sapiens	119-124
26373796-6	2015	In addition, PGRN-deficient adipocytes were more refractory to tunicamycin- or dexamethasone-induced insulin resistance, indicating the causative role of the TNFR1 pathway in the action of PGRN.	Tunicamycin	63-74	granulin	Mus musculus	13-17
26355342-8	2015	In livers from obese mice, administration of LPS or tunicamycin results in IRE1alpha and PERK activation, leading to the overexpression of CHOP.	Tunicamycin	52-63	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	75-84
26548430-3	2016	The INS-1 islet cell line was treated with various concentrations of tunicamycin to establish the ERS model.	Tunicamycin	69-80	insulin 1	Rattus norvegicus	4-9
26548430-5	2016	The ERS model induced by tunicamycin showed significantly increased expression of binding immunoglobulin protein (BIP)/glucose-regulated protein 78 (Grp78), which is a marker for ERS, and the expression of Erp29 was also increased at the mRNA and protein levels.	Tunicamycin	25-36	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	82-112
26548430-5	2016	The ERS model induced by tunicamycin showed significantly increased expression of binding immunoglobulin protein (BIP)/glucose-regulated protein 78 (Grp78), which is a marker for ERS, and the expression of Erp29 was also increased at the mRNA and protein levels.	Tunicamycin	25-36	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	114-117
26548430-5	2016	The ERS model induced by tunicamycin showed significantly increased expression of binding immunoglobulin protein (BIP)/glucose-regulated protein 78 (Grp78), which is a marker for ERS, and the expression of Erp29 was also increased at the mRNA and protein levels.	Tunicamycin	25-36	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	149-154
26548430-5	2016	The ERS model induced by tunicamycin showed significantly increased expression of binding immunoglobulin protein (BIP)/glucose-regulated protein 78 (Grp78), which is a marker for ERS, and the expression of Erp29 was also increased at the mRNA and protein levels.	Tunicamycin	25-36	endoplasmic reticulum protein 29	Rattus norvegicus	206-211
26610463-8	2015	Treatment with UP resulted in reduced increment of ATF6 and CHOP, and recovered the decrease of phosphorylation of Akt/mTOR by tunicamycin and the increment of autophagy.	Tunicamycin	127-138	thymoma viral proto-oncogene 1	Mus musculus	115-118
26610463-8	2015	Treatment with UP resulted in reduced increment of ATF6 and CHOP, and recovered the decrease of phosphorylation of Akt/mTOR by tunicamycin and the increment of autophagy.	Tunicamycin	127-138	mechanistic target of rapamycin kinase	Mus musculus	119-123
26599511-6	2015	TGF-beta and tunicamycin promoted MUC5AC induction after 72 h in human bronchial airway epithelial BEAS-2B cells, which was dampened by 20 muM kaempferol.	Tunicamycin	13-24	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	34-40
26599511-7	2015	Kaempferol inhibited tunicamycin-induced ER stress of airway epithelial cells through disturbing the activation of the ER transmembrane sensor ATF6 and IRE1alpha.	Tunicamycin	21-32	activating transcription factor 6	Mus musculus	143-147
26599511-7	2015	Kaempferol inhibited tunicamycin-induced ER stress of airway epithelial cells through disturbing the activation of the ER transmembrane sensor ATF6 and IRE1alpha.	Tunicamycin	21-32	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	152-161
26599511-8	2015	Additionally, this compound demoted the induction of ER chaperones such as GRP78 and HSP70 and the splicing of XBP-1 mRNA by tunicamycin.	Tunicamycin	125-136	X-box binding protein 1	Mus musculus	111-116
26599511-10	2015	TGF-beta and tunicamycin induced TRAF2 with JNK activation and such induction was deterred by kaempferol.	Tunicamycin	13-24	TNF receptor-associated factor 2	Mus musculus	33-38
26599511-10	2015	TGF-beta and tunicamycin induced TRAF2 with JNK activation and such induction was deterred by kaempferol.	Tunicamycin	13-24	mitogen-activated protein kinase 8	Mus musculus	44-47
26599511-11	2015	The inhibition of JNK activation encumbered the XBP-1 mRNA splicing and MUC5AC induction by tunicamycin and TGF-beta.	Tunicamycin	92-103	mitogen-activated protein kinase 8	Mus musculus	18-21
26599511-11	2015	The inhibition of JNK activation encumbered the XBP-1 mRNA splicing and MUC5AC induction by tunicamycin and TGF-beta.	Tunicamycin	92-103	mucin 5, subtypes A and C, tracheobronchial/gastric	Mus musculus	72-78
26599396-11	2015	In contrast, inhibition of glycosylation by treatment with tunicamycin dramatically reduced membrane translocation of intracellular hNIS, resulting in reduced radioiodine uptake.	Tunicamycin	59-70	solute carrier family 5 member 5	Homo sapiens	132-136
26449458-5	2015	Treatment of C2C12 myotubes with palmitate or tunicamycin significantly increased the expression of musclin as well as ER stress-related genes, but treatment with oleate did not.	Tunicamycin	46-57	osteocrin	Homo sapiens	100-107
26449458-6	2015	Pre-treatment of C2C12 myotubes with 4-phenyl butyrate suppressed the expression of ER stress-related genes, simultaneously, resulting in decreased expression of the musclin gene induced by palmitate or tunicamycin.	Tunicamycin	203-214	osteocrin	Homo sapiens	166-173
28955811-4	2016	Partial or non-glycosylated forms of a secreted form of hCES2 have been obtained by three approaches: (i) enzymatic deglycosylation with peptide N-glycosidase F; (ii) incubation with the inhibitor tunicamycin; ii) site directed mutagenesis of each or both N-glycosylation sites.	Tunicamycin	197-208	carboxylesterase 2	Homo sapiens	56-61
28955811-6	2016	On the other hand, tunicamycin led to decreased levels of secreted hCES2 but the enzyme was still active.	Tunicamycin	19-30	carboxylesterase 2	Homo sapiens	67-72
26498681-2	2015	In this study, results showed that tunicamycin, an inhibitor of N-glycosylation, synergistically enhanced the antitumor activity of trastuzumab against HER2-overexpressing breast cancer cells through induction of cell cycle arrest and apoptosis.	Tunicamycin	35-46	erb-b2 receptor tyrosine kinase 2	Homo sapiens	152-156
26498681-3	2015	Combined treatment of tunicamycin with trastuzumab dramatically decreased the expression of EGFR family and its down signaling pathway in SKBR3 and MCF-7/HER2 cells.	Tunicamycin	22-33	epidermal growth factor receptor	Homo sapiens	92-96
26498681-3	2015	Combined treatment of tunicamycin with trastuzumab dramatically decreased the expression of EGFR family and its down signaling pathway in SKBR3 and MCF-7/HER2 cells.	Tunicamycin	22-33	erb-b2 receptor tyrosine kinase 2	Homo sapiens	154-158
26498681-4	2015	Tunicamycin dose-dependently inhibited tumor growth in both of SKBR3 xenografts and MCF-7/HER2 xenografts.	Tunicamycin	0-11	erb-b2 receptor tyrosine kinase 2	Homo sapiens	90-94
26498681-5	2015	Optimal tunicamycin without inducing ER stress in liver tissue significantly increased the antitumor effect of trastuzumab in MCF-7/HER2 xenografts.	Tunicamycin	8-19	erb-b2 receptor tyrosine kinase 2	Homo sapiens	132-136
26419589-11	2015	FADD-DN also attenuated tunicamycin-induced UPR and ER stress.	Tunicamycin	24-35	Fas associated via death domain	Homo sapiens	0-4
26540043-4	2015	MEAO inhibited the tunicamycin-induced increase in luciferase activity of ER stress-reporter constructs containing ER stress response element and ATF6 response element.	Tunicamycin	19-30	activating transcription factor 6	Homo sapiens	146-150
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	87-92
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
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	X-box binding protein 1	Homo sapiens	104-109
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	113-124	X-box binding protein 1	Homo sapiens	104-109
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	113-124	X-box binding protein 1	Homo sapiens	104-109
26540043-10	2015	Alismol, a guaiane-type sesquiterpenes in Alisma orientale, inhibited GRP78 expression in tunicamycin-treated HepG2 cells.	Tunicamycin	90-101	heat shock protein family A (Hsp70) member 5	Homo sapiens	70-75
26329269-0	2015	Duhuo Jisheng decoction inhibits endoplasmic reticulum stress in chondrocytes induced by tunicamycin through the downregulation of miR-34a.	Tunicamycin	89-100	microRNA 34a	Homo sapiens	131-138
26192086-4	2015	ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression.	Tunicamycin	20-31	SMAD family member 2	Homo sapiens	77-84
26192086-4	2015	ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression.	Tunicamycin	20-31	catenin beta 1	Homo sapiens	140-152
26192086-4	2015	ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression.	Tunicamycin	20-31	snail family transcriptional repressor 1	Homo sapiens	157-162
26192086-4	2015	ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression.	Tunicamycin	33-35	SMAD family member 2	Homo sapiens	77-84
26192086-4	2015	ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression.	Tunicamycin	33-35	catenin beta 1	Homo sapiens	140-152
26192086-4	2015	ER stress inducers, tunicamycin (TM) and thapsigargin (TG), induced EMT with Smad2/3 phosphorylation, an increased nuclear translocation of beta-catenin and Snail expression.	Tunicamycin	33-35	snail family transcriptional repressor 1	Homo sapiens	157-162
26151415-9	2015	Molecularly, tunicamycin (100 ng/ml) increased the levels of GRP78 and CHOP 6 h after administration.	Tunicamycin	13-24	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	61-66
26151415-9	2015	Molecularly, tunicamycin (100 ng/ml) increased the levels of GRP78 and CHOP 6 h after administration.	Tunicamycin	13-24	DNA-damage inducible transcript 3	Rattus norvegicus	71-75
26429299-7	2015	Tunicamycin greatly increased both mRNA and protein levels of GRP78.	Tunicamycin	0-11	heat shock protein 5	Mus musculus	62-67
26361146-8	2015	Tunicamycin-exposed islets from NLRP3 KO mice exhibited similar levels of ER stress and apoptosis induction as islets from WT (Ins2(+/+); NLRP3(+/+)) mice.	Tunicamycin	0-11	NLR family, pyrin domain containing 3	Mus musculus	32-37
26254015-3	2015	The expression of ANGPTL8 was significantly increased in HepG2 cells exposed to palmitic acid, tunicamycin, or T0901317, and was reversed in cells treated with AICAR.	Tunicamycin	95-106	angiopoietin like 8	Homo sapiens	18-25
26254015-3	2015	The expression of ANGPTL8 was significantly increased in HepG2 cells exposed to palmitic acid, tunicamycin, or T0901317, and was reversed in cells treated with AICAR.	Tunicamycin	95-106	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	160-165
26254015-4	2015	Palmitic acid, tunicamycin, and T0901317 increased LXRalpha and SREBP-1c mRNA expression.	Tunicamycin	15-26	nuclear receptor subfamily 1 group H member 3	Homo sapiens	51-59
26254015-4	2015	Palmitic acid, tunicamycin, and T0901317 increased LXRalpha and SREBP-1c mRNA expression.	Tunicamycin	15-26	sterol regulatory element binding transcription factor 1	Homo sapiens	64-72
26448323-7	2015	Inhibition of endoplasmic reticulum (ER) stress with chemical chaperones partially blocked ischemic injury-induced CXCL10 upregulation, whereas induction of ER stress with tunicamycin enhanced CXCL10 expression in retina and primary retinal ganglion cells.	Tunicamycin	172-183	chemokine (C-X-C motif) ligand 10	Mus musculus	193-199
26444017-2	2015	We demonstrate that the ER stress inducer tunicamycin triggers an unfolded protein response, upregulates ER chaperone Grp78, and activates the autophagy pathway in renal tubular epithelial cells in culture.	Tunicamycin	42-53	heat shock protein 5	Mus musculus	118-123
26444017-7	2015	In mouse kidney, similarly to renal epithelial cells in culture, tunicamycin triggered ER stress, markedly upregulated Grp78, and activated autophagy without impairing the autophagic flux.	Tunicamycin	65-76	heat shock protein 5	Mus musculus	119-124
25968954-6	2015	Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity.	Tunicamycin	10-21	BCL2-associated X protein	Mus musculus	105-108
25968954-6	2015	Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity.	Tunicamycin	10-21	caspase 9	Mus musculus	110-119
25968954-6	2015	Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity.	Tunicamycin	10-21	caspase 12	Mus musculus	125-135
25968954-6	2015	Moreover, tunicamycin challenge dramatically facilitated myocardial apoptosis as manifested by increased Bax, caspase 9, and caspase 12 protein levels, as well as elevated caspase 3 activity.	Tunicamycin	10-21	caspase 3	Mus musculus	172-181
26355342-8	2015	In livers from obese mice, administration of LPS or tunicamycin results in IRE1alpha and PERK activation, leading to the overexpression of CHOP.	Tunicamycin	52-63	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	89-93
26355342-8	2015	In livers from obese mice, administration of LPS or tunicamycin results in IRE1alpha and PERK activation, leading to the overexpression of CHOP.	Tunicamycin	52-63	DNA-damage inducible transcript 3	Mus musculus	139-143
26049021-3	2015	Here we investigated gene expression profiles under ER stress in melanoma cells and found that IDH1 was dramatically increased with ER stress induced by tunicamycin.	Tunicamycin	153-164	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	95-99
26100023-8	2015	Thus, the spatiotemporal regulation of Rab7 activity during tunicamycin-induced autophagy is regulated by LRRK1.	Tunicamycin	60-71	RAB7, member RAS oncogene family	Mus musculus	39-43
26172539-6	2015	Moreover, the transcription factor ATF4 is found to mediate both the apoptosis induced by 2-DG and the glycosylation inhibitor tunicamycin, as well as the necrosis provoked by glucose withdrawal.	Tunicamycin	127-138	activating transcription factor 4	Homo sapiens	35-39
25801913-5	2015	HDAC4 knockdown showed modest cell growth inhibition; however, it markedly enhanced cytotoxicity induced by either tunicamycin or carfilzomib (CFZ), associated with upregulating ATF4 and CHOP.	Tunicamycin	115-126	histone deacetylase 4	Homo sapiens	0-5
26100023-8	2015	Thus, the spatiotemporal regulation of Rab7 activity during tunicamycin-induced autophagy is regulated by LRRK1.	Tunicamycin	60-71	leucine-rich repeat kinase 1	Mus musculus	106-111
26080997-7	2015	Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta.	Tunicamycin	177-188	sterol regulatory element binding transcription factor 1	Mus musculus	97-140
26080997-7	2015	Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta.	Tunicamycin	177-188	sterol regulatory element binding transcription factor 1	Mus musculus	142-149
26080997-7	2015	Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta.	Tunicamycin	177-188	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	155-164
26080997-7	2015	Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta.	Tunicamycin	177-188	sterol regulatory element binding transcription factor 1	Mus musculus	260-267
26080997-7	2015	Interestingly, n-3 PUFAs attenuated the nuclear translocation of lipogenic transcription factors sterol regulatory element-binding protein-1 (SREBP-1) and C/EBPbeta, induced by tunicamycin or HFD, suggesting that n-3 PUFAs suppress ER stress via modulation of SREBP-1 and C/EBPbeta.	Tunicamycin	177-188	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	272-281
26137860-7	2015	However, when Hrd1 was knocked down, thapsigargin and tunicamycin dramatically decreased ERAD, while increasing maladaptive ER stress proteins and cell death.	Tunicamycin	54-65	synovial apoptosis inhibitor 1, synoviolin	Mus musculus	14-18
26317416-5	2015	Block of core glycosylation with tunicamycin demonstrated that changes in plasma membrane CaSR levels were due to differences in exocytic rate.	Tunicamycin	33-44	calcium sensing receptor	Homo sapiens	90-94
26288094-6	2015	Here we demonstrate that guanabenz is protective in fibroblasts expressing G93A mutant SOD1 when they are exposed to tunicamycin mediated ER stress.	Tunicamycin	117-128	superoxide dismutase 1, soluble	Mus musculus	87-91
26349962-3	2015	Tunicamycin blocks the first step of P-gp (glycoprotein P) and BCRP (breast cancer resistance protein) N-glycosylation, which is a very important modification for the activity and cellular localisation of these proteins.	Tunicamycin	0-11	phosphoglycolate phosphatase	Homo sapiens	37-41
26079879-4	2015	In this study, the results showed that tunicamycin decreased insulin-stimulated Akt phosphorylation, but promoted the phosphorylation of protein kinase R-like ER protein kinase (PERK) time-dependently in C2C12 cells.	Tunicamycin	39-50	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	137-176
26079879-4	2015	In this study, the results showed that tunicamycin decreased insulin-stimulated Akt phosphorylation, but promoted the phosphorylation of protein kinase R-like ER protein kinase (PERK) time-dependently in C2C12 cells.	Tunicamycin	39-50	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	178-182
26079879-5	2015	Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently.	Tunicamycin	198-209	heat shock protein 5	Mus musculus	42-72
26079879-5	2015	Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently.	Tunicamycin	198-209	heat shock protein 5	Mus musculus	74-77
26079879-5	2015	Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently.	Tunicamycin	198-209	heat shock protein 5	Mus musculus	109-114
26079879-5	2015	Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently.	Tunicamycin	198-209	X-box binding protein 1	Mus musculus	147-170
26079879-5	2015	Consistently, ERS gene markers, including binding immunoglobulin protein (BIP)/glucose regulated protein 78 (GRP78) expression and the splicing of X box binding protein 1 (XBP-1), were activated by tunicamycin time-dependently.	Tunicamycin	198-209	X-box binding protein 1	Mus musculus	172-177
26079879-8	2015	A strong phosphorylation of inositol-requiring enzyme 1 (IRE-1), c-JUN NH2-terminal kinase (JNK), and insulin receptor substrate 1 (IRS-1) serine, and simultaneously, a dramatic decrease of IRS-1 tyrosine phosphorylation were observed in the presence of tunicamycin, leading to a blockade of insulin signaling, which was reversed by melatonin pretreatment.	Tunicamycin	254-265	insulin receptor substrate 1	Mus musculus	132-137
26079879-8	2015	A strong phosphorylation of inositol-requiring enzyme 1 (IRE-1), c-JUN NH2-terminal kinase (JNK), and insulin receptor substrate 1 (IRS-1) serine, and simultaneously, a dramatic decrease of IRS-1 tyrosine phosphorylation were observed in the presence of tunicamycin, leading to a blockade of insulin signaling, which was reversed by melatonin pretreatment.	Tunicamycin	254-265	insulin receptor substrate 1	Mus musculus	190-195
26079879-10	2015	Therefore, these results demonstrated that melatonin pretreatment inhibited the activated role of tunicamycin on ERS and insulin resistance through melatonin receptor-mediated IRE-1/JNK/IRS-1 insulin signaling in skeletal muscle cells.	Tunicamycin	98-109	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	176-181
26079879-10	2015	Therefore, these results demonstrated that melatonin pretreatment inhibited the activated role of tunicamycin on ERS and insulin resistance through melatonin receptor-mediated IRE-1/JNK/IRS-1 insulin signaling in skeletal muscle cells.	Tunicamycin	98-109	mitogen-activated protein kinase 8	Mus musculus	182-185
26079879-10	2015	Therefore, these results demonstrated that melatonin pretreatment inhibited the activated role of tunicamycin on ERS and insulin resistance through melatonin receptor-mediated IRE-1/JNK/IRS-1 insulin signaling in skeletal muscle cells.	Tunicamycin	98-109	insulin receptor substrate 1	Mus musculus	186-191
25972450-8	2015	This in vivo finding is corroborated by the in vitro study showing that cultured cardiac fibroblasts treated with recombinant sFRP2 protein exhibited progressive increase in the expression and activity of TNAP, which was completely abrogated by cycloheximide or tunicamycin.	Tunicamycin	262-273	secreted frizzled-related protein 2	Mus musculus	126-131
26022098-6	2015	We hypothesized that TN-induced activation of p38 MAPK signaling pathway is responsible for cell death.	Tunicamycin	21-23	mitogen-activated protein kinase 14	Homo sapiens	46-49
26349962-3	2015	Tunicamycin blocks the first step of P-gp (glycoprotein P) and BCRP (breast cancer resistance protein) N-glycosylation, which is a very important modification for the activity and cellular localisation of these proteins.	Tunicamycin	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	63-67
26349962-3	2015	Tunicamycin blocks the first step of P-gp (glycoprotein P) and BCRP (breast cancer resistance protein) N-glycosylation, which is a very important modification for the activity and cellular localisation of these proteins.	Tunicamycin	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	69-101
26349962-11	2015	Western blot analysis showed that, in LoVo/Dx and W1PR cells, tunicamycin treatment resulted in the expression of a 70kDa P-gp protein instead of the mature 170kDa P-gp.	Tunicamycin	62-73	phosphoglycolate phosphatase	Homo sapiens	122-126
26349962-11	2015	Western blot analysis showed that, in LoVo/Dx and W1PR cells, tunicamycin treatment resulted in the expression of a 70kDa P-gp protein instead of the mature 170kDa P-gp.	Tunicamycin	62-73	phosphoglycolate phosphatase	Homo sapiens	164-168
26349962-13	2015	In tunicamycin-treated W1TR cells, the size of the BCRP protein did not differ from that of its native unglycosylated form.	Tunicamycin	3-14	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	51-55
26349962-14	2015	In tunicamycin-treated A2780T1 cells, BCRP expression was completely inhibited, but pre-treatment with MG132 or BMA suppressed the effect of tunicamycin.	Tunicamycin	3-14	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-42
26349962-15	2015	Immunocytochemistry analysis indicated that tunicamycin only affected the translocation of P-gp but not that of BCRP.	Tunicamycin	44-55	phosphoglycolate phosphatase	Homo sapiens	91-95
26065400-7	2015	Then we explored the role of IRE1-XBP1-snail pathway in transforming growth factor (TGF)-beta1/tunicamycin (TM)-induced EMT.	Tunicamycin	95-106	X-box binding protein 1	Rattus norvegicus	34-38
25713411-11	2015	The potent ER stress inducers (thapsigargin and tunicamycin) directly decreased precursor and mature forms of integrin-beta1 and led appearance of unglycosylated core protein of integrin-beta1.	Tunicamycin	48-59	integrin subunit beta 1	Rattus norvegicus	110-124
25713411-11	2015	The potent ER stress inducers (thapsigargin and tunicamycin) directly decreased precursor and mature forms of integrin-beta1 and led appearance of unglycosylated core protein of integrin-beta1.	Tunicamycin	48-59	integrin subunit beta 1	Rattus norvegicus	178-192
25824433-8	2015	Tunicamycin treatment of oocytes expressing Cav1.2/WT mimicked the effects of the quadruple mutations.	Tunicamycin	0-11	calcium channel, voltage-dependent, L type, alpha 1C subunit S homeolog	Xenopus laevis	44-50
26447625-6	2015	Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P&lt;0.05; IL-1b, 16.063.40, t =7.93, P&lt;0.05; IL-6, 31.1610.60, t=5.08, P&lt;0.05).	Tunicamycin	0-11	tumor necrosis factor	Mus musculus	68-72
26447625-6	2015	Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P&lt;0.05; IL-1b, 16.063.40, t =7.93, P&lt;0.05; IL-6, 31.1610.60, t=5.08, P&lt;0.05).	Tunicamycin	0-11	interleukin 6	Mus musculus	74-78
26447625-6	2015	Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P&lt;0.05; IL-1b, 16.063.40, t =7.93, P&lt;0.05; IL-6, 31.1610.60, t=5.08, P&lt;0.05).	Tunicamycin	0-11	interleukin 1 beta	Mus musculus	83-88
26447625-6	2015	Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P&lt;0.05; IL-1b, 16.063.40, t =7.93, P&lt;0.05; IL-6, 31.1610.60, t=5.08, P&lt;0.05).	Tunicamycin	0-11	tumor necrosis factor	Mus musculus	101-105
26447625-6	2015	Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P&lt;0.05; IL-1b, 16.063.40, t =7.93, P&lt;0.05; IL-6, 31.1610.60, t=5.08, P&lt;0.05).	Tunicamycin	0-11	interleukin 1 beta	Mus musculus	138-143
26447625-6	2015	Tunicamycin significantly enhanced the LPS-induced up-regulation of TNFa, IL-6 and IL-1b expression (TNFa, 1.44+/-0.38, t=2.8, P&lt;0.05; IL-1b, 16.063.40, t =7.93, P&lt;0.05; IL-6, 31.1610.60, t=5.08, P&lt;0.05).	Tunicamycin	0-11	interleukin 6	Mus musculus	176-180
26140985-0	2015	Nuclear versus cytosolic activity of the yeast Hog1 MAP kinase in response to osmotic and tunicamycin-induced ER stress.	Tunicamycin	90-101	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	47-51
26227493-4	2015	RTN1 overexpression in renal cells induces ER stress and apoptosis, whereas RTN1 knockdown attenuates tunicamycin-induced and hyperglycaemia-induced ER stress and apoptosis.	Tunicamycin	102-113	reticulon 1	Mus musculus	76-80
25889874-4	2015	AtBiP3 promoter activity clearly reflected the effects of inducers of ER stress, such as tunicamycin, dithiothreitol, and salicylic acid.	Tunicamycin	89-100	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	0-6
25881988-7	2015	Tunicamycin treatment increased (P &lt; 0.01) and TUDCA treatment decreased (P &lt; 0.01) the expression level of ER chaperones, GRP78 and GRP94.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	129-134
25881988-7	2015	Tunicamycin treatment increased (P &lt; 0.01) and TUDCA treatment decreased (P &lt; 0.01) the expression level of ER chaperones, GRP78 and GRP94.	Tunicamycin	0-11	heat shock protein 90 beta family member 1	Homo sapiens	139-144
26100877-7	2015	Endogenous PAR1 rendered deficient in glycosylation using tunicamycin, a glycoprotein synthesis inhibitor, also exhibited increased PI signaling and diminished RhoA activation opposite to native receptor.	Tunicamycin	58-69	coagulation factor II thrombin receptor	Homo sapiens	11-15
25808625-4	2015	Sphk2, a major isotype of sphingosine kinase in the liver, was transcriptionally up-regulated by tunicamycin and lipopolysaccharides.	Tunicamycin	97-108	sphingosine kinase 2	Mus musculus	0-5
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	17-28	activating transcription factor 4	Homo sapiens	100-104
25737469-3	2015	We studied the role of GADD34 on the induction of autophagy and/or apoptosis by NaF- or tunicamycin-induced ER-stress in HepG2 cells transfected with GADD34 siRNA.	Tunicamycin	88-99	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	23-29
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	17-28	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	42-46
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	17-28	eukaryotic translation initiation factor 2A	Homo sapiens	70-79
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
25737469-6	2015	After 4 h, GADD34 mRNA expression was also increased by NaF and tunicamycin.	Tunicamycin	64-75	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	11-17
25737469-7	2015	Suppression of GADD34 by GADD34 siRNA increased ATF4 expression in both NaF- and tunicamycin-treated cells.	Tunicamycin	81-92	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	15-21
25737469-7	2015	Suppression of GADD34 by GADD34 siRNA increased ATF4 expression in both NaF- and tunicamycin-treated cells.	Tunicamycin	81-92	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	25-31
25737469-7	2015	Suppression of GADD34 by GADD34 siRNA increased ATF4 expression in both NaF- and tunicamycin-treated cells.	Tunicamycin	81-92	activating transcription factor 4	Homo sapiens	48-52
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	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	4-10
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
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	activating transcription factor 4	Homo sapiens	76-80
25896661-5	2015	MATERIALS AND METHODS: Treatment of endoplasmic stress inducers, thapsigargin and tunicamycin, inhibited adipocyte differentiation, stimulated Smile mRNA expression, and repressed the expression of adiponectin (Adipoq) in 3T3-L1 pre-adipocyte.	Tunicamycin	82-93	CREB/ATF bZIP transcription factor	Mus musculus	143-148
25896661-5	2015	MATERIALS AND METHODS: Treatment of endoplasmic stress inducers, thapsigargin and tunicamycin, inhibited adipocyte differentiation, stimulated Smile mRNA expression, and repressed the expression of adiponectin (Adipoq) in 3T3-L1 pre-adipocyte.	Tunicamycin	82-93	adiponectin, C1Q and collagen domain containing	Mus musculus	198-209
25896661-5	2015	MATERIALS AND METHODS: Treatment of endoplasmic stress inducers, thapsigargin and tunicamycin, inhibited adipocyte differentiation, stimulated Smile mRNA expression, and repressed the expression of adiponectin (Adipoq) in 3T3-L1 pre-adipocyte.	Tunicamycin	82-93	adiponectin, C1Q and collagen domain containing	Mus musculus	211-217
25926156-8	2015	Finally, we investigated the levels of TMEM132A mRNA and protein after exposure to five different neurotoxic stimuli, including thapsigargin, tunicamycin, serum starvation, homocysteine, and hydrogen peroxide.	Tunicamycin	142-153	transmembrane protein 132A	Mus musculus	39-47
25241896-6	2015	UDP-GlcNAc is essential for N-linked glycosylation occurring in the endoplasmic reticulum (ER) and high UAP1 expression associates with resistance against inhibitors of N-linked glycosylation (tunicamycin and 2-deoxyglucose) but not with a general ER stress-inducing agent, the calcium ionophore A23187.	Tunicamycin	193-204	UDP-N-acetylglucosamine pyrophosphorylase 1	Homo sapiens	104-108
26109405-6	2015	The expression of iRhom1 was increased by endoplasmic reticulum (ER) stressors, such as thapsigargin and tunicamycin, leading to the enhancement of proteasome activity, especially in ER-containing microsomes.	Tunicamycin	105-116	rhomboid 5 homolog 1	Homo sapiens	18-24
26194078-7	2015	Exendin-4 also reduced the expression of SEPP1 and fetuin-A in cells treated with tunicamycin, an ER stress inducer.	Tunicamycin	82-93	selenoprotein P	Homo sapiens	41-46
26194078-7	2015	Exendin-4 also reduced the expression of SEPP1 and fetuin-A in cells treated with tunicamycin, an ER stress inducer.	Tunicamycin	82-93	alpha 2-HS glycoprotein	Homo sapiens	51-59
25827060-4	2015	Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages.	Tunicamycin	48-59	TNF superfamily member 10	Homo sapiens	127-132
25827060-4	2015	Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages.	Tunicamycin	48-59	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	303-308
25827060-4	2015	Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages.	Tunicamycin	61-63	TNF superfamily member 10	Homo sapiens	127-132
25827060-4	2015	Here, we demonstrate that thapsigargin (TG) and tunicamycin (TM), two ERS inducers activated macrophages were able to increase TRAIL mRNA and protein expression in RAW264.7 macrophages, the culture supernatant of THP-1 cells, and mouse peritoneal macrophages, indicating that ERS as a potent inducer of TRAIL transcription and expression in macrophages.	Tunicamycin	61-63	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	303-308
25855079-7	2015	Inhibition of glycosylation by tunicamycin significantly decreased ASBT activity and shifted ASBT bands to ~30 kDa, representing a deglycosylated protein.	Tunicamycin	31-42	solute carrier family 10 member 2	Homo sapiens	67-71
25855079-7	2015	Inhibition of glycosylation by tunicamycin significantly decreased ASBT activity and shifted ASBT bands to ~30 kDa, representing a deglycosylated protein.	Tunicamycin	31-42	solute carrier family 10 member 2	Homo sapiens	93-97
25996208-4	2015	In addition, the compound decreased tunicamycin-induced GRP78 promoter activity in a dose dependent manner without inducing significant inhibition of luciferase activity and cell growth for 6 and 12 h. Moreover, the compound decreased the expression of GRP78, CHOP, XBP-1, and suppressed XBP-1, and reduced phosphorylation of IRE1alpha in FaO rat liver cells.	Tunicamycin	36-47	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	56-61
25996208-4	2015	In addition, the compound decreased tunicamycin-induced GRP78 promoter activity in a dose dependent manner without inducing significant inhibition of luciferase activity and cell growth for 6 and 12 h. Moreover, the compound decreased the expression of GRP78, CHOP, XBP-1, and suppressed XBP-1, and reduced phosphorylation of IRE1alpha in FaO rat liver cells.	Tunicamycin	36-47	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	253-258
25996208-4	2015	In addition, the compound decreased tunicamycin-induced GRP78 promoter activity in a dose dependent manner without inducing significant inhibition of luciferase activity and cell growth for 6 and 12 h. Moreover, the compound decreased the expression of GRP78, CHOP, XBP-1, and suppressed XBP-1, and reduced phosphorylation of IRE1alpha in FaO rat liver cells.	Tunicamycin	36-47	DNA-damage inducible transcript 3	Rattus norvegicus	260-264
25996208-4	2015	In addition, the compound decreased tunicamycin-induced GRP78 promoter activity in a dose dependent manner without inducing significant inhibition of luciferase activity and cell growth for 6 and 12 h. Moreover, the compound decreased the expression of GRP78, CHOP, XBP-1, and suppressed XBP-1, and reduced phosphorylation of IRE1alpha in FaO rat liver cells.	Tunicamycin	36-47	X-box binding protein 1	Rattus norvegicus	266-271
25996208-4	2015	In addition, the compound decreased tunicamycin-induced GRP78 promoter activity in a dose dependent manner without inducing significant inhibition of luciferase activity and cell growth for 6 and 12 h. Moreover, the compound decreased the expression of GRP78, CHOP, XBP-1, and suppressed XBP-1, and reduced phosphorylation of IRE1alpha in FaO rat liver cells.	Tunicamycin	36-47	X-box binding protein 1	Rattus norvegicus	288-293
25923692-3	2015	We aimed to investigate the impact on LOX-1 expression by tunicamycin (TM)-induced ER stress and to determine the effect of HDL on TM-affected LOX-1 expression in hepatic L02 cells.	Tunicamycin	58-69	oxidized low density lipoprotein receptor 1	Homo sapiens	38-43
25923692-9	2015	Knock down of IRE1 or XBP-1 effectively restored LOX-1 expression and improved lipid uptake in TM-treated cells.	Tunicamycin	95-97	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	14-18
25923692-9	2015	Knock down of IRE1 or XBP-1 effectively restored LOX-1 expression and improved lipid uptake in TM-treated cells.	Tunicamycin	95-97	X-box binding protein 1	Homo sapiens	22-27
25727012-5	2015	In vivo study indicates that administration of the ER stressor tunicamycin in mice led to increased expression of beta-klotho in the liver.	Tunicamycin	63-74	klotho beta	Mus musculus	114-125
25620058-6	2015	Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice.	Tunicamycin	0-11	activating transcription factor 6	Mus musculus	140-144
25537833-8	2015	Fgf21-null mice exhibited increased expression of ER stress marker genes and augmented hepatic lipid accumulation after tunicamycin treatment.	Tunicamycin	120-131	fibroblast growth factor 21	Mus musculus	0-5
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
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	151-156
25417142-0	2015	Wogonin protects rat dorsal root ganglion neurons against tunicamycin-induced ER stress through the PERK-eIF2alpha-ATF4 signaling pathway.	Tunicamycin	58-69	eukaryotic translation initiation factor 2A	Rattus norvegicus	105-114
25417142-0	2015	Wogonin protects rat dorsal root ganglion neurons against tunicamycin-induced ER stress through the PERK-eIF2alpha-ATF4 signaling pathway.	Tunicamycin	58-69	activating transcription factor 4	Rattus norvegicus	115-119
25711465-0	2015	Melatonin-mediated Bim up-regulation and cyclooxygenase-2 (COX-2) down-regulation enhances tunicamycin-induced apoptosis in MDA-MB-231 cells.	Tunicamycin	91-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	41-57
25711465-0	2015	Melatonin-mediated Bim up-regulation and cyclooxygenase-2 (COX-2) down-regulation enhances tunicamycin-induced apoptosis in MDA-MB-231 cells.	Tunicamycin	91-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	59-64
25711465-4	2015	Melatonin up-regulates pro-apoptotic protein Bim expression at the transcriptional levels in the presence of tunicamycin.	Tunicamycin	109-120	BCL2 like 11	Homo sapiens	45-48
25711465-5	2015	Melatonin inhibits tunicamycin-induced COX-2 expression in MDA-MB-231 cells.	Tunicamycin	19-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	39-44
25711465-6	2015	Furthermore, inhibition of COX-2 activity using the COX-2 inhibitor, NS398, increases tunicamycin-induced apoptosis.	Tunicamycin	86-97	prostaglandin-endoperoxide synthase 2	Homo sapiens	27-32
25711465-6	2015	Furthermore, inhibition of COX-2 activity using the COX-2 inhibitor, NS398, increases tunicamycin-induced apoptosis.	Tunicamycin	86-97	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-57
25711465-9	2015	In addition, melatonin blocked tunicamycin-induced NF-kappaB transcriptional activity, p65 nuclear translocation, and p38 MAPK activation.	Tunicamycin	31-42	RELA proto-oncogene, NF-kB subunit	Homo sapiens	87-90
25711465-9	2015	In addition, melatonin blocked tunicamycin-induced NF-kappaB transcriptional activity, p65 nuclear translocation, and p38 MAPK activation.	Tunicamycin	31-42	mitogen-activated protein kinase 14	Homo sapiens	118-121
25711465-11	2015	Taken together, our results suggest that melatonin enhances antitumor function through up-regulation of Bim expression and down-regulation of COX-2 expression in tunicamycin-treated MDA-MB-231 cells.	Tunicamycin	162-173	prostaglandin-endoperoxide synthase 2	Homo sapiens	142-147
25620058-6	2015	Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice.	Tunicamycin	0-11	heat shock protein 5	Mus musculus	166-171
25620058-6	2015	Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice.	Tunicamycin	0-11	heat shock protein 90, beta (Grp94), member 1	Mus musculus	173-178
25620058-6	2015	Tunicamycin caused UPR in the cerebral cortex, hippocampus and cerebellum of mice of PD4 and PD12, which was evident by the upregulation of ATF6, XBP1s, p-eIF2alpha, GRP78, GRP94 and MANF, but failed to induce UPR in the brain of PD25 mice.	Tunicamycin	0-11	mesencephalic astrocyte-derived neurotrophic factor	Mus musculus	183-187
25620058-8	2015	In PD4 mice, tunicamycin-induced caspase-3 activation was observed in layer II of the parietal and optical cortex, CA1-CA3 and the subiculum of the hippocampus, the cerebellar external germinal layer and the superior/inferior colliculus.	Tunicamycin	13-24	caspase 3	Mus musculus	33-42
25620058-8	2015	In PD4 mice, tunicamycin-induced caspase-3 activation was observed in layer II of the parietal and optical cortex, CA1-CA3 and the subiculum of the hippocampus, the cerebellar external germinal layer and the superior/inferior colliculus.	Tunicamycin	13-24	carbonic anhydrase 1	Mus musculus	115-122
25620058-9	2015	Tunicamycin-induced caspase-3 activation was also shown on PD12 but to a much lesser degree and mainly located in the dentate gyrus of the hippocampus, deep cerebellar nuclei and pons.	Tunicamycin	0-11	caspase 3	Mus musculus	20-29
25660457-7	2015	We also demonstrated that expression of miR-23a stimulated with tunicamycin was rescued by melatonin treatment, resulting in reduced ER stress in primary hepatocytes.	Tunicamycin	64-75	microRNA 23a	Homo sapiens	40-47
25660451-6	2015	GLP-1 (7-36) prevented H2O2-, l-glutamate-, tunicamycin-, thapsigargin-, and amyloid beta1-42-induced neuronal cell death in a concentration-dependent manner.	Tunicamycin	44-55	glucagon	Mus musculus	0-5
25249581-8	2015	ASK1 knockdown in C17.2 neural stem cells diminished high glucose- or tunicamycin-induced IRE1alpha activation, which further supports our hypothesis that ASK1 plays a causal role in diabetes-induced ER stress and apoptosis.	Tunicamycin	70-81	mitogen-activated protein kinase kinase kinase 5	Mus musculus	0-4
25249581-8	2015	ASK1 knockdown in C17.2 neural stem cells diminished high glucose- or tunicamycin-induced IRE1alpha activation, which further supports our hypothesis that ASK1 plays a causal role in diabetes-induced ER stress and apoptosis.	Tunicamycin	70-81	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	90-99
25249581-8	2015	ASK1 knockdown in C17.2 neural stem cells diminished high glucose- or tunicamycin-induced IRE1alpha activation, which further supports our hypothesis that ASK1 plays a causal role in diabetes-induced ER stress and apoptosis.	Tunicamycin	70-81	mitogen-activated protein kinase kinase kinase 5	Mus musculus	155-159
25573487-8	2015	On the other hand inhibition of elongation of N-glycosylation by tunicamycin (TM) resulted in inhibition of Phaseolus vulgaris-L (L-PHA) lectin-binding activity and inhibited cell adhesion to galectin-8, laminin and fibronectin.	Tunicamycin	65-76	galectin 8	Homo sapiens	192-202
25667230-5	2015	We also show that CIA2-deficient cells display an increased resistance to tunicamycin-induced endoplasmic reticulum (ER) stress, as evidenced by the upregulated splicing of the mRNA of HAC1, which encodes a functional transcription factor that regulates the transcription of unfolded protein response (UPR) target genes, suggesting enhanced intracellular UPR activity.	Tunicamycin	74-85	transcription factor HAC1	Saccharomyces cerevisiae S288C	185-189
25573487-8	2015	On the other hand inhibition of elongation of N-glycosylation by tunicamycin (TM) resulted in inhibition of Phaseolus vulgaris-L (L-PHA) lectin-binding activity and inhibited cell adhesion to galectin-8, laminin and fibronectin.	Tunicamycin	65-76	fibronectin 1	Homo sapiens	216-227
24691093-3	2015	Fibroblasts from the skin of two such mutants (Snell dwarf and PAPP-A knockout) were found to have higher levels of ATF4 protein and expression of several ATF4 target genes in responses to amino acid withdrawal, cadmium, hydrogen peroxide, and tunicamycin.	Tunicamycin	244-255	pregnancy-associated plasma protein A	Mus musculus	63-69
24691093-3	2015	Fibroblasts from the skin of two such mutants (Snell dwarf and PAPP-A knockout) were found to have higher levels of ATF4 protein and expression of several ATF4 target genes in responses to amino acid withdrawal, cadmium, hydrogen peroxide, and tunicamycin.	Tunicamycin	244-255	activating transcription factor 4	Mus musculus	155-159
25405329-7	2015	Furthermore, pretreatment with tunicamycin significantly attenuated the induction of proinflammatory cytokines and CD40, by LDL.	Tunicamycin	31-42	CD40 molecule	Homo sapiens	115-119
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	58-62
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	eukaryotic translation initiation factor 2A	Homo sapiens	67-76
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	136-141
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
25428129-6	2015	Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K.	Tunicamycin	49-60	mechanistic target of rapamycin kinase	Homo sapiens	15-19
25428129-6	2015	Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K.	Tunicamycin	49-60	mechanistic target of rapamycin kinase	Homo sapiens	112-116
25428129-6	2015	Interestingly, mTOR was activated rapidly during tunicamycin treatment, as indicated by phosphorylation of both mTOR and p70S6K.	Tunicamycin	49-60	ribosomal protein S6 kinase B1	Homo sapiens	121-127
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	mechanistic target of rapamycin kinase	Homo sapiens	14-18
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	78-82
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
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	123-128
25539857-7	2015	The Cox-2 response to PFF was fourfold decreased in cells from old bones (p &lt; 0.001), while tunicamycin decreased PFF-induced Cox-2 expression by threefold in cells from adult bones (p &lt; 0.01).	Tunicamycin	95-106	prostaglandin-endoperoxide synthase 2	Mus musculus	129-134
24356728-0	2015	Unfolded protein response inducers tunicamycin and dithiothreitol promote myeloma cell differentiation mediated by XBP-1.	Tunicamycin	35-46	X-box binding protein 1	Homo sapiens	115-120
24356728-4	2015	Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity.	Tunicamycin	62-73	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	132-136
24356728-4	2015	Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity.	Tunicamycin	62-73	X-box binding protein 1	Homo sapiens	137-142
24356728-4	2015	Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity.	Tunicamycin	62-73	X-box binding protein 1	Homo sapiens	232-237
24356728-4	2015	Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity.	Tunicamycin	75-77	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	132-136
24356728-4	2015	Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity.	Tunicamycin	75-77	X-box binding protein 1	Homo sapiens	137-142
24356728-4	2015	Herein, we used low-dose pharmacological UPR inducers such as tunicamycin (TM) and dithiothreitol (DTT) to efficiently activate the IRE1-XBP-1 pathway in myeloma cells characterized by transcriptional expression increase in spliced XBP-1 and molecular chaperons, accompanied by significant differentiation and maturation of these myeloma cells, without concomitant cytotoxicity.	Tunicamycin	75-77	X-box binding protein 1	Homo sapiens	232-237
25389134-6	2015	Tunicamycin treatment selectively reduced R345W F3 secretion by 87% (vs. WT F3).	Tunicamycin	0-11	EGF containing fibulin extracellular matrix protein 1	Homo sapiens	48-50
25389134-6	2015	Tunicamycin treatment selectively reduced R345W F3 secretion by 87% (vs. WT F3).	Tunicamycin	0-11	EGF containing fibulin extracellular matrix protein 1	Homo sapiens	76-78
25736111-0	2015	[Role of KA1 receptor in excitotoxic neurodegeneration in mouse hippocampus triggered by kainic acid- or tunicamycin-induced endoplasmic reticulum stress].	Tunicamycin	105-116	glutamate receptor, ionotropic, kainate 4	Mus musculus	9-12
25492867-4	2015	In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78).	Tunicamycin	143-154	patatin-like phospholipase domain containing 8	Rattus norvegicus	56-66
25492867-4	2015	In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78).	Tunicamycin	143-154	activating transcription factor 6	Rattus norvegicus	177-210
25492867-4	2015	In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78).	Tunicamycin	143-154	activating transcription factor 6	Rattus norvegicus	212-216
25492867-4	2015	In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78).	Tunicamycin	143-154	heat shock protein 90 beta family member 1	Rattus norvegicus	254-282
25492867-4	2015	In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78).	Tunicamycin	143-154	heat shock protein 90 beta family member 1	Rattus norvegicus	284-289
25492867-4	2015	In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78).	Tunicamycin	143-154	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	295-323
25492867-4	2015	In cultured rat GECs, overexpression of the full-length iPLA2gamma, but not a mutant iPLA2gamma that fails to associate with the ER, augmented tunicamycin-induced activation of activating transcription factor-6 (ATF6) and induction of the ER chaperones, glucose-regulated protein 94 (GRP94) and glucose-regulated protein 78 (GRP78).	Tunicamycin	143-154	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	325-330
25492867-6	2015	Tunicamycin-induced cytotoxicity was reduced in GECs expressing iPLA2gamma, and the cytoprotection was reversed by dominant-negative ATF6.	Tunicamycin	0-11	patatin-like phospholipase domain containing 8	Rattus norvegicus	64-74
25492867-6	2015	Tunicamycin-induced cytotoxicity was reduced in GECs expressing iPLA2gamma, and the cytoprotection was reversed by dominant-negative ATF6.	Tunicamycin	0-11	activating transcription factor 6	Rattus norvegicus	133-137
25492867-7	2015	GECs from iPLA2gamma knock-out mice showed blunted ATF6 activation and chaperone up-regulation in response to tunicamycin.	Tunicamycin	110-121	patatin-like phospholipase domain containing 8	Mus musculus	10-20
25494629-4	2014	RESULTS: We provide first evidence that SND1 promoter activity is increased in human liver cancer cells upon exposure to thapsigargin or tunicamycin or by ectopic expression of ATF6, a crucial transcription factor in the unfolded protein response triggered by ER stress.	Tunicamycin	137-148	staphylococcal nuclease and tudor domain containing 1	Homo sapiens	40-44
26237103-6	2015	An isolated homozygous mutant of AGB1, agb1-3, was more sensitive to the tunicamycin-induced ER stress compared to the wild type and the other loss-of-function mutants of G protein subunits.	Tunicamycin	73-84	GTP binding protein beta 1	Arabidopsis thaliana	33-37
26237103-6	2015	An isolated homozygous mutant of AGB1, agb1-3, was more sensitive to the tunicamycin-induced ER stress compared to the wild type and the other loss-of-function mutants of G protein subunits.	Tunicamycin	73-84	GTP binding protein beta 1	Arabidopsis thaliana	39-43
26018731-2	2015	Here we report that RIPK1 functions as an important prosurvival mechanism in melanoma cells undergoing pharmacological ER stress induced by tunicamycin (TM) or thapsigargin (TG) through activation of autophagy.	Tunicamycin	140-151	receptor interacting serine/threonine kinase 1	Homo sapiens	20-25
26018731-2	2015	Here we report that RIPK1 functions as an important prosurvival mechanism in melanoma cells undergoing pharmacological ER stress induced by tunicamycin (TM) or thapsigargin (TG) through activation of autophagy.	Tunicamycin	153-155	receptor interacting serine/threonine kinase 1	Homo sapiens	20-25
24865476-15	2015	Imatinib-induced cell survival of tunicamycin-treated cells was partially mediated by ERK activation.	Tunicamycin	34-45	Eph receptor B1	Rattus norvegicus	86-89
25823847-4	2015	METHODS: THP-1 and HT-29 IECs were stimulated with 2 microg/ml tunicamycin (TNM) for the indicated periods of time.	Tunicamycin	63-74	GLI family zinc finger 2	Homo sapiens	9-14
25630719-10	2015	In vitro, ER stress induced by tunicamycin synergistically increased LPS-triggered pro-inflammatory cytokine induction and promoted the activation of nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) pathway in bone marrow-derived macrophages; moreover, tunicamycin also cooperated with TNF-alpha to increase hepatocyte apoptosis.	Tunicamycin	31-42	tumor necrosis factor	Mus musculus	315-324
25494629-6	2014	Quantitative real-time PCR revealed a near 3 fold increase in SND1 mRNA expression by either of the stress-inducers; whereas SND1 protein was maximally upregulated (3.4-fold) in cells exposed to tunicamycin, a protein glycosylation inhibitor.	Tunicamycin	195-206	staphylococcal nuclease and tudor domain containing 1	Homo sapiens	62-66
25494629-6	2014	Quantitative real-time PCR revealed a near 3 fold increase in SND1 mRNA expression by either of the stress-inducers; whereas SND1 protein was maximally upregulated (3.4-fold) in cells exposed to tunicamycin, a protein glycosylation inhibitor.	Tunicamycin	195-206	staphylococcal nuclease and tudor domain containing 1	Homo sapiens	125-129
25126734-0	2014	Endoplasmic reticulum stress induced by tunicamycin and thapsigargin protects against transient ischemic brain injury: Involvement of PARK2-dependent mitophagy.	Tunicamycin	40-51	parkin RBR E3 ubiquitin protein ligase	Mus musculus	134-139
25231320-0	2014	Tunicamycin-induced ER stress regulates chemokine CCL5 expression and secretion via STAT3 followed by decreased transmigration of MCF-7 breast cancer cells.	Tunicamycin	0-11	C-C motif chemokine ligand 5	Homo sapiens	50-54
25231320-0	2014	Tunicamycin-induced ER stress regulates chemokine CCL5 expression and secretion via STAT3 followed by decreased transmigration of MCF-7 breast cancer cells.	Tunicamycin	0-11	signal transducer and activator of transcription 3	Homo sapiens	84-89
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	C-C motif chemokine ligand 5	Homo sapiens	96-100
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	signal transducer and activator of transcription 3	Homo sapiens	102-107
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
25231320-7	2014	Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site.	Tunicamycin	10-21	C-C motif chemokine ligand 5	Homo sapiens	30-34
25231320-7	2014	Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site.	Tunicamycin	10-21	signal transducer and activator of transcription 3	Homo sapiens	105-110
25231320-7	2014	Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site.	Tunicamycin	10-21	signal transducer and activator of transcription 3	Homo sapiens	114-119
25231320-7	2014	Moreover, tunicamycin-induced CCL5 expression was positively related to upregulation of unphosphorylated STAT3 (U-STAT3) but negatively related to STAT3 phosphorylation at the Tyr705 site.	Tunicamycin	10-21	signal transducer and activator of transcription 3	Homo sapiens	114-119
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	45-50
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
25360516-4	2014	The blocking of cell surface GRP78 by anti-GRP78 antibody prevented apoptosis, suggesting that induction of cell surface GRP78 by doxorubicin and tunicamycin is required for apoptosis.	Tunicamycin	146-157	heat shock protein family A (Hsp70) member 5	Homo sapiens	29-34
25360516-4	2014	The blocking of cell surface GRP78 by anti-GRP78 antibody prevented apoptosis, suggesting that induction of cell surface GRP78 by doxorubicin and tunicamycin is required for apoptosis.	Tunicamycin	146-157	heat shock protein family A (Hsp70) member 5	Homo sapiens	43-48
25360516-4	2014	The blocking of cell surface GRP78 by anti-GRP78 antibody prevented apoptosis, suggesting that induction of cell surface GRP78 by doxorubicin and tunicamycin is required for apoptosis.	Tunicamycin	146-157	heat shock protein family A (Hsp70) member 5	Homo sapiens	43-48
25457612-8	2014	This mechanism is potentially involved in mTORC1 regulation by amino acids, rotenone, and tunicamycin, connecting stress response with mTORC1 inhibition.	Tunicamycin	90-101	CREB regulated transcription coactivator 1	Mus musculus	42-48
25457612-8	2014	This mechanism is potentially involved in mTORC1 regulation by amino acids, rotenone, and tunicamycin, connecting stress response with mTORC1 inhibition.	Tunicamycin	90-101	CREB regulated transcription coactivator 1	Mus musculus	135-141
25106896-7	2014	Tunicamycin-induced ER stress altered reactive oxygen species (ROS) (6.34-fold ), membrane potential (4.1-fold ), mitochondrial biogenesis (2.4-fold ), and adiponectin secretion (3.5-fold ).	Tunicamycin	0-11	adiponectin, C1Q and collagen domain containing	Homo sapiens	156-167
24983772-0	2014	Histone H3K4 methyltransferase Mll1 regulates protein glycosylation and tunicamycin-induced apoptosis through transcriptional regulation.	Tunicamycin	72-83	lysine methyltransferase 2A	Homo sapiens	31-35
24983772-4	2014	Here, we find that Mll1 deficiency enhances UPR and apoptosis induced by the glycosylation inhibitor TM (tunicamycin).	Tunicamycin	105-116	lysine methyltransferase 2A	Homo sapiens	19-23
25816608-7	2014	At the same time, the induction of endoplasmic reticulum stress by tunicamycin in glioma cells with suppressed activity of ERN1 endoribonuclease decreases the expression level of PRPS1 and PRPS2 genes only.	Tunicamycin	67-78	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	123-127
25816608-7	2014	At the same time, the induction of endoplasmic reticulum stress by tunicamycin in glioma cells with suppressed activity of ERN1 endoribonuclease decreases the expression level of PRPS1 and PRPS2 genes only.	Tunicamycin	67-78	phosphoribosyl pyrophosphate synthetase 1	Homo sapiens	179-184
25816608-7	2014	At the same time, the induction of endoplasmic reticulum stress by tunicamycin in glioma cells with suppressed activity of ERN1 endoribonuclease decreases the expression level of PRPS1 and PRPS2 genes only.	Tunicamycin	67-78	phosphoribosyl pyrophosphate synthetase 2	Homo sapiens	189-194
25170079-5	2014	Intraperitoneal administration of the ER stressor tunicamycin in mice resulted in hepatic steatosis, accompanied by activation of the three canonical UPR branches and increased the expression of FGF21.	Tunicamycin	50-61	fibroblast growth factor 21	Mus musculus	195-200
25170079-7	2014	Administration of recombinant FGF21 in mice alleviated tunicamycin-induced liver steatosis, in parallel with reduced eIF2alpha-ATF4-CHOP signaling.	Tunicamycin	55-66	fibroblast growth factor 21	Mus musculus	30-35
25340554-3	2014	In this study, we examined the biological significance of gp130 glycosylation using tunicamycin (Tm), an inhibitor of enzyme involved in N-linked glycosylation.	Tunicamycin	84-95	interleukin 6 cytokine family signal transducer	Homo sapiens	58-63
25340554-3	2014	In this study, we examined the biological significance of gp130 glycosylation using tunicamycin (Tm), an inhibitor of enzyme involved in N-linked glycosylation.	Tunicamycin	97-99	interleukin 6 cytokine family signal transducer	Homo sapiens	58-63
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	microRNA 615	Homo sapiens	16-23
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
25112878-5	2014	Of these mutants, pro3 was the most sensitive to tunicamycin and was rescued by anaerobic growth conditions or reduced thiol reagents.	Tunicamycin	49-60	pyrroline-5-carboxylate reductase	Saccharomyces cerevisiae S288C	18-22
25063273-5	2014	PPARbeta/delta activation also prevented thapsigargin- and tunicamycin-induced ER stress in human and murine skeletal muscle cells.	Tunicamycin	59-70	peroxisome proliferator activated receptor delta	Homo sapiens	0-8
25011082-6	2014	In comparison to NSCLC cells with functional LKB1, treatment of NSCLC cells lacking LKB1 with the ER stress activators (ERSA), tunicamycin, brefeldin A or 2DG, resulted in aggravation of ER stress, increased cytotoxicity, and evidence of ER stress-mediated cell death.	Tunicamycin	127-138	serine/threonine kinase 11	Homo sapiens	84-88
25035425-4	2014	We report here that Lmf1 expression is induced by ER stress in various cell lines and in tunicamycin (TM)-injected mice.	Tunicamycin	89-100	lipase maturation factor 1	Mus musculus	20-24
25092289-6	2014	Also, the addition of the TGF-beta inhibitor SB431542 and the Wnt/beta-catenin antagonist IWP-2 negated the endodermal differentiation of ESCs mediated by thapsigargin and tunicamycin.	Tunicamycin	172-183	catenin (cadherin associated protein), beta 1	Mus musculus	66-78
25228093-6	2014	The protein and mRNA expression levels of MICA/B in SMMC7721 and HepG2 cells treated by tunicamycin were evaluated by flow cytometry, Western Blot and RT-PCR.	Tunicamycin	88-99	MHC class I polypeptide-related sequence A	Homo sapiens	42-46
25108065-8	2014	Additionally, although progesterone secretion and levels of steroidogenic enzymes decreased following intra-peritoneal injection of Tunicamycin, an ER stress inducer, the expression of Grp78/Bip, p50ATF6, and CHOP dramatically increased.	Tunicamycin	132-143	heat shock protein 5	Mus musculus	185-190
25108065-8	2014	Additionally, although progesterone secretion and levels of steroidogenic enzymes decreased following intra-peritoneal injection of Tunicamycin, an ER stress inducer, the expression of Grp78/Bip, p50ATF6, and CHOP dramatically increased.	Tunicamycin	132-143	heat shock protein 5	Mus musculus	191-194
25108065-8	2014	Additionally, although progesterone secretion and levels of steroidogenic enzymes decreased following intra-peritoneal injection of Tunicamycin, an ER stress inducer, the expression of Grp78/Bip, p50ATF6, and CHOP dramatically increased.	Tunicamycin	132-143	DNA-damage inducible transcript 3	Mus musculus	209-213
25232251-3	2014	The N-/O-glycosylation inhibitors (tunicamycin and benzyl-N-acetyl-alpha-galactosaminide) were then used to interfere with KL-6/MUC1 glycosylation in two pancreatic carcinoma cell lines, and the effects on KL-6/MUC1 expression, and cell adhesion and invasion were determined.	Tunicamycin	35-46	mucin 1, cell surface associated	Homo sapiens	123-127
25232251-3	2014	The N-/O-glycosylation inhibitors (tunicamycin and benzyl-N-acetyl-alpha-galactosaminide) were then used to interfere with KL-6/MUC1 glycosylation in two pancreatic carcinoma cell lines, and the effects on KL-6/MUC1 expression, and cell adhesion and invasion were determined.	Tunicamycin	35-46	mucin 1, cell surface associated	Homo sapiens	128-132
24723324-5	2014	We evaluated whether neuronal differentiation and dendrite outgrowth were regulated by HRD1, a ubiquitin ligase that was induced under mild conditions of tunicamycin-induced ER stress.	Tunicamycin	154-165	synovial apoptosis inhibitor 1, synoviolin	Mus musculus	87-91
24838315-9	2014	Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction.	Tunicamycin	78-89	mucin 1, cell surface associated	Homo sapiens	28-32
24838315-9	2014	Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction.	Tunicamycin	78-89	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	154-157
24838315-9	2014	Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction.	Tunicamycin	78-89	mucin 1, cell surface associated	Homo sapiens	158-162
24838315-9	2014	Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction.	Tunicamycin	78-89	galectin 3	Homo sapiens	165-175
24838315-9	2014	Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction.	Tunicamycin	78-89	mucin 1, cell surface associated	Homo sapiens	158-162
24838315-9	2014	Chemical deglycosylation of MUC1 using a mixture of N-glycosylation inhibitor tunicamycin and O-glycosylation inhibitor benzyl-alpha-GalNAc disrupted the Src/MUC1-C/galectin-3/EGFR complexes and thereby abolished smoke-induced MUC1-C-TyrP and MUC1-C/p120ctn interaction.	Tunicamycin	78-89	mucin 1, cell surface associated	Homo sapiens	158-162
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
24962313-8	2014	We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6.	Tunicamycin	31-42	X-box binding protein 1	Homo sapiens	81-85
24962313-8	2014	We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6.	Tunicamycin	31-42	X-box binding protein 1	Homo sapiens	87-92
24962313-8	2014	We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6.	Tunicamycin	31-42	activating transcription factor 6	Homo sapiens	106-139
24962313-8	2014	We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6.	Tunicamycin	31-42	activating transcription factor 6	Homo sapiens	141-145
24962313-8	2014	We also found that propofol or tunicamycin alone increased the levels of spliced XBP1 (XBP1s) and cleaved activating transcription factor 6 (ATF6), an active form of ATF6.	Tunicamycin	31-42	activating transcription factor 6	Homo sapiens	166-170
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	growth differentiation factor 10	Homo sapiens	21-24
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
24962313-10	2014	Knockdown endogenous BiP with siRNA abolished the suppression of propofol on tunicamycin-mediated activation of CHOP and caspase-3.	Tunicamycin	77-88	caspase 3	Homo sapiens	121-130
24962313-11	2014	Meanwhile, knockdown BiP attenuated the protective effects of propofol on the neural cells exposed to tunicamycin.	Tunicamycin	102-113	growth differentiation factor 10	Homo sapiens	21-24
24970053-9	2014	Hence, various concentrations of tunicamycin were used to treat the cells in order to study its influence on CD147 N-glycosylation and MMP-2 expression.	Tunicamycin	33-44	basigin (Ok blood group)	Homo sapiens	109-114
24970053-9	2014	Hence, various concentrations of tunicamycin were used to treat the cells in order to study its influence on CD147 N-glycosylation and MMP-2 expression.	Tunicamycin	33-44	matrix metallopeptidase 2	Homo sapiens	135-140
25035425-4	2014	We report here that Lmf1 expression is induced by ER stress in various cell lines and in tunicamycin (TM)-injected mice.	Tunicamycin	102-104	lipase maturation factor 1	Mus musculus	20-24
25023286-5	2014	However, these changes were countered by Bcl-xL induction, which is necessary to protect differentiating cells both from ER stress-induced death by tunicamycin and from the death signals inherent in differentiation.	Tunicamycin	148-159	BCL2-like 1	Mus musculus	41-47
24357007-6	2014	Tunicamycin and thapsigargin, compounds known to induce ER stress, also decreased the SCD protein.	Tunicamycin	0-11	stearoyl-CoA desaturase	Homo sapiens	86-89
24784707-8	2014	This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected.	Tunicamycin	68-79	mitogen-activated protein kinase 8	Homo sapiens	88-111
24813659-3	2014	Gemigliptin significantly decreased the tunicamycin-mediated increase in glucose regulated protein 78 (GRP78) expression and ER stress-mediated signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C-EBP homologous protein (CHOP) and inositol-requiring enzyme 1alpha (IRE1alpha)/c-Jun N-terminal kinase (JNK)-p38.	Tunicamycin	40-51	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	73-101
24813659-3	2014	Gemigliptin significantly decreased the tunicamycin-mediated increase in glucose regulated protein 78 (GRP78) expression and ER stress-mediated signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C-EBP homologous protein (CHOP) and inositol-requiring enzyme 1alpha (IRE1alpha)/c-Jun N-terminal kinase (JNK)-p38.	Tunicamycin	40-51	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	103-108
24813659-3	2014	Gemigliptin significantly decreased the tunicamycin-mediated increase in glucose regulated protein 78 (GRP78) expression and ER stress-mediated signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C-EBP homologous protein (CHOP) and inositol-requiring enzyme 1alpha (IRE1alpha)/c-Jun N-terminal kinase (JNK)-p38.	Tunicamycin	40-51	DNA-damage inducible transcript 3	Rattus norvegicus	232-256
24813659-3	2014	Gemigliptin significantly decreased the tunicamycin-mediated increase in glucose regulated protein 78 (GRP78) expression and ER stress-mediated signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C-EBP homologous protein (CHOP) and inositol-requiring enzyme 1alpha (IRE1alpha)/c-Jun N-terminal kinase (JNK)-p38.	Tunicamycin	40-51	DNA-damage inducible transcript 3	Rattus norvegicus	258-262
24813659-3	2014	Gemigliptin significantly decreased the tunicamycin-mediated increase in glucose regulated protein 78 (GRP78) expression and ER stress-mediated signaling molecules such as protein kinase RNA-like endoplasmic reticulum kinase (PERK)/C-EBP homologous protein (CHOP) and inositol-requiring enzyme 1alpha (IRE1alpha)/c-Jun N-terminal kinase (JNK)-p38.	Tunicamycin	40-51	mitogen activated protein kinase 14	Rattus norvegicus	343-346
24813659-6	2014	The reduction in tunicamycin-induced GRP78 level and PERK/CHOP pathway activity by gemigliptin was reversed after treatment with Akt inhibitor.	Tunicamycin	17-28	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	37-42
24813659-6	2014	The reduction in tunicamycin-induced GRP78 level and PERK/CHOP pathway activity by gemigliptin was reversed after treatment with Akt inhibitor.	Tunicamycin	17-28	DNA-damage inducible transcript 3	Rattus norvegicus	58-62
24813659-6	2014	The reduction in tunicamycin-induced GRP78 level and PERK/CHOP pathway activity by gemigliptin was reversed after treatment with Akt inhibitor.	Tunicamycin	17-28	AKT serine/threonine kinase 1	Rattus norvegicus	129-132
24807724-5	2014	CRT was also found to be of high importance for proper oligomerization of the viral structural proteins VP26 and VP28, and when CRT glycosylation was blocked with tunicamycin, a significant decrease in both viral replication and assembly was detected.	Tunicamycin	163-174	calreticulin	Homo sapiens	0-3
24807724-5	2014	CRT was also found to be of high importance for proper oligomerization of the viral structural proteins VP26 and VP28, and when CRT glycosylation was blocked with tunicamycin, a significant decrease in both viral replication and assembly was detected.	Tunicamycin	163-174	calreticulin	Homo sapiens	128-131
24973711-7	2014	We show that chemical ER stress inducers, such as tunicamycin or thapsigargin, enhanced IR-induced caspase 3 activation and DNA fragmentation in intestinal epithelial cells.	Tunicamycin	50-61	caspase 3	Rattus norvegicus	99-108
25064675-6	2014	Treatment of larvae or adult fish with tunicamycin induces ER stress and upregulates the expression of several key components of the gp78 ERAD complex in the liver.	Tunicamycin	39-50	autocrine motility factor receptor a	Danio rerio	133-137
25064675-7	2014	Moreover, liver-specific overexpression of the dominant-negative form of gp78 (gp78-R2M) renders liver more sensitive to tunicamycin-induced ER stress and enhances the expression of sterol response element binding protein (Srebp)-target genes, which was largely suppressed in fish overexpressing wild-type gp78.	Tunicamycin	121-132	autocrine motility factor receptor a	Danio rerio	73-77
25064675-7	2014	Moreover, liver-specific overexpression of the dominant-negative form of gp78 (gp78-R2M) renders liver more sensitive to tunicamycin-induced ER stress and enhances the expression of sterol response element binding protein (Srebp)-target genes, which was largely suppressed in fish overexpressing wild-type gp78.	Tunicamycin	121-132	autocrine motility factor receptor a	Danio rerio	79-83
25064675-7	2014	Moreover, liver-specific overexpression of the dominant-negative form of gp78 (gp78-R2M) renders liver more sensitive to tunicamycin-induced ER stress and enhances the expression of sterol response element binding protein (Srebp)-target genes, which was largely suppressed in fish overexpressing wild-type gp78.	Tunicamycin	121-132	autocrine motility factor receptor a	Danio rerio	79-83
25026174-5	2014	Tunicamycin or brefeldin A, two ER stress inducers, increased APE1 and GRP78, an ER stress marker, expression in HepG2 and Huh-7 cells.	Tunicamycin	0-11	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	62-66
25026174-5	2014	Tunicamycin or brefeldin A, two ER stress inducers, increased APE1 and GRP78, an ER stress marker, expression in HepG2 and Huh-7 cells.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	71-76
24982359-4	2014	MATERIALS AND METHODS: GRP78 was over-expressed in A549 cells with 2-deoxyglucose (2-dG) or tunicamycin (TM) treatments for 48 h and subsequently exposed to cisplatin for 2 h. Viability of these cells was determined at 0, 12, 24, 36 and 48 h afterwards.	Tunicamycin	92-103	heat shock protein family A (Hsp70) member 5	Homo sapiens	23-28
24982359-4	2014	MATERIALS AND METHODS: GRP78 was over-expressed in A549 cells with 2-deoxyglucose (2-dG) or tunicamycin (TM) treatments for 48 h and subsequently exposed to cisplatin for 2 h. Viability of these cells was determined at 0, 12, 24, 36 and 48 h afterwards.	Tunicamycin	105-107	heat shock protein family A (Hsp70) member 5	Homo sapiens	23-28
24722832-0	2014	Overexpression of CREB protein protects from tunicamycin-induced apoptosis in various rat cell types.	Tunicamycin	45-56	cAMP responsive element binding protein 1	Rattus norvegicus	18-22
24722832-4	2014	The significance of the ubiquitously expressed transcription factor CREB is demonstrated in prolonged, tunicamycin (TM)-induced ER stress in this study.	Tunicamycin	103-114	cAMP responsive element binding protein 1	Rattus norvegicus	68-72
24722832-4	2014	The significance of the ubiquitously expressed transcription factor CREB is demonstrated in prolonged, tunicamycin (TM)-induced ER stress in this study.	Tunicamycin	116-118	cAMP responsive element binding protein 1	Rattus norvegicus	68-72
24604564-5	2014	GRP78 protein levels were similar in the tunicamycin (Tm), salubrinal, and SP600125 groups, but were lower in cells treated with SN50.	Tunicamycin	41-52	heat shock protein family A (Hsp70) member 5	Homo sapiens	0-5
25050111-0	2014	IRE1alpha knockdown rescues tunicamycin-induced developmental defects and apoptosis in Xenopus laevis.	Tunicamycin	28-39	endoplasmic reticulum to nucleus signaling 1 S homeolog	Xenopus laevis	0-9
24784707-8	2014	This was supported by the finding that RvD1 significantly inhibited tunicamycin-induced c-Jun N-terminal kinase (JNK) expression, although P38 and ERK1/2 phosphorylation were not affected.	Tunicamycin	68-79	mitogen-activated protein kinase 8	Homo sapiens	113-116
24963635-9	2014	The endoplasmic reticulum (ER) stress-inducing reagent tunicamycin induced OPN mRNA expression in A549, MLE12 and HPAEpiC, and OPN mRNA expression was induced via activation of the ERK-dependent signaling pathway in A549 and MLE12.	Tunicamycin	55-66	secreted phosphoprotein 1	Homo sapiens	75-78
24963635-9	2014	The endoplasmic reticulum (ER) stress-inducing reagent tunicamycin induced OPN mRNA expression in A549, MLE12 and HPAEpiC, and OPN mRNA expression was induced via activation of the ERK-dependent signaling pathway in A549 and MLE12.	Tunicamycin	55-66	secreted phosphoprotein 1	Homo sapiens	127-130
24963635-9	2014	The endoplasmic reticulum (ER) stress-inducing reagent tunicamycin induced OPN mRNA expression in A549, MLE12 and HPAEpiC, and OPN mRNA expression was induced via activation of the ERK-dependent signaling pathway in A549 and MLE12.	Tunicamycin	55-66	mitogen-activated protein kinase 1	Homo sapiens	181-184
24945938-6	2014	Treatment of ECs with tunicamycin, an N-glycosylation inhibitor, suppressed CD62P (P-selectin) expression on the cell surface as well as the 140 kDa form in the cytoplasm.	Tunicamycin	22-33	selectin, platelet	Mus musculus	76-81
24945938-6	2014	Treatment of ECs with tunicamycin, an N-glycosylation inhibitor, suppressed CD62P (P-selectin) expression on the cell surface as well as the 140 kDa form in the cytoplasm.	Tunicamycin	22-33	selectin, platelet	Mus musculus	83-93
24945938-8	2014	Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression.	Tunicamycin	94-105	thymoma viral proto-oncogene 1	Mus musculus	116-119
24945938-8	2014	Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression.	Tunicamycin	94-105	thymoma viral proto-oncogene 1	Mus musculus	116-119
24945938-8	2014	Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression.	Tunicamycin	186-197	coagulation factor II	Mus musculus	0-8
24945938-8	2014	Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression.	Tunicamycin	186-197	selectin, platelet	Mus musculus	27-37
24945938-8	2014	Thrombin, which stimulates P-selectin expression on ECs, induced AKT phosphorylation, whereas tunicamycin inhibited AKT phosphorylation, suggesting that AKT signaling is involved in the tunicamycin-mediated inhibition of P-selectin expression.	Tunicamycin	186-197	selectin, platelet	Mus musculus	221-231
24944523-3	2014	METHODS: Cancer cells were treated with tunicamycin (TM) for 8 and 24 h. The expression of Derlin-1 and autophagy-related genes was determined by western blot.	Tunicamycin	40-51	derlin 1	Homo sapiens	91-99
24944523-3	2014	METHODS: Cancer cells were treated with tunicamycin (TM) for 8 and 24 h. The expression of Derlin-1 and autophagy-related genes was determined by western blot.	Tunicamycin	53-55	derlin 1	Homo sapiens	91-99
24652289-7	2014	Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1).	Tunicamycin	57-68	insulin	Homo sapiens	122-129
24892553-5	2014	(i) Tunicamycin induced ER stress as measured by increased mRNA and protein levels of glucose-regulated protein 78 kDa, P-eIF2alpha, activating transcription factor 4, C/EBP homologous protein, and cell death.	Tunicamycin	4-15	eukaryotic translation initiation factor 2A	Rattus norvegicus	122-131
24892553-5	2014	(i) Tunicamycin induced ER stress as measured by increased mRNA and protein levels of glucose-regulated protein 78 kDa, P-eIF2alpha, activating transcription factor 4, C/EBP homologous protein, and cell death.	Tunicamycin	4-15	activating transcription factor 4	Rattus norvegicus	133-166
24892553-5	2014	(i) Tunicamycin induced ER stress as measured by increased mRNA and protein levels of glucose-regulated protein 78 kDa, P-eIF2alpha, activating transcription factor 4, C/EBP homologous protein, and cell death.	Tunicamycin	4-15	CCAAT/enhancer binding protein gamma	Rattus norvegicus	168-173
24576409-6	2014	Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expressions enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation.	Tunicamycin	95-106	mitogen-activated protein kinase 14	Mus musculus	33-36
24576409-6	2014	Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expressions enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation.	Tunicamycin	95-106	DNA-damage inducible transcript 3	Mus musculus	58-62
24576409-6	2014	Interestingly, the inhibition of p38 MAPK pathway reduced CHOP and Bip expressions enhanced by tunicamycin and restored eNOS promoter activation as well as phosphorylation.	Tunicamycin	95-106	heat shock protein 5	Mus musculus	67-70
24888588-4	2014	In addition, we found that experimental induction of ER stress by tunicamycin injections in mice results in a block of pro-B-cell to pre-B-cell differentiation specifically in Mzb1(-/-) mice.	Tunicamycin	66-77	marginal zone B and B1 cell-specific protein 1	Mus musculus	176-180
25033633-8	2014	Under stress conditions, the FCM assay showed that cell percentage of S phases increased, whereas that of G1 phases decreased in the IRE1alpha group (P &lt; 0.05) compared with the control group of tunicamycin (TM) treatment.	Tunicamycin	198-209	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	133-142
25033633-8	2014	Under stress conditions, the FCM assay showed that cell percentage of S phases increased, whereas that of G1 phases decreased in the IRE1alpha group (P &lt; 0.05) compared with the control group of tunicamycin (TM) treatment.	Tunicamycin	211-213	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	133-142
24714921-3	2014	Following treatment of the cells with the ER stress inducers, thapsigargin (TG) or tunicamycin (TM), the lentiviral short hairpin RNA (shRNA)-mediated knockdown of Ufm1 increased the apoptosis of Raw264.7 cells.	Tunicamycin	83-94	ubiquitin-fold modifier 1	Mus musculus	164-168
24714921-3	2014	Following treatment of the cells with the ER stress inducers, thapsigargin (TG) or tunicamycin (TM), the lentiviral short hairpin RNA (shRNA)-mediated knockdown of Ufm1 increased the apoptosis of Raw264.7 cells.	Tunicamycin	96-98	ubiquitin-fold modifier 1	Mus musculus	164-168
24714921-5	2014	The overexpression of Ufm1 induced by lentiviral infection in the Raw264.7 cells treated with the ER stress inducers, TG or TM, resulted in the opposite effect.	Tunicamycin	124-126	ubiquitin-fold modifier 1	Mus musculus	22-26
24666819-8	2014	The induction of the UPR by tunicamycin was accompanied by activation of NF-kappaB in NSC34 cells and motor neurons.	Tunicamycin	28-39	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	73-82
24652289-7	2014	Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1).	Tunicamycin	57-68	insulin receptor substrate 1	Homo sapiens	157-161
24652289-7	2014	Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1).	Tunicamycin	57-68	insulin receptor substrate 1	Homo sapiens	175-179
24652289-7	2014	Metabolic stress modeled by anisomycin, thapsigargin, or tunicamycin increased many of the same Ser(P)/Thr(P) residues as insulin, some of which (Ser(P)-302(Irs1), Ser(P)-307(Irs1), and four others) correlated significantly with impaired insulin-stimulated Tyr(P)(Irs1).	Tunicamycin	57-68	insulin receptor substrate 1	Homo sapiens	175-179
24412219-6	2014	Tunicamycin to inhibit glycosylation reduced SGLT1 activity comparable to that seen with L-NAME treatment.	Tunicamycin	0-11	solute carrier family 5 member 1	Rattus norvegicus	45-50
24370996-6	2014	As a result of impaired ATF6 activation, dermal fibroblasts and adult thyrocytes from ERp29(-/-) mice display significantly lower apoptosis sensitivities when treated with tunicamycin and hydrogen peroxide.	Tunicamycin	172-183	endoplasmic reticulum protein 29	Mus musculus	86-91
24412219-8	2014	Immunoblots of luminal membranes from tunicamycin treated or L-NAME treated IEC-18 cells showed a decrease in the apparent molecular size of SGLT1 protein to 62 and 67 kD, respectively suggesting an alteration in protein glycosylation.	Tunicamycin	38-49	solute carrier family 5 member 1	Rattus norvegicus	141-146
24589479-5	2014	Upon induction of autophagy, by using amino acid deprivation as well as tunicamycin, we found that GD3 ganglioside, considered as a paradigmatic raft constituent, actively contributed to the biogenesis and maturation of autophagic vacuoles.	Tunicamycin	72-83	GRDX	Homo sapiens	99-102
24743137-6	2014	Time-lapse confocal microscopy indicated that A1AT co-localized with Golgi in the endothelium whilst inhibition of the classical secretory pathway with tunicamycin significantly increased intracellular retention of A1AT.	Tunicamycin	152-163	serpin family A member 1	Homo sapiens	215-219
24468888-11	2014	In addition, induction of ER stress by tunicamycin resulted in significantly increased expression of pro-inflammatory molecules such as IL-1beta and TNF-alpha in cultured inflammatory FLS.	Tunicamycin	39-50	interleukin 1 beta	Rattus norvegicus	136-144
24468888-11	2014	In addition, induction of ER stress by tunicamycin resulted in significantly increased expression of pro-inflammatory molecules such as IL-1beta and TNF-alpha in cultured inflammatory FLS.	Tunicamycin	39-50	tumor necrosis factor	Rattus norvegicus	149-158
24576488-0	2014	Inhibition of inducible nitric oxide synthase and interleukin-1beta expression by tunicamycin in cultured glial cells exposed to lipopolysaccharide.	Tunicamycin	82-93	nitric oxide synthase 2	Homo sapiens	14-45
24576488-0	2014	Inhibition of inducible nitric oxide synthase and interleukin-1beta expression by tunicamycin in cultured glial cells exposed to lipopolysaccharide.	Tunicamycin	82-93	interleukin 1 beta	Homo sapiens	50-67
24583133-7	2014	In vitro, treatment of RAW264.7 macrophages with tunicamycin, and subsequently stimulation with lipopolysaccharide (LPS) and interferon (IFN)-gamma enhances MIP2 mRNA und protein expression compared to proinflammatory stimulation alone.	Tunicamycin	49-60	chemokine (C-X-C motif) ligand 2	Mus musculus	157-161
24482374-9	2014	Metformin and PPARdelta agonist GW1516 reversed tunicamycin (ER stress inducer)-induced ER stress, oxidative stress, and impairment of endothelium-dependent relaxation in mouse aortae as well as NO production in mouse aortic endothelial cells.	Tunicamycin	48-59	peroxisome proliferator activator receptor delta	Mus musculus	14-23
24389415-4	2014	Tunicamycin, an inducer of endoplasmic reticulum stress, stimulated SMILE expression.	Tunicamycin	0-11	CREB/ATF bZIP transcription factor	Mus musculus	68-73
24583133-8	2014	However, LPS/IFNgamma induced vascular endothelial growth factor (VEGF) production was blunted by tunicamycin induced-ER stress.	Tunicamycin	98-109	interferon gamma	Mus musculus	13-21
24583133-8	2014	However, LPS/IFNgamma induced vascular endothelial growth factor (VEGF) production was blunted by tunicamycin induced-ER stress.	Tunicamycin	98-109	vascular endothelial growth factor A	Mus musculus	30-64
24583133-8	2014	However, LPS/IFNgamma induced vascular endothelial growth factor (VEGF) production was blunted by tunicamycin induced-ER stress.	Tunicamycin	98-109	vascular endothelial growth factor A	Mus musculus	66-70
24663680-6	2014	Experiments using tunicamycin, an inhibitor of N-glycosylation, indicated that the N-glycosylation of hKv1.5 is more effective at 28 C than at 37 C. Finally, the hypothermic treatment also rescued the protein expression and currents of trafficking-defective hKv1.5 mutants.	Tunicamycin	18-29	potassium voltage-gated channel subfamily A member 5	Homo sapiens	102-108
24667182-7	2014	In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt).	Tunicamycin	80-91	heat shock protein 5	Mus musculus	138-143
24667182-7	2014	In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt).	Tunicamycin	80-91	phosphatidylethanolamine N-methyltransferase	Mus musculus	205-209
24667182-7	2014	In mProx24 renal proximal tubular cells, the treatment with ER-stress inducers, tunicamycin and thapsigargin, increased the expression of GRP78, which was reduced by transfection of a shRNA lentivirus for Pemt (shRNA-Pemt).	Tunicamycin	80-91	phosphatidylethanolamine N-methyltransferase	Mus musculus	211-221
24647338-7	2014	Expression of p85beta was significantly more decreased under treatment with melatonin and thapsigargin or tunicamycin plus the PI3K inhibitors LY294002 or wortmannin than under treatment with only melatonin or a PI3K inhibitor.	Tunicamycin	106-117	phosphoinositide-3-kinase regulatory subunit 2	Mus musculus	14-21
24647338-8	2014	The PI3K downstream target p-Akt (Ser473, Thr308) showed significantly decreased expression under treatment with melatonin and thapsigargin or tunicamycin plus PI3K inhibitors than under treatment with melatonin or PI3K inhibitors only.	Tunicamycin	143-154	thymoma viral proto-oncogene 1	Mus musculus	29-32
24366244-0	2014	Inhibition of serine/threonine protein phosphatase PP1 protects cardiomyocytes from tunicamycin-induced apoptosis and I/R through the upregulation of p-eIF2alpha.	Tunicamycin	84-95	neuropeptide Y receptor Y4	Rattus norvegicus	51-54
24366244-0	2014	Inhibition of serine/threonine protein phosphatase PP1 protects cardiomyocytes from tunicamycin-induced apoptosis and I/R through the upregulation of p-eIF2alpha.	Tunicamycin	84-95	eukaryotic translation initiation factor 2A	Rattus norvegicus	152-161
24605085-9	2014	To discriminate between these possibilities, HEK293 cells expressing TRPM4 WT were treated with tunicamycin, an inhibitor of glycosylation.	Tunicamycin	96-107	transient receptor potential cation channel subfamily M member 4	Homo sapiens	69-74
24605085-10	2014	In contrast to N-glycosylation signal abolishment by mutagenesis, tunicamycin treatment led to an increase in the TRPM4-mediated current.	Tunicamycin	66-77	transient receptor potential cation channel subfamily M member 4	Homo sapiens	114-119
24520378-8	2014	Molecularly, baicalin ameliorated tunicamycin-induced ER stress by downregulation of CHOP.	Tunicamycin	34-45	DNA-damage inducible transcript 3	Rattus norvegicus	85-89
24520378-9	2014	In addition, baicalin inverted tunicamycin-induced decreases of eNOS mRNA and protein levels, phospho eNOS and NO production through CHOP pathway.	Tunicamycin	31-42	nitric oxide synthase 3	Rattus norvegicus	64-68
24520378-9	2014	In addition, baicalin inverted tunicamycin-induced decreases of eNOS mRNA and protein levels, phospho eNOS and NO production through CHOP pathway.	Tunicamycin	31-42	nitric oxide synthase 3	Rattus norvegicus	102-106
24520378-9	2014	In addition, baicalin inverted tunicamycin-induced decreases of eNOS mRNA and protein levels, phospho eNOS and NO production through CHOP pathway.	Tunicamycin	31-42	DNA-damage inducible transcript 3	Rattus norvegicus	133-137
24315873-4	2014	Treatment with tunicamycin (TM), an ER stress inducer, increased ATF3 expression in the preosteoblast cell line, MC3T3-E1.	Tunicamycin	15-26	activating transcription factor 3	Mus musculus	65-69
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	263-274	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	80-89
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	263-274	activating transcription factor 6	Homo sapiens	94-98
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	263-274	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	203-212
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	263-274	activating transcription factor 6	Homo sapiens	217-221
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	276-278	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	80-89
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	276-278	activating transcription factor 6	Homo sapiens	94-98
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	276-278	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	203-212
24240056-4	2014	In contrast to an initial increase followed by rapid reduction in activation of IRE1alpha and ATF6 signaling in control cells that were relatively sensitive to ER stress-induced apoptosis, activation of IRE1alpha and ATF6 by the pharmacological ER stress inducer tunicamycin (TM) or thapsigargin (TG) persisted in melanoma cells.	Tunicamycin	276-278	activating transcription factor 6	Homo sapiens	217-221
24275540-8	2014	SelS protein expression was unaffected by enterocytic differentiation but increased in response to selenium supplementation and after treatment with the ER stress inducer tunicamycin.	Tunicamycin	171-182	selenoprotein S	Homo sapiens	0-4
23921951-6	2014	Similar to knockdown of glucose-regulated protein 78 (GRP78), inhibition of XBP1 decelerated melanoma cell proliferation and enhanced apoptosis induced by the pharmacological ER stress inducers tunicamycin and thapasigargin.	Tunicamycin	194-205	X-box binding protein 1	Homo sapiens	76-80
24699413-0	2014	The Batten disease gene CLN3 confers resistance to endoplasmic reticulum stress induced by tunicamycin.	Tunicamycin	91-102	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	24-28
24465394-9	2014	PST also inhibited the up-regulation of GRP78 expression during UPR activation (by tunicamycin) in hepatocytes.	Tunicamycin	83-94	heat shock protein 5	Mus musculus	40-45
24125761-8	2014	The treatment of wild-type AADAC-expressing HuH-7 cells with tunicamycin, which produces unglycosylated protein, decreased AADAC enzyme activity.	Tunicamycin	61-72	arylacetamide deacetylase	Homo sapiens	27-32
24125761-8	2014	The treatment of wild-type AADAC-expressing HuH-7 cells with tunicamycin, which produces unglycosylated protein, decreased AADAC enzyme activity.	Tunicamycin	61-72	arylacetamide deacetylase	Homo sapiens	123-128
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
24315873-4	2014	Treatment with tunicamycin (TM), an ER stress inducer, increased ATF3 expression in the preosteoblast cell line, MC3T3-E1.	Tunicamycin	28-30	activating transcription factor 3	Mus musculus	65-69
24309597-6	2014	Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance.	Tunicamycin	0-11	insulin	Homo sapiens	80-87
24575364-9	2014	(3) Induction of ERSR stress by tunicamycin in H9C2 resulted in the upregulation of ERSR stress response genes along with downregulation of adiponectin, adiponectin receptors 1 and 2, and Serca2A.	Tunicamycin	32-43	adiponectin, C1Q and collagen domain containing	Mus musculus	140-151
24575364-9	2014	(3) Induction of ERSR stress by tunicamycin in H9C2 resulted in the upregulation of ERSR stress response genes along with downregulation of adiponectin, adiponectin receptors 1 and 2, and Serca2A.	Tunicamycin	32-43	adiponectin receptor 1	Mus musculus	153-182
24575364-9	2014	(3) Induction of ERSR stress by tunicamycin in H9C2 resulted in the upregulation of ERSR stress response genes along with downregulation of adiponectin, adiponectin receptors 1 and 2, and Serca2A.	Tunicamycin	32-43	ATPase, Ca++ transporting, cardiac muscle, slow twitch 2	Mus musculus	188-195
24418603-5	2014	Quantitative RT-PCR assays showed that the metabolic stressors histidinol and tunicamycin increased ATF4 levels and up-regulated ALT2 in HepG2 and Huh7 cells.	Tunicamycin	78-89	activating transcription factor 4	Homo sapiens	100-104
24418603-5	2014	Quantitative RT-PCR assays showed that the metabolic stressors histidinol and tunicamycin increased ATF4 levels and up-regulated ALT2 in HepG2 and Huh7 cells.	Tunicamycin	78-89	glutamic--pyruvic transaminase 2	Homo sapiens	129-133
24418603-7	2014	Moreover, ATF4 silencing prevented the activating effect of histidinol and tunicamycin on ATF4 and ALT2 expression.	Tunicamycin	75-86	activating transcription factor 4	Homo sapiens	10-14
24418603-7	2014	Moreover, ATF4 silencing prevented the activating effect of histidinol and tunicamycin on ATF4 and ALT2 expression.	Tunicamycin	75-86	activating transcription factor 4	Homo sapiens	90-94
24418603-7	2014	Moreover, ATF4 silencing prevented the activating effect of histidinol and tunicamycin on ATF4 and ALT2 expression.	Tunicamycin	75-86	glutamic--pyruvic transaminase 2	Homo sapiens	99-103
25229868-6	2014	The interaction with Cne1p was abrogated by the addition of tunicamycin, an inhibitor of N-glycosylation, indicating that N-linked carbohydrates might be necessary for protein binding to Cne1p.	Tunicamycin	60-71	calnexin	Saccharomyces cerevisiae S288C	21-26
25229868-6	2014	The interaction with Cne1p was abrogated by the addition of tunicamycin, an inhibitor of N-glycosylation, indicating that N-linked carbohydrates might be necessary for protein binding to Cne1p.	Tunicamycin	60-71	calnexin	Saccharomyces cerevisiae S288C	187-192
24309597-7	2014	Moreover, disturbance of autophagy and insulin sensitivity induced by tunicamycin can be effectively corrected by the addition of osteocalcin in an NFkappaB-dependent manner in vitro.	Tunicamycin	70-81	bone gamma-carboxyglutamate protein	Homo sapiens	130-141
25011668-7	2014	Most interestingly, GLUT4 gene expression induced by 4-PBA was not associated with ER stress even in the presence of tunicamycin, an ER stress inducer.	Tunicamycin	117-128	solute carrier family 2 member 4	Homo sapiens	20-25
24309597-6	2014	Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance.	Tunicamycin	0-11	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	155-159
24309597-6	2014	Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance.	Tunicamycin	0-11	mitogen-activated protein kinase 8	Homo sapiens	160-163
24309597-6	2014	Tunicamycin-induced ER stress in adipocytes can trigger autophagic response and insulin insensitivity that was partially attributed to the upregulation of IRE1-JNK pathway, whereas autophagy deficiency resulted in ER stress and impaired insulin signaling, further supporting the crucial roles of autophagy in ER stress and insulin resistance.	Tunicamycin	0-11	insulin	Homo sapiens	237-244
24309597-7	2014	Moreover, disturbance of autophagy and insulin sensitivity induced by tunicamycin can be effectively corrected by the addition of osteocalcin in an NFkappaB-dependent manner in vitro.	Tunicamycin	70-81	insulin	Homo sapiens	39-46
24787918-4	2014	As endoplasmic reticulum (ER) stress was reported in the early stage of AD, we injected tunicamycin, an ER stress inducer, into the lateral ventricular of rats and 48 hours later found in the other three brain regions but not cerebellum, increasing of binding immunoglobulin protein with the increased phosphorylation of pancreatic ER kinase, inositol-requiring enzyme 1, and activating transcription factor 6.	Tunicamycin	88-99	activating transcription factor 6	Rattus norvegicus	343-409
24787918-6	2014	The synapse-associated proteins, GluR2, PSD95, and synapsin1, were found decreased in the hippocampus after tunicamycin exposure.	Tunicamycin	108-119	glutamate ionotropic receptor AMPA type subunit 2	Rattus norvegicus	33-38
24787918-6	2014	The synapse-associated proteins, GluR2, PSD95, and synapsin1, were found decreased in the hippocampus after tunicamycin exposure.	Tunicamycin	108-119	discs large MAGUK scaffold protein 4	Rattus norvegicus	40-45
24787918-6	2014	The synapse-associated proteins, GluR2, PSD95, and synapsin1, were found decreased in the hippocampus after tunicamycin exposure.	Tunicamycin	108-119	synapsin I	Rattus norvegicus	51-60
24863135-8	2014	RESULTS: Chemical ER stress inducers such as tunicamycin (TM, 0.2 muM) and thapsigargin (TG, 0.2 muM) induced EMT, as shown by upregulation of alpha-smooth muscle actin and downregulation of E-cadherin.	Tunicamycin	45-56	cadherin 1	Homo sapiens	191-201
24863135-8	2014	RESULTS: Chemical ER stress inducers such as tunicamycin (TM, 0.2 muM) and thapsigargin (TG, 0.2 muM) induced EMT, as shown by upregulation of alpha-smooth muscle actin and downregulation of E-cadherin.	Tunicamycin	58-60	cadherin 1	Homo sapiens	191-201
24056124-5	2013	Tunicamycin also inhibited the expression of inflammatory molecule mRNAs induced by stimulation of TLR2 (with lipoteichoic acid) or TLR3 (with polyinosinic:polycytidylic acid), which do not require myeloid differentiation protein-2 (MD2) for their activation.	Tunicamycin	0-11	toll-like receptor 3	Mus musculus	132-136
23884247-6	2014	From various stimuli tested, 12-O-tetradecanoylphorbol-13-acetate and tunicamycin affected SKI-1 expression.	Tunicamycin	70-81	membrane bound transcription factor peptidase, site 1	Homo sapiens	91-96
24314051-4	2013	A complete deletion of L7 in Sec61p resulted in viable, cold- and tunicamycin-hypersensitive yeast cells with strong defects in posttranslational protein import of soluble proteins into the ER, and in ERAD of soluble substrates.	Tunicamycin	66-77	translocon subunit SEC61	Saccharomyces cerevisiae S288C	29-35
24056124-0	2013	Tunicamycin inhibits Toll-like receptor-activated inflammation in RAW264.7 cells by suppression of NF-kappaB and c-Jun activity via a mechanism that is independent of ER-stress and N-glycosylation.	Tunicamycin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	99-108
24056124-0	2013	Tunicamycin inhibits Toll-like receptor-activated inflammation in RAW264.7 cells by suppression of NF-kappaB and c-Jun activity via a mechanism that is independent of ER-stress and N-glycosylation.	Tunicamycin	0-11	jun proto-oncogene	Mus musculus	113-118
24056124-5	2013	Tunicamycin also inhibited the expression of inflammatory molecule mRNAs induced by stimulation of TLR2 (with lipoteichoic acid) or TLR3 (with polyinosinic:polycytidylic acid), which do not require myeloid differentiation protein-2 (MD2) for their activation.	Tunicamycin	0-11	lymphocyte antigen 96	Mus musculus	233-236
24056124-6	2013	Moreover, inhibition of LPS-induced iNOS expression was not inhibited by castanospermine, another N-glycosylation inhibitor, suggesting that the inhibitory effect of tunicamycin on LPS-induced iNOS induction is likely independent of MD2 N-glycosylation.	Tunicamycin	166-177	nitric oxide synthase 2, inducible	Mus musculus	36-40
24056124-6	2013	Moreover, inhibition of LPS-induced iNOS expression was not inhibited by castanospermine, another N-glycosylation inhibitor, suggesting that the inhibitory effect of tunicamycin on LPS-induced iNOS induction is likely independent of MD2 N-glycosylation.	Tunicamycin	166-177	nitric oxide synthase 2, inducible	Mus musculus	193-197
24056124-7	2013	Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter.	Tunicamycin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	45-54
24056124-7	2013	Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter.	Tunicamycin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	117-120
24056124-7	2013	Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter.	Tunicamycin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	151-154
24056124-7	2013	Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter.	Tunicamycin	0-11	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	159-162
24056124-7	2013	Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter.	Tunicamycin	0-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	170-179
24056124-7	2013	Tunicamycin inhibited nuclear factor-kappaB (NF-kappaB) activity by suppressing LPS-induced nuclear translocation of p50 and subsequent DNA binding of p50 and p65 to the NF-kappaB site of the iNOS promoter.	Tunicamycin	0-11	nitric oxide synthase 2, inducible	Mus musculus	192-196
24056124-8	2013	Tunicamycin also inhibited the transcriptional activity of a cAMP-response element (CRE) reporter, possibly by inhibiting c-Jun activation.	Tunicamycin	0-11	jun proto-oncogene	Mus musculus	122-127
24056124-9	2013	Therefore, we conclude that tunicamycin represses TLR-induced inflammation through suppression of NF-kappaB and CRE activity via a mechanism that is independent of ER-stress and N-glycosylation.	Tunicamycin	28-39	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	98-107
24142515-5	2013	In A549 cells, inhibition of glycosylation by tunicamycin increased the electrophoretic mobility (Mr) and reduced the expression level of wild-type ABCA3 in a dose-dependent manner.	Tunicamycin	46-57	ATP binding cassette subfamily A member 3	Homo sapiens	148-153
24130050-0	2013	Tunicamycin potentiates cisplatin anticancer efficacy through the DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma.	Tunicamycin	0-11	dolichyl-phosphate (UDP-N-acetylglucosamine) acetylglucosaminephosphotransferase 1 (GlcNAc-1-P transferase)	Mus musculus	66-72
24130050-0	2013	Tunicamycin potentiates cisplatin anticancer efficacy through the DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma.	Tunicamycin	0-11	thymoma viral proto-oncogene 1	Mus musculus	73-76
24130050-0	2013	Tunicamycin potentiates cisplatin anticancer efficacy through the DPAGT1/Akt/ABCG2 pathway in mouse Xenograft models of human hepatocellular carcinoma.	Tunicamycin	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	77-82
24130050-6	2013	The N-linked glycosylation (NLG) inhibitor tunicamycin dramatically reduced ABCG2 expression, altered its subcellular localization, and reversed its drug efflux effect in multiple hepatocellular carcinoma cell lines.	Tunicamycin	43-54	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	76-81
24130050-10	2013	Finally, the CDDP treatment combined with UDP-GlcNAc-dolichol-phosphate N-acetylglucosamine-1 phosphate transferase (DPAGT1) knockdown recapitulated the effect observed when CDDP was used in combination with tunicamycin.	Tunicamycin	208-219	dolichyl-phosphate (UDP-N-acetylglucosamine) acetylglucosaminephosphotransferase 1 (GlcNAc-1-P transferase)	Mus musculus	117-123
24130050-11	2013	In summary, our results suggest that tunicamycin may reverse the drug resistance and improve the efficacy of combination treatments for hepatocellular carcinomas by targeting the DPAGT1/Akt/ABCG2 pathway.	Tunicamycin	37-48	dolichyl-phosphate (UDP-N-acetylglucosamine) acetylglucosaminephosphotransferase 1 (GlcNAc-1-P transferase)	Mus musculus	179-185
24130050-11	2013	In summary, our results suggest that tunicamycin may reverse the drug resistance and improve the efficacy of combination treatments for hepatocellular carcinomas by targeting the DPAGT1/Akt/ABCG2 pathway.	Tunicamycin	37-48	thymoma viral proto-oncogene 1	Mus musculus	186-189
24130050-11	2013	In summary, our results suggest that tunicamycin may reverse the drug resistance and improve the efficacy of combination treatments for hepatocellular carcinomas by targeting the DPAGT1/Akt/ABCG2 pathway.	Tunicamycin	37-48	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	190-195
24142703-6	2013	The pathogenic yeast Candida albicans carries only one homolog of Kch1/Kch2, and homozygous knock-out mutants were similarly deficient in the activation of HACS during the responses to tunicamycin.	Tunicamycin	185-196	Kch1p	Saccharomyces cerevisiae S288C	66-70
24142703-6	2013	The pathogenic yeast Candida albicans carries only one homolog of Kch1/Kch2, and homozygous knock-out mutants were similarly deficient in the activation of HACS during the responses to tunicamycin.	Tunicamycin	185-196	pheromone-regulated K(+) transporter PRM6	Saccharomyces cerevisiae S288C	71-75
24130050-7	2013	Furthermore, tunicamycin reduced the expression levels of several CSC markers and suppressed the tumorigenicity of CD133(+) CSCs.	Tunicamycin	13-24	prominin 1	Mus musculus	115-120
24130050-8	2013	Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr.	Tunicamycin	0-11	proliferating cell nuclear antigen	Mus musculus	53-87
24130050-8	2013	Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr.	Tunicamycin	0-11	proliferating cell nuclear antigen	Mus musculus	89-93
24130050-8	2013	Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr.	Tunicamycin	0-11	poly (ADP-ribose) polymerase family, member 1	Mus musculus	136-140
24130050-8	2013	Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr.	Tunicamycin	0-11	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	201-206
24130050-8	2013	Tunicamycin combined with cisplatin (CDDP) inhibited proliferating cell nuclear antigen (PCNA) expression and increased the cleavage of PARP; this effect was partially rescued by the overexpression of ABCG2 or Akt-myr.	Tunicamycin	0-11	thymoma viral proto-oncogene 1	Mus musculus	210-213
24146856-9	2013	The ER-stress inducer tunicamycin increased gp96-expression in a concentration- and time-dependent manner.	Tunicamycin	22-33	heat shock protein 90 beta family member 1	Homo sapiens	44-48
23537529-9	2013	Moreover, OLFP significantly attenuated the tunicamycin-induced expression of the ER stress marker BiP (immunoglobulin heavy chain-binding protein) in the cells.	Tunicamycin	44-55	heat shock protein 5	Mus musculus	99-102
23537529-9	2013	Moreover, OLFP significantly attenuated the tunicamycin-induced expression of the ER stress marker BiP (immunoglobulin heavy chain-binding protein) in the cells.	Tunicamycin	44-55	heat shock protein 5	Mus musculus	104-146
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	nitric oxide synthase 2, inducible	Mus musculus	93-114
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	nitric oxide synthase 2, inducible	Mus musculus	116-120
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	prostaglandin-endoperoxide synthase 2	Mus musculus	123-139
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	prostaglandin-endoperoxide synthase 2	Mus musculus	141-146
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	interleukin 1 beta	Mus musculus	149-167
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	interleukin 1 beta	Mus musculus	169-177
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	tumor necrosis factor	Mus musculus	183-210
24056124-2	2013	Tunicamycin caused a reduction in LPS-induced nitric oxide (NO) production and expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), interleukin-1 beta (IL-1beta) and tumor necrosis factor alpha (TNF-alpha).	Tunicamycin	0-11	tumor necrosis factor	Mus musculus	212-221
24056124-5	2013	Tunicamycin also inhibited the expression of inflammatory molecule mRNAs induced by stimulation of TLR2 (with lipoteichoic acid) or TLR3 (with polyinosinic:polycytidylic acid), which do not require myeloid differentiation protein-2 (MD2) for their activation.	Tunicamycin	0-11	toll-like receptor 2	Mus musculus	99-103
23958596-9	2013	The WT transfectants treated with tunicamycin markedly lost LPLA2 activity.	Tunicamycin	34-45	phospholipase A2 group XV	Homo sapiens	60-65
24008518-9	2013	Protein levels of both p53 and glucosidase II were increased in response to UV irradiation but decreased in response to tunicamycin-induced ER stress.	Tunicamycin	120-131	tumor protein p53	Homo sapiens	23-26
24204574-8	2013	In fact, peritoneal macrophages isolated from Herp-deficient mice and RAW264.7 macrophages in which Herp was eliminated with a siRNA expressed lower levels of mRNA for inflammatory cytokines when they were treated with tunicamycin.	Tunicamycin	219-230	homocysteine-inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1	Mus musculus	46-50
24204574-8	2013	In fact, peritoneal macrophages isolated from Herp-deficient mice and RAW264.7 macrophages in which Herp was eliminated with a siRNA expressed lower levels of mRNA for inflammatory cytokines when they were treated with tunicamycin.	Tunicamycin	219-230	homocysteine-inducible, endoplasmic reticulum stress-inducible, ubiquitin-like domain member 1	Mus musculus	100-104
24204775-9	2013	Treatment of C2C12 myotubes with the ER-stressor tunicamycin resulted in the accumulation of reactive oxygen species (ROS), leading to the activation of protein expression of PTP1B.	Tunicamycin	49-60	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	175-180
24204775-10	2013	Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFkappaB p65 and was required for ER stress-mediated expression of PTP1B.	Tunicamycin	13-24	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	83-91
24204775-10	2013	Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFkappaB p65 and was required for ER stress-mediated expression of PTP1B.	Tunicamycin	13-24	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	92-95
24204775-10	2013	Furthermore, tunicamycin-induced ROS production activated nuclear translocation of NFkappaB p65 and was required for ER stress-mediated expression of PTP1B.	Tunicamycin	13-24	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	150-155
23911939-5	2013	The trafficking and glycosylation inhibitors brefeldin, monensin and tunicamycin substantially reduced cleavage and release of the N-terminal ectodomain of FLT1 and inhibited secretion of the isoforms of sFLT1.	Tunicamycin	69-80	fms related receptor tyrosine kinase 1	Homo sapiens	156-160
24021650-2	2013	We show that the ER stress inducer tunicamycin stimulates selective degradation of Rad51 via the 26S proteasome, impairing DSB repair and enhancing radiosensitivity in human lung cancer A549 cells.	Tunicamycin	35-46	RAD51 recombinase	Homo sapiens	83-88
23816873-9	2013	Administration of ER stress inducer, tunicamycin along with cold hypoxic stress, caused a discernible increase in protein oxidation and GRP78 expression, along with a significant elevation in proteasome and apoptotic activity.	Tunicamycin	37-48	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	136-141
23318453-11	2013	Ectopic expression of RRBP1 alleviated apoptosis that was induced by the ER-stress agent tunicamycin, 2-deoxy-D-glucose (2DG) or doxorubicin via enhancing GRP78 protein expression.	Tunicamycin	89-100	ribosome binding protein 1	Homo sapiens	22-27
23711292-0	2013	Inhibition of x-box binding protein 1 reduces tunicamycin-induced apoptosis in aged murine macrophages.	Tunicamycin	46-57	X-box binding protein 1	Mus musculus	14-37
23711292-5	2013	Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin.	Tunicamycin	193-204	X-box binding protein 1	Mus musculus	27-50
23711292-5	2013	Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin.	Tunicamycin	193-204	X-box binding protein 1	Mus musculus	52-56
23711292-5	2013	Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin.	Tunicamycin	193-204	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	84-93
23711292-5	2013	Reduced gene expression of x-box binding protein 1 (XBP1), a downstream effector of IRE1alpha, enhanced p-IRE1alpha levels and reduced apoptosis in aged, but not young macrophages treated with tunicamycin.	Tunicamycin	193-204	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	106-115
23707365-9	2013	Tunicamycin upregulated StARD1 expression and this outcome was abrogated by tauroursodeoxycholic acid.	Tunicamycin	0-11	steroidogenic acute regulatory protein	Mus musculus	24-30
23811795-4	2013	This effect was reversed by glycosyltransferase inactive mutant Mgat5 L188R transfection, alpha-mannosidase II inhibitor swainsonine treatment and N-acetyl glucosamine (GlcNAc) phosphotransferase (GPT) inhibitor tunicamycin administration.	Tunicamycin	212-223	alpha-1,6-mannosylglycoprotein 6-beta-N-acetylglucosaminyltransferase	Homo sapiens	64-69
24304569-5	2013	Similarly, inhibition of ET-1 receptors fully restored the impairment of acetylcholine-mediated relaxation induced by ER stress (maximal relaxation: control = 94+-2%, tunicamycin = 76+-5%, tunicamycin + tezosentan = 90+-3).	Tunicamycin	167-178	endothelin 1	Rattus norvegicus	25-29
24304569-5	2013	Similarly, inhibition of ET-1 receptors fully restored the impairment of acetylcholine-mediated relaxation induced by ER stress (maximal relaxation: control = 94+-2%, tunicamycin = 76+-5%, tunicamycin + tezosentan = 90+-3).	Tunicamycin	189-200	endothelin 1	Rattus norvegicus	25-29
24045949-5	2013	Tunicamycin, which induces ER stress, significantly suppressed PAC1 gene expression, and salubrinal, a selective inhibitor of the protein kinase RNA-like endoplasmic reticulum kinase signaling pathway of ER stress, blocked the suppression.	Tunicamycin	0-11	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	63-67
24045949-6	2013	In luciferase reporter assay, we found that two Sp1 sites were involved in suppression of PAC1 gene expression due to tunicamycin or OGD.	Tunicamycin	118-129	adenylate cyclase activating polypeptide 1 receptor 1	Mus musculus	90-94
24012670-4	2013	Like other chaperones (e.g., GRP94 and GRP78), calumenin expression was highly upregulated during ERS induced by 10 mug/ml tunicamycin, but attenuated in the presence of 500 muM PBA, the chemical chaperone in neonatal rat ventricular cardiomyocytes (NRVCs).	Tunicamycin	123-134	calumenin	Rattus norvegicus	47-56
23811795-4	2013	This effect was reversed by glycosyltransferase inactive mutant Mgat5 L188R transfection, alpha-mannosidase II inhibitor swainsonine treatment and N-acetyl glucosamine (GlcNAc) phosphotransferase (GPT) inhibitor tunicamycin administration.	Tunicamycin	212-223	N-acetylglucosamine-1-phosphate transferase subunits alpha and beta	Homo sapiens	147-195
23711089-8	2013	Simultaneously, the expression of phosphorylated AKT (p-AKT) was elevated in HepG2 and SMMC-7721 cells given tunicamycin but reduced in the presence of melatonin.	Tunicamycin	109-120	AKT serine/threonine kinase 1	Homo sapiens	49-52
23711089-8	2013	Simultaneously, the expression of phosphorylated AKT (p-AKT) was elevated in HepG2 and SMMC-7721 cells given tunicamycin but reduced in the presence of melatonin.	Tunicamycin	109-120	AKT serine/threonine kinase 1	Homo sapiens	56-59
23711134-10	2013	In tunicamycin treatment, HuD and insulin proteins showed similar expression tendencies.	Tunicamycin	3-14	insulin	Homo sapiens	34-41
23999590-7	2013	Moreover, icariin inhibited upregulation of endoplasmic reticulum markers, GRP78, GRP94 and CHOP, elicited by tunicamycin.	Tunicamycin	110-121	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	75-80
23999590-7	2013	Moreover, icariin inhibited upregulation of endoplasmic reticulum markers, GRP78, GRP94 and CHOP, elicited by tunicamycin.	Tunicamycin	110-121	DNA-damage inducible transcript 3	Rattus norvegicus	92-96
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	activating transcription factor 4	Homo sapiens	113-117
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
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	activating transcription factor 4	Homo sapiens	0-4
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	activating transcription factor 4	Homo sapiens	92-96
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	activating transcription factor 4	Homo sapiens	92-96
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
23976981-4	2013	Tunicamycin-induced death of SH-SY5H cells was prevented by terminal aromatic substituted butyric or valeric acids, in association with a decrease in the mRNA expression of stress-related factors, and in the accumulation of the ATF4 protein.	Tunicamycin	0-11	activating transcription factor 4	Homo sapiens	228-232
23774476-2	2013	The present study demonstrated that treatment with 1-10 mug/ml tunicamycin, a potent revulsant of ER stress, drastically induced TXNIP expression accompanied by the generation of cleaved caspase-3 as an indicator of apoptosis in SK-N-SH human neuroblastoma cells.	Tunicamycin	63-74	thioredoxin interacting protein	Homo sapiens	129-134
23774476-5	2013	Co-treatment of SK-N-SH cells with 100 muM nobiletin and 1 mug/ml tunicamycin for 24h strongly suppressed apoptosis and increased TXNIP expression induced by 1 mug/ml tunicamycin treatment alone.	Tunicamycin	66-77	thioredoxin interacting protein	Homo sapiens	130-135
23774476-5	2013	Co-treatment of SK-N-SH cells with 100 muM nobiletin and 1 mug/ml tunicamycin for 24h strongly suppressed apoptosis and increased TXNIP expression induced by 1 mug/ml tunicamycin treatment alone.	Tunicamycin	167-178	thioredoxin interacting protein	Homo sapiens	130-135
23615711-5	2013	Chac1 mRNA expression was also induced immediately following treatment with tunicamycin (Tm) and brefeldin A.	Tunicamycin	76-87	ChaC, cation transport regulator 1	Mus musculus	0-5
23319378-10	2013	Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP.	Tunicamycin	40-51	regulated endocrine-specific protein 18	Mus musculus	81-87
23319378-10	2013	Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP.	Tunicamycin	40-51	heat shock protein 5	Mus musculus	128-131
23319378-10	2013	Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP.	Tunicamycin	40-51	heat shock protein 90, beta (Grp94), member 1	Mus musculus	133-138
23319378-10	2013	Moreover, ERS inducer--thapsigargin and tunicamycin, decreased the expression of RESP18, which is different from the changes of BiP, GRP94, and CHOP.	Tunicamycin	40-51	DNA-damage inducible transcript 3	Mus musculus	144-148
33209651-8	2013	The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252).	Tunicamycin	20-31	cyclin D1	Mus musculus	93-102
33209651-8	2013	The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252).	Tunicamycin	20-31	cyclin-dependent kinase 4	Mus musculus	107-111
33209651-8	2013	The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252).	Tunicamycin	20-31	cyclin D1	Mus musculus	116-125
33209651-8	2013	The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252).	Tunicamycin	20-31	cyclin-dependent kinase 4	Mus musculus	134-138
33209651-8	2013	The nano-formulated Tunicamycin blocked the cell cycle progression by inhibiting either both cyclin D1 and CDK4, or cyclin D1, or the CDK4 expression as well as the expression of phospho Rb (serine-229/threonine-252).	Tunicamycin	20-31	RB transcriptional corepressor 1	Mus musculus	187-189
33209651-12	2013	Down regulated expression of caspase-9 and caspase-3 proposes a non-canonical pathway of cell death during "ER stress" induced by nano-formulated Tunicamycin.	Tunicamycin	146-157	caspase 9	Mus musculus	29-38
33209651-12	2013	Down regulated expression of caspase-9 and caspase-3 proposes a non-canonical pathway of cell death during "ER stress" induced by nano-formulated Tunicamycin.	Tunicamycin	146-157	caspase 3	Mus musculus	43-52
23737521-5	2013	Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor.	Tunicamycin	13-24	prion protein	Homo sapiens	83-87
23904594-4	2013	An endoplasmic reticulum stress inducer tunicamycin replicated the effect of NOC18 with regard to decrease of orexin-IR neurons and formation of aggregates.	Tunicamycin	40-51	hypocretin	Mus musculus	110-116
23894433-8	2013	Using cell lines, DNAJB3 protein was reduced following treatment with palmitate and tunicamycin which is suggestive of the link between the expression of DNAJB3 and the activation of the endoplasmic reticulum stress.	Tunicamycin	84-95	DnaJ heat shock protein family (Hsp40) member B3	Homo sapiens	18-24
23894433-8	2013	Using cell lines, DNAJB3 protein was reduced following treatment with palmitate and tunicamycin which is suggestive of the link between the expression of DNAJB3 and the activation of the endoplasmic reticulum stress.	Tunicamycin	84-95	DnaJ heat shock protein family (Hsp40) member B3	Homo sapiens	154-160
23737521-5	2013	Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor.	Tunicamycin	13-24	endoplasmic reticulum lectin 1	Homo sapiens	139-145
23737521-5	2013	Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor.	Tunicamycin	13-24	growth arrest and DNA damage inducible beta	Homo sapiens	147-154
23737521-5	2013	Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor.	Tunicamycin	13-24	sestrin 2	Homo sapiens	156-161
23665163-9	2013	Interestingly, PADI4 was up-regulated by various stresses such as H2O2, acrylamide, and tunicamycin in neuroblastoma SK-N-SH cells but inhibited by RG.	Tunicamycin	88-99	peptidyl arginine deiminase 4	Homo sapiens	15-20
23737521-5	2013	Brefeldin A, tunicamycin, and thapsigargin ER stressors induced gene expression of PRNP and four randomly chosen ERSE-26-containing genes, ERLEC1, GADD45B, SESN2, and SLC38A5, in primary human neuron cultures or in the breast carcinoma MCF-7 cell line, although the level of the response depends on the gene analyzed, the genetic background of the cells, the cell type, and the ER stressor.	Tunicamycin	13-24	solute carrier family 38 member 5	Homo sapiens	167-174
23434931-4	2013	In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis.	Tunicamycin	93-104	transcription factor 7 like 2	Homo sapiens	128-134
23434931-4	2013	In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis.	Tunicamycin	93-104	vascular endothelial growth factor A	Homo sapiens	139-144
23434931-4	2013	In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis.	Tunicamycin	93-104	transcription factor 7 like 2	Homo sapiens	234-240
23434931-4	2013	In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis.	Tunicamycin	93-104	vascular endothelial growth factor A	Homo sapiens	256-261
23434931-4	2013	In lymphoblastoid cells induced to undergo endoplasmic reticulum (ER) stress by treatment of tunicamycin, higher fold change of TCF7L2 and VEGFA mRNA levels were observed in rs7903146-TT cells than in rs7903146-CC cells (P = 0.02 for TCF7L2; P = 0.004 for VEGFA), suggesting that ER stress plays a role in PDR pathogenesis.	Tunicamycin	93-104	PDR	Homo sapiens	306-309
23826334-5	2013	Wild type levels of tunicamycin sensitivity were restored in iph1 null cells when the TORC1 complex was inhibited by rapamycin or by heat inactivation of the Tor2 kinase.	Tunicamycin	20-31	CREB regulated transcription coactivator 1	Homo sapiens	86-91
23580093-6	2013	Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells.	Tunicamycin	186-197	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	46-73
23580093-6	2013	Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells.	Tunicamycin	186-197	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	75-80
23580093-6	2013	Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells.	Tunicamycin	199-201	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	46-73
23580093-6	2013	Meanwhile, ER stress inhibitor salubrinal- or inositol-requiring enzyme 1 (IRE-1) shRNA silencing inhibited oridonin"s anti-HuH-6 effects, while ER stress inducers thapsigargin (Tg) and tunicamycin (Tm) mimicked oridonin"s actions on HuH-6 cells.	Tunicamycin	199-201	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	75-80
23708521-5	2013	Consistent with these results in vivo, the addition of osteocalcin reversed autophagy and ER stress and restored defective insulin sensitivity in vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs) in the presence of tunicamycin or in knockout XBP-1 (a transcription factor which mediates ER stress response) cells or in Atg7(-/-) cells.	Tunicamycin	240-251	bone gamma-carboxyglutamate protein 2	Mus musculus	55-66
23755268-6	2013	We show that VCD was highly cytotoxic only under hypoglycemic conditions, but not in the presence of normal glucose levels, and VCD blocked GRP78 expression only when glycolysis was impaired (due to hypoglycemia or the presence of the glycolysis inhibitor 2-deoxyglucose), but not when GRP78 was induced by other means (hypoxia, thapsigargin, tunicamycin).	Tunicamycin	343-354	heat shock protein family A (Hsp70) member 5	Homo sapiens	140-145
23448571-3	2013	In the present study, we showed that pretreatment with FGF-2 decreased the inhibition of DNA synthesis and induction of apoptosis by two different ER stress inducers, TM (tunicamycin) and TG (thapsigargin), in both human hepatoblastoma HepG2 cells and breast cancer MCF-7 cells.	Tunicamycin	167-169	fibroblast growth factor 2	Homo sapiens	55-60
23313043-9	2013	An insulin-resistant state was induced by exposing cells to 5mug/ml of tunicamycin as indicated by decreased insulin-mediated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and glucose uptake.	Tunicamycin	71-82	insulin receptor substrate 1	Mus musculus	154-182
23313043-9	2013	An insulin-resistant state was induced by exposing cells to 5mug/ml of tunicamycin as indicated by decreased insulin-mediated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and glucose uptake.	Tunicamycin	71-82	insulin receptor substrate 1	Mus musculus	184-189
23146721-7	2013	Simultaneous activation of WT KIT and treatment with endoplasmic reticulum (ER) inhibitors, tunicamycin or brefeldin A induced a complete inhibition of membrane expression of the 145 kDa form of KIT.	Tunicamycin	92-103	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	195-198
23665024-7	2013	Tunicamycin, an established ER stress inducer, increased vascular cellular adhesion molecule (VCAM)-1 expression in endothelial cells.	Tunicamycin	0-11	vascular cell adhesion molecule 1	Homo sapiens	57-101
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
23724116-6	2013	In addition, tunicamycin inhibited the androgen-induced expression of AR target genes KLK3 and CaMKK2 by 50%.	Tunicamycin	13-24	kallikrein related peptidase 3	Homo sapiens	86-90
23724116-6	2013	In addition, tunicamycin inhibited the androgen-induced expression of AR target genes KLK3 and CaMKK2 by 50%.	Tunicamycin	13-24	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	95-101
23724116-11	2013	Confocal imaging revealed that androgen induced plasma-membrane localization of IGF-1R was blocked by tunicamycin.	Tunicamycin	102-113	insulin like growth factor 1 receptor	Homo sapiens	80-86
23624196-6	2013	The secretion and mRNA expression levels of pro-inflammatory cytokines were increased by tunicamycin, and this stimulation was significantly suppressed by an overexpression of CDNF, demonstrating that CDNF plays an important role in astrocyte inflammation and functioning by resisting ER stress.	Tunicamycin	89-100	cerebral dopamine neurotrophic factor	Homo sapiens	201-205
23618865-0	2013	A sigma-1 receptor antagonist (NE-100) prevents tunicamycin-induced cell death via GRP78 induction in hippocampal cells.	Tunicamycin	48-59	sigma non-opioid intracellular receptor 1	Mus musculus	2-18
23618865-0	2013	A sigma-1 receptor antagonist (NE-100) prevents tunicamycin-induced cell death via GRP78 induction in hippocampal cells.	Tunicamycin	48-59	heat shock protein 5	Mus musculus	83-88
23500541-4	2013	Here, we find that ER stress induced by 2-DG as well as tunicamycin activates AMPK via Ca2+-CaMKKbeta leading to stimulation of autophagy.	Tunicamycin	56-67	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	92-101
23448571-3	2013	In the present study, we showed that pretreatment with FGF-2 decreased the inhibition of DNA synthesis and induction of apoptosis by two different ER stress inducers, TM (tunicamycin) and TG (thapsigargin), in both human hepatoblastoma HepG2 cells and breast cancer MCF-7 cells.	Tunicamycin	171-182	fibroblast growth factor 2	Homo sapiens	55-60
23518711-9	2013	Quantitative reverse transcriptase polymerase chain reaction demonstrated that Atf5alpha is the most abundant transcript in adult mouse encephalon and injection of the endoplasmic reticulum stress inducer tunicamycin into adult mouse brain increased neuronal ATF5 levels.	Tunicamycin	205-216	activating transcription factor 5	Mus musculus	259-263
23373714-1	2013	BACKGROUND AND PURPOSE: Endoplasmic reticulum (ER) stress has been implicated in the pathogeneses of insulin resistance and type 2 diabetes, and extracellular signal-regulated kinase (ERK) antagonist is an insulin sensitizer that can restore muscle insulin responsiveness in both tunicamycin-treated muscle cells and type 2 diabetic mice.	Tunicamycin	280-291	mitogen-activated protein kinase 1	Mus musculus	145-182
23373714-1	2013	BACKGROUND AND PURPOSE: Endoplasmic reticulum (ER) stress has been implicated in the pathogeneses of insulin resistance and type 2 diabetes, and extracellular signal-regulated kinase (ERK) antagonist is an insulin sensitizer that can restore muscle insulin responsiveness in both tunicamycin-treated muscle cells and type 2 diabetic mice.	Tunicamycin	280-291	mitogen-activated protein kinase 1	Mus musculus	184-187
23460517-4	2013	Hepatocyte-specific mutation of STAT3 prevented the induction of these secretory pathways during pneumonia, with similar results observed following pharmacological activation of ER stress by using tunicamycin.	Tunicamycin	197-208	signal transducer and activator of transcription 3	Mus musculus	32-37
23473976-6	2013	RESULTS: The result showed that tunicamycin activated p38 mitogen-activated protein kinase (MAPK), while inflammatory cytokines activated p38 MAPK and NFkappaB.	Tunicamycin	32-43	mitogen-activated protein kinase 14	Homo sapiens	54-90
23473976-6	2013	RESULTS: The result showed that tunicamycin activated p38 mitogen-activated protein kinase (MAPK), while inflammatory cytokines activated p38 MAPK and NFkappaB.	Tunicamycin	32-43	mitogen-activated protein kinase 14	Homo sapiens	54-57
23537656-8	2013	OxLDL stimulated apoE and CETP secretion, while tunicamycin determined a reduction of the secreted apoE and CETP, both in control and lipid-loaded macrophages.	Tunicamycin	48-59	apolipoprotein E	Homo sapiens	99-103
23537656-8	2013	OxLDL stimulated apoE and CETP secretion, while tunicamycin determined a reduction of the secreted apoE and CETP, both in control and lipid-loaded macrophages.	Tunicamycin	48-59	cholesteryl ester transfer protein	Homo sapiens	108-112
23537656-9	2013	The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages.	Tunicamycin	46-57	HDL3	Homo sapiens	16-20
23537656-9	2013	The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages.	Tunicamycin	46-57	eukaryotic translation initiation factor 2A	Homo sapiens	146-156
23537656-9	2013	The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages.	Tunicamycin	46-57	apolipoprotein E	Homo sapiens	215-219
23537656-9	2013	The addition of HDL3 to the culture medium of tunicamycin-treated cells induced: (i) the reduction of ER stress, expressed as decreased levels of eIF-2alpha and SAPK/JNK, and (ii) a partial recovery of the secreted apoE and CETP levels in lipid-loaded macrophages.	Tunicamycin	46-57	cholesteryl ester transfer protein	Homo sapiens	224-228
23261264-2	2013	Expression of VvACBP was detected in grape leaves exposed to tunicamycin-induced endoplasmic reticulum (ER) stress as well as cold and heat shock treatments.	Tunicamycin	61-72	acyl-CoA-binding domain-containing protein 3-like	Vitis vinifera	14-20
23364800-7	2013	Similarly, the induction of apoptosis was higher in tunicamycin-treated male mice, as measured by the activation of Bax and caspase-3.	Tunicamycin	52-63	BCL2-associated X protein	Mus musculus	116-119
23364800-7	2013	Similarly, the induction of apoptosis was higher in tunicamycin-treated male mice, as measured by the activation of Bax and caspase-3.	Tunicamycin	52-63	caspase 3	Mus musculus	124-133
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	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	78-83
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	AKT serine/threonine kinase 1	Homo sapiens	112-115
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
23385868-6	2013	Our results show that tunicamycin triggered ER stress in myoblasts and led to an increase in protein synthesis via a decorin-dependent pathway.	Tunicamycin	22-33	decorin	Homo sapiens	117-124
23638076-8	2013	We demonstrated that endoplasmic reticulum (ER) stress, an important mediator in diabetes-associated complications, was inducible in vitro in normal NK cells and that tunicamycin treatment resulted in a significant decrease in NKG2D expression (P&lt;0.05).	Tunicamycin	167-178	killer cell lectin like receptor K1	Homo sapiens	227-232
23403944-6	2013	Thapsigargin or tunicamycin was used to induce ER stress in human cells expressing the leptin receptor.	Tunicamycin	16-27	leptin	Homo sapiens	87-93
23756390-8	2013	Decreased COX-2 after GS-HCl was caused by N-glycosylation inhibition as much as tunicamycin.	Tunicamycin	81-92	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	10-15
23316062-6	2013	Interestingly, tunicamycin-induced cardiomyocyte mechanical anomalies and cell death were ablated by the CaMKII inhibitor KN93, in a manner reminiscent of catalase.	Tunicamycin	15-26	calcium/calmodulin-dependent protein kinase II gamma	Mus musculus	105-111
23313137-9	2013	Treatment with tunicamycin, an endoplasmic reticulum stress inducer, increased cleaved caspase-3 and -8 levels in Nogo-B KO MF-HSCs compared with WT MF-HSCs (P &lt; 0.01).	Tunicamycin	15-26	caspase 8	Mus musculus	87-103
23313137-9	2013	Treatment with tunicamycin, an endoplasmic reticulum stress inducer, increased cleaved caspase-3 and -8 levels in Nogo-B KO MF-HSCs compared with WT MF-HSCs (P &lt; 0.01).	Tunicamycin	15-26	reticulon 4	Mus musculus	114-120
23178931-9	2013	Cultured myotubes exhibited increased levels of PTP1B in response to tunicamycin treatment.	Tunicamycin	69-80	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	48-53
23178931-12	2013	However, tunicamycin-induced phosphorylation of eukaryotic initiation factor 2alpha and c-Jun NH(2)-terminal kinase-2 were significantly attenuated in the Ptp1b knockout mice.	Tunicamycin	9-20	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	155-160
23178931-13	2013	Treatment with TUDCA or silencing of PTP1B reversed tunicamycin-induced blunted myotube glucose uptake.	Tunicamycin	52-63	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	37-42
23270862-5	2013	A spontaneous onset of apoptotic cell death of granulosa cells was induced by thapsigargin or tunicamycin treatment in vitro, which was closely related to the increase of LRF, Luman, CCAAT/enhancer-binding protein homologous protein, and caspase-12 mRNA.	Tunicamycin	94-105	CREB3 regulatory factor	Mus musculus	171-174
23270862-5	2013	A spontaneous onset of apoptotic cell death of granulosa cells was induced by thapsigargin or tunicamycin treatment in vitro, which was closely related to the increase of LRF, Luman, CCAAT/enhancer-binding protein homologous protein, and caspase-12 mRNA.	Tunicamycin	94-105	cAMP responsive element binding protein 3	Mus musculus	176-181
23270862-5	2013	A spontaneous onset of apoptotic cell death of granulosa cells was induced by thapsigargin or tunicamycin treatment in vitro, which was closely related to the increase of LRF, Luman, CCAAT/enhancer-binding protein homologous protein, and caspase-12 mRNA.	Tunicamycin	94-105	caspase 12	Mus musculus	238-248
23242184-3	2013	Here we showed that ER stress induced by tunicamycin or thapsigargin suppressed inducible (CoCl(2) or hypoxia) transcription of erythropoietin (EPO), a representative HIF target gene, in HepG2.	Tunicamycin	41-52	erythropoietin	Rattus norvegicus	128-142
23242184-3	2013	Here we showed that ER stress induced by tunicamycin or thapsigargin suppressed inducible (CoCl(2) or hypoxia) transcription of erythropoietin (EPO), a representative HIF target gene, in HepG2.	Tunicamycin	41-52	erythropoietin	Rattus norvegicus	144-147
23242184-9	2013	Induction of ER stress in rat liver and kidney by tunicamycin decreased the hepatic and renal mRNA and plasma level of EPO.	Tunicamycin	50-61	erythropoietin	Rattus norvegicus	119-122
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	eukaryotic translation initiation factor 2A	Homo sapiens	71-80
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
23041155-4	2012	In mouse cultured hippocampal HT22 cells, imipramine inhibited cell death and caspase-3 activation induced by tunicamycin, although it did not alter the elevated expressions of 78 kDa glucose-regulated protein (GRP78) and C/EBP-homologous protein (CHOP).	Tunicamycin	110-121	caspase 3	Mus musculus	78-87
23123503-4	2013	Moreover, intraperitoneal injection of the ER stressor tunicamycin induced hepatic Fgf21 expression in mice and resulted in marked elevation of serum FGF21 levels.	Tunicamycin	55-66	fibroblast growth factor 21	Mus musculus	150-155
23379566-7	2013	The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription.	Tunicamycin	49-60	gastrin releasing peptide	Homo sapiens	18-21
23379566-7	2013	The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription.	Tunicamycin	49-60	X-box binding protein 1	Homo sapiens	92-96
23379566-7	2013	The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription.	Tunicamycin	49-60	activating transcription factor 4	Homo sapiens	98-102
23379566-7	2013	The expression of GRP in HL-7702 cells inhibited tunicamycin triggered ER stress-associated XBP1, ATF4, and TRAF2 mRNA transcription.	Tunicamycin	49-60	TNF receptor associated factor 2	Homo sapiens	108-113
23010535-4	2013	Here we report that activation of the UPR response by tunicamycin (TM), an ER stress inducer, leads to accumulation of p27 and G1 cell cycle arrest in melanoma cells.	Tunicamycin	54-65	dynactin subunit 6	Homo sapiens	119-122
23010535-4	2013	Here we report that activation of the UPR response by tunicamycin (TM), an ER stress inducer, leads to accumulation of p27 and G1 cell cycle arrest in melanoma cells.	Tunicamycin	67-69	dynactin subunit 6	Homo sapiens	119-122
23711492-5	2013	RESULTS: Elevated Klotho levels in HK-2 cells decreased expression of ER stress markers phospho--IRE1, XBP-1s, BiP, CHOP, pJNK, and phospho-p38, all of which were elevated in response to tunicamycin and/or thapsigargin.	Tunicamycin	187-198	klotho	Homo sapiens	18-24
23123503-4	2013	Moreover, intraperitoneal injection of the ER stressor tunicamycin induced hepatic Fgf21 expression in mice and resulted in marked elevation of serum FGF21 levels.	Tunicamycin	55-66	fibroblast growth factor 21	Mus musculus	83-88
23291236-7	2013	We demonstrated that lipin-1 expression was suppressed by the treatment with ER stress inducers (tunicamycin and thapsigargin) at transcriptional level.	Tunicamycin	97-108	lipin 1	Homo sapiens	21-28
23123183-9	2013	Administration of tunicamycin to wild-type mice caused intestinal ER stress, which increased when IL-10R1 was blocked.	Tunicamycin	18-29	interleukin 10 receptor, alpha	Mus musculus	98-105
23123183-10	2013	In LS174T cells, induction of ER stress with tunicamycin and misfolding of MUC2 were reduced by administration of IL-10; this reduction required STAT1 and STAT3.	Tunicamycin	45-56	interleukin 10	Homo sapiens	114-119
23123183-11	2013	In LS174T cells incubated with tunicamycin, IL-10 up-regulated genes involved in MUC2 folding and in ER-associated degradation and maintained correct folding of MUC2, its transport from the ER, and its O-glycosylation and secretion.	Tunicamycin	31-42	interleukin 10	Homo sapiens	44-49
23123183-11	2013	In LS174T cells incubated with tunicamycin, IL-10 up-regulated genes involved in MUC2 folding and in ER-associated degradation and maintained correct folding of MUC2, its transport from the ER, and its O-glycosylation and secretion.	Tunicamycin	31-42	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	81-85
23123183-11	2013	In LS174T cells incubated with tunicamycin, IL-10 up-regulated genes involved in MUC2 folding and in ER-associated degradation and maintained correct folding of MUC2, its transport from the ER, and its O-glycosylation and secretion.	Tunicamycin	31-42	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	161-165
23201481-5	2013	Thapsigargin induced retrotranslocation and rapid degradation of clusterin from the endoplasmic reticulum, whereas tunicamycin failed to degrade but rather retained clusterin in the endoplasmic reticulum.	Tunicamycin	115-126	clusterin	Homo sapiens	165-174
23106379-7	2013	hnRNP A1 mediates the increase of SREBP-1a protein level and SREBP-1a IRES activity in Hep G2 cells and in rat hepatocytes upon tunicamycin- and thapsigargin-induced ER stress.	Tunicamycin	128-139	heterogeneous nuclear ribonucleoprotein A1	Homo sapiens	0-8
23544152-5	2013	Tunicamycin or thapsigargin was injected into the intravitreal body of oxygen-induced retinopathy (OIR) model mice at postnatal day 14 (P14) and retinal neovascularization was quantified at P17.	Tunicamycin	0-11	family with sequence similarity 72, member A	Mus musculus	190-193
23544152-8	2013	Tunicamycin enhanced the expression of BiP in HRMEC at both the mRNA level and at the protein level on the cell surface, and increased the formation of a BiP/T-cadherin immunocomplex.	Tunicamycin	0-11	heat shock protein 5	Mus musculus	39-42
23544152-8	2013	Tunicamycin enhanced the expression of BiP in HRMEC at both the mRNA level and at the protein level on the cell surface, and increased the formation of a BiP/T-cadherin immunocomplex.	Tunicamycin	0-11	heat shock protein 5	Mus musculus	154-157
23544152-8	2013	Tunicamycin enhanced the expression of BiP in HRMEC at both the mRNA level and at the protein level on the cell surface, and increased the formation of a BiP/T-cadherin immunocomplex.	Tunicamycin	0-11	cadherin 13	Mus musculus	158-168
23457489-3	2013	Therefore, in order to explore the molecular mechanisms by which CLU inhibited ER stress-induced apoptosis, HCC cell lines were treated with tunicamycin (TN), an ER stress inducer.	Tunicamycin	141-152	clusterin	Homo sapiens	65-68
23457489-3	2013	Therefore, in order to explore the molecular mechanisms by which CLU inhibited ER stress-induced apoptosis, HCC cell lines were treated with tunicamycin (TN), an ER stress inducer.	Tunicamycin	154-156	clusterin	Homo sapiens	65-68
23437357-8	2013	In this study, eIF3a was down-regulated and recruited into stress granules by iron depletion as well as by the classical stress-inducers, hypoxia and tunicamycin.	Tunicamycin	150-161	eukaryotic translation initiation factor 3 subunit J	Homo sapiens	15-20
23359526-6	2013	14-3-3zeta overexpressing mice were potently protected against cell death caused by intracerebroventricular injection of the ER stressor tunicamycin.	Tunicamycin	137-148	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide	Mus musculus	0-10
22821029-9	2012	Real-time polymerase chain reaction revealed that ERGIC-53 along with several chaperone proteins was up-regulated after tunicamycin treatment; however, the expression of VIPL was unchanged.	Tunicamycin	120-131	lectin, mannose binding 1	Homo sapiens	50-58
22661239-9	2012	Furthermore, whilst hsp-4 was strongly induced by tunicamycin, pre-exposure of C. elegans to low doses of tunicamycin followed by ethanol was not sufficient to induce an additive ER stress response.	Tunicamycin	50-61	Endoplasmic reticulum chaperone BiP homolog;Heat shock 70 kDa protein D	Caenorhabditis elegans	20-25
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	mitogen-activated protein kinase 9	Homo sapiens	108-133
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	mitogen-activated protein kinase 9	Homo sapiens	135-139
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	231-234
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
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
22776647-9	2012	Similarly to the inhibition of OxPAPC effects, knockdown of miR-663 suppressed elevation of ATF4, VEGF and TRIB in response to another inducer of UPR, tunicamycin.	Tunicamycin	151-162	microRNA 663a	Homo sapiens	60-67
23041155-5	2012	Interestingly, in such cells application of imipramine normalized the expression of the sigma-1 receptor, which was decreased by treatment with tunicamycin alone.	Tunicamycin	144-155	sigma non-opioid intracellular receptor 1	Mus musculus	88-104
23041155-6	2012	Additionally, NE-100, a selective sigma-1 receptor antagonist, abolished the protective effect of imipramine against such tunicamycin-induced cell death.	Tunicamycin	122-133	sigma non-opioid intracellular receptor 1	Mus musculus	34-50
23041155-8	2012	Furthermore, in anesthetized mice intracerebroventricular administration of tunicamycin decreased the number of neuronal cells in the hippocampus, particularly in the CA1 and dentate gyrus (DG) areas, and 7 days" imipramine treatment (10mg/kg/day; i.p.)	Tunicamycin	76-87	carbonic anhydrase 1	Mus musculus	167-170
22893028-11	2012	In contrast, tunicamycin activated a balanced adaptive UPR in association with the maintenance of Xbp1 splicing.	Tunicamycin	13-24	X-box binding protein 1	Mus musculus	98-102
22841895-2	2012	In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation.	Tunicamycin	23-34	toll-like receptor 4	Mus musculus	117-120
22841895-2	2012	In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation.	Tunicamycin	23-34	nitric oxide synthase 2, inducible	Mus musculus	131-162
22841895-2	2012	In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation.	Tunicamycin	23-34	nitric oxide synthase 2, inducible	Mus musculus	164-168
22841895-2	2012	In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation.	Tunicamycin	36-38	toll-like receptor 4	Mus musculus	117-120
22841895-2	2012	In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation.	Tunicamycin	36-38	nitric oxide synthase 2, inducible	Mus musculus	131-162
22841895-2	2012	In this study we found tunicamycin (TM) and brefeldin A (BFA), two ER stressors, could attenuate lipopolysaccharide (LPS)-elicited inducible nitric oxide synthase (iNOS) gene expression in murine RAW264.7 macrophages, and this effect was not resulting from the effects on IKK or MAPKs activation.	Tunicamycin	36-38	nitric oxide synthase 2, inducible	Mus musculus	164-168
22923171-0	2012	Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis             is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13             proteins in Caki-2 renal carcinoma cells.	Tunicamycin	15-26	ADAM metallopeptidase domain 10	Homo sapiens	146-152
23028052-7	2012	In contrast, other forms of ER stress (e.g., tunicamycin treatment) promote IRF3 phosphorylation independently of stimulator of IFN gene and TANK-binding kinase 1.	Tunicamycin	45-56	interferon regulatory factor 3	Mus musculus	76-80
23028052-7	2012	In contrast, other forms of ER stress (e.g., tunicamycin treatment) promote IRF3 phosphorylation independently of stimulator of IFN gene and TANK-binding kinase 1.	Tunicamycin	45-56	TANK-binding kinase 1	Mus musculus	141-162
23028052-8	2012	Rather, IRF3 activation by tunicamycin and 2-deoxyglucose was inhibited by 4-(2-aminoethyl)-benzenesulfonyl fluoride hydrochloride, a serine protease inhibitor that blocks activating transcription factor 6 processing.	Tunicamycin	27-38	interferon regulatory factor 3	Mus musculus	8-12
22821197-6	2012	Treatment with tunicamycin, an inhibitor of protein glycosylation, led to the accumulation of the unglycosylated form of TMEM132A in inverse proportion to the glycosylated form; however, both forms were localized at the cell surface at almost equal rates.	Tunicamycin	15-26	transmembrane protein 132A	Homo sapiens	121-129
22923171-0	2012	Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis             is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13             proteins in Caki-2 renal carcinoma cells.	Tunicamycin	15-26	matrix metallopeptidase 9	Homo sapiens	154-159
22923171-0	2012	Suppression of tunicamycin-induced CD44v6 ectodomain shedding and apoptosis             is correlated with temporal expression patterns of active ADAM10, MMP-9 and MMP-13             proteins in Caki-2 renal carcinoma cells.	Tunicamycin	15-26	matrix metallopeptidase 13	Homo sapiens	164-170
22923171-3	2012	Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain.	Tunicamycin	21-32	caspase 3	Homo sapiens	87-96
22923171-3	2012	Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain.	Tunicamycin	21-32	poly(ADP-ribose) polymerase 1	Homo sapiens	98-104
22923171-3	2012	Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain.	Tunicamycin	34-36	caspase 3	Homo sapiens	87-96
22923171-3	2012	Exposure of cells to tunicamycin (TM)-induced apoptosis was accompanied by cleavage of caspase-3, PARP-1 and CD44v6 ectodomain.	Tunicamycin	34-36	poly(ADP-ribose) polymerase 1	Homo sapiens	98-104
22923171-5	2012	Furthermore, induction of matrix metallo-proteinase (MMP)-13, MMP-9 and ADAM10 expression was highly stimulated by tunicamycin in a time- and dose-dependent manner.	Tunicamycin	115-126	matrix metallopeptidase 9	Homo sapiens	62-67
22923171-5	2012	Furthermore, induction of matrix metallo-proteinase (MMP)-13, MMP-9 and ADAM10 expression was highly stimulated by tunicamycin in a time- and dose-dependent manner.	Tunicamycin	115-126	ADAM metallopeptidase domain 10	Homo sapiens	72-78
22959925-4	2012	Here, we investigated the role of Nrf2 in tunicamycin-induced ER stress using a murine insulinoma beta-cell line, betaTC-6.	Tunicamycin	42-53	nuclear factor, erythroid derived 2, like 2	Mus musculus	34-38
22959925-5	2012	shRNA-mediated silencing of Nrf2 expression in betaTC-6 cells significantly increased tunicamycin-induced cytotoxicity, elevated the expression of the pro-apoptotic ER stress marker Chop10, and inhibited tunicamycin-inducible expression of the proteasomal catalytic subunits Psmb5 and Psmb6.	Tunicamycin	86-97	nuclear factor, erythroid derived 2, like 2	Mus musculus	28-32
22959925-5	2012	shRNA-mediated silencing of Nrf2 expression in betaTC-6 cells significantly increased tunicamycin-induced cytotoxicity, elevated the expression of the pro-apoptotic ER stress marker Chop10, and inhibited tunicamycin-inducible expression of the proteasomal catalytic subunits Psmb5 and Psmb6.	Tunicamycin	204-215	nuclear factor, erythroid derived 2, like 2	Mus musculus	28-32
22959925-7	2012	D3T pretreatment reduced tunicamycin cytotoxicity and attenuated the tunicamycin-inducible Chop10 and protein kinase RNA-activated-like ER kinase (Perk).	Tunicamycin	69-80	DNA-damage inducible transcript 3	Mus musculus	91-97
22959925-7	2012	D3T pretreatment reduced tunicamycin cytotoxicity and attenuated the tunicamycin-inducible Chop10 and protein kinase RNA-activated-like ER kinase (Perk).	Tunicamycin	69-80	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	102-145
22959925-7	2012	D3T pretreatment reduced tunicamycin cytotoxicity and attenuated the tunicamycin-inducible Chop10 and protein kinase RNA-activated-like ER kinase (Perk).	Tunicamycin	69-80	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	147-151
22705154-3	2012	Here, we show that bestrophin-3 (Best-3), a protein previously associated with Ca(2+)-activated Cl(-) channel activity, is upregulated by the ER stressors, thapsigargin (TG), tunicamycin (TUN) and the toxic metal Cd(2+).	Tunicamycin	175-186	bestrophin 3	Rattus norvegicus	19-31
23000413-4	2012	In the present study, the results from the cell culture experiments were extended to show that tunicamycin-mediated ER stress in the liver in vivo also induces REDD1 gene expression.	Tunicamycin	95-106	DNA damage inducible transcript 4	Homo sapiens	160-165
23082053-3	2012	RESULTS: Tunicamycin and PNGase F treatment markedly inhibited Axl glycoprotein synthesis and expression, proliferation, invasion, and lymphatic metastasis both in vitro and in vivo.	Tunicamycin	9-20	AXL receptor tyrosine kinase	Mus musculus	63-66
22705154-3	2012	Here, we show that bestrophin-3 (Best-3), a protein previously associated with Ca(2+)-activated Cl(-) channel activity, is upregulated by the ER stressors, thapsigargin (TG), tunicamycin (TUN) and the toxic metal Cd(2+).	Tunicamycin	175-186	bestrophin 3	Rattus norvegicus	33-39
23038705-3	2012	We found that p53 ablation resulted in a profound sensitivity to tunicamycin that was associated with liver dysfunction, ground glass hepatocyte (GGH) development and nuclear atypia/dysplasia.	Tunicamycin	65-76	transformation related protein 53, pseudogene	Mus musculus	14-17
23038705-5	2012	Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism.	Tunicamycin	0-11	heat shock protein 5	Mus musculus	35-38
23038705-5	2012	Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism.	Tunicamycin	0-11	heat shock protein 5	Mus musculus	39-44
23038705-5	2012	Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism.	Tunicamycin	0-11	heat shock protein 90, beta (Grp94), member 1	Mus musculus	49-54
22821808-0	2012	Tunicamycin inhibits PDGF-BB-induced proliferation and migration of vascular smooth muscle cells through induction of HO-1.	Tunicamycin	0-11	heme oxygenase 1	Homo sapiens	118-122
22781655-4	2012	Retinal pigment epithelial (RPE) cells from alphaB crystallin (-/-) mice, and human RPE cells transfected with alphaB crystallin siRNA, are more vulnerable to ER stress induced by tunicamycin.	Tunicamycin	180-191	crystallin, alpha B	Mus musculus	111-128
23038705-7	2012	The cytoprotective effects of p53 were confirmed by cell viability studies, indicating that p53 deficiency conferred sensitivity against tunicamycin.	Tunicamycin	137-148	transformation related protein 53, pseudogene	Mus musculus	30-33
23038705-7	2012	The cytoprotective effects of p53 were confirmed by cell viability studies, indicating that p53 deficiency conferred sensitivity against tunicamycin.	Tunicamycin	137-148	transformation related protein 53, pseudogene	Mus musculus	92-95
22664345-4	2012	By preincubation with mPL, the cell viabilities were significantly increased in TM or TG treated cells, and caspase-12 activated cells induced by TM or TG treatment were significantly decreased.	Tunicamycin	80-82	myeloproliferative leukemia virus oncogene	Mus musculus	22-25
22664345-4	2012	By preincubation with mPL, the cell viabilities were significantly increased in TM or TG treated cells, and caspase-12 activated cells induced by TM or TG treatment were significantly decreased.	Tunicamycin	146-148	myeloproliferative leukemia virus oncogene	Mus musculus	22-25
22664345-4	2012	By preincubation with mPL, the cell viabilities were significantly increased in TM or TG treated cells, and caspase-12 activated cells induced by TM or TG treatment were significantly decreased.	Tunicamycin	146-148	caspase 12	Mus musculus	108-118
22956603-8	2012	Human SEMA4A mutants were expressed in zebrafish embryos with tunicamycin and mRNA of DNA damage-inducible transcript 3 (ddit3) was measured as an ER stress marker.	Tunicamycin	62-73	semaphorin 4A	Homo sapiens	6-12
22571197-5	2012	The lung cancer cell line A549, the gastric carcinoma cell line MKN1 and the immortal cell line HEK (human embryonic kidney)-293 exhibit reduced TGF-beta signalling when either treated with two inhibitors, including tunicamycin (a potent N-linked glycosylation inhibitor) and kifunensine [an inhibitor of ER (endoplasmic reticulum) and Golgi mannosidase I family members], or introduced with a non-glycosylated mutant version of TbetaRII.	Tunicamycin	216-227	transforming growth factor beta 1	Homo sapiens	145-153
22571197-5	2012	The lung cancer cell line A549, the gastric carcinoma cell line MKN1 and the immortal cell line HEK (human embryonic kidney)-293 exhibit reduced TGF-beta signalling when either treated with two inhibitors, including tunicamycin (a potent N-linked glycosylation inhibitor) and kifunensine [an inhibitor of ER (endoplasmic reticulum) and Golgi mannosidase I family members], or introduced with a non-glycosylated mutant version of TbetaRII.	Tunicamycin	216-227	transforming growth factor beta receptor 2	Homo sapiens	429-437
23038705-5	2012	Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism.	Tunicamycin	0-11	transformation related protein 53, pseudogene	Mus musculus	87-90
23038705-5	2012	Tunicamycin administration induced BiP/GRP78 and GRP94 expression more potently in the p53-deficient mice than in controls and elevated phosphatidylcholine, the major lipid of ER, by a p53-dependent mechanism.	Tunicamycin	0-11	transformation related protein 53, pseudogene	Mus musculus	185-188
22545589-6	2012	We examined whether the induction of ER stress using tunicamycin, thapsigargin, or palmitate alters the messenger RNA (mRNA) and protein expression of adiponectin and the mRNA expression of chaperones ERP44 and ERO1 in adult-derived human adipocyte stem (ADHAS) cells.	Tunicamycin	53-64	adiponectin, C1Q and collagen domain containing	Homo sapiens	151-162
22545589-6	2012	We examined whether the induction of ER stress using tunicamycin, thapsigargin, or palmitate alters the messenger RNA (mRNA) and protein expression of adiponectin and the mRNA expression of chaperones ERP44 and ERO1 in adult-derived human adipocyte stem (ADHAS) cells.	Tunicamycin	53-64	endoplasmic reticulum protein 44	Homo sapiens	201-206
22545589-9	2012	Our studies indicate that: (1) ER stress markers were increased to a higher degree using tunicamycin or thapsigargin compared to palmitate; (2) ER stress significantly decreased adiponectin mRNA in response to tunicamycin and thapsigargin, but palmitate did not decrease adiponectin mRNA levels.	Tunicamycin	89-100	adiponectin, C1Q and collagen domain containing	Homo sapiens	178-189
22545589-9	2012	Our studies indicate that: (1) ER stress markers were increased to a higher degree using tunicamycin or thapsigargin compared to palmitate; (2) ER stress significantly decreased adiponectin mRNA in response to tunicamycin and thapsigargin, but palmitate did not decrease adiponectin mRNA levels.	Tunicamycin	210-221	adiponectin, C1Q and collagen domain containing	Homo sapiens	178-189
22545589-9	2012	Our studies indicate that: (1) ER stress markers were increased to a higher degree using tunicamycin or thapsigargin compared to palmitate; (2) ER stress significantly decreased adiponectin mRNA in response to tunicamycin and thapsigargin, but palmitate did not decrease adiponectin mRNA levels.	Tunicamycin	210-221	adiponectin, C1Q and collagen domain containing	Homo sapiens	271-282
22430940-7	2012	In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively.	Tunicamycin	29-40	heat shock protein 5	Mus musculus	81-86
22430940-7	2012	In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively.	Tunicamycin	29-40	DNA-damage inducible transcript 3	Mus musculus	101-105
22430940-7	2012	In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively.	Tunicamycin	29-40	milk fat globule EGF and factor V/VIII domain containing	Mus musculus	107-110
22430940-7	2012	In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively.	Tunicamycin	29-40	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	178-183
22430940-7	2012	In vitro study revealed that tunicamycin significantly upregulated the levels of GRP78, p-eIF2alpha, CHOP, p47(phox) NADPH oxidase and 4-hydroxynonenal, which was exacerbated by ALDH2 knockdown and abolished by ALDH2 overexpression, respectively.	Tunicamycin	29-40	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	211-216
22430940-8	2012	Overexpression of ALDH2 abrogated tunicamycin-induced dephosphorylation Akt.	Tunicamycin	34-45	aldehyde dehydrogenase 2, mitochondrial	Mus musculus	18-23
22430940-8	2012	Overexpression of ALDH2 abrogated tunicamycin-induced dephosphorylation Akt.	Tunicamycin	34-45	thymoma viral proto-oncogene 1	Mus musculus	72-75
22573382-3	2012	In this study, we report lipid accumulation, sterol regulatory element-binding protein-2 (SREBP-2) expression, and ER stress in proximal tubules of kidneys from mice treated with the classic ER stressor tunicamycin (Tm) or in human renal biopsy specimens showing CsA-induced nephrotoxicity.	Tunicamycin	203-214	sterol regulatory element binding factor 2	Mus musculus	45-88
22573382-3	2012	In this study, we report lipid accumulation, sterol regulatory element-binding protein-2 (SREBP-2) expression, and ER stress in proximal tubules of kidneys from mice treated with the classic ER stressor tunicamycin (Tm) or in human renal biopsy specimens showing CsA-induced nephrotoxicity.	Tunicamycin	216-218	sterol regulatory element binding factor 2	Mus musculus	90-97
22573382-3	2012	In this study, we report lipid accumulation, sterol regulatory element-binding protein-2 (SREBP-2) expression, and ER stress in proximal tubules of kidneys from mice treated with the classic ER stressor tunicamycin (Tm) or in human renal biopsy specimens showing CsA-induced nephrotoxicity.	Tunicamycin	216-218	heat shock protein family A (Hsp70) member 9	Homo sapiens	263-266
22742743-10	2012	Using the DPAGT1-specific inhibitor tunicamycin, we show that DPAGT1 is required for efficient glycosylation of acetylcholine-receptor subunits and for efficient export of acetylcholine receptors to the cell surface.	Tunicamycin	36-47	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	10-16
22742743-10	2012	Using the DPAGT1-specific inhibitor tunicamycin, we show that DPAGT1 is required for efficient glycosylation of acetylcholine-receptor subunits and for efficient export of acetylcholine receptors to the cell surface.	Tunicamycin	36-47	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	62-68
22539597-8	2012	Infusion of tunicamycin in control mice induced ER stress in aorta and MRA, and reduced EDR by a TGF-beta1-dependent mechanism in aorta and reactive oxygen species-dependent mechanism in MRA.	Tunicamycin	12-23	transforming growth factor, beta 1	Mus musculus	97-106
22852048-4	2012	Toyocamycin was shown to suppress thapsigargin-, tunicamycin- and 2-deoxyglucose-induced XBP1 mRNA splicing in HeLa cells without affecting activating transcription factor 6 (ATF6) and PKR-like ER kinase (PERK) activation.	Tunicamycin	49-60	X-box binding protein 1	Homo sapiens	89-93
22426894-0	2012	Tunicamycin sensitizes human prostate cells to TRAIL-induced apoptosis             by upregulation of TRAIL receptors and downregulation of cIAP2.	Tunicamycin	0-11	TNF superfamily member 10	Homo sapiens	47-52
22740470-5	2012	The important ER stress regulator 78 kDa glucose-regulated protein (GRP-78 or BiP) was highly upregulated together with several proteins that have been found to form a multiprotein complex with BiP including cyclophilin B, DnaJ homolog subfamily B member 11, endoplasmin, hypoxia upregulated protein 1, protein disulfide isomerase and protein disulfide isomerase A4 upon tunicamycin-induced ER stress.	Tunicamycin	371-382	heat shock protein family A (Hsp70) member 5	Homo sapiens	68-74
22740470-5	2012	The important ER stress regulator 78 kDa glucose-regulated protein (GRP-78 or BiP) was highly upregulated together with several proteins that have been found to form a multiprotein complex with BiP including cyclophilin B, DnaJ homolog subfamily B member 11, endoplasmin, hypoxia upregulated protein 1, protein disulfide isomerase and protein disulfide isomerase A4 upon tunicamycin-induced ER stress.	Tunicamycin	371-382	heat shock protein family A (Hsp70) member 5	Homo sapiens	78-81
22740470-5	2012	The important ER stress regulator 78 kDa glucose-regulated protein (GRP-78 or BiP) was highly upregulated together with several proteins that have been found to form a multiprotein complex with BiP including cyclophilin B, DnaJ homolog subfamily B member 11, endoplasmin, hypoxia upregulated protein 1, protein disulfide isomerase and protein disulfide isomerase A4 upon tunicamycin-induced ER stress.	Tunicamycin	371-382	heat shock protein family A (Hsp70) member 5	Homo sapiens	194-197
22740470-6	2012	Furthermore, seven aminoacyl-tRNA synthetases and five proteins belonging to the Sec61 complex were increased in response to tunicamycin-induced ER stress.	Tunicamycin	125-136	SEC61 translocon subunit alpha 1	Homo sapiens	81-86
22497927-8	2012	Tunicamycin, a classical ER stress inductor, also impaired ABCA-1 expression and cholesterol efflux (showing a decrease of 61% and 82%, respectively), confirming the deleterious effect of ER stress in macrophage cholesterol accumulation.	Tunicamycin	0-11	ATP binding cassette subfamily A member 1	Homo sapiens	59-65
22459357-0	2012	Tunicamycin produces TDP-43 cytoplasmic inclusions in cultured brain organotypic slices.	Tunicamycin	0-11	TAR DNA binding protein	Mus musculus	21-27
22459357-10	2012	The induction of TDP-43 cytoplasmic translocation in cerebrocortical slice cultures by tunicamycin provides a platform for further mechanistic investigations of pathological processing of TDP-43.	Tunicamycin	87-98	TAR DNA binding protein	Mus musculus	17-23
22459357-10	2012	The induction of TDP-43 cytoplasmic translocation in cerebrocortical slice cultures by tunicamycin provides a platform for further mechanistic investigations of pathological processing of TDP-43.	Tunicamycin	87-98	TAR DNA binding protein	Mus musculus	188-194
25657664-0	2012	Low levels of Bax inhibitor-1 gene expression increase tunicamycin-induced apoptosis in human neuroblastoma SY5Y cells.	Tunicamycin	55-66	transmembrane BAX inhibitor motif containing 6	Homo sapiens	14-29
25657664-2	2012	In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment.	Tunicamycin	26-37	transmembrane BAX inhibitor motif containing 6	Homo sapiens	120-135
25657664-2	2012	In control SH-SY5Y cells, tunicamycin treatment induced endoplasmic reticulum stress-mediated apoptosis; however, after Bax inhibitor-1 gene knockdown, cell survival rates were significantly decreased and the degree of apoptosis was significantly increased following tunicamycin treatment.	Tunicamycin	267-278	transmembrane BAX inhibitor motif containing 6	Homo sapiens	120-135
22511781-3	2012	We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1.	Tunicamycin	71-82	mitofusin 2	Mus musculus	140-144
22511781-3	2012	We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1.	Tunicamycin	71-82	OPA1, mitochondrial dynamin like GTPase	Mus musculus	245-249
22511781-3	2012	We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1.	Tunicamycin	71-82	collapsin response mediator protein 1	Mus musculus	251-255
22511781-3	2012	We report here that induction of ER stress with either thapsigargin or tunicamycin in mouse embryonic fibroblasts leads to up-regulation of Mfn2 mRNA and protein levels with no change in the expression of the mitochondrial shaping factors Mfn1, Opa1, Drp1, and Fis1.	Tunicamycin	71-82	fission, mitochondrial 1	Mus musculus	261-265
21922249-11	2012	GRP78 expression and xbp-1 mRNA splicing were enhanced significantly in the presence of IFN-gamma/TNF-alpha and tunicamycin, and they could be dampened by BBR.	Tunicamycin	112-123	heat shock protein family A (Hsp70) member 5	Homo sapiens	0-5
21922249-11	2012	GRP78 expression and xbp-1 mRNA splicing were enhanced significantly in the presence of IFN-gamma/TNF-alpha and tunicamycin, and they could be dampened by BBR.	Tunicamycin	112-123	X-box binding protein 1	Homo sapiens	21-26
22426894-0	2012	Tunicamycin sensitizes human prostate cells to TRAIL-induced apoptosis             by upregulation of TRAIL receptors and downregulation of cIAP2.	Tunicamycin	0-11	TNF superfamily member 10	Homo sapiens	102-107
22532439-5	2012	Spontaneous apoptosis was also observed in vitro in granulosa cells induced by serum deprivation or by the ER stress agent tunicamycin, both inducing similar increases in DDIT3 mRNA.	Tunicamycin	123-134	DNA damage-inducible transcript 3 protein	Capra hircus	171-176
22699051-4	2012	The expressions of Bax, Bcl-2, and GRP78 in cells treated with 3 micromol/L tunicamycin with or without 6.00 micromol/L cisplatin were measured with Western blotting.	Tunicamycin	76-87	BCL2 associated X, apoptosis regulator	Homo sapiens	19-22
22699051-4	2012	The expressions of Bax, Bcl-2, and GRP78 in cells treated with 3 micromol/L tunicamycin with or without 6.00 micromol/L cisplatin were measured with Western blotting.	Tunicamycin	76-87	heat shock protein family A (Hsp70) member 5	Homo sapiens	35-40
22699051-9	2012	Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3.	Tunicamycin	14-25	caspase 3	Homo sapiens	233-242
22699051-9	2012	Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3.	Tunicamycin	154-165	heat shock protein family A (Hsp70) member 5	Homo sapiens	197-203
22699051-9	2012	Compared with tunicamycin and cisplatin alone, the combined treatment significantly increased Bax expression and decreased Bcl-2 expression in the cells; tunicamycin up-regulated the expression of GRP-78 and enhanced the activity of caspase-3.	Tunicamycin	154-165	caspase 3	Homo sapiens	233-242
22699051-10	2012	CONCLUSION: Tunicamycin can inhibit the proliferation of CNE-1 and CNE-2 cells and enhance cisplatin-induced cell death, the mechanism of which may involve excessive endoplasmic reticulum stress response and increased activity of caspase-3.	Tunicamycin	12-23	caspase 3	Homo sapiens	230-239
22335396-1	2012	Arabidopsis bZIP28, an ER membrane-associated transcription factor, is activated in response to conditions that induce ER stress-adverse environmental conditions or exposure to ER stress agents such as tunicamycin and dithiothreitol.	Tunicamycin	202-213	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	12-18
22524620-6	2012	Treatments of hPBMCs with tunicamycin and deglycosylation enzymes that removed the carbohydrate moieties reduced the secretion of IFN-gamma induction from hPBMCs.	Tunicamycin	26-37	interferon gamma	Homo sapiens	130-139
22328531-7	2012	The Orm2 protein level responds to ER stress conditions, increasing when cells are treated with tunicamycin or DTT, agents that induce the unfolded protein response (UPR).	Tunicamycin	96-107	sphingolipid homeostasis protein ORM2	Saccharomyces cerevisiae S288C	4-8
22593433-1	2012	BACKGROUND/AIM: Blocking N-glycosylation of the epidermal growth factor receptor (EGFR) by tunicamycin inhibits its cellular accumulation.	Tunicamycin	91-102	epidermal growth factor receptor	Cricetulus griseus	48-80
22593433-1	2012	BACKGROUND/AIM: Blocking N-glycosylation of the epidermal growth factor receptor (EGFR) by tunicamycin inhibits its cellular accumulation.	Tunicamycin	91-102	epidermal growth factor receptor	Cricetulus griseus	82-86
22426894-0	2012	Tunicamycin sensitizes human prostate cells to TRAIL-induced apoptosis             by upregulation of TRAIL receptors and downregulation of cIAP2.	Tunicamycin	0-11	baculoviral IAP repeat containing 3	Homo sapiens	140-145
22426894-1	2012	The addition of tunicamycin to prostate cancer cells enhances cell death mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Tunicamycin	16-27	TNF superfamily member 10	Homo sapiens	85-140
22426894-1	2012	The addition of tunicamycin to prostate cancer cells enhances cell death mediated by tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).	Tunicamycin	16-27	TNF superfamily member 10	Homo sapiens	142-147
22426894-2	2012	In this study, we investigated whether tunicamycin, an endoplasmic reticulum stress inducer, can potentiate TRAIL-induced apoptosis in human prostate cancer cells.	Tunicamycin	39-50	TNF superfamily member 10	Homo sapiens	108-113
22426894-4	2012	The combined treatment with tunicamycin and TRAIL significantly induced apoptosis, and stimulated caspase-3, -8 and -9 activity, as well as the cleavage of poly (ADP-ribose) polymerase.	Tunicamycin	28-39	caspase 3	Homo sapiens	98-118
22426894-4	2012	The combined treatment with tunicamycin and TRAIL significantly induced apoptosis, and stimulated caspase-3, -8 and -9 activity, as well as the cleavage of poly (ADP-ribose) polymerase.	Tunicamycin	28-39	poly(ADP-ribose) polymerase 1	Homo sapiens	156-184
22426894-5	2012	We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2).	Tunicamycin	14-25	TNF superfamily member 10	Homo sapiens	35-40
22426894-5	2012	We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2).	Tunicamycin	14-25	TNF receptor superfamily member 10a	Homo sapiens	82-102
22426894-5	2012	We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2).	Tunicamycin	14-25	baculoviral IAP repeat containing 3	Homo sapiens	137-170
22426894-5	2012	We found that tunicamycin promoted TRAIL-induced apoptosis by the upregulation of death receptor (DR)4 and DR5 and the downregulation of cellular inhibitor of apoptosis 2 (cIAP2).	Tunicamycin	14-25	baculoviral IAP repeat containing 3	Homo sapiens	172-177
22374970-6	2012	Strikingly, exposure of HepG2 cells to prolonged mild ER stress activation induced by low levels of thapsigargin, tunicamycin, or palmitate augmented insulin-stimulated Akt phosphorylation.	Tunicamycin	114-125	insulin	Homo sapiens	150-157
22466652-7	2012	Treating WT mice with the ER stressor tunicamycin led to marked repression of hepatic sortilin-1 expression, while administration of the chemical chaperone PBA to ob/ob mice led to amelioration of ER stress, increased sortilin-1 expression, and reduced apoB and triglyceride secretion.	Tunicamycin	38-49	sortilin 1	Mus musculus	86-96
22326432-7	2012	In cultured cardiac myocytes, treatment with the ER stressor, tunicamycin, or with adenovirus encoding activated ATF6 decreased miR-455 and increased Calr levels, consistent with the effects of ATF6 on miR-455 and Calr, in vivo.	Tunicamycin	62-73	microRNA 455	Mus musculus	128-135
22326432-7	2012	In cultured cardiac myocytes, treatment with the ER stressor, tunicamycin, or with adenovirus encoding activated ATF6 decreased miR-455 and increased Calr levels, consistent with the effects of ATF6 on miR-455 and Calr, in vivo.	Tunicamycin	62-73	calreticulin	Mus musculus	150-154
22326432-7	2012	In cultured cardiac myocytes, treatment with the ER stressor, tunicamycin, or with adenovirus encoding activated ATF6 decreased miR-455 and increased Calr levels, consistent with the effects of ATF6 on miR-455 and Calr, in vivo.	Tunicamycin	62-73	calreticulin	Mus musculus	214-218
22648618-6	2012	In vivo retinal damage in mice following intravitreous injection of tunicamycin was evaluated by counting the cell numbers in the ganglion cell layer (GCL) and measuring the thickness of outer nuclear layer (ONL).	Tunicamycin	68-79	germ cell-less, spermatogenesis associated 1	Mus musculus	151-154
22648618-10	2012	A-ext., bixin, and Bx-1 significantly inhibited the tunicamycin-induced loss of cells from the GCL, and these materials also suppressed the tunicamycin-induced thinning of ONL.	Tunicamycin	52-63	germ cell-less, spermatogenesis associated 1	Mus musculus	95-98
22190710-6	2012	Tunicamycin, an ER stress inducer, induced active XBP1 protein in nuclei of 4-cell embryos.	Tunicamycin	0-11	X-box binding protein 1	Homo sapiens	50-54
22427561-9	2012	GlcN and tunicamycin reduced the molecular mass of TNF-alpha-induced ICAM-1 in ARPE-19 cells.	Tunicamycin	9-20	tumor necrosis factor	Homo sapiens	51-60
22427561-9	2012	GlcN and tunicamycin reduced the molecular mass of TNF-alpha-induced ICAM-1 in ARPE-19 cells.	Tunicamycin	9-20	intercellular adhesion molecule 1	Homo sapiens	69-75
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.	Tunicamycin	97-108	prostaglandin-endoperoxide synthase 2	Homo sapiens	32-37
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.	Tunicamycin	97-108	prostaglandin-endoperoxide synthase 2	Homo sapiens	59-64
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.	Tunicamycin	97-108	prostaglandin-endoperoxide synthase 2	Homo sapiens	59-64
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	prostaglandin-endoperoxide synthase 2	Homo sapiens	92-97
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.	Tunicamycin	33-44	BCL2 apoptosis regulator	Homo sapiens	197-202
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	BCL2 associated X, apoptosis regulator	Homo sapiens	203-206
22442073-4	2012	Inhibiting glycosylation with tunicamycin reduced ASIC1a surface trafficking, dendritic targeting, and acid-activated current density.	Tunicamycin	30-41	acid-sensing (proton-gated) ion channel 1	Mus musculus	50-56
22215650-9	2012	Tunicamycin significantly upregulated IL-12p40 expression in adipocytes, and IL-12 addition increased ER stress gene expression; conversely, LSF, an IL-12 signaling inhibitor, and an IL-12p40-neutralizing antibody attenuated tunicamycin-induced ER stress.	Tunicamycin	0-11	interleukin 12b	Mus musculus	38-46
22215650-9	2012	Tunicamycin significantly upregulated IL-12p40 expression in adipocytes, and IL-12 addition increased ER stress gene expression; conversely, LSF, an IL-12 signaling inhibitor, and an IL-12p40-neutralizing antibody attenuated tunicamycin-induced ER stress.	Tunicamycin	225-236	interleukin 12b	Mus musculus	183-191
22215680-9	2012	Further, ER stress-inducing agents, including tunicamycin and thapsigargin, induced the expression of CSE in ATF4(+/+) MEFs.	Tunicamycin	46-57	cystathionase (cystathionine gamma-lyase)	Mus musculus	102-105
22215680-9	2012	Further, ER stress-inducing agents, including tunicamycin and thapsigargin, induced the expression of CSE in ATF4(+/+) MEFs.	Tunicamycin	46-57	activating transcription factor 4	Mus musculus	109-113
22215680-10	2012	Consistent with ATF4(-/-) MEFs, CSE(-/-) MEFs showed significantly greater apoptosis when treated with tunicamycin, thapsigargin, and l-Hcy, compared with CSE(+/+) MEFs.	Tunicamycin	103-114	cystathionase (cystathionine gamma-lyase)	Mus musculus	32-35
21790829-8	2012	In human neuroblastoma cells exposed to Abeta, tunicamycin or H2O2, PACT and pPKR concentrations are increased.	Tunicamycin	47-58	amyloid beta precursor protein	Homo sapiens	40-45
21790829-8	2012	In human neuroblastoma cells exposed to Abeta, tunicamycin or H2O2, PACT and pPKR concentrations are increased.	Tunicamycin	47-58	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	68-72
22219379-6	2012	Kar2p-sfGFP mobility decreases upon treatment with tunicamycin or dithiothreitol, consistent with increased levels of unfolded proteins and the incorporation of Kar2p-sfGFP into slower-diffusing complexes.	Tunicamycin	51-62	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	0-5
22219379-6	2012	Kar2p-sfGFP mobility decreases upon treatment with tunicamycin or dithiothreitol, consistent with increased levels of unfolded proteins and the incorporation of Kar2p-sfGFP into slower-diffusing complexes.	Tunicamycin	51-62	Hsp70 family ATPase KAR2	Saccharomyces cerevisiae S288C	161-166
22323590-5	2012	After SMCs were exposed to A23187, thapsigargin, or tunicamycin, intracellular calcium level was increased, and CSE translocated from the cytosol to mitochondria.	Tunicamycin	52-63	cystathionine gamma-lyase	Homo sapiens	112-115
22227571-8	2012	Corroborating this, tunicamycin, a selective inhibitor of N-linked glycosylation, abolished MICA/B surface expression without compromising activation of MICA promoter activity.	Tunicamycin	20-31	MHC class I polypeptide-related sequence A	Homo sapiens	92-96
22281494-2	2012	Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes.	Tunicamycin	29-40	insulin	Homo sapiens	80-87
22281494-2	2012	Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes.	Tunicamycin	29-40	insulin receptor substrate 1	Homo sapiens	125-130
22281494-2	2012	Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes.	Tunicamycin	29-40	mechanistic target of rapamycin kinase	Homo sapiens	178-182
22281494-2	2012	Pretreatment with 5mug/ml of tunicamycin or 600nM thapsigargin for 3h decreased insulin-mediated tyrosine phosphorylation of IRS-1 and glucose uptake, and increased the level of mTOR/S6K1 phosphorylation in L6 myotubes.	Tunicamycin	29-40	ribosomal protein S6 kinase B1	Homo sapiens	183-187
21909975-3	2011	In vitro, IMD(1-53) (10(-9), 10(-8), and 10(-7) mol/l) directly inhibited the upregulation of ERS markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein, and caspase-12 induced by the ERS inducers tunicamycin (Tm, 10 mg/ml) or dithiothreitol (DTT, 2 mmol/l) in cardiac tissue.	Tunicamycin	238-249	adrenomedullin 2	Rattus norvegicus	10-13
22063270-9	2012	Furthermore, over-expression of NSMase2 in ER-stressed BAEC lowered cholesterol levels to within control levels as well as nearly doubled the NO production, restoring it to ~74% and 68% of controls using tunicamycin and palmitate, respectively.	Tunicamycin	204-215	sphingomyelin phosphodiesterase 3	Homo sapiens	32-39
22006247-6	2012	RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt).	Tunicamycin	50-61	insulin	Homo sapiens	72-79
22006247-6	2012	RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt).	Tunicamycin	50-61	thymoma viral proto-oncogene 1	Mus musculus	109-112
22006247-6	2012	RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt).	Tunicamycin	50-61	thymoma viral proto-oncogene 1	Mus musculus	117-120
22006247-6	2012	RESULTS: Incubation of myotubes with palmitate or tunicamycin inhibited insulin-stimulated protein kinase B (PKB)/ v-akt murine thymoma viral oncogene homologue 1 (Akt).	Tunicamycin	50-61	thymoma viral proto-oncogene 1	Mus musculus	164-167
22006247-10	2012	Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation.	Tunicamycin	8-19	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	55-82
22006247-10	2012	Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation.	Tunicamycin	8-19	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	84-89
22006247-10	2012	Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation.	Tunicamycin	8-19	mitogen-activated protein kinase 8	Homo sapiens	118-121
22006247-10	2012	Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation.	Tunicamycin	8-19	insulin receptor substrate 1	Homo sapiens	169-197
22006247-10	2012	Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation.	Tunicamycin	8-19	insulin receptor substrate 1	Homo sapiens	199-204
22006247-10	2012	Indeed, tunicamycin induced a robust activation of the inositol-requiring enzyme 1 (IRE-1)/c-JUN NH2-terminal kinase (JNK) pathway, leading to serine phosphorylation of insulin receptor substrate 1 (IRS-1) and a decrease in IRS-1 tyrosine phosphorylation.	Tunicamycin	8-19	insulin receptor substrate 1	Homo sapiens	224-229
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	119-125
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	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	127-136
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
22550476-7	2012	While glucolipotoxicity/tunicamycin increased oxidative stress, ER stress, mRNA expression of TRPC-6, and programmed the THP-1 monocytes towards apoptosis, all these molecular perturbations were resisted by PBA.	Tunicamycin	24-35	transient receptor potential cation channel subfamily C member 6	Homo sapiens	94-100
22550476-7	2012	While glucolipotoxicity/tunicamycin increased oxidative stress, ER stress, mRNA expression of TRPC-6, and programmed the THP-1 monocytes towards apoptosis, all these molecular perturbations were resisted by PBA.	Tunicamycin	24-35	GLI family zinc finger 2	Homo sapiens	121-126
23251594-12	2012	Finally, ER stress induced by tunicamycin was ameliorated by mechanical strain as demonstrated by decreased C/EBPbeta, increased BiP and decreased CHOP protein expression.	Tunicamycin	30-41	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	108-117
23251594-12	2012	Finally, ER stress induced by tunicamycin was ameliorated by mechanical strain as demonstrated by decreased C/EBPbeta, increased BiP and decreased CHOP protein expression.	Tunicamycin	30-41	heat shock protein 5	Mus musculus	129-132
23251594-12	2012	Finally, ER stress induced by tunicamycin was ameliorated by mechanical strain as demonstrated by decreased C/EBPbeta, increased BiP and decreased CHOP protein expression.	Tunicamycin	30-41	DNA-damage inducible transcript 3	Mus musculus	147-151
23209735-12	2012	The significant enhancement in PERK, ATF6 phosphorylated IRE1, BiP and cleaved caspase-3 expression induced by brefeldin A and tunicamycin was partly prevented by glutamine.	Tunicamycin	127-138	activating transcription factor 6	Rattus norvegicus	37-41
23209735-12	2012	The significant enhancement in PERK, ATF6 phosphorylated IRE1, BiP and cleaved caspase-3 expression induced by brefeldin A and tunicamycin was partly prevented by glutamine.	Tunicamycin	127-138	growth differentiation factor 10	Rattus norvegicus	63-66
23209735-12	2012	The significant enhancement in PERK, ATF6 phosphorylated IRE1, BiP and cleaved caspase-3 expression induced by brefeldin A and tunicamycin was partly prevented by glutamine.	Tunicamycin	127-138	caspase 3	Rattus norvegicus	79-88
22912727-7	2012	Interestingly, nuclear translocation of procaspase-3 (proCASP3) was observed in cells either overexpressing TRB3 or under tunicamycin-induced ER stress.	Tunicamycin	122-133	caspase 3	Homo sapiens	40-52
22912727-7	2012	Interestingly, nuclear translocation of procaspase-3 (proCASP3) was observed in cells either overexpressing TRB3 or under tunicamycin-induced ER stress.	Tunicamycin	122-133	caspase 3	Homo sapiens	54-62
22815824-8	2012	Compared with wild type mice, CHOP-/- mice showed an enhanced hippocampal cell apoptosis, worse performance in memory-related behavioral tests, and attenuated IRE-1 expression under tunicamycin treatment.	Tunicamycin	182-193	DNA-damage inducible transcript 3	Mus musculus	30-34
22815824-8	2012	Compared with wild type mice, CHOP-/- mice showed an enhanced hippocampal cell apoptosis, worse performance in memory-related behavioral tests, and attenuated IRE-1 expression under tunicamycin treatment.	Tunicamycin	182-193	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	159-164
22662196-5	2012	COS-7 cells transfected with chIL2/15Rbeta produced proteins of approximately 75 and 62.5 kDa under normal and tunicamycin-treated conditions, respectively.	Tunicamycin	111-122	chitinase 3 like 2	Homo sapiens	29-34
22359644-10	2012	Consistently, IRE1a is preferentially required for bZIP60 splicing upon pathogen infection, while IRE1b plays a major role in bZIP60 processing upon Tunicamycin (Tm)-induced stress.	Tunicamycin	149-160	inositol requiring 1-1	Arabidopsis thaliana	98-103
22359644-10	2012	Consistently, IRE1a is preferentially required for bZIP60 splicing upon pathogen infection, while IRE1b plays a major role in bZIP60 processing upon Tunicamycin (Tm)-induced stress.	Tunicamycin	149-160	basic region/leucine zipper motif 60	Arabidopsis thaliana	126-132
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	113-117
21954231-6	2012	Treatment of neuronal cells with ER stress insults, tunicamycin and thapsigargin, increased mtHTT aggregation via IRE1 activation.	Tunicamycin	52-63	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	114-118
22460328-4	2012	Here hyperphosphorylation of tau, activation of glycogen synthase kinase-3beta (GSK-3beta), and elevation of Bip were induced by ventricular infusion of ER stressors, tunicamycin (TM) and thapsigargin (TG), in rats.	Tunicamycin	167-178	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	109-112
22460328-4	2012	Here hyperphosphorylation of tau, activation of glycogen synthase kinase-3beta (GSK-3beta), and elevation of Bip were induced by ventricular infusion of ER stressors, tunicamycin (TM) and thapsigargin (TG), in rats.	Tunicamycin	180-182	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	109-112
22859938-6	2012	Tunicamycin or brefeldin A, two ER stress inducers, increased p53 expression in MCF-7 and Hela cells.	Tunicamycin	0-11	tumor protein p53	Homo sapiens	62-65
22808162-7	2012	Tunicamycin (TM), an ER stress inducer used as a positive control, promoted an increase in the density of nuclear XBP-1 at the one-cell and two-cell stages.	Tunicamycin	0-11	X-box binding protein 1	Mus musculus	114-119
22808162-9	2012	Conversely, high concentrations of TM or sorbitol led to reduced nuclear XBP-1 density and significant ER stress-induced apoptosis.	Tunicamycin	35-37	X-box binding protein 1	Mus musculus	73-78
22662254-8	2012	In 3T3-L1 adipocytes, 11beta-HSD1 mRNA levels were down-regulated following induction of ER stress by tunicamycin but were up-regulated following inhibition of mTOR by rapamycin.	Tunicamycin	102-113	hydroxysteroid 11-beta dehydrogenase 1	Mus musculus	22-33
22936838-2	2012	Its impairment by tunicamycin [a competitive inhibitor of N-acetylglucosaminyl 1-phosphate transferase (GPT)] has been known to inhibit neo-vascularization (i.e., angiogenesis) in humanized breast tumor due to an induction of ER stress-mediated unfolded protein response (UPR).	Tunicamycin	18-29	glutamic--pyruvic transaminase	Homo sapiens	104-107
22192458-9	2011	RESULTS: Tunicamycin treatment of ALK-positive NB cells resulted in a hypoglycosylated ALK band and in decreased amounts of mature full size receptor.	Tunicamycin	9-20	ALK receptor tyrosine kinase	Homo sapiens	34-37
22192458-9	2011	RESULTS: Tunicamycin treatment of ALK-positive NB cells resulted in a hypoglycosylated ALK band and in decreased amounts of mature full size receptor.	Tunicamycin	9-20	ALK receptor tyrosine kinase	Homo sapiens	87-90
22013072-5	2011	Down-regulation of CerS6/C(16)-ceramide, and not its further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).	Tunicamycin	165-176	ceramide synthase 6	Homo sapiens	19-24
22013072-5	2011	Down-regulation of CerS6/C(16)-ceramide, and not its further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).	Tunicamycin	165-176	activating transcription factor 6	Homo sapiens	120-125
22013072-6	2011	Induction of WT-CerS6 expression, but not its mutant, or ectopic expression of the dominant-negative mutant form of ATF-6 protected cells from apoptosis in response to CerS6 knockdown and tunicamycin or SAHA treatment.	Tunicamycin	188-199	activating transcription factor 6	Homo sapiens	116-121
21909975-3	2011	In vitro, IMD(1-53) (10(-9), 10(-8), and 10(-7) mol/l) directly inhibited the upregulation of ERS markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein, and caspase-12 induced by the ERS inducers tunicamycin (Tm, 10 mg/ml) or dithiothreitol (DTT, 2 mmol/l) in cardiac tissue.	Tunicamycin	251-253	adrenomedullin 2	Rattus norvegicus	10-13
21986529-8	2011	In addition, chromatin immunoprecipitation analysis demonstrated that both tunicamycin treatment and ATF3 overexpression inhibited the recruitment of p300 to PDX-1 on the insulin promoter in MIN6N8 cells.	Tunicamycin	75-86	E1A binding protein p300	Mus musculus	150-154
21986529-8	2011	In addition, chromatin immunoprecipitation analysis demonstrated that both tunicamycin treatment and ATF3 overexpression inhibited the recruitment of p300 to PDX-1 on the insulin promoter in MIN6N8 cells.	Tunicamycin	75-86	pancreatic and duodenal homeobox 1	Mus musculus	158-163
21542787-2	2011	RESULTS: Wild-type and transgenic mice with cardiac-specific overexpression of the active mutant of Akt (Myr-Akt) were subjected to the ER stress inducer tunicamycin (1 or 3 mg/kg).	Tunicamycin	154-165	thymoma viral proto-oncogene 1	Mus musculus	100-103
21542787-6	2011	Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA.	Tunicamycin	15-26	thymoma viral proto-oncogene 1	Mus musculus	49-52
21542787-6	2011	Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA.	Tunicamycin	15-26	glycogen synthase kinase 3 beta	Mus musculus	79-109
21542787-6	2011	Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA.	Tunicamycin	15-26	glycogen synthase kinase 3 beta	Mus musculus	111-119
21542787-6	2011	Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA.	Tunicamycin	15-26	glycogen synthase kinase 3 beta	Mus musculus	147-155
21542787-6	2011	Treatment with tunicamycin also dephosphorylated Akt and its downstream signal glycogen synthase kinase 3beta (GSK3beta) (leading to activation of GSK3beta), the effect of which was abrogated by Akt activation and TUDCA.	Tunicamycin	15-26	thymoma viral proto-oncogene 1	Mus musculus	195-198
21932778-5	2011	Experiments using the drug tunicamycin to inhibit the N-linked glycosylation of glypican-1 showed that secretion of anchorless glypican-1 was reduced and that the protein did not accumulate inside the cells.	Tunicamycin	27-38	glypican 1	Homo sapiens	80-90
21932778-5	2011	Experiments using the drug tunicamycin to inhibit the N-linked glycosylation of glypican-1 showed that secretion of anchorless glypican-1 was reduced and that the protein did not accumulate inside the cells.	Tunicamycin	27-38	glypican 1	Homo sapiens	127-137
22118540-0	2011	Tunicamycin negatively regulates BMP2-induced osteoblast differentiation through CREBH expression in MC3T3E1 cells.	Tunicamycin	0-11	bone morphogenetic protein 2	Mus musculus	33-37
22118540-0	2011	Tunicamycin negatively regulates BMP2-induced osteoblast differentiation through CREBH expression in MC3T3E1 cells.	Tunicamycin	0-11	cAMP responsive element binding protein 3-like 3	Mus musculus	81-86
22118540-4	2011	In the present study, tunicamycin increased the level of CREBH activation (cleavage) as well as mRNA expression in osteoblast cells.	Tunicamycin	22-33	cAMP responsive element binding protein 3-like 3	Mus musculus	57-62
22118540-7	2011	In addition, inhibition of CREBH expression using siRNA reversed the tunicamycin-suppressed ALP and OC expression.	Tunicamycin	69-80	cAMP responsive element binding protein 3-like 3	Mus musculus	27-32
22340178-2	2011	The present study was designed to characterize the function-unknown gene, C6orf120, and elucidates its primary role in tunicamycin-induced CD4(+) T apoptosis.	Tunicamycin	119-130	chromosome 6 open reading frame 120	Homo sapiens	74-82
22340178-2	2011	The present study was designed to characterize the function-unknown gene, C6orf120, and elucidates its primary role in tunicamycin-induced CD4(+) T apoptosis.	Tunicamycin	119-130	CD4 molecule	Homo sapiens	139-142
21970967-3	2011	Using the rat C6 glioma cell line and flow cytometry, we assessed GRP78 expression following tunicamycin- and glutamate-induced ER stress.	Tunicamycin	93-104	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	66-71
21970967-5	2011	Annexin V and propidium iodide labeling revealed cells transiently expressing GRP78 prior to injury were protected against high-concentrations of tunicamycin and glutamate within 72 h. Our findings support the hypothesis that GRP78 inhibits cell death associated with ER stress.	Tunicamycin	146-157	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	78-83
21970967-5	2011	Annexin V and propidium iodide labeling revealed cells transiently expressing GRP78 prior to injury were protected against high-concentrations of tunicamycin and glutamate within 72 h. Our findings support the hypothesis that GRP78 inhibits cell death associated with ER stress.	Tunicamycin	146-157	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	226-231
22118540-7	2011	In addition, inhibition of CREBH expression using siRNA reversed the tunicamycin-suppressed ALP and OC expression.	Tunicamycin	69-80	bone gamma-carboxyglutamate protein 2	Mus musculus	100-102
21752865-6	2011	Treatment of HEK293 (human embryonic kidney) cells expressing BRI2 with the N-glycosylation inhibitor tunicamycin or mutation of Asn170 to alanine reduced its molecular mass by ~2 kDa.	Tunicamycin	102-113	integral membrane protein 2B	Homo sapiens	62-66
21677259-4	2011	Under cellular stress induced by hypoxia (1% O(2) or CoCl(2) treatment) or tunicamycin, Prdx6-deficient cells exhibited aberrant activation of ER stress-responsive genes/protein with higher expression of ROS, and died with apoptosis.	Tunicamycin	75-86	peroxiredoxin 6	Homo sapiens	88-93
21677259-5	2011	Wild-type cells exposed to tunicamycin or hypoxia remained relatively insensitive with lower expression of ROS and ER-responsive genes than did Prdx6-deficient cells, but upregulation of ER stress responsive proteins or chaperones mimicked the UPR response of Prdx6-deficient or aging cells.	Tunicamycin	27-38	peroxiredoxin 6	Homo sapiens	144-149
21677259-5	2011	Wild-type cells exposed to tunicamycin or hypoxia remained relatively insensitive with lower expression of ROS and ER-responsive genes than did Prdx6-deficient cells, but upregulation of ER stress responsive proteins or chaperones mimicked the UPR response of Prdx6-deficient or aging cells.	Tunicamycin	27-38	peroxiredoxin 6	Homo sapiens	260-265
21832078-2	2011	We demonstrate that CAMP mRNA and protein expression increase in epithelial cells (human primary keratinocytes, HaCaT keratinocytes, and HeLa cells), but not in myeloid (U937 and HL-60) cells, following ER stress generated by two mechanistically different, pharmacological stressors, thapsigargin or tunicamycin.	Tunicamycin	300-311	cathelicidin antimicrobial peptide	Homo sapiens	20-24
21896647-7	2011	Treatment with ER stressors, tunicamycin or DTT, rapidly decreased BiP-GFP mobility in mHtt striatal cells and accelerated UPR activation compared with wild-type cells.	Tunicamycin	29-40	heat shock protein family A (Hsp70) member 5	Homo sapiens	67-70
21896647-7	2011	Treatment with ER stressors, tunicamycin or DTT, rapidly decreased BiP-GFP mobility in mHtt striatal cells and accelerated UPR activation compared with wild-type cells.	Tunicamycin	29-40	huntingtin	Mus musculus	87-91
21712074-4	2011	Here we found that application of endoplasmic reticulum stress inducers such as tunicamycin (that prevents protein N-glycosylation) and thapsigargin (that inhibits Ca2+-ATPase) to organotypic slice cultures of the hypothalamus caused preferential loss of orexin-immunoreactive neurons, as compared to melanin-concentrating hormone- or calcitonin gene-related peptide-immunoreactive neurons.	Tunicamycin	80-91	hypocretin neuropeptide precursor	Homo sapiens	255-261
21712074-5	2011	The decrease in orexin-immunoreactive neurons at early time points (6-24 h) was not accompanied by induction of cell death as indicated by the absence of caspase-3 activation and no significant change in the number of NeuN-positive cells, whereas sustained treatment with tunicamycin for 72 h induced cell death.	Tunicamycin	272-283	hypocretin neuropeptide precursor	Homo sapiens	16-22
21712074-7	2011	In addition, inhibition of axonal transport by colchicine and inhibition of proteasomal activity by MG132 significantly prevented the decrease in orexin immunoreactivity by tunicamycin.	Tunicamycin	173-184	hypocretin neuropeptide precursor	Homo sapiens	146-152
21841811-7	2011	RESULTS: Tunicamycin-induced chronic ER stress attenuated IR tyrosine phosphorylation in a time-dependent manner, whereas over-expression of ATF6 protected IR from desensitization.	Tunicamycin	9-20	insulin receptor	Homo sapiens	58-60
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
21605081-3	2011	The aim of the present study was to investigate the role of L-PTP1B (liver-specific PTP1B) in chronically HFD (high-fat diet) and pharmacologically induced (tunicamycin and thapsigargin) ER-stress response signalling in vitro and in vivo.	Tunicamycin	157-168	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	62-67
21605081-3	2011	The aim of the present study was to investigate the role of L-PTP1B (liver-specific PTP1B) in chronically HFD (high-fat diet) and pharmacologically induced (tunicamycin and thapsigargin) ER-stress response signalling in vitro and in vivo.	Tunicamycin	157-168	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	84-89
21762510-4	2011	RESULTS: Expression in the presence of either tunicamycin or furin inhibitor showed that a substantial portion of recombinant intracellular E1 and precursor E3E2 was glycosylated, but that a smaller fraction of E3E2 was processed by furin into mature E3 and E2.	Tunicamycin	46-57	small nucleolar RNA, H/ACA box 73A	Homo sapiens	140-161
21640381-5	2011	In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH).	Tunicamycin	39-50	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	136-186
21640381-5	2011	In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH).	Tunicamycin	39-50	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	256-265
21640381-5	2011	In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH).	Tunicamycin	39-50	activating transcription factor 6	Homo sapiens	268-301
21640381-5	2011	In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH).	Tunicamycin	39-50	activating transcription factor 6	Homo sapiens	303-307
21640381-5	2011	In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH).	Tunicamycin	39-50	cAMP responsive element binding protein 3 like 3	Homo sapiens	381-386
21640381-9	2011	Moreover, in mice treated with the ER stress inducer tunicamycin, CORM administration reduced serum levels of CRP and the expression of CRP mRNA in the liver.	Tunicamycin	53-64	C-reactive protein, pentraxin-related	Mus musculus	110-113
21640381-9	2011	Moreover, in mice treated with the ER stress inducer tunicamycin, CORM administration reduced serum levels of CRP and the expression of CRP mRNA in the liver.	Tunicamycin	53-64	C-reactive protein, pentraxin-related	Mus musculus	136-139
21731954-6	2011	HAC1 is central to the unfolded protein response (UPR) and in its absence, i.e. the absence of UPR, emc1Delta-, emc3Delta-, emc4Delta-, emc5Delta-hac1Delta double mutants were specifically hypersensitive to ER-stress (tunicamycin) lending credence to the usefulness of the high content microscope screening for discovery of functional effects of single mutants.	Tunicamycin	218-229	transcription factor HAC1	Saccharomyces cerevisiae S288C	0-4
21535396-8	2011	RESULTS: Tunicamycin treatment reduced TF activity at the endothelial cell surface; however, this reduction was found to be the result of decreased TF protein production in tunicamycin-treated cells.	Tunicamycin	9-20	coagulation factor III, tissue factor	Homo sapiens	39-41
21535396-8	2011	RESULTS: Tunicamycin treatment reduced TF activity at the endothelial cell surface; however, this reduction was found to be the result of decreased TF protein production in tunicamycin-treated cells.	Tunicamycin	9-20	coagulation factor III, tissue factor	Homo sapiens	148-150
21535396-8	2011	RESULTS: Tunicamycin treatment reduced TF activity at the endothelial cell surface; however, this reduction was found to be the result of decreased TF protein production in tunicamycin-treated cells.	Tunicamycin	173-184	coagulation factor III, tissue factor	Homo sapiens	148-150
21677192-0	2011	A haploid genetic screen identifies the major facilitator domain containing 2A (MFSD2A) transporter as a key mediator in the response to tunicamycin.	Tunicamycin	137-148	major facilitator superfamily domain containing 2A	Homo sapiens	80-86
21677192-1	2011	Tunicamycin (TM) inhibits eukaryotic asparagine-linked glycosylation, protein palmitoylation, ganglioside production, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity, and cell wall biosynthesis in bacteria.	Tunicamycin	0-11	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	142-189
21677192-1	2011	Tunicamycin (TM) inhibits eukaryotic asparagine-linked glycosylation, protein palmitoylation, ganglioside production, proteoglycan synthesis, 3-hydroxy-3-methylglutaryl coenzyme-A reductase activity, and cell wall biosynthesis in bacteria.	Tunicamycin	13-15	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	142-189
21725197-6	2011	NTSR-1 glycosylation was confirmed by pharmacological (tunicamycin) and chemical (PGNaseF and O-type glycosidase) approaches.	Tunicamycin	55-66	neurotensin receptor 1	Homo sapiens	0-6
21736484-3	2011	The leakage of EC-SOD through the retinal endothelial cell layer was elevated by the treatment with thapsigargin or tunicamycin.	Tunicamycin	116-127	superoxide dismutase 3	Homo sapiens	15-21
21640381-5	2011	In HepG2 cells, ER stress triggered by tunicamycin, thapsigargin and homocysteine markedly induced CRP expression and the activation of protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring transmembrane kinase/endonuclease 1alpha (IRE1alpha), activating transcription factor 6 (ATF6), and hepatocyte-specific cyclic AMP response element binding protein H (CREBH).	Tunicamycin	39-50	C-reactive protein	Homo sapiens	99-102
21676868-7	2011	A 3.8-fold increased expression of TSP-1, an endogenous angiogenesis inhibitor in Matrigel(TM) implants correlated with that in tunicamycin (32 h)-treated capillary endothelial cells.	Tunicamycin	128-139	tumor suppressor region 1	Mus musculus	35-40
21538441-5	2011	The prolonged treatment of wild-type larvae with tunicamycin (TN), which caused chronic ER stress, phenocopied foigr.	Tunicamycin	49-60	trafficking protein particle complex subunit 11	Danio rerio	111-116
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
21294793-8	2011	Although tunicamycin upregulated XBP1 splicing in cultured chondrocytes, its impact on XBP1 splicing was weakened at higher concentrations.	Tunicamycin	9-20	X-box binding protein 1	Homo sapiens	33-37
21294793-8	2011	Although tunicamycin upregulated XBP1 splicing in cultured chondrocytes, its impact on XBP1 splicing was weakened at higher concentrations.	Tunicamycin	9-20	X-box binding protein 1	Homo sapiens	87-91
21527262-4	2011	Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL).	Tunicamycin	140-142	heat shock protein 90 beta family member 1	Homo sapiens	86-91
21389343-8	2011	However, tunicamycin-induced HSPA5 expression was significantly lowered in these cells when pretreated with E(2) (P &lt; 0.01 and P &lt; 0.05, respectively).	Tunicamycin	9-20	heat shock protein family A (Hsp70) member 5	Homo sapiens	29-34
21439722-3	2011	PrP(C) confers resistance against oxidative stress-apoptosis as indicated by MTT assay, Annexin V-FITC/PI and DCFH-DA staining, but this property is abolished upon N-glycosylation inhibition by tunicamycin.	Tunicamycin	194-205	prion protein	Homo sapiens	0-6
20927523-0	2011	Inhibition of N-linked glycosylation by tunicamycin induces E-cadherin-mediated cell-cell adhesion and inhibits cell proliferation in undifferentiated human colon cancer cells.	Tunicamycin	40-51	cadherin 1	Homo sapiens	60-70
20927523-9	2011	Interestingly, tunicamycin, but not swainsonine, was able to induce functional E-cadherin-mediated cell-cell adhesion in undifferentiated HCT-116 cells, as shown by the increased association of E-cadherin with the actin cytoskeleton.	Tunicamycin	15-26	cadherin 1	Homo sapiens	79-89
20927523-9	2011	Interestingly, tunicamycin, but not swainsonine, was able to induce functional E-cadherin-mediated cell-cell adhesion in undifferentiated HCT-116 cells, as shown by the increased association of E-cadherin with the actin cytoskeleton.	Tunicamycin	15-26	cadherin 1	Homo sapiens	194-204
21527262-4	2011	Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL).	Tunicamycin	127-138	heat shock protein family A (Hsp70) member 5	Homo sapiens	47-81
21527262-4	2011	Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL).	Tunicamycin	127-138	heat shock protein 90 beta family member 1	Homo sapiens	86-91
21527262-4	2011	Time-dependent induction of the ER chaperones, glucose-regulated protein (GRP) 78 and GRP94, was observed after treatment with tunicamycin (TM) (80 mug/mL).	Tunicamycin	140-142	heat shock protein family A (Hsp70) member 5	Homo sapiens	47-81
21454560-8	2011	Inhibitors of N-linked glycosylation (tunicamycin, deoxymannojirimycin, and deoxynojirimycin) also markedly attenuated the inhibitory effect of IGF-I on beta-glycerophosphate-induced mineralization (p &lt; 0.05) and activation of Akt and MAPK.	Tunicamycin	38-49	insulin like growth factor 1	Homo sapiens	144-149
22093624-9	2011	With exposure to tunicamycin (3 micromol/L) for 12, 24, 36 hours the Bim protein levels were not increased in Mel-RM and MM200 cells.	Tunicamycin	17-28	BCL2 like 11	Homo sapiens	69-72
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
21605547-5	2011	TUDCA efficiently inhibited the expression of UPR dependent genes like GRP78 triggered by the ER stressor tunicamycin in the small intestinal epithelial cell line Mode-K. TUDCA inhibited upstream signaling events in all three branches of the UPR cascade and diminished binding of UPR activated transcription factors to the grp78 promoter.	Tunicamycin	106-117	heat shock protein family A (Hsp70) member 5	Homo sapiens	71-76
21605547-5	2011	TUDCA efficiently inhibited the expression of UPR dependent genes like GRP78 triggered by the ER stressor tunicamycin in the small intestinal epithelial cell line Mode-K. TUDCA inhibited upstream signaling events in all three branches of the UPR cascade and diminished binding of UPR activated transcription factors to the grp78 promoter.	Tunicamycin	106-117	heat shock protein family A (Hsp70) member 5	Homo sapiens	323-328
21600878-4	2011	In this work, we have examined the effect of metformin on the expression of UPR-related markers (GRP94 and CHOP) induced by glucosamine (GlcN), 2-deoxyglucose (2-DOG) and tunicamycin (TUNI) in renal proximal tubular epithelial cells and in murine mesangial cells.	Tunicamycin	171-182	heat shock protein 90 beta family member 1	Canis lupus familiaris	97-102
20726815-7	2011	Tunicamycin and thapsigargin, irrespective of the dose, induced sufficient ER stress, as evidenced by the increased phosphorylation or activation of eIF2alpha and PERK.	Tunicamycin	0-11	eukaryotic translation initiation factor 2A	Rattus norvegicus	149-158
21252914-3	2011	We demonstrate here that AMF/PGI also protects against thapsigargin (TG)- and tunicamycin (TUN)-induced ER stress and apoptosis.	Tunicamycin	78-89	glucose-6-phosphate isomerase	Homo sapiens	29-32
21252914-3	2011	We demonstrate here that AMF/PGI also protects against thapsigargin (TG)- and tunicamycin (TUN)-induced ER stress and apoptosis.	Tunicamycin	91-94	glucose-6-phosphate isomerase	Homo sapiens	29-32
21279413-8	2011	These antibodies also reacted to a glycosylation-disturbed full-length nephrin protein (inhibited by tunicamycin), but did not react to either a native nephrin protein or a fully glycosylated conformational nephrin protein.	Tunicamycin	101-112	NPHS1 adhesion molecule, nephrin	Rattus norvegicus	71-78
21590646-6	2011	After exposure to TN, phospho-Akt protein levels were repressed whereas total Akt protein levels were not changed.	Tunicamycin	18-20	AKT serine/threonine kinase 1	Rattus norvegicus	30-33
21590646-6	2011	After exposure to TN, phospho-Akt protein levels were repressed whereas total Akt protein levels were not changed.	Tunicamycin	18-20	AKT serine/threonine kinase 1	Rattus norvegicus	78-81
21590646-8	2011	After LY294002 administration in non-TN-treated cells, cell viability was reduced, and CHOP and Bax protein levels were elevated, and Bcl-2 protein levels were reduced.	Tunicamycin	37-39	DNA-damage inducible transcript 3	Rattus norvegicus	87-91
21590646-8	2011	After LY294002 administration in non-TN-treated cells, cell viability was reduced, and CHOP and Bax protein levels were elevated, and Bcl-2 protein levels were reduced.	Tunicamycin	37-39	BCL2 associated X, apoptosis regulator	Rattus norvegicus	96-99
21590646-8	2011	After LY294002 administration in non-TN-treated cells, cell viability was reduced, and CHOP and Bax protein levels were elevated, and Bcl-2 protein levels were reduced.	Tunicamycin	37-39	BCL2, apoptosis regulator	Rattus norvegicus	134-139
21310902-6	2011	On stress induction, HTRA1 and VEGFA were upregulated in human fetal RPE cells treated by tunicamycin and dithiothreitol, but reduced after treatment by MG132.	Tunicamycin	90-101	HtrA serine peptidase 1	Homo sapiens	21-26
21310902-6	2011	On stress induction, HTRA1 and VEGFA were upregulated in human fetal RPE cells treated by tunicamycin and dithiothreitol, but reduced after treatment by MG132.	Tunicamycin	90-101	vascular endothelial growth factor A	Homo sapiens	31-36
21216966-6	2011	PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress.	Tunicamycin	78-89	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	0-5
21242807-1	2011	We investigated the effects of endoplasmic reticulum (ER) stress inducers thapsigargin (TG) and tunicamycin (Tm) on immunostimulant lipopolysaccharide/interferon (LPS/IFN)-induced expression of isoform of nitric oxide synthase (iNOS) and nitric oxide (NO) production in vascular smooth muscle cells.	Tunicamycin	96-107	interferon regulatory factor 6	Homo sapiens	132-170
21308740-4	2011	Monolayer cultures treated with ER stressors glucose withdrawal (-Glu), tunicamycin (TN), or thapsigargin (TG) up-regulated Grp78 and Gadd153, demonstrating a complete ER stress response.	Tunicamycin	72-83	heat shock protein family A (Hsp70) member 5	Bos taurus	124-129
21308740-4	2011	Monolayer cultures treated with ER stressors glucose withdrawal (-Glu), tunicamycin (TN), or thapsigargin (TG) up-regulated Grp78 and Gadd153, demonstrating a complete ER stress response.	Tunicamycin	85-87	heat shock protein family A (Hsp70) member 5	Bos taurus	124-129
21245056-11	2011	SAM treatment also reduced tumour necrosis factor-alpha-induced reactive oxygen species and tunicamycin-induced GRP78 expression in VSMCs.	Tunicamycin	92-103	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	112-117
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
21321189-5	2011	The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner.	Tunicamycin	4-15	X-box binding protein 1	Mus musculus	36-59
21321189-5	2011	The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner.	Tunicamycin	4-15	heat shock protein 5	Mus musculus	78-83
21321189-5	2011	The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner.	Tunicamycin	4-15	DNA-damage inducible transcript 3	Mus musculus	88-92
21321189-5	2011	The tunicamycin-induced splicing of X-box binding protein-1 and expression of GRP78 and CHOP were reduced by resveratrol in cultured cells in a SIRT1-dependent manner.	Tunicamycin	4-15	sirtuin 1	Mus musculus	144-149
21321189-6	2011	Conversely, SIRT1-deficient mouse embryonic fibroblasts challenged with tunicamycin exhibited markedly increased mTORC1 activity and impaired ER homeostasi and insulin signaling.	Tunicamycin	72-83	CREB regulated transcription coactivator 1	Mus musculus	113-119
21360721-5	2011	Treatment of McA-RH7777 cells with 4-phenyl butyric acid, a chemical ER stress inhibitor, prevented glucosamine- and tunicamycin-induced increases in GRP78 and phosphorylated eIF2alpha, rescued newly synthesized [(35) S]-labeled apoB100, and substantially blocked the colocalization of apoB with GFP-LC3.	Tunicamycin	117-128	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	150-155
21360721-5	2011	Treatment of McA-RH7777 cells with 4-phenyl butyric acid, a chemical ER stress inhibitor, prevented glucosamine- and tunicamycin-induced increases in GRP78 and phosphorylated eIF2alpha, rescued newly synthesized [(35) S]-labeled apoB100, and substantially blocked the colocalization of apoB with GFP-LC3.	Tunicamycin	117-128	eukaryotic translation initiation factor 2A	Rattus norvegicus	175-184
21360721-5	2011	Treatment of McA-RH7777 cells with 4-phenyl butyric acid, a chemical ER stress inhibitor, prevented glucosamine- and tunicamycin-induced increases in GRP78 and phosphorylated eIF2alpha, rescued newly synthesized [(35) S]-labeled apoB100, and substantially blocked the colocalization of apoB with GFP-LC3.	Tunicamycin	117-128	apolipoprotein B	Rattus norvegicus	229-236
21360721-5	2011	Treatment of McA-RH7777 cells with 4-phenyl butyric acid, a chemical ER stress inhibitor, prevented glucosamine- and tunicamycin-induced increases in GRP78 and phosphorylated eIF2alpha, rescued newly synthesized [(35) S]-labeled apoB100, and substantially blocked the colocalization of apoB with GFP-LC3.	Tunicamycin	117-128	apolipoprotein B	Rattus norvegicus	229-233
22069719-7	2011	However, RTA inhibited both phosphorylation of inositol-requiring enzyme 1 (IRE1) and splicing of X-box binding protein1 mRNA by the UPR-inducing agent tunicamycin (Tm).	Tunicamycin	152-163	RNA binding fox-1 homolog 2	Homo sapiens	9-12
22069719-7	2011	However, RTA inhibited both phosphorylation of inositol-requiring enzyme 1 (IRE1) and splicing of X-box binding protein1 mRNA by the UPR-inducing agent tunicamycin (Tm).	Tunicamycin	152-163	X-box binding protein 1	Homo sapiens	98-120
21241252-5	2011	Tunicamycin-treated Bak-/-Bax-/- cells remain viable, but cease growth, arresting in G1-phase and undergoing autophagy in the absence of apoptosis.	Tunicamycin	0-11	BCL2 antagonist/killer 1	Homo sapiens	20-23
21241252-5	2011	Tunicamycin-treated Bak-/-Bax-/- cells remain viable, but cease growth, arresting in G1-phase and undergoing autophagy in the absence of apoptosis.	Tunicamycin	0-11	BCL2 associated X, apoptosis regulator	Homo sapiens	26-29
21241252-11	2011	Importantly, the effects of tunicamycin on cellular metabolic processes may be related to a reduction in cell-surface GLUT1 (glucose transporter 1) levels which, in turn, may reflect decreased Akt signalling.	Tunicamycin	28-39	solute carrier family 2 member 1	Homo sapiens	118-123
21241252-11	2011	Importantly, the effects of tunicamycin on cellular metabolic processes may be related to a reduction in cell-surface GLUT1 (glucose transporter 1) levels which, in turn, may reflect decreased Akt signalling.	Tunicamycin	28-39	solute carrier family 2 member 1	Homo sapiens	125-146
21216966-6	2011	PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress.	Tunicamycin	78-89	protein tyrosine phosphatase, non-receptor type 2	Mus musculus	24-29
21216966-6	2011	PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress.	Tunicamycin	78-89	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	98-102
21216966-6	2011	PTP1B overexpression or TCPTP knockdown in MIN6 cells mitigated palmitate- or tunicamycin-induced PERK/eIF2alpha ER stress signaling, whereas PTP1B deficiency enhanced ER stress.	Tunicamycin	78-89	eukaryotic translation initiation factor 2A	Mus musculus	103-112
21151176-6	2011	The combination of ER stress inducers (such as THAPS or tunicamycin) and CDDP effectively induced the translocation of CRT to the plasma membrane, as well as immunogenic cell death, although ER stress or CDDP alone was insufficient to induce CRT exposure and immunogenic cell death.	Tunicamycin	56-67	calreticulin	Homo sapiens	119-122
21126579-12	2011	Tunicamycin prevented OCTN2 glycosylation, but it did not impair maturation to the plasma membrane.	Tunicamycin	0-11	solute carrier family 22 member 5	Homo sapiens	22-27
21029237-6	2011	In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA.	Tunicamycin	26-37	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	63-66
21029237-6	2011	In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA.	Tunicamycin	26-37	glycogen synthase kinase 3 alpha	Homo sapiens	68-77
21029237-6	2011	In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA.	Tunicamycin	26-37	microtubule associated protein tau	Homo sapiens	89-92
21029237-6	2011	In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA.	Tunicamycin	26-37	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	151-154
21029237-6	2011	In SH-SY5Y cell cultures, tunicamycin and Abeta(1-42) activate PKR, GSK-3beta and induce tau phosphorylation and all these processes are attenuated by PKR inhibitors or PKR siRNA.	Tunicamycin	26-37	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	151-154
21029237-7	2011	Our results demonstrate that neuronal PKR co-localizes with GSK-3beta and tau in AD brains and is able to modulate GSK-3beta activation, tau phosphorylation and apoptosis in neuroblastoma cells exposed to tunicamycin or Abeta.	Tunicamycin	205-216	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	38-41
20526696-4	2011	Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection.	Tunicamycin	92-103	prion protein	Homo sapiens	17-20
20526696-4	2011	Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection.	Tunicamycin	92-103	prion protein	Homo sapiens	29-32
20526696-4	2011	Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection.	Tunicamycin	92-103	prion protein	Homo sapiens	29-32
20526696-4	2011	Cells expressing PrP-PG9 and PrP-PG12 were sensitive to endoplasmic reticulum (ER) stimuli, tunicamycin, and brefeldin A. ER-stress-related proteins, Grp94, XBP1, TRAF2, and CHOP, were significantly increased in cells expressing PrP-PG9 and PrP-PG12, while Grp78 increased markedly 12 h and pro-caspase-12 decreased sharply 20 h post-transfection.	Tunicamycin	92-103	prion protein	Homo sapiens	29-32
21150875-2	2011	Since tumor necrosis factor alpha (TNFalpha) plays a role in acute kidney injury, and induces ER stress and cell death in vitro, we examined the contribution of TNFalpha to acute kidney ER stress induced by tunicamycin.	Tunicamycin	207-218	tumor necrosis factor	Mus musculus	161-169
21150875-3	2011	Contrary to expectation, tunicamycin caused much more severe kidney injury in TNFalpha-/- than in wild-type mice.	Tunicamycin	25-36	tumor necrosis factor	Mus musculus	78-86
21150875-5	2011	Reconstitution of TNFalpha-/- mice with TNFalpha 24 h before tunicamycin injection reversed the susceptibility.	Tunicamycin	61-72	tumor necrosis factor	Mus musculus	18-26
21150875-6	2011	When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1).	Tunicamycin	56-67	tumor necrosis factor	Mus musculus	5-13
21150875-6	2011	When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1).	Tunicamycin	56-67	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	102-107
21150875-6	2011	When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1).	Tunicamycin	56-67	tumor necrosis factor	Mus musculus	160-168
21150875-6	2011	When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1).	Tunicamycin	56-67	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	188-202
21150875-6	2011	When TNFalpha-receptor-deficient mice were treated with tunicamycin, severe renal injury developed in TNFR1-/- but not TNFR2-/- mice, suggesting this aspect of TNFalpha action was through TNF receptor-1 (TNFR1).	Tunicamycin	56-67	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	204-209
21150875-9	2011	Finally, treatment of proximal tubule cells isolated from TNFR1-/- mice with an inhibitor of eIF2alpha phosphatase increased the levels of phosphorylated eIF2alpha and substantially reduced tunicamycin-induced cell death.	Tunicamycin	190-201	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	58-63
21150875-9	2011	Finally, treatment of proximal tubule cells isolated from TNFR1-/- mice with an inhibitor of eIF2alpha phosphatase increased the levels of phosphorylated eIF2alpha and substantially reduced tunicamycin-induced cell death.	Tunicamycin	190-201	eukaryotic translation initiation factor 2A	Mus musculus	93-102
21490406-4	2011	Here, we report that acylated ghrelin inhibited tunicamycin- or thapsigargin-triggered ER stress-induced apoptotic cell death in primary rat cortical neurons.	Tunicamycin	48-59	ghrelin and obestatin prepropeptide	Rattus norvegicus	30-37
20970123-2	2011	Inhibition of CD44 N- and O-linked glycosylation by using tunicamycin and/or B-GalNAc statistically significantly inhibited endometrial cell attachment to peritoneal mesothelial cells, suggesting a role in establishment of early endometriotic lesions.	Tunicamycin	58-69	CD44 molecule (Indian blood group)	Homo sapiens	14-18
21087599-7	2011	In parental HL60 cells, ABC50 KD increased sensitivity to Ec, thapsigargin and tunicamycin but not to serum withdrawal or etoposide.	Tunicamycin	79-90	ATP binding cassette subfamily F member 1	Homo sapiens	24-29
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
21168844-10	2011	Nicorandil significantly attenuated tunicamycin-induced CHOP upregulation in cultured THP-1 macrophages.	Tunicamycin	36-47	GLI family zinc finger 2	Homo sapiens	86-91
21298055-6	2011	Analyses of the cell viabilities in the presences of tunicamycin and brefeldin A revealed that expressions of PrP-KDEL and PrP-3AV sensitized the transfected cells to ER stress stimuli.	Tunicamycin	53-64	prion protein	Homo sapiens	110-113
21298055-6	2011	Analyses of the cell viabilities in the presences of tunicamycin and brefeldin A revealed that expressions of PrP-KDEL and PrP-3AV sensitized the transfected cells to ER stress stimuli.	Tunicamycin	53-64	pre-mRNA processing factor 3	Homo sapiens	123-128
21184741-7	2011	Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1.	Tunicamycin	65-76	derlin 1	Homo sapiens	22-30
21184741-7	2011	Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1.	Tunicamycin	65-76	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	103-107
21184741-7	2011	Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1.	Tunicamycin	65-76	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	187-191
21184741-7	2011	Notably, knockdown of Derlin-1 also stabilized the expression of tunicamycin-induced deglycosylated WT BCRP protein, implying the importance of glycosylation state for the recognition of BCRP by Derlin-1.	Tunicamycin	65-76	derlin 1	Homo sapiens	195-203
21490406-6	2011	Ghrelin suppressed tunicamycin- or thapsigargin-induced upregulation and nuclear translocation of C/EBP homologous protein (CHOP).	Tunicamycin	19-30	DNA-damage inducible transcript 3	Rattus norvegicus	98-122
21490406-6	2011	Ghrelin suppressed tunicamycin- or thapsigargin-induced upregulation and nuclear translocation of C/EBP homologous protein (CHOP).	Tunicamycin	19-30	DNA-damage inducible transcript 3	Rattus norvegicus	124-128
21490406-7	2011	Ghrelin also inhibited tunicamycin or thapsigargin induction of PRK-like ER kinase (PERK), eukaryotic translation initiation factor-2alpha (eIF2alpha) and activating transcription factor (ATF) 4.	Tunicamycin	23-34	eukaryotic translation initiation factor 2A	Rattus norvegicus	91-138
21490406-7	2011	Ghrelin also inhibited tunicamycin or thapsigargin induction of PRK-like ER kinase (PERK), eukaryotic translation initiation factor-2alpha (eIF2alpha) and activating transcription factor (ATF) 4.	Tunicamycin	23-34	eukaryotic translation initiation factor 2A	Rattus norvegicus	140-149
21490406-7	2011	Ghrelin also inhibited tunicamycin or thapsigargin induction of PRK-like ER kinase (PERK), eukaryotic translation initiation factor-2alpha (eIF2alpha) and activating transcription factor (ATF) 4.	Tunicamycin	23-34	activating transcription factor 4	Rattus norvegicus	155-194
21490406-8	2011	Exposure of cells to tunicamycin or thapsigargin resulted in nuclear translocation of forkhead box protein O1 (Foxo1), which was reduced by pretreatment with ghrelin.	Tunicamycin	21-32	forkhead box O1	Rattus norvegicus	86-109
21490406-8	2011	Exposure of cells to tunicamycin or thapsigargin resulted in nuclear translocation of forkhead box protein O1 (Foxo1), which was reduced by pretreatment with ghrelin.	Tunicamycin	21-32	forkhead box O1	Rattus norvegicus	111-116
21490406-8	2011	Exposure of cells to tunicamycin or thapsigargin resulted in nuclear translocation of forkhead box protein O1 (Foxo1), which was reduced by pretreatment with ghrelin.	Tunicamycin	21-32	ghrelin and obestatin prepropeptide	Rattus norvegicus	158-165
21432213-5	2011	RESULTS: Gene expression analysis revealed that Ire1beta was up-regulated in astrocytes exposed to aluminum while Ire1alpha was up-regulated by tunicamycin.	Tunicamycin	144-155	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	114-123
22174631-0	2011	Tunicamycin depresses P-glycoprotein glycosylation without an effect on its membrane localization and drug efflux activity in L1210 cells.	Tunicamycin	0-11	phosphoglycolate phosphatase	Mus musculus	22-36
22174631-8	2011	Tunicamycin inhibited P-gp N-glycosylation in both of the P-gp-positive cells.	Tunicamycin	0-11	phosphoglycolate phosphatase	Mus musculus	22-26
22174631-10	2011	The present paper brings evidence that independently on the mode of P-gp expression (selection with drugs or transfection with a gene encoding P-gp) in L1210 cells, tunicamycin induces inhibition of N-glycosylation of this protein, without altering its function as plasma membrane drug efflux pump.	Tunicamycin	165-176	phosphoglycolate phosphatase	Mus musculus	68-72
22174631-10	2011	The present paper brings evidence that independently on the mode of P-gp expression (selection with drugs or transfection with a gene encoding P-gp) in L1210 cells, tunicamycin induces inhibition of N-glycosylation of this protein, without altering its function as plasma membrane drug efflux pump.	Tunicamycin	165-176	phosphoglycolate phosphatase	Mus musculus	143-147
21282934-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 9	Homo sapiens	64-73
21282934-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 4	Homo sapiens	78-87
21282934-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 4	Homo sapiens	111-120
21282934-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 9	Homo sapiens	138-147
32272543-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 9	Homo sapiens	64-73
32272543-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 4	Homo sapiens	78-87
32272543-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 4	Homo sapiens	111-120
32272543-2	2011	Tunicamycin, which is known to induce ER stress, activated both caspase-9 and caspase-4, and the activation of caspase-4 preceded that of caspase-9.	Tunicamycin	0-11	caspase 9	Homo sapiens	138-147
20974203-5	2011	Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity.	Tunicamycin	60-71	heat shock protein family A (Hsp70) member 5	Homo sapiens	87-92
20974203-5	2011	Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity.	Tunicamycin	60-71	activating transcription factor 4	Homo sapiens	112-116
20974203-5	2011	Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity.	Tunicamycin	73-75	heat shock protein family A (Hsp70) member 5	Homo sapiens	87-92
20974203-5	2011	Pretreatment with ER stress inducers, thapsigargin (Tg) and tunicamycin (Tm), promoted GRP78 mRNA induction and ATF4 translation, which are ER stress markers, under our experimental conditions and protected against the cytotoxicity.	Tunicamycin	73-75	activating transcription factor 4	Homo sapiens	112-116
22073243-12	2011	We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms.	Tunicamycin	109-120	UDP-Glucose Glycoprotein glucosylTransferase	Caenorhabditis elegans	19-26
22073243-12	2011	We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms.	Tunicamycin	109-120	UDP-Glucose Glycoprotein glucosylTransferase	Caenorhabditis elegans	31-38
22073243-12	2011	We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms.	Tunicamycin	109-120	UDP-Glucose Glycoprotein glucosylTransferase	Caenorhabditis elegans	169-175
22073243-12	2011	We found that both CeUGGT1 and CeUGGT2 play a protective role under ER stress conditions, since 10 microg/ml tunicamycin arrested development at the L2/L3 stage of both uggt-1(RNAi) and uggt-2(RNAi) but not of control worms.	Tunicamycin	109-120	UDP-Glucose Glycoprotein glucosylTransferase	Caenorhabditis elegans	186-192
21698202-4	2011	METHODS: Muscle cells were incubated overnight with tunicamycin or thapsigargin to induce ER stress and the activation of the unfolded protein response, mTORC1 activity at baseline and following insulin and amino acids, as well as amino acid transport were determined.	Tunicamycin	52-63	CREB regulated transcription coactivator 1	Mus musculus	153-159
21698202-7	2011	The leucine (2.5-5 mM)-induced phosphorylation of S6K1 on the other hand was repressed by low concentrations of both tunicamycin and thapsigargin.	Tunicamycin	117-128	ribosomal protein S6 kinase B1	Homo sapiens	50-54
21698202-10	2011	Tunicamycin and thapsigargin both decreased the basal phosphorylation state of PRAS40.	Tunicamycin	0-11	AKT1 substrate 1	Homo sapiens	79-85
22355548-2	2011	We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type.	Tunicamycin	118-129	Endoribonuclease/protein kinase IRE1-like protein	Arabidopsis thaliana	45-50
22355548-2	2011	We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type.	Tunicamycin	118-129	inositol requiring 1-1	Arabidopsis thaliana	55-60
22355548-2	2011	We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type.	Tunicamycin	118-129	Endoribonuclease/protein kinase IRE1-like protein	Arabidopsis thaliana	62-67
22355548-2	2011	We found that a double mutant of Arabidopsis IRE1A and IRE1B (ire1a/ire1b) is more sensitive to the ER stress inducer tunicamycin than the wild-type.	Tunicamycin	118-129	inositol requiring 1-1	Arabidopsis thaliana	68-73
20826801-9	2010	Interestingly, in cells treated with tunicamycin, SIRPalpha dimerization but not CD47 binding was inhibited, suggesting that a SIRPalpha dimer is probably bivalent.	Tunicamycin	37-48	signal regulatory protein alpha	Homo sapiens	50-59
20826801-9	2010	Interestingly, in cells treated with tunicamycin, SIRPalpha dimerization but not CD47 binding was inhibited, suggesting that a SIRPalpha dimer is probably bivalent.	Tunicamycin	37-48	signal regulatory protein alpha	Homo sapiens	127-136
20631254-4	2010	In this report, we burdened mice with intraperitoneal injection of the ER stress-inducing reagent tunicamycin and found that wild-type mice were able to recover from the insult, whereas ATF6alpha-knockout mice exhibited liver dysfunction and steatosis.	Tunicamycin	98-109	activating transcription factor 6	Mus musculus	186-195
21064031-8	2010	Altered UPR signaling in livers of CD154KO mice was confirmed in tunicamycin (TM) challenge experiments.	Tunicamycin	65-76	CD40 ligand	Mus musculus	35-42
20933500-4	2010	Here we showed that several well-characterized ER stress inducers (thapsigargin, tunicamycin, and dithiothreitol) increase the expression of TLR2 in epithelial cells.	Tunicamycin	81-92	toll-like receptor 2	Mus musculus	141-145
20933500-6	2010	Furthermore, there was significant increase of TLR2 mRNA level in the livers of tunicamycin-treated mice and high-fat diet-fed mice, suggesting an impact of ER stress in vivo on the expression of TLR2.	Tunicamycin	80-91	toll-like receptor 2	Mus musculus	47-51
20933500-6	2010	Furthermore, there was significant increase of TLR2 mRNA level in the livers of tunicamycin-treated mice and high-fat diet-fed mice, suggesting an impact of ER stress in vivo on the expression of TLR2.	Tunicamycin	80-91	toll-like receptor 2	Mus musculus	196-200
20501874-7	2010	In C(2)C(12) muscle cells, tunicamycin, thapsigargin, and palmitic acid all increased UPR markers and decreased phosphorylation of S6K1 (P &lt; 0.05).	Tunicamycin	27-38	ribosomal protein S6 kinase, polypeptide 1	Mus musculus	131-135
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
21076579-5	2010	METHODS: The effects of tunicamycin and thapsigargin on insulin and TRB3 expression in INS-1 cells were measured by Northern and Western blot analysis, respectively.	Tunicamycin	24-35	insulin	Homo sapiens	56-63
21076579-5	2010	METHODS: The effects of tunicamycin and thapsigargin on insulin and TRB3 expression in INS-1 cells were measured by Northern and Western blot analysis, respectively.	Tunicamycin	24-35	tribbles pseudokinase 3	Rattus norvegicus	68-72
21076579-8	2010	RESULTS: The treatment of INS-1 cells with tunicamycin and thapsigargin decreased insulin mRNA expression, but increased TRB3 protein expression.	Tunicamycin	43-54	tribbles pseudokinase 3	Rattus norvegicus	121-125
20886113-4	2010	METHODOLOGY: Forced expression of Hr by transfection decreased the number of apoptotic nuclei, levels of caspase-3 activity, and cytosolic cytochrome C in COS cells exposed to staurosporine and tunicamycin.	Tunicamycin	194-205	lysine demethylase and nuclear receptor corepressor	Mus musculus	34-36
20688044-9	2010	COX-2 downregulation by E5 could be overcome by thapsigargin or tunicamycin treatments, which initiate ER stress via calcium fluxes and abnormal protein glycosylation respectively, making it unlikely that E5 specifically tempers these pathways.	Tunicamycin	64-75	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5
20685651-3	2010	We found that overexpression of lipid-anchored Rheb enhanced the apoptotic effects induced by UV light, TNFalpha, or tunicamycin in an mTOR complex 1 (mTORC1)-dependent manner.	Tunicamycin	117-128	Ras homolog, mTORC1 binding	Homo sapiens	47-51
20685651-3	2010	We found that overexpression of lipid-anchored Rheb enhanced the apoptotic effects induced by UV light, TNFalpha, or tunicamycin in an mTOR complex 1 (mTORC1)-dependent manner.	Tunicamycin	117-128	mechanistic target of rapamycin kinase	Homo sapiens	135-139
20685651-3	2010	We found that overexpression of lipid-anchored Rheb enhanced the apoptotic effects induced by UV light, TNFalpha, or tunicamycin in an mTOR complex 1 (mTORC1)-dependent manner.	Tunicamycin	117-128	CREB regulated transcription coactivator 1	Mus musculus	151-157
20692228-3	2010	The results showed that SelK was regulated by ER stress agents, Tunicamycin (Tm) and beta-Mercaptoethanol (beta-ME), in HepG2 cells.	Tunicamycin	64-75	selenoprotein K	Homo sapiens	24-28
20628148-8	2010	Manipulating ER signaling by siRNA down-regulation of BiP/GRP78 or treating B-CLL cells with 2 well-known ER stress-inducers, tunicamycin and thapsigargin, increases their apoptosis.	Tunicamycin	126-137	heat shock protein family A (Hsp70) member 5	Homo sapiens	58-63
20354865-5	2010	Using transfected Chinese hamster ovary (CHO) cells to reconstitute Kv4 complex, we show that the pharmacological inhibition of DPP10 glycosylation by tunicamycin and neuraminidase affects transient outward potassium current (I (to)) kinetics.	Tunicamycin	151-162	inactive dipeptidyl peptidase 10	Cricetulus griseus	128-133
20618991-9	2010	N-glycosylation inhibitor tunicamycin was used to deglycosylate the integrin beta1 subunit.	Tunicamycin	26-37	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	77-82
20407008-4	2010	In this work, we demonstrated that tunicamycin inhibition of glycosylation of the GLP-1 receptor expressed in CHO cells interfered with biosynthesis and intracellular trafficking, thereby eliminating natural ligand binding.	Tunicamycin	35-46	glucagon	Homo sapiens	82-87
20354865-9	2010	The effects of tunicamycin on the native I (to) currents of human atrial myocytes expressing DPP10 were similar to those of the KV4.3/KChIP2/DPP10 complex in CHO cells.	Tunicamycin	15-26	dipeptidyl peptidase like 10	Homo sapiens	93-98
20368330-3	2010	ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells.	Tunicamycin	42-53	matrix metallopeptidase 3	Mus musculus	88-93
20368330-3	2010	ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells.	Tunicamycin	42-53	matrix metallopeptidase 3	Mus musculus	88-91
20368330-3	2010	ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells.	Tunicamycin	42-53	matrix metallopeptidase 3	Mus musculus	158-163
20368330-3	2010	ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells.	Tunicamycin	55-57	matrix metallopeptidase 3	Mus musculus	88-93
20368330-3	2010	ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells.	Tunicamycin	55-57	matrix metallopeptidase 3	Mus musculus	88-91
20368330-3	2010	ER stress induced by brefeldin A (BFA) or tunicamycin (TM) increases gene expression of MMP-3, selectively among various MMP subtypes, and the active form of MMP-3 (actMMP-3) in the brain-derived CATH.a cells.	Tunicamycin	55-57	matrix metallopeptidase 3	Mus musculus	158-163
20235094-5	2010	These transcripts and Nrf2 (Nfe2l2) were increased by systemic application of tunicamycin or the selective olfactotoxic chemical methimazole.	Tunicamycin	78-89	nuclear factor, erythroid derived 2, like 2	Mus musculus	22-26
20235094-5	2010	These transcripts and Nrf2 (Nfe2l2) were increased by systemic application of tunicamycin or the selective olfactotoxic chemical methimazole.	Tunicamycin	78-89	nuclear factor, erythroid derived 2, like 2	Mus musculus	28-34
20631306-7	2010	Depleting MD-2 using small interfering RNA or blocking the N-glycosylation of cells using tunicamycin blocked membrane trafficking of TLR4.	Tunicamycin	90-101	toll-like receptor 4	Mus musculus	134-138
20513236-8	2010	The thapsigargin- and tunicamycin-induced UPR (unfolded protein response) also increased SREBP-1 expression in Hep G2 cells, through the cap-independent translation mediated by IRES.	Tunicamycin	22-33	sterol regulatory element binding transcription factor 1	Homo sapiens	89-96
20460427-4	2010	RESULTS: N-glycosylation of CN-1 was either inhibited by tunicamycin in pCSII-CN-1-transfected Cos-7 cells or by stepwise deletion of its three putative N-glycosylation sites.	Tunicamycin	57-68	carnosine dipeptidase 1	Homo sapiens	28-32
20460427-7	2010	Tunicamycin completely inhibited CN-1 secretion.	Tunicamycin	0-11	carnosine dipeptidase 1	Homo sapiens	33-37
20457808-3	2010	Knockdown of the oxidase Nox4, expressed on ER endomembranes, or expression of ER-targeted catalase blocked ER H(2)O(2) production by tunicamycin and Tat and prevented the UPR following exposure to these two agonists, but not to thapsigargin or dithiothreitol.	Tunicamycin	134-145	NADPH oxidase 4	Homo sapiens	25-29
20430884-0	2010	The activity of yeast Hog1 MAPK is required during endoplasmic reticulum stress induced by tunicamycin exposure.	Tunicamycin	91-102	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	22-26
20430884-5	2010	Strains lacking the MAPK Hog1p displayed sensitivity to tunicamycin or beta-mercaptoethanol, whereas hyperactivation of the pathway enhanced their resistance.	Tunicamycin	56-67	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	25-30
20430884-7	2010	Northern blot analysis demonstrated that Hog1p controls the tunicamycin-induced transcriptional change of GPD1 and that wild-type cells exposed to the drug accumulated glycerol in a Hog1p-dependent manner.	Tunicamycin	60-71	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	41-46
20430884-7	2010	Northern blot analysis demonstrated that Hog1p controls the tunicamycin-induced transcriptional change of GPD1 and that wild-type cells exposed to the drug accumulated glycerol in a Hog1p-dependent manner.	Tunicamycin	60-71	glycerol-3-phosphate dehydrogenase (NAD(+)) GPD1	Saccharomyces cerevisiae S288C	106-110
20430884-7	2010	Northern blot analysis demonstrated that Hog1p controls the tunicamycin-induced transcriptional change of GPD1 and that wild-type cells exposed to the drug accumulated glycerol in a Hog1p-dependent manner.	Tunicamycin	60-71	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	182-187
20413434-9	2010	Molecular analyses of tunicamycin-treated tumors showed reduced levels of EGFR and Met, two RTKs overexpressed in gliomas.	Tunicamycin	22-33	epidermal growth factor receptor	Homo sapiens	74-78
20450227-7	2010	In further support of a role for glycosylation in receptor function, treatment of RAW 264.7 macrophages with the N-linked glycosylation synthesis inhibitor tunicamycin attenuates P2X(7) agonist-induced, but not phorbol ester-induced, ERK1/2 phosphorylation.	Tunicamycin	156-167	purinergic receptor P2X 7	Homo sapiens	179-185
20450227-7	2010	In further support of a role for glycosylation in receptor function, treatment of RAW 264.7 macrophages with the N-linked glycosylation synthesis inhibitor tunicamycin attenuates P2X(7) agonist-induced, but not phorbol ester-induced, ERK1/2 phosphorylation.	Tunicamycin	156-167	mitogen-activated protein kinase 3	Homo sapiens	234-240
20354865-6	2010	Tunicamycin completely blocked DPP10 glycosylation and reduced DPP10 cell surface expression.	Tunicamycin	0-11	inactive dipeptidyl peptidase 10	Cricetulus griseus	31-36
20354865-6	2010	Tunicamycin completely blocked DPP10 glycosylation and reduced DPP10 cell surface expression.	Tunicamycin	0-11	inactive dipeptidyl peptidase 10	Cricetulus griseus	63-68
20005867-5	2010	Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells.	Tunicamycin	19-30	ATP binding cassette subfamily C member 1	Homo sapiens	228-232
20146743-1	2010	EOS1 is required for tolerance to oxidative stress in Saccharomyces cerevisiae; mutants are defective in the gene sensitive to hydrogen peroxide and tolerant to tunicamycin.	Tunicamycin	161-172	Eos1p	Saccharomyces cerevisiae S288C	0-4
19951703-6	2010	To evaluate the role of glycosylation in the enzyme activity, we produced unglycosylated UGT1A9 by treating HEK293 cells transiently transfected with expression plasmid with tunicamycin.	Tunicamycin	174-185	UDP glucuronosyltransferase family 1 member A9	Homo sapiens	89-95
19838798-0	2010	Tunicamycin-induced cell death in the trigeminal ganglion is suppressed by nerve growth factor in the mouse embryo.	Tunicamycin	0-11	nerve growth factor	Mus musculus	75-94
19838798-1	2010	The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry.	Tunicamycin	43-54	nerve growth factor	Mus musculus	14-33
19838798-1	2010	The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry.	Tunicamycin	43-54	nerve growth factor	Mus musculus	35-38
19838798-1	2010	The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry.	Tunicamycin	56-58	nerve growth factor	Mus musculus	14-33
19838798-1	2010	The effect of nerve growth factor (NGF) on tunicamycin (Tm)-treated neurons in the trigeminal ganglion was investigated by use of caspase-3 immunohistochemistry.	Tunicamycin	56-58	nerve growth factor	Mus musculus	35-38
20005867-5	2010	Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells.	Tunicamycin	19-30	ATP binding cassette subfamily C member 4	Homo sapiens	237-241
20005867-5	2010	Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells.	Tunicamycin	19-30	ATP binding cassette subfamily C member 1	Homo sapiens	306-310
20005867-5	2010	Pre-treatment with tunicamycin, which inhibits the biosynthesis of N-linked oligosaccharides, decreased the accumulation of Pt in sensitive cells exposed to oxaliplatin or cisplatin and increased the electrophoretic mobility of MRP1 and MRP4, reproducing the association between decreased glycosylation of MRP1 and MRP4 and decreased Pt accumulation observed in the resistant IGROV-1/OHP cells.	Tunicamycin	19-30	ATP binding cassette subfamily C member 4	Homo sapiens	315-319
20348923-5	2010	Mice with deletion of p85alpha in liver (L-Pik3r1(-/-)) show a similar attenuated UPR after tunicamycin administration, leading to an increased inflammatory response.	Tunicamycin	92-103	phosphoinositide-3-kinase regulatory subunit 1	Mus musculus	22-30
20080976-2	2010	IFRD1 mRNA and protein are elevated in tunicamycin-treated human kidney epithelial cells via stabilization of the mRNA.	Tunicamycin	39-50	interferon related developmental regulator 1	Homo sapiens	0-5
20231441-5	2010	Treatment with an inducer of UPR, tunicamycin, resulted in accelerated cell death of AtBAG7-null mutants.	Tunicamycin	34-45	BCL-2-associated athanogene 7	Arabidopsis thaliana	85-91
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
20305782-8	2010	A marked increase in PARM-1 expression was observed in response to ER stress inducers such as thapsigargin and tunicamycin, which also induced apoptotic cell death.	Tunicamycin	111-122	prostate androgen-regulated mucin-like protein 1	Rattus norvegicus	21-27
19961488-10	2010	Exposure of cells to the endoplasmic reticulum stress inducers thapsigargin and tunicamycin also led to cell apoptosis, which was modulated by Cx43 levels in a way similar to MG132.	Tunicamycin	80-91	gap junction protein, alpha 1	Mus musculus	143-147
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	growth differentiation factor 10	Homo sapiens	161-164
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	AKT serine/threonine kinase 1	Homo sapiens	221-224
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	mitogen-activated protein kinase 1	Homo sapiens	229-232
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	AKT serine/threonine kinase 1	Homo sapiens	264-267
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	mitogen-activated protein kinase 1	Homo sapiens	337-340
20007973-5	2010	FLS2 tolerated mild underglycosylation occurring in stt3a but was sensitive to severe underglycosylation induced by tunicamycin treatment.	Tunicamycin	116-127	Leucine-rich receptor-like protein kinase family protein	Arabidopsis thaliana	0-4
19834331-7	2010	TUDCA treatment inhibited tunicamycin-induced ER stress as evidenced by the attenuation of phosphorylation of eukaryotic translation initiation factor-2a and glucose reactive protein-78.	Tunicamycin	26-37	eukaryotic translation initiation factor 2A	Homo sapiens	110-153
19901967-9	2010	TCTP also protects cells against the proapoptotic effects of tunicamycin and etoposide, but not against those of arsenite.	Tunicamycin	61-72	tumor protein, translationally-controlled 1	Homo sapiens	0-4
20104019-3	2010	Three widely used ER stress inducers including tunicamycin, DTT and MG132 led to the conversion of LC3-I to LC3-II , a commonly used marker of autophagy, as well as the downregulation of mTOR concurrently.	Tunicamycin	47-58	mechanistic target of rapamycin kinase	Homo sapiens	187-191
19782129-5	2010	Tunicamycin prevented the N-linked glycosylation and maturation of PDGFRbeta as well as its activation by PDGF-BB.	Tunicamycin	0-11	platelet derived growth factor receptor beta	Homo sapiens	67-76
19782129-6	2010	However, upon tunicamycin treatment, DRD4 continued to signal to ERK1/2 in a tyrphostin A9-sensitive manner.	Tunicamycin	14-25	dopamine receptor D4	Homo sapiens	37-41
19782129-6	2010	However, upon tunicamycin treatment, DRD4 continued to signal to ERK1/2 in a tyrphostin A9-sensitive manner.	Tunicamycin	14-25	mitogen-activated protein kinase 3	Homo sapiens	65-71
21140004-7	2010	Our data showed that blocking of N-glycan transfer to the nascent polypeptide chain with the antibiotic tunicamycin resulted in the loss of E1 and E2.	Tunicamycin	104-115	small nucleolar RNA, H/ACA box 73A	Homo sapiens	140-149
20944397-6	2010	In agreement with increases of TIN1 transcripts, the TIN1 protein accumulated in response to tunicamycin treatment.	Tunicamycin	93-104	tunicamycin induced protein	Arabidopsis thaliana	31-35
20944397-6	2010	In agreement with increases of TIN1 transcripts, the TIN1 protein accumulated in response to tunicamycin treatment.	Tunicamycin	93-104	tunicamycin induced protein	Arabidopsis thaliana	53-57
20511722-3	2010	Here we show that tunicamycin, an antibiotic promoting ER stress, suppresses the expression of p21, a tumor suppressor that induces cell cycle arrest and inhibits apoptosis.	Tunicamycin	18-29	cyclin dependent kinase inhibitor 1A	Homo sapiens	95-98
20511722-5	2010	Consistently with these findings, siRNA-mediated inhibition of p21 levels restored the sensitivity of CHOP-deficient cells to tunicamycin.	Tunicamycin	126-137	cyclin dependent kinase inhibitor 1A	Homo sapiens	63-66
20164584-4	2010	Tunicamycin treatment caused a doubling of PSEN1 holoprotein production in HEK293 cells and an increase in holoprotein production to approximately 180% in GOTO human neuroblastoma and KNS-42 human glioma cell lines, without changing the amounts of PSEN1 N- or C-terminal fragments.	Tunicamycin	0-11	presenilin 1	Homo sapiens	43-48
20164584-4	2010	Tunicamycin treatment caused a doubling of PSEN1 holoprotein production in HEK293 cells and an increase in holoprotein production to approximately 180% in GOTO human neuroblastoma and KNS-42 human glioma cell lines, without changing the amounts of PSEN1 N- or C-terminal fragments.	Tunicamycin	0-11	presenilin 1	Homo sapiens	248-253
20164584-6	2010	HEK293 cells that stably overexpressed PSEN1 holoprotein showed increased resistance to ER stress induced by tunicamycin, but they did not show resistance to ER stress caused by thapsigargin, a specific inhibitor of sarco ER calcium-ATPase (SERCA).	Tunicamycin	109-120	presenilin 1	Homo sapiens	39-44
20164584-7	2010	In wild-type HEK293 cells under ER stress induced by tunicamycin, an increased amount of SERCA interacted with PSEN1 holoprotein.	Tunicamycin	53-64	presenilin 1	Homo sapiens	111-116
19773801-8	2010	ER stress agent tunicamycin induced ARMET and CHOP expressions in the primary cultured neurons.	Tunicamycin	16-27	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	36-41
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
19773801-9	2010	Treatment with recombinant human ARMET promoted neuron proliferation and prevented from neuron apoptosis induced by tunicamycin.	Tunicamycin	116-127	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	33-38
20022931-4	2010	Western blot analyses performed with or without endoglycosidase H, peptide:N-glycosidase F or tunicamycin treatments and site-directed mutagenesis revealed that MC2R was glycosylated in the N-terminal domain at its two putative N-glycosylation sites (Asn(12)-Asn(13)-Thr(14) and Asn(17)-Asn(18)-Ser(19)).	Tunicamycin	94-105	melanocortin 2 receptor	Homo sapiens	161-165
19783479-6	2010	These studies uncovered PknB/Stk and Stp as modulators of cell wall structure and susceptibility to cell wall-acting antibiotics such as certain beta-lactams and tunicamycin.	Tunicamycin	162-173	macrophage stimulating 1 receptor (c-met-related tyrosine kinase)	Mus musculus	29-32
19875812-5	2010	Mesangial cells preferentially induced C/EBPbeta after exposure to thapsigargin or tunicamycin; induction of C/EBPdelta was modest and transient, and expression of C/EBPalpha was absent.	Tunicamycin	83-94	CCAAT/enhancer binding protein (C/EBP), beta	Mus musculus	39-48
19841481-7	2009	Consistent with a synthetic impairment between challenged ER function and inositol deprivation, increased expression of NTE1 improved the growth of cells exposed to tunicamycin in the absence of inositol.	Tunicamycin	165-176	lysophospholipase	Saccharomyces cerevisiae S288C	120-124
19909340-5	2009	When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38.	Tunicamycin	101-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	5-10
19909340-5	2009	When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38.	Tunicamycin	101-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	167-172
19909340-5	2009	When ABCG2 wild type-expressing cells were incubated with various N-linked glycosylation inhibitors, tunicamycin profoundly suppressed the protein expression level of ABCG2 and, accordingly, reduced the ABCG2-mediated cellular resistance to the cancer chemotherapeutic SN-38.	Tunicamycin	101-112	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	167-172
19643964-8	2009	The induced caspase-4 and caspase-3 activities by tunicamycin and the stimulated IL-8 protein expression by IL-1beta were markedly reduced by caspase-4 inhibitor Z-LEVD-fmk.	Tunicamycin	50-61	caspase 4	Homo sapiens	12-21
19643964-8	2009	The induced caspase-4 and caspase-3 activities by tunicamycin and the stimulated IL-8 protein expression by IL-1beta were markedly reduced by caspase-4 inhibitor Z-LEVD-fmk.	Tunicamycin	50-61	caspase 3	Homo sapiens	26-35
19643964-9	2009	Although caspase-4 inhibitor Z-LEVD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tunicamycin-induced hRPE apoptotic cell death by 59% and 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis.	Tunicamycin	90-101	caspase 4	Homo sapiens	9-18
19643964-9	2009	Although caspase-4 inhibitor Z-LEVD-fmk and caspase-1 and -4 inhibitor Z-YVAD-fmk reduced tunicamycin-induced hRPE apoptotic cell death by 59% and 86%, respectively, pan-caspase inhibitor Z-VAD-fmk completely abolished the induced apoptosis.	Tunicamycin	90-101	caspase 1	Homo sapiens	44-60
19643964-8	2009	The induced caspase-4 and caspase-3 activities by tunicamycin and the stimulated IL-8 protein expression by IL-1beta were markedly reduced by caspase-4 inhibitor Z-LEVD-fmk.	Tunicamycin	50-61	caspase 4	Homo sapiens	142-151
19242657-0	2009	Tunicamycin suppresses cisplatin-induced HepG2 cell apoptosis via enhancing p53 protein nuclear export.	Tunicamycin	0-11	tumor protein p53	Homo sapiens	76-79
19739097-11	2009	In addition, blockage of N-glycosylation by treatment with tunicamycin eliminated 17 kDa form of intracellular IL-13, but failed to promote IL-13 secretion in BSMC.	Tunicamycin	59-70	interleukin 13	Homo sapiens	111-116
19502591-5	2009	ER stress agents thapsigargin and tunicamycin suppressed AdipoR2 and pAMPK levels in Huh7 cells, while fenofibrate and the chemical chaperone 4-phenylbutyrate (PBA) prevented these changes.	Tunicamycin	34-45	adiponectin receptor 2	Homo sapiens	57-64
19741092-7	2009	However, we show that TMX-class I HC interaction is enhanced during tunicamycin-induced ER stress, and TMX prevents the ER-to-cytosol retrotranslocation of misfolded class I HC targeted for proteasomal degradation.	Tunicamycin	68-79	thioredoxin related transmembrane protein 1	Homo sapiens	22-25
19777212-0	2009	Tunicamycin induces resistance to camptothecin and etoposide in human hepatocellular carcinoma cells: role of cell-cycle arrest and GRP78.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	132-137
19777212-11	2009	Furthermore, the cells transfected with GRP78 siRNA were partly resistant to tunicamycin-induced apoptosis but not the inhibitory effect on cell-cycle regulators indicating that GRP78 and G1 arrest are two independent factors to tunicamycin-induced resistance mechanism.	Tunicamycin	77-88	heat shock protein family A (Hsp70) member 5	Homo sapiens	40-45
19777212-11	2009	Furthermore, the cells transfected with GRP78 siRNA were partly resistant to tunicamycin-induced apoptosis but not the inhibitory effect on cell-cycle regulators indicating that GRP78 and G1 arrest are two independent factors to tunicamycin-induced resistance mechanism.	Tunicamycin	229-240	heat shock protein family A (Hsp70) member 5	Homo sapiens	40-45
19777212-12	2009	In conclusion, the data suggest that tunicamycin induces the resistance to topoisomerase inhibitors through GRP78 up-regulation and G1 arrest of the cell cycle.	Tunicamycin	37-48	heat shock protein family A (Hsp70) member 5	Homo sapiens	108-113
19699254-4	2009	Capsaicin also induced degradation of tumor suppressor p53; this effect was enhanced by the ER stressor tunicamycin.	Tunicamycin	104-115	tumor protein p53	Homo sapiens	55-58
19825181-6	2009	Three generations of barcode microarrays at 30, 8 and 5 microm features sizes independently identified the primary target of tunicamycin to be ALG7.	Tunicamycin	125-136	UDP-N-acetylglucosamine--dolichyl-phosphate N-acetylglucosaminephosphotransferase	Saccharomyces cerevisiae S288C	143-147
19640905-6	2009	In the present study, we show that alpha-actinin-4 K256E upregulates grp94 and CHOP expression in COS cells and significantly exacerbates induction of bip and CHOP in GEC in the presence of tunicamycin.	Tunicamycin	190-201	actinin alpha 4	Homo sapiens	35-50
19561031-4	2009	Our data show that the proteolytic cleavage of the rodent Muc3 SEA module was partially prevented by treatment with tunicamycin, an inhibitor of N-glycosylation.	Tunicamycin	116-127	MUC3	Homo sapiens	58-62
19615339-3	2009	CRELD2 mRNA is also shown to be immediately induced by treatment with the ER stress-inducing reagents tunicamycin and brefeldin A.	Tunicamycin	102-113	cysteine-rich with EGF-like domains 2	Mus musculus	0-6
19650649-6	2009	To address the role of Sep15 in protein folding, we analyzed changes in Sep15 expression in murine fibroblast NIH3T3 cells in response to tunicamycin, brefeldin A (brefA), thapsigargin, and DTT that lead to accumulation of unfolded proteins within the ER.	Tunicamycin	138-149	selenoprotein F	Mus musculus	72-77
19282840-6	2009	Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro.	Tunicamycin	97-108	CCAAT enhancer binding protein beta	Homo sapiens	238-247
19282840-6	2009	Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro.	Tunicamycin	97-108	Kruppel like factor 4	Homo sapiens	249-253
19282840-6	2009	Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro.	Tunicamycin	97-108	ATP binding cassette subfamily A member 12	Homo sapiens	259-265
19282840-6	2009	Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro.	Tunicamycin	110-112	CCAAT enhancer binding protein beta	Homo sapiens	238-247
19282840-6	2009	Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro.	Tunicamycin	110-112	Kruppel like factor 4	Homo sapiens	249-253
19282840-6	2009	Furthermore, microarray analyses and quantitative PCR revealed that ER stress-inducing reagents, tunicamycin (TU), thapsigargin, and brefeldin A, altered the expression of genes essential for human epidermal KC differentiation, including C/EBPbeta, KLF4, and ABCA12 in vitro.	Tunicamycin	110-112	ATP binding cassette subfamily A member 12	Homo sapiens	259-265
19411306-0	2009	Knockdown of ERp57 increases BiP/GRP78 induction and protects against hyperoxia and tunicamycin-induced apoptosis.	Tunicamycin	84-95	protein disulfide isomerase family A member 3	Homo sapiens	13-18
19411306-6	2009	Transient transfection of ERp57 small interfering RNA significantly knocked down ERp57 expression and reduced hyperoxia- or tunicamycin-induced apoptosis in human endothelial cells.	Tunicamycin	124-135	protein disulfide isomerase family A member 3	Homo sapiens	26-31
19411306-8	2009	The activation of caspase-3 induced by hyperoxia or tunicamycin was diminished and immunoglobulin heavy chain-binding protein/glucose-regulated protein 78-kDa (BiP/GRP78) induction was increased in ERp57 knockdown cells.	Tunicamycin	52-63	caspase 3	Homo sapiens	18-27
19411306-9	2009	Overexpression of ERp57 exacerbated hyperoxia- or tunicamycin-induced apoptosis in human endothelial cells.	Tunicamycin	50-61	protein disulfide isomerase family A member 3	Homo sapiens	18-23
19411306-11	2009	Overexpression of ERp57 also augmented tunicamycin-induced caspase-3 activation and reduced BiP/GRP78 induction.	Tunicamycin	39-50	protein disulfide isomerase family A member 3	Homo sapiens	18-23
19411306-11	2009	Overexpression of ERp57 also augmented tunicamycin-induced caspase-3 activation and reduced BiP/GRP78 induction.	Tunicamycin	39-50	caspase 3	Homo sapiens	59-68
19411306-13	2009	It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction.	Tunicamycin	85-96	protein disulfide isomerase family A member 3	Homo sapiens	29-34
19411306-13	2009	It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction.	Tunicamycin	85-96	caspase 3	Homo sapiens	132-141
19411306-13	2009	It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction.	Tunicamycin	85-96	heat shock protein family A (Hsp70) member 5	Homo sapiens	172-175
19411306-13	2009	It appears that knockdown of ERp57 confers cellular protection against hyperoxia- or tunicamycin-induced apoptosis by inhibition of caspase-3 activation and stimulation of BiP/GRP78 induction.	Tunicamycin	85-96	heat shock protein family A (Hsp70) member 5	Homo sapiens	176-181
19443639-6	2009	Bsg isolated from HL-60 cells bound to E-selectin, and tunicamycin treatment to abolish N-linked glycans from Bsg abrogated this binding.	Tunicamycin	55-66	basigin (Ok blood group)	Homo sapiens	110-113
19650649-7	2009	We show that expression of this protein is transcriptionally up-regulated in response to adaptive UPR caused by tunicamycin and brefA, whereas acute ER stress caused by DTT and thapsigargin leads to rapid and specific degradation of Sep15 by proteasomes.	Tunicamycin	112-123	selenoprotein F	Mus musculus	233-238
19724688-4	2009	This was primarily because of the inhibition of Mcl-1 by obatoclax, in that cotreatment with TM and another BH3 mimetic ABT737, which does not antagonize Mcl-1, caused only minimal increases in apoptosis.	Tunicamycin	93-95	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	48-53
19501045-5	2009	In neuroepithelial cells treated with tunicamycin, an N-glycosylation inhibitor, unglycosylated form of gp130 was detected.	Tunicamycin	38-49	interleukin 6 signal transducer	Mus musculus	104-109
19130057-0	2009	Activation of ER stress and inhibition of EGFR N-glycosylation by tunicamycin enhances susceptibility of human non-small cell lung cancer cells to erlotinib.	Tunicamycin	66-77	epidermal growth factor receptor	Homo sapiens	42-46
19130057-5	2009	We found that tunicamycin generated an aglycosylated form of 130 kDa EGFR.	Tunicamycin	14-25	epidermal growth factor receptor	Homo sapiens	69-73
19130057-6	2009	Tunicamycin additionally affected EGFR activation and subcellular localization.	Tunicamycin	0-11	epidermal growth factor receptor	Homo sapiens	34-38
19130057-7	2009	Interestingly, the combination of tunicamycin and erlotinib caused more inhibitory effect on EGFR phosphorylation than that of erlotinib alone.	Tunicamycin	34-45	epidermal growth factor receptor	Homo sapiens	93-97
19130057-9	2009	CONCLUSIONS: Overall, our data demonstrate that tunicamycin significantly enhances the susceptibility of lung cancer cells to erlotinib, particularly sensitizing resistant cell lines to erlotinib, and that such sensitization may be associated with activation of the ER stress pathway and with inhibition of EGFR N-glycosylation.	Tunicamycin	48-59	epidermal growth factor receptor	Homo sapiens	307-311
19492336-4	2009	Incubation of mesangial cells with ER stress-inducing agents (thapsigargin, tunicamycin, and AB(5) subtilase cytotoxin) resulted in a decrease in connexin 43 (Cx43) expression at both protein and mRNA levels.	Tunicamycin	76-87	gap junction protein alpha 1	Homo sapiens	146-157
19492336-4	2009	Incubation of mesangial cells with ER stress-inducing agents (thapsigargin, tunicamycin, and AB(5) subtilase cytotoxin) resulted in a decrease in connexin 43 (Cx43) expression at both protein and mRNA levels.	Tunicamycin	76-87	gap junction protein alpha 1	Homo sapiens	159-163
19242657-4	2009	In order to further explore the mechanism underlying tumor resistance to cisplatin, we observed that increased nuclear export of endogenous p53 protein by pharmacological inducers of ER stress, such as tunicamycin, was associated with the suppression of cisplatin-induced apoptosis.	Tunicamycin	202-213	tumor protein p53	Homo sapiens	140-143
19251702-6	2009	Conversely, the hypersensitivity of lrk-1 mutant animals to the endoplasmic reticulum stressor tunicamycin was reduced in a pink-1 mutant background.	Tunicamycin	95-106	Leucine-rich repeat serine/threonine-protein kinase 1	Caenorhabditis elegans	36-41
19251702-6	2009	Conversely, the hypersensitivity of lrk-1 mutant animals to the endoplasmic reticulum stressor tunicamycin was reduced in a pink-1 mutant background.	Tunicamycin	95-106	PTEN induced kinase 1	Homo sapiens	124-130
19276076-8	2009	Mesangial cell cultures treated with poly(I:C) or tunicamycin in normal glucose media synthesized monocyte-adhesive hyaluronan matrices but with concurrent down-regulation of cyclin D3.	Tunicamycin	50-61	cyclin D3	Rattus norvegicus	175-184
19406177-7	2009	Furthermore, in vitro, ghrelin directly inhibited the myocardial ERS response induced by tunicamycin or dithiothreitol in rat cardiac tissue.	Tunicamycin	89-100	ghrelin and obestatin prepropeptide	Rattus norvegicus	23-30
19582722-7	2009	The 2-D apoB profile obtained from the media of HepG2 cells treated in the presence of agents (tunicamycin and glucosamine) known to modulate the PTM of apoB was distinct from that of control cells.	Tunicamycin	95-106	apolipoprotein B	Homo sapiens	8-12
19582722-7	2009	The 2-D apoB profile obtained from the media of HepG2 cells treated in the presence of agents (tunicamycin and glucosamine) known to modulate the PTM of apoB was distinct from that of control cells.	Tunicamycin	95-106	apolipoprotein B	Homo sapiens	153-157
19424594-5	2009	Importantly, both PI3K inhibitor LY294002 and dominant-negative Akt construct promoted tunicamycin- and thapsigargin-induced ERK phosphorylation.	Tunicamycin	87-98	AKT serine/threonine kinase 1	Homo sapiens	64-67
19424594-5	2009	Importantly, both PI3K inhibitor LY294002 and dominant-negative Akt construct promoted tunicamycin- and thapsigargin-induced ERK phosphorylation.	Tunicamycin	87-98	mitogen-activated protein kinase 1	Homo sapiens	125-128
19454717-8	2009	The suppression of NF-kappaB was reproduced by other inducers of UPR including AB(5) subtilase cytotoxin, tunicamycin, thapsigargin, and A23187.	Tunicamycin	106-117	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	19-28
19347031-3	2009	We targeted Bcl-2 to mitochondria or endoplasmic reticulum (ER) and induced apoptosis using several apoptotic stimuli that initiate ER and/or mitochondrial signaling pathways (UV radiation, TNF and cycloheximide, staurosporine, thapsigargin and tunicamycin).	Tunicamycin	245-256	BCL2 apoptosis regulator	Homo sapiens	12-17
19307757-0	2009	Tunicamycin enhances TRAIL-induced apoptosis by inhibition of cyclin D1 and the subsequent downregulation of survivin.	Tunicamycin	0-11	TNF superfamily member 10	Homo sapiens	21-26
19307757-0	2009	Tunicamycin enhances TRAIL-induced apoptosis by inhibition of cyclin D1 and the subsequent downregulation of survivin.	Tunicamycin	0-11	cyclin D1	Homo sapiens	62-71
19307757-3	2009	In this study, we showed that tunicamycin, a naturally occurring antibiotic, was a potent enhancer of TRAIL-induced apoptosis through downregulation of survivin.	Tunicamycin	30-41	TNF superfamily member 10	Homo sapiens	102-107
19307757-4	2009	The tunicamycin-mediated sensitization to TRAIL was efficiently reduced by forced expression of survivin, suggesting that the sensitization was mediated at least in part through inhibition of survivin expression.	Tunicamycin	4-15	TNF superfamily member 10	Homo sapiens	42-47
19307757-5	2009	Tunicamycin also repressed expression of cyclin D1, a cell cycle regulator commonly overexpressed in thyroid carcinoma.	Tunicamycin	0-11	cyclin D1	Homo sapiens	41-50
19307757-6	2009	Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin.	Tunicamycin	182-193	cyclin D1	Homo sapiens	161-170
19307757-6	2009	Furthermore, silencing cyclin D1 by RNA interference reduced survivin expression and sensitized thyroid cancer cells to TRAIL; in contrast, forced expression of cyclin D1 attenuated tunicamycin-potentiated TRAIL-induced apoptosis via over-riding downregulation of survivin.	Tunicamycin	182-193	TNF superfamily member 10	Homo sapiens	206-211
19307757-7	2009	Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin.	Tunicamycin	44-55	TNF superfamily member 10	Homo sapiens	65-70
19307757-7	2009	Collectively, our results demonstrated that tunicamycin promoted TRAIL-induced apoptosis, at least in part, by inhibiting the expression of cyclin D1 and subsequent survivin.	Tunicamycin	44-55	cyclin D1	Homo sapiens	140-149
18661133-7	2009	Cytotoxicity of two agents, cytochalasin H and tunicamycin, identified through the COMPARE analysis of KSR1 expression and drug sensitivity, was also examined in wild type (KSR(+/+)) mouse embryo fibroblasts (MEFs) and MEFs deficient in KSR1 expression (KSR1(-/-)).	Tunicamycin	47-58	kinase suppressor of ras 1	Mus musculus	103-107
19369942-2	2009	We found that the FG-specific Kss1 MAPK is activated by a combination of an O-glycosylation defect caused by disruption of the gene encoding the protein O-mannosyltransferase Pmt4, and an N-glycosylation defect induced by tunicamycin.	Tunicamycin	222-233	mitogen-activated serine/threonine-protein kinase KSS1	Saccharomyces cerevisiae S288C	30-34
19360472-3	2009	The nuclear translocation of DHFR protein during apoptosis was independent of the cellular context, but it was more sensitive in cell death induction by DNA damaging agents such as doxorubicin, etoposide and ultraviolent radiation than endoplasmic reticulum stressors (brefeldin-A and tunicamycin) and anti-microtubule agents (paclitaxel and nocodozole).	Tunicamycin	285-296	dihydrofolate reductase	Homo sapiens	29-33
19188482-3	2009	Tunicamycin caused early activation of caspase-2, -3, -4, and -8, followed by apoptosis, whereas caspase-9 was slowly activated.	Tunicamycin	0-11	caspase 2	Homo sapiens	39-64
19188482-5	2009	Tunicamycin induced apoptosis independently of the mitochondrial pathway but caused lysosomal destabilization followed by lysosomal membrane permeabilization (LMP), cathepsin B relocation from lysosomes to the cytosol, and caspase-8 and -3 activation.	Tunicamycin	0-11	cathepsin B	Homo sapiens	165-176
19188482-5	2009	Tunicamycin induced apoptosis independently of the mitochondrial pathway but caused lysosomal destabilization followed by lysosomal membrane permeabilization (LMP), cathepsin B relocation from lysosomes to the cytosol, and caspase-8 and -3 activation.	Tunicamycin	0-11	caspase 8	Homo sapiens	223-239
19188482-9	2009	Activating GSK-3beta caused K562 cells to be susceptible to tunicamycin-induced apoptosis.	Tunicamycin	60-71	glycogen synthase kinase 3 beta	Homo sapiens	11-20
19338771-5	2009	Tunicamycin-evoked changes in cellular Ca2+ fluxes coincided with decreased glycosylation of STIM1 protein.	Tunicamycin	0-11	stromal interaction molecule 1	Homo sapiens	93-98
18661133-10	2009	In addition, the sensitivity to cytochalasin H and tunicamycin of breast cancer cell lines with low KSR1 expression, (HS578T and MDA-MB-231/ATCC), was increased relative to the sensitivity of breast cancer cells with higher levels of KSR1 (MCF7).	Tunicamycin	51-62	kinase suppressor of ras 1	Homo sapiens	100-104
18661133-10	2009	In addition, the sensitivity to cytochalasin H and tunicamycin of breast cancer cell lines with low KSR1 expression, (HS578T and MDA-MB-231/ATCC), was increased relative to the sensitivity of breast cancer cells with higher levels of KSR1 (MCF7).	Tunicamycin	51-62	kinase suppressor of ras 1	Homo sapiens	234-238
19367787-2	2009	In the present study we propose that the cytoprotective effects attributed to 17beta-estradiol and tunicamycin in an in vivo rodent model of ischemia are reflected by changes in neuronal tissue levels of m-calpain, HSP70, GRP94 and GRP78.	Tunicamycin	99-110	calpain 2	Rattus norvegicus	204-213
19367787-2	2009	In the present study we propose that the cytoprotective effects attributed to 17beta-estradiol and tunicamycin in an in vivo rodent model of ischemia are reflected by changes in neuronal tissue levels of m-calpain, HSP70, GRP94 and GRP78.	Tunicamycin	99-110	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	215-220
19367787-2	2009	In the present study we propose that the cytoprotective effects attributed to 17beta-estradiol and tunicamycin in an in vivo rodent model of ischemia are reflected by changes in neuronal tissue levels of m-calpain, HSP70, GRP94 and GRP78.	Tunicamycin	99-110	heat shock protein 90 beta family member 1	Rattus norvegicus	222-227
19367787-2	2009	In the present study we propose that the cytoprotective effects attributed to 17beta-estradiol and tunicamycin in an in vivo rodent model of ischemia are reflected by changes in neuronal tissue levels of m-calpain, HSP70, GRP94 and GRP78.	Tunicamycin	99-110	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	232-237
19367787-7	2009	Pretreatment with 50 microg/kg tunicamycin significantly reduced HSP70 in cortical tissue samples taken from sham-operated rats and appeared to attenuate the threshold for activation of m-calpain in rats undergoing 4 h of MCAO.	Tunicamycin	31-42	heat shock protein family A (Hsp70) member 1B	Rattus norvegicus	65-70
19367787-7	2009	Pretreatment with 50 microg/kg tunicamycin significantly reduced HSP70 in cortical tissue samples taken from sham-operated rats and appeared to attenuate the threshold for activation of m-calpain in rats undergoing 4 h of MCAO.	Tunicamycin	31-42	calpain 2	Rattus norvegicus	186-195
19367787-8	2009	Lastly, a combined treatment in which rats undergoing MCAO were pretreated with both tunicamycin (24 h prior) and 17beta-estradiol (30 min prior) was associated with an attenuated stress response as indicated by reduced expression of GRP78 and GRP94 when compared to saline-treated controls.	Tunicamycin	85-96	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	234-239
19367787-8	2009	Lastly, a combined treatment in which rats undergoing MCAO were pretreated with both tunicamycin (24 h prior) and 17beta-estradiol (30 min prior) was associated with an attenuated stress response as indicated by reduced expression of GRP78 and GRP94 when compared to saline-treated controls.	Tunicamycin	85-96	heat shock protein 90 beta family member 1	Rattus norvegicus	244-249
18661133-7	2009	Cytotoxicity of two agents, cytochalasin H and tunicamycin, identified through the COMPARE analysis of KSR1 expression and drug sensitivity, was also examined in wild type (KSR(+/+)) mouse embryo fibroblasts (MEFs) and MEFs deficient in KSR1 expression (KSR1(-/-)).	Tunicamycin	47-58	kinase suppressor of ras 1	Mus musculus	103-106
18661133-8	2009	These studies demonstrated enhanced sensitivity, as well as increased ERK activation, in KSR(-/-) MEFs following exposure to tunicamycin or cytochalasin H compared to KSR(+/+) MEFs.	Tunicamycin	125-136	kinase suppressor of ras 1	Homo sapiens	89-92
18661133-9	2009	Furthermore, restoration of KSR1 expression in KSR(-/-) MEFs following stable transduction of cells with a KSR1 expression vector, enhanced sensitivity of cells to tunicamycin and cytochalasin H and decreased ERK1/2 activation following exposure to these drugs.	Tunicamycin	164-175	kinase suppressor of ras 1	Homo sapiens	28-32
18661133-9	2009	Furthermore, restoration of KSR1 expression in KSR(-/-) MEFs following stable transduction of cells with a KSR1 expression vector, enhanced sensitivity of cells to tunicamycin and cytochalasin H and decreased ERK1/2 activation following exposure to these drugs.	Tunicamycin	164-175	kinase suppressor of ras 1	Homo sapiens	28-31
19122239-4	2009	ERdj5 promoted apoptosis in tunicamycin, thapsigargin, and bortezomib-treated cells.	Tunicamycin	28-39	DnaJ heat shock protein family (Hsp40) member C10	Homo sapiens	0-5
19302790-3	2009	X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts.	Tunicamycin	95-106	X-box binding protein 1	Homo sapiens	0-15
19302790-3	2009	X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts.	Tunicamycin	95-106	X-box binding protein 1	Homo sapiens	17-22
19302790-3	2009	X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts.	Tunicamycin	95-106	heat shock protein family A (Hsp70) member 5	Homo sapiens	34-39
19302790-3	2009	X-box protein-1 (XBP-1) splicing, GRP78 expression and caspase-12 activation were increased by tunicamycin or IR in Atm-deficient AT5BIVA fibroblasts.	Tunicamycin	95-106	ATM serine/threonine kinase	Homo sapiens	116-119
19302790-4	2009	Activation of caspase-12 and caspase-3 by tunicamycin was significantly reduced in cells transfected with wild-type Atm (AT5BIVA/wtATM).	Tunicamycin	42-53	caspase 3	Homo sapiens	29-38
19302790-4	2009	Activation of caspase-12 and caspase-3 by tunicamycin was significantly reduced in cells transfected with wild-type Atm (AT5BIVA/wtATM).	Tunicamycin	42-53	ATM serine/threonine kinase	Homo sapiens	116-119
19302790-4	2009	Activation of caspase-12 and caspase-3 by tunicamycin was significantly reduced in cells transfected with wild-type Atm (AT5BIVA/wtATM).	Tunicamycin	42-53	ATM serine/threonine kinase	Homo sapiens	121-134
19302790-5	2009	Atm knockdown by siRNA, however, noticeably elevated ER-stress and chemosensitivity to tunicamycin.	Tunicamycin	87-98	ATM serine/threonine kinase	Homo sapiens	0-3
19100962-4	2009	Both thapsigargin and tunicamycin elevated the mRNA level of MMP13 and phosphorylation of p38 MAPK.	Tunicamycin	22-33	matrix metallopeptidase 13	Homo sapiens	61-66
19100962-4	2009	Both thapsigargin and tunicamycin elevated the mRNA level of MMP13 and phosphorylation of p38 MAPK.	Tunicamycin	22-33	mitogen-activated protein kinase 14	Homo sapiens	90-93
18990090-8	2009	Lastly, the ER stressors tunicamycin, thapsigargin and Brefeldin A were found to inhibit basal Nrf1 activity by approximately 25%, and almost completely prevented induction of Nrf1-mediated transactivation by tBHQ.	Tunicamycin	25-36	nuclear respiratory factor 1	Rattus norvegicus	95-99
18990090-8	2009	Lastly, the ER stressors tunicamycin, thapsigargin and Brefeldin A were found to inhibit basal Nrf1 activity by approximately 25%, and almost completely prevented induction of Nrf1-mediated transactivation by tBHQ.	Tunicamycin	25-36	nuclear respiratory factor 1	Rattus norvegicus	176-180
19005738-4	2009	GDNF secretion was augmented by stimulation with high potassium, while it was inhibited by treatment with either tunicamycin, an inhibitor of protein glycosylation, or brefeldin A, a disturbing factor of ER-Golgi transport.	Tunicamycin	113-124	glial cell derived neurotrophic factor	Homo sapiens	0-4
19180501-10	2009	Incubation with 2 agents that induce endoplasmic reticulum stress, tunicamycin and thapsigargin, increased TRB3 levels in normal cells.	Tunicamycin	67-78	tribbles pseudokinase 3	Homo sapiens	107-111
19166345-12	2009	Inhibition of hH(4)R glycosylation by tunicamycin reduced the [(3)H]HA binding B(max) value.	Tunicamycin	38-49	histamine receptor H4	Homo sapiens	14-20
18840095-2	2009	The present study shows that ASNS (asparagine synthetase) transcription activity was up-regulated in HepG2 cells treated with the UPR activators thapsigargin and tunicamycin.	Tunicamycin	162-173	asparagine synthetase (glutamine-hydrolyzing)	Homo sapiens	29-33
18840095-2	2009	The present study shows that ASNS (asparagine synthetase) transcription activity was up-regulated in HepG2 cells treated with the UPR activators thapsigargin and tunicamycin.	Tunicamycin	162-173	asparagine synthetase (glutamine-hydrolyzing)	Homo sapiens	35-56
19302790-0	2009	ATM blocks tunicamycin-induced endoplasmic reticulum stress.	Tunicamycin	11-22	ATM serine/threonine kinase	Homo sapiens	0-3
19302790-2	2009	We present here conclusive data showing that ATM blocks ER-stress induced by tunicamycin or ionizing radiation (IR).	Tunicamycin	77-88	ATM serine/threonine kinase	Homo sapiens	45-48
19567124-6	2009	The GRP78 expression level of the tunicamycin group was 4.9 times as high as that of the control group, and the CHOP expression level of the tunicamycin group was 3.1 times as high as hat of the control group.	Tunicamycin	34-45	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	4-9
19567124-6	2009	The GRP78 expression level of the tunicamycin group was 4.9 times as high as that of the control group, and the CHOP expression level of the tunicamycin group was 3.1 times as high as hat of the control group.	Tunicamycin	141-152	DNA-damage inducible transcript 3	Rattus norvegicus	112-116
19567124-7	2009	SERCA2a overexpression was found to relieve the expression of GRP78 induced by hypoxia and tunicamycin (49.1% and 50.4% decrease respectively), and to inhibit the activation of CHOP (52.7% and 66.1% decrease respectively).	Tunicamycin	91-102	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	62-67
19567124-9	2009	Compared with the tunicamycin group, the protein expression levels of GRP78 and CHOP of the SERCA2a overexpression + tunicamycin group were significantly lower by 50.4% and 66.1% respectively, the apoptotic rate was significantly lower by 54.0%, and the cardiomyocyte survival rate was significantly higher by 6.7% (all P &lt; 0.05).	Tunicamycin	18-29	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	70-75
19567124-9	2009	Compared with the tunicamycin group, the protein expression levels of GRP78 and CHOP of the SERCA2a overexpression + tunicamycin group were significantly lower by 50.4% and 66.1% respectively, the apoptotic rate was significantly lower by 54.0%, and the cardiomyocyte survival rate was significantly higher by 6.7% (all P &lt; 0.05).	Tunicamycin	18-29	DNA-damage inducible transcript 3	Rattus norvegicus	80-84
19567124-9	2009	Compared with the tunicamycin group, the protein expression levels of GRP78 and CHOP of the SERCA2a overexpression + tunicamycin group were significantly lower by 50.4% and 66.1% respectively, the apoptotic rate was significantly lower by 54.0%, and the cardiomyocyte survival rate was significantly higher by 6.7% (all P &lt; 0.05).	Tunicamycin	117-128	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	70-75
19567124-9	2009	Compared with the tunicamycin group, the protein expression levels of GRP78 and CHOP of the SERCA2a overexpression + tunicamycin group were significantly lower by 50.4% and 66.1% respectively, the apoptotic rate was significantly lower by 54.0%, and the cardiomyocyte survival rate was significantly higher by 6.7% (all P &lt; 0.05).	Tunicamycin	117-128	DNA-damage inducible transcript 3	Rattus norvegicus	80-84
18978361-0	2009	Tunicamycin enhances the apoptosis induced by tumor necrosis factor-related apoptosis-inducing ligand in endometriotic stromal cells.	Tunicamycin	0-11	TNF superfamily member 10	Homo sapiens	46-101
18978361-2	2009	In the present study, the effect of tunicamycin, a possible apoptosis enhancer, on TRAIL-induced apoptosis in endometriotic stromal cells (ESC) was determined.	Tunicamycin	36-47	TNF superfamily member 10	Homo sapiens	83-88
18978361-8	2009	RESULTS: Tunicamycin increases both DR5 mRNA (P &lt; 0.005) and TRAIL-induced apoptosis (P &lt; 0.0001) in ESC.	Tunicamycin	9-20	TNF receptor superfamily member 10b	Homo sapiens	36-39
18978361-8	2009	RESULTS: Tunicamycin increases both DR5 mRNA (P &lt; 0.005) and TRAIL-induced apoptosis (P &lt; 0.0001) in ESC.	Tunicamycin	9-20	TNF superfamily member 10	Homo sapiens	64-69
18978361-9	2009	The increase in TRAIL-induced apoptosis in ESC by tunicamycin was suppressed (P &lt; 0.05) by z-VAD-fmk.	Tunicamycin	50-61	TNF superfamily member 10	Homo sapiens	16-21
18978361-10	2009	Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin.	Tunicamycin	43-54	TNF receptor superfamily member 10b	Homo sapiens	18-21
18978361-10	2009	Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin.	Tunicamycin	43-54	TNF receptor superfamily member 10b	Homo sapiens	75-78
18978361-10	2009	Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin.	Tunicamycin	146-157	TNF receptor superfamily member 10b	Homo sapiens	18-21
18978361-10	2009	Transfection with DR5 siRNA suppressed the tunicamycin-induced increase in DR5 mRNA and abrogated the up-regulation of TRAIL-induced apoptosis by tunicamycin.	Tunicamycin	146-157	TNF superfamily member 10	Homo sapiens	119-124
18814142-4	2009	Exposure to adrenaline not only increased cAMP formation, phosphorylation of cAMP responsive element (CRE) binding protein (CREB) on serine133 and CRE reporter activity in a manner sensitive to propranolol, but also rendered C3H10T1/2 cells resistant to the cytotoxicity of hydrogen peroxide, but not of either 2,4-dinitirophenol or tunicamycin.	Tunicamycin	333-344	cAMP responsive element binding protein 1	Mus musculus	124-128
19026635-5	2009	In the present study, we show that glycosylation is an essential requirement for surface nucleolin expression, since it is prevented when cells are cultured in the presence of tunicamycin, an inhibitor of N-glycosylation.	Tunicamycin	176-187	nucleolin	Homo sapiens	89-98
18981290-5	2009	Tunicamycin treatment markedly decreased the secretion of ADAMTS13 into the culture medium of transfected cells.	Tunicamycin	0-11	A disintegrin and metalloproteinase with thrombospondin motifs 13	Cricetulus griseus	58-66
19047052-10	2009	We have found that Nrf3 is activated by the ER stressors tunicamycin and brefeldin A, and that NHB1 is required for this response.	Tunicamycin	57-68	nuclear factor, erythroid derived 2, like 3	Mus musculus	19-23
19007793-6	2009	Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis.	Tunicamycin	86-97	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	18-21
19007793-6	2009	Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis.	Tunicamycin	86-97	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	26-30
19007793-6	2009	Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis.	Tunicamycin	86-97	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	123-127
19007793-6	2009	Reconstitution of PKR and PACT expression in the null cells renders them sensitive to tunicamycin, thus demonstrating that PACT-induced PKR activation plays an essential function in induction of apoptosis.	Tunicamycin	86-97	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	136-139
19239156-6	2009	After tunicamycin-mediated ERS, the expression of the key molecular chaperone, Bip, increased in both cell lines.	Tunicamycin	6-17	heat shock protein 5	Mus musculus	79-82
19124762-3	2009	Priming of the cells with ER stress inducers (tunicamycin, thapsigargin, A23187, and AB5 subtilase cytotoxin) caused blunted induction of MCP-1 in response to TNF-alpha, IL-1beta, macrophage-derived factors, or bystander macrophages.	Tunicamycin	46-57	C-C motif chemokine ligand 2	Homo sapiens	138-143
19124762-3	2009	Priming of the cells with ER stress inducers (tunicamycin, thapsigargin, A23187, and AB5 subtilase cytotoxin) caused blunted induction of MCP-1 in response to TNF-alpha, IL-1beta, macrophage-derived factors, or bystander macrophages.	Tunicamycin	46-57	tumor necrosis factor	Homo sapiens	159-168
19124762-3	2009	Priming of the cells with ER stress inducers (tunicamycin, thapsigargin, A23187, and AB5 subtilase cytotoxin) caused blunted induction of MCP-1 in response to TNF-alpha, IL-1beta, macrophage-derived factors, or bystander macrophages.	Tunicamycin	46-57	interleukin 1 beta	Homo sapiens	170-178
19239156-7	2009	The chaperone, GRP94, responded differently to extended tunicamycin treatment, with protein levels remaining largely unchanged in 3T3L1 cells but falling in C2C12 cells.	Tunicamycin	56-67	heat shock protein 90, beta (Grp94), member 1	Mus musculus	15-20
18801901-4	2009	Our results demonstrated that tribbles-related protein 3 (TRB3), which is a target gene of CHOP, was responsible for tunicamycin (an ER stress inducer)-induced apoptosis.	Tunicamycin	117-128	tribbles pseudokinase 3	Rattus norvegicus	30-56
18801901-4	2009	Our results demonstrated that tribbles-related protein 3 (TRB3), which is a target gene of CHOP, was responsible for tunicamycin (an ER stress inducer)-induced apoptosis.	Tunicamycin	117-128	tribbles pseudokinase 3	Rattus norvegicus	58-62
18801901-4	2009	Our results demonstrated that tribbles-related protein 3 (TRB3), which is a target gene of CHOP, was responsible for tunicamycin (an ER stress inducer)-induced apoptosis.	Tunicamycin	117-128	DNA-damage inducible transcript 3	Rattus norvegicus	91-95
18691157-2	2008	Addressing the cytoprotective functions of PON2, we observed that PON2 overexpression provided significant resistance to ER-stress-induced caspase 3 activation when the ER stress was induced by interference with protein modification (by tunicamycin or dithiothreitol), but not when ER stress was induced by disturbance of Ca(2+) homoeostasis (by thapsigargin or A23187).	Tunicamycin	237-248	paraoxonase 2	Homo sapiens	66-70
19007793-0	2009	Essential role of PACT-mediated PKR activation in tunicamycin-induced apoptosis.	Tunicamycin	50-61	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	18-22
19007793-0	2009	Essential role of PACT-mediated PKR activation in tunicamycin-induced apoptosis.	Tunicamycin	50-61	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	32-35
19007793-3	2009	In this study, we examined the involvement of double-stranded RNA (dsRNA)-activated protein kinase (PKR) and its protein activator PACT in tunicamycin-induced apoptosis.	Tunicamycin	139-150	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	100-103
19007793-3	2009	In this study, we examined the involvement of double-stranded RNA (dsRNA)-activated protein kinase (PKR) and its protein activator PACT in tunicamycin-induced apoptosis.	Tunicamycin	139-150	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	131-135
19007793-4	2009	We demonstrate for the first time that PACT is phosphorylated in response to tunicamycin and is responsible for PKR activation by direct interaction.	Tunicamycin	77-88	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	39-43
19007793-4	2009	We demonstrate for the first time that PACT is phosphorylated in response to tunicamycin and is responsible for PKR activation by direct interaction.	Tunicamycin	77-88	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	112-115
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	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	13-17
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	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	26-29
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	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	95-99
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	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	111-114
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	eukaryotic translation initiation factor 2A	Homo sapiens	183-192
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
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
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	152-163	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	13-17
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	152-163	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	26-29
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	152-163	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	111-114
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	152-163	protein activator of interferon induced protein kinase EIF2AK2	Homo sapiens	13-17
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	152-163	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	26-29
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	152-163	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	111-114
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	167-178	heat shock protein 5	Mus musculus	83-88
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	167-178	heat shock protein 5	Mus musculus	90-132
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	167-178	heat shock protein 5	Mus musculus	134-137
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	167-178	heat shock protein 5	Mus musculus	139-142
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	252-263	heat shock protein 5	Mus musculus	83-88
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	252-263	heat shock protein 5	Mus musculus	90-132
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	252-263	heat shock protein 5	Mus musculus	134-137
18757512-1	2009	PURPOSE: The effect of a preferential inducer of 78 kDa glucose-regulated protein (GRP78)/immunoglobulin heavy-chain binding protein (BiP; BiP inducer X, BIX) against tunicamycin-induced cell death in RGC-5 (a rat ganglion cell line), and also against tunicamycin- or N-methyl-D-aspartate (NMDA)-induced retinal damage in mice was evaluated.	Tunicamycin	252-263	heat shock protein 5	Mus musculus	139-142
18757512-3	2009	The effect of BIX on tunicamycin (at 2 microg/mL)-induced damage was evaluated by measuring the cell-death rate and CHOP protein expression.	Tunicamycin	21-32	DNA-damage inducible transcript 3	Mus musculus	116-120
18757512-5	2009	The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression.	Tunicamycin	35-46	germ cell-less, spermatogenesis associated 1	Mus musculus	123-126
18757512-5	2009	The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression.	Tunicamycin	35-46	deoxynucleotidyltransferase, terminal	Mus musculus	139-180
18757512-5	2009	The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression.	Tunicamycin	35-46	deoxynucleotidyltransferase, terminal	Mus musculus	182-185
18757512-5	2009	The retinal cell damage induced by tunicamycin (1 microg) or NMDA (40 nmol) was assessed by examining ganglion cell layer (GCL) cell loss, terminal deoxyribonucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining, and CHOP protein expression.	Tunicamycin	35-46	DNA-damage inducible transcript 3	Mus musculus	241-245
18757512-7	2009	BIX (1 and 5 microM) significantly reduced tunicamycin-induced cell death, and BIX (5 microM) significantly reduced tunicamycin-induced CHOP protein expression.	Tunicamycin	116-127	DNA-damage inducible transcript 3	Mus musculus	136-140
18757512-9	2009	Co-administration of BIX (5 nmol) significantly reduced both the retinal cell death and the CHOP protein expression in GCL induced by intravitreal injection of tunicamycin or NMDA.	Tunicamycin	160-171	DNA-damage inducible transcript 3	Mus musculus	92-96
18757512-9	2009	Co-administration of BIX (5 nmol) significantly reduced both the retinal cell death and the CHOP protein expression in GCL induced by intravitreal injection of tunicamycin or NMDA.	Tunicamycin	160-171	germ cell-less, spermatogenesis associated 1	Mus musculus	119-122
19028522-4	2009	Pretreatment with 100 microM alpha-mannosidase inhibitor 1-deoxymannojirimycin (DMJ) in PC-12 cells significantly attenuated the cytotoxicity by ER stressors tunicamycin (TM), thapsigargin (TG), and amyloid beta1-42 (Abeta1-42), and reduced caspase-3 activation by TM and TG.	Tunicamycin	171-173	caspase 3	Rattus norvegicus	241-250
18691157-4	2008	However, only tunicamycin and dithiothreitol resulted in increased PON2 mRNA and protein levels.	Tunicamycin	14-25	paraoxonase 2	Homo sapiens	67-71
18778408-5	2008	Interestingly, when cells are depleted of cholesterol and treated with tunicamycin, treatments that by themselves do not affect PLAP sorting, PLAP is not able to oligomerize and is missorted to the basolateral surface, thus supporting an indirect role of N-glycosylation, possibly mediated by a raft-associated glycosylated interactor.	Tunicamycin	71-82	alkaline phosphatase, placental	Homo sapiens	142-146
18791174-4	2008	Effects of tunicamycin and thapsigargin on IL-1beta- and TNF-alpha-stimulated MCP-1 mRNA expression and protein production were further examined by RT-PCR and ELISA, respectively.	Tunicamycin	11-22	interleukin 1 beta	Homo sapiens	43-51
18791174-4	2008	Effects of tunicamycin and thapsigargin on IL-1beta- and TNF-alpha-stimulated MCP-1 mRNA expression and protein production were further examined by RT-PCR and ELISA, respectively.	Tunicamycin	11-22	tumor necrosis factor	Homo sapiens	57-66
18791174-4	2008	Effects of tunicamycin and thapsigargin on IL-1beta- and TNF-alpha-stimulated MCP-1 mRNA expression and protein production were further examined by RT-PCR and ELISA, respectively.	Tunicamycin	11-22	C-C motif chemokine ligand 2	Homo sapiens	78-83
18791174-8	2008	Compared to Cys and IL-10, the ER stress activators tunicamycin and thapsigargin were even more potent enhancers of hRPE caspase-12S gene expression.	Tunicamycin	52-63	ribulose-5-phosphate-3-epimerase	Homo sapiens	116-120
18626793-6	2008	Since PAC1-R mRNA expression was induced by NGF, PACAP exhibited neuroprotective effect against tunicamycin-induced cell death in the differentiated PC12 cells.	Tunicamycin	96-107	ADCYAP receptor type I	Rattus norvegicus	6-12
18799549-6	2008	In tumor necrosis factor (TNF)-alpha-treated cells, suppression of MCP-1 by indomethacin was inversely correlated with induction of UPR, and other inducers of UPR including tunicamycin, thapsigargin, and A23187 reproduced the suppressive effect.	Tunicamycin	173-184	tumor necrosis factor	Mus musculus	3-36
18626793-6	2008	Since PAC1-R mRNA expression was induced by NGF, PACAP exhibited neuroprotective effect against tunicamycin-induced cell death in the differentiated PC12 cells.	Tunicamycin	96-107	adenylate cyclase activating polypeptide 1	Rattus norvegicus	49-54
19017746-6	2008	The bZIP60 protein resides in the ER membrane under unstressed condition and is cleaved in response to ER stress caused by either tunicamycin or DTT.	Tunicamycin	130-141	basic region/leucine zipper motif 60	Arabidopsis thaliana	4-10
18650099-7	2008	Following tunicamycin treatment the secretion of additional proteins as well as ER-resident chaperones from the Hsp70 and Hsp90 families outside the protoplasts was noted.	Tunicamycin	10-21	heat shock protein 70	Arabidopsis thaliana	112-117
18768906-4	2008	Tunicamycin treatment or expression in the stt3a-2 mutant relieved the folding block, and migration to Golgi stacks resumed.	Tunicamycin	0-11	staurosporin and temperature sensitive 3-like A	Arabidopsis thaliana	43-48
18503006-8	2008	Grx6 and Grx7 have measurable oxidoreductase activity in vivo, which is increased in the presence of tunicamycin.	Tunicamycin	101-112	glutathione-disulfide reductase GRX6	Saccharomyces cerevisiae S288C	0-4
18847488-4	2008	RESULTS: Tunicamycin treatment demonstrated that human OSTalpha is glycosylated.	Tunicamycin	9-20	solute carrier family 51 subunit alpha	Homo sapiens	55-63
18847488-6	2008	Immunofluorescence of both cells indicated that, in the presence of OSTbeta, the alpha subunit could still be expressed on the plasma membrane after tunicamycin treatment.	Tunicamycin	149-160	solute carrier family 51 subunit beta	Homo sapiens	68-75
18838865-3	2008	Here, we show by epistatic analysis that p53 inhibition results in a maximum level of autophagy that cannot be further enhanced by a variety of different autophagy inducers including lithium, tunicamycin-induced stress of the endoplasmic reticulum (ER) or inhibition of Bcl-2 and Bcl-X(L) with the BH3 mimetic ABT737.	Tunicamycin	192-203	tumor protein p53	Homo sapiens	41-44
18838865-4	2008	Chemical inducers of autophagy (including rapamycin, lithium, tunicamycin and ABT737) induced rapid depletion of the p53 protein.	Tunicamycin	62-73	tumor protein p53	Homo sapiens	117-120
18701708-8	2008	Apoptotic death caused by tunicamycin was dramatically reduced in a strain expressing endogenous levels of calnexin lacking its TM and cytosolic tail.	Tunicamycin	26-37	calnexin	Homo sapiens	107-115
18839021-2	2008	METHODS: rNav1.3 was expressed in Xenopus oocyte, with glycosylation inhibition by using tunicamycin.	Tunicamycin	89-100	sodium voltage-gated channel alpha subunit 3	Rattus norvegicus	9-16
18718935-4	2008	Tunicamycin treatment of Arabidopsis cells, which causes ER stress, led to up-regulation of AtERdj3A, AtERdj3B, AtP58(IPK) and AtERdj2B.	Tunicamycin	0-11	DNAJ heat shock N-terminal domain-containing protein	Arabidopsis thaliana	92-100
18718935-4	2008	Tunicamycin treatment of Arabidopsis cells, which causes ER stress, led to up-regulation of AtERdj3A, AtERdj3B, AtP58(IPK) and AtERdj2B.	Tunicamycin	0-11	DNAJ heat shock family protein	Arabidopsis thaliana	102-110
18718935-4	2008	Tunicamycin treatment of Arabidopsis cells, which causes ER stress, led to up-regulation of AtERdj3A, AtERdj3B, AtP58(IPK) and AtERdj2B.	Tunicamycin	0-11	DnaJ / Sec63 Brl domains-containing protein	Arabidopsis thaliana	127-135
18549807-2	2008	In HEK293-corin cells, the inhibition of N-glycosylation, with tunicamycin, reduced the cell-surface expression of murine corin, but did not alter the total expression.	Tunicamycin	63-74	corin, serine peptidase	Mus musculus	10-15
18549807-2	2008	In HEK293-corin cells, the inhibition of N-glycosylation, with tunicamycin, reduced the cell-surface expression of murine corin, but did not alter the total expression.	Tunicamycin	63-74	corin, serine peptidase	Mus musculus	122-127
18549807-3	2008	Therefore, tunicamycin treatment likely caused the intracellular accumulation of non-glycosylated corin.	Tunicamycin	11-22	corin, serine peptidase	Mus musculus	98-103
18549807-4	2008	Tunicamycin treatment also significantly reduced corin activity (pro-ANP cleavage) in these cells.	Tunicamycin	0-11	corin, serine peptidase	Mus musculus	49-54
18701495-3	2008	Inhibition of Mcl-1 by small interference RNA (siRNA) rendered melanoma cells sensitive to apoptosis induced by the ER stress inducers thapsigargin and tunicamycin, but this sensitization was partially reversed by siRNA knockdown of PUMA or Noxa, as shown in Mcl-1-deficient melanoma cells.	Tunicamycin	152-163	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
18604159-6	2008	Several distinct autophagy inducers (e.g., starvation, rapamycin, lithium, tunicamycin and thapsigargin) stimulate the rapid degradation of p53.	Tunicamycin	75-86	tumor protein p53	Homo sapiens	140-143
18690846-3	2008	Immunoblots of whole cell lysates, subcellular fractionation and tunicamycin treatment of human tumor cells indicated that 4Ig-hB7H3 is a approximately 100-kDa N-linked glycosylated membrane protein.	Tunicamycin	65-76	CD276 molecule	Homo sapiens	123-132
18788711-3	2008	Both Chinese propolis and chrysin concentration-dependently inhibited such cell death, the tunicamycin-induced activation of caspase-3, and the effects of tunicamycin on mitochondria [release of cytochrome c into the cytosol and disruption of the mitochondrial membrane potential (DeltaPsim)].	Tunicamycin	91-102	caspase 3	Homo sapiens	125-134
18788711-3	2008	Both Chinese propolis and chrysin concentration-dependently inhibited such cell death, the tunicamycin-induced activation of caspase-3, and the effects of tunicamycin on mitochondria [release of cytochrome c into the cytosol and disruption of the mitochondrial membrane potential (DeltaPsim)].	Tunicamycin	155-166	cytochrome c, somatic	Homo sapiens	195-207
18704925-7	2008	However, upon treatment with tunicamycin, which induces an endoplasmic reticulum (ER)-stress response, CrebH(-/-) mice displayed reduced expression of acute phase response proteins.	Tunicamycin	29-40	cAMP responsive element binding protein 3-like 3	Mus musculus	103-108
18628206-7	2008	Expression of ERp16 in HeLa cells inhibited the induction of apoptosis by agents that elicit ER stress, including brefeldin A, tunicamycin, and dithiothreitol.	Tunicamycin	127-138	thioredoxin domain containing 12	Homo sapiens	14-19
18602013-2	2008	We have characterized the global transcriptional response of Candida albicans to ER stresses (dithiothreitol and tunicamycin) and established the impact of the transcription factor Hac1 upon this response.	Tunicamycin	113-124	transcription factor HAC1	Saccharomyces cerevisiae S288C	181-185
18682497-5	2008	Unglycosylated CFTR, generated by removal of glycosylation sites or treatment of cells with the N-glycosylation inhibitor tunicamycin, did not bind calnexin, but did traffic to the cell surface and exhibited chloride channel activity.	Tunicamycin	122-133	CF transmembrane conductance regulator	Homo sapiens	15-19
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
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	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	157-161
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	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	163-169
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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	175-179
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	X-box binding protein 1	Homo sapiens	195-199
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	eukaryotic translation initiation factor 2A	Homo sapiens	268-277
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	mitogen-activated protein kinase 8	Homo sapiens	279-283
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	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	289-294
18555216-9	2008	In contrast, tunicamycin (TM) strongly inhibited N-glycans incorporation into OA protein.	Tunicamycin	13-24	glycoprotein (transmembrane) nmb	Mus musculus	78-80
18555216-9	2008	In contrast, tunicamycin (TM) strongly inhibited N-glycans incorporation into OA protein.	Tunicamycin	26-28	glycoprotein (transmembrane) nmb	Mus musculus	78-80
18503006-8	2008	Grx6 and Grx7 have measurable oxidoreductase activity in vivo, which is increased in the presence of tunicamycin.	Tunicamycin	101-112	glutathione-disulfide reductase GRX7	Saccharomyces cerevisiae S288C	9-13
18503006-8	2008	Grx6 and Grx7 have measurable oxidoreductase activity in vivo, which is increased in the presence of tunicamycin.	Tunicamycin	101-112	oxidoreductase	Saccharomyces cerevisiae S288C	30-44
18561914-8	2008	Overexpression of Armet/MANF inhibited cell proliferation and improved cell viability under glucose-free conditions and tunicamycin treatment.	Tunicamycin	120-131	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	18-23
18477628-7	2008	We observed that nicotine suppressed the Tm-induced, but not Tg-induced, splicing of XBP1 mRNA, and also suppressed the Tm-induced, but not Tg-induced, production of cleaved ATF6 in PC12 cells.	Tunicamycin	41-43	X-box binding protein 1	Rattus norvegicus	85-89
18561914-8	2008	Overexpression of Armet/MANF inhibited cell proliferation and improved cell viability under glucose-free conditions and tunicamycin treatment.	Tunicamycin	120-131	mesencephalic astrocyte derived neurotrophic factor	Homo sapiens	24-28
18600068-0	2008	Tunicamycin-induced ER stress upregulates the expression of mitochondrial HtrA2 and promotes apoptosis through the cytosolic release of HtrA2.	Tunicamycin	0-11	HtrA serine peptidase 2	Homo sapiens	74-79
18376137-6	2008	We showed that during induction of autophagy by rapamycin, tunicamycin or starvation to amino acids, fluorescence intensity of GFP-LC3 is reduced in a time-dependent manner.	Tunicamycin	59-70	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	131-134
18339707-7	2008	In addition, it was found that DHCR24 exerted cytoprotective effects in the tunicamycin-induced endoplasmic reticulum stress by eliminating ROS.	Tunicamycin	76-87	24-dehydrocholesterol reductase	Mus musculus	31-37
18466333-4	2008	Treatment of cultures with the endoplasmic reticulum (ER) stressor tunicamycin caused an increase in levels of 14-3-3 zeta within the ER-containing microsomal fraction, along with up-regulation of Lys-Asp-Glu-Leu-containing proteins and calnexin, and the selective death of dentate granule cells.	Tunicamycin	67-78	tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, zeta polypeptide	Mus musculus	111-122
18308848-4	2008	Silencing of MEKK-1 gene expression in betaTC-6 and human dispersed islet cells, using in vitro-generated diced small interfering RNA, resulted in protection from DETA/NO, STZ, H2O2, and tunicamycin induced cell death.	Tunicamycin	187-198	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	13-19
18064635-10	2008	Taking into account that induction of ER stress by tunicamycin and brefeldin A, without altering intracellular calcium concentrations, also increased HIF-1alpha mRNA, suggests that ER stress pathways enhanced transcription of HIF-1alpha mRNA.	Tunicamycin	51-62	hypoxia inducible factor 1 subunit alpha	Homo sapiens	150-160
18064635-10	2008	Taking into account that induction of ER stress by tunicamycin and brefeldin A, without altering intracellular calcium concentrations, also increased HIF-1alpha mRNA, suggests that ER stress pathways enhanced transcription of HIF-1alpha mRNA.	Tunicamycin	51-62	hypoxia inducible factor 1 subunit alpha	Homo sapiens	226-236
18600068-0	2008	Tunicamycin-induced ER stress upregulates the expression of mitochondrial HtrA2 and promotes apoptosis through the cytosolic release of HtrA2.	Tunicamycin	0-11	HtrA serine peptidase 2	Homo sapiens	136-141
18600068-3	2008	In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm.	Tunicamycin	157-168	HtrA serine peptidase 2	Homo sapiens	52-57
18600068-3	2008	In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm.	Tunicamycin	157-168	HtrA serine peptidase 2	Homo sapiens	253-258
18600068-3	2008	In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm.	Tunicamycin	170-172	HtrA serine peptidase 2	Homo sapiens	52-57
18600068-3	2008	In the present study, we have demonstrated that the HtrA2 protein level was gradually and significantly increased by up to 10-fold in the mitochondria under tunicamycin (Tm)-induced ER stress, which eventually promoted cell death through the release of HtrA2 into the cytoplasm.	Tunicamycin	170-172	HtrA serine peptidase 2	Homo sapiens	253-258
18211961-10	2008	The thyroid-specific and epithelial dedifferentiation by thapsigargin or tunicamycin were completely prevented by the PP2 inhibitor of Src-family kinases and by stable expression of a dominant-negative Src.	Tunicamycin	73-84	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	135-138
18425424-6	2008	Inhibition of N-glycosylation by tunicamycin reduced both the enzymatic activity of extracellular NEP2 and the molecular size of intracellular NEP2.	Tunicamycin	33-44	membrane metallo-endopeptidase-like 1	Mus musculus	98-102
18425424-6	2008	Inhibition of N-glycosylation by tunicamycin reduced both the enzymatic activity of extracellular NEP2 and the molecular size of intracellular NEP2.	Tunicamycin	33-44	membrane metallo-endopeptidase-like 1	Mus musculus	143-147
18379069-4	2008	Using primary cultured rat cortical neurons, we here examined whether expression of PLC-beta 1 and -gamma 1 was altered in ER stress-loaded neurons induced by tunicamycin (Tm).	Tunicamycin	159-170	phospholipase C beta 1	Rattus norvegicus	84-107
18379069-4	2008	Using primary cultured rat cortical neurons, we here examined whether expression of PLC-beta 1 and -gamma 1 was altered in ER stress-loaded neurons induced by tunicamycin (Tm).	Tunicamycin	172-174	phospholipase C beta 1	Rattus norvegicus	84-107
18216284-5	2008	We showed that ER stress induced by tunicamycin or high temperature resulted in increased transcription of apy-1.	Tunicamycin	36-47	Apyrase apy-1	Caenorhabditis elegans	107-112
18198352-9	2008	Finally, MIN6 cells depleted of GRP78 were more susceptible to tunicamycin-induced apoptosis but not to palmitate-induced apoptosis compared with control cells.	Tunicamycin	63-74	heat shock protein 5	Mus musculus	32-37
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.	Tunicamycin	338-349	heat shock protein family A (Hsp70) member 5	Homo sapiens	258-263
18436549-8	2008	The Atcrt1a mutants exhibited increased sensitivity to the drug tunicamycin, an inducer of the unfolded protein response.	Tunicamycin	64-75	calreticulin 1a	Arabidopsis thaliana	4-11
18436549-9	2008	We therefore conclude that AtCRT1a is an alleviator of the tunicamycin-induced unfolded protein response, and propose that the use of the mouse crt-/- fibroblasts as a calreticulin expression system may prove useful to assess functionalities of calreticulins from different species.	Tunicamycin	59-70	calreticulin 1a	Arabidopsis thaliana	27-34
18356160-5	2008	Induction of ER stress by treatment with either thapsigargin or tunicamycin activated autophagy in immortalized hepatocytes as monitored by the conversion LC3-I to LC3-II, clustering of LC3 into dot-like cytoplasmic structures, and electron microscopic detection of autophagosomes.	Tunicamycin	64-75	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	155-158
18356160-5	2008	Induction of ER stress by treatment with either thapsigargin or tunicamycin activated autophagy in immortalized hepatocytes as monitored by the conversion LC3-I to LC3-II, clustering of LC3 into dot-like cytoplasmic structures, and electron microscopic detection of autophagosomes.	Tunicamycin	64-75	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	164-167
18356160-5	2008	Induction of ER stress by treatment with either thapsigargin or tunicamycin activated autophagy in immortalized hepatocytes as monitored by the conversion LC3-I to LC3-II, clustering of LC3 into dot-like cytoplasmic structures, and electron microscopic detection of autophagosomes.	Tunicamycin	64-75	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	164-167
18483264-5	2008	Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation.	Tunicamycin	44-55	epidermal growth factor receptor	Homo sapiens	105-109
18483264-5	2008	Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation.	Tunicamycin	44-55	erb-b2 receptor tyrosine kinase 2	Homo sapiens	111-116
18483264-5	2008	Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation.	Tunicamycin	44-55	erb-b2 receptor tyrosine kinase 3	Homo sapiens	118-123
18483264-5	2008	Using the N-linked glycosylation inhibitor, tunicamycin, we show that expression levels of several RTKS (EGFR, ErbB2, ErbB3, and IGF-IR) are exquisitely sensitive to inhibition of N-linked glycosylation.	Tunicamycin	44-55	insulin like growth factor 1 receptor	Homo sapiens	129-135
18395193-2	2008	We evaluated the effect of a selective inducer of immunoglobulin heavy chain binding protein (BiP) (BiP inducer X; BIX) against both tunicamycin-induced cell death (in SH-SY5Y cells) and the effects of global transient forebrain ischemia (in gerbils).	Tunicamycin	133-144	heat shock protein family A (Hsp70) member 5	Homo sapiens	50-92
18395193-2	2008	We evaluated the effect of a selective inducer of immunoglobulin heavy chain binding protein (BiP) (BiP inducer X; BIX) against both tunicamycin-induced cell death (in SH-SY5Y cells) and the effects of global transient forebrain ischemia (in gerbils).	Tunicamycin	133-144	heat shock protein family A (Hsp70) member 5	Homo sapiens	94-97
17624530-9	2008	In addition, IPI-504 also blocks the tunicamycin-induced phosphorylation of eIF2 by PERK.	Tunicamycin	37-48	eukaryotic translation initiation factor 2 subunit beta	Homo sapiens	76-80
17624530-9	2008	In addition, IPI-504 also blocks the tunicamycin-induced phosphorylation of eIF2 by PERK.	Tunicamycin	37-48	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	84-88
18649184-6	2008	The temporal differences of Panx1 trafficking correlate with spatial differences of intracellular localizations induced by Golgi blockage by Brefeldin-A or glycosylation prevention by tunicamycin.	Tunicamycin	184-195	pannexin 1	Homo sapiens	28-33
18256359-7	2008	Of note, pretreatment with tunicamycin or thapsigargin decreased the excessive ER stress-induced intracellular signaling observed in anti-Thy1 nephritis.	Tunicamycin	27-38	Thy-1 cell surface antigen	Rattus norvegicus	138-142
18280615-3	2008	Analysis of propidium iodide uptake showed that TM-induced neuronal death in a concentration-dependent manner (20-80 microg/mL) and that the rank order of vulnerability among hippocampal subregions was dentate gyrus (DG)&gt;CA1&gt;CA3.	Tunicamycin	48-50	carbonic anhydrase 1	Rattus norvegicus	224-227
18280615-3	2008	Analysis of propidium iodide uptake showed that TM-induced neuronal death in a concentration-dependent manner (20-80 microg/mL) and that the rank order of vulnerability among hippocampal subregions was dentate gyrus (DG)&gt;CA1&gt;CA3.	Tunicamycin	48-50	carbonic anhydrase 3	Rattus norvegicus	231-234
18375764-4	2008	We show that deglycosylation of cell surface proteins by glycosidase treatment, or inhibition of protein N-glycosylation by tunicamycin, ablates CyaA binding and penetration of CD11b-expressing cells.	Tunicamycin	124-135	integrin subunit alpha M	Homo sapiens	177-182
17988239-9	2008	Provoking SA in vitro in the presence of the N-linked glycosylation blocker tunicamycin abrogated the activity-dependent increase of HCN1/HCN2 heteromerization.	Tunicamycin	76-87	hyperpolarization activated cyclic nucleotide gated potassium channel 1	Homo sapiens	133-137
17988239-9	2008	Provoking SA in vitro in the presence of the N-linked glycosylation blocker tunicamycin abrogated the activity-dependent increase of HCN1/HCN2 heteromerization.	Tunicamycin	76-87	hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2	Homo sapiens	138-142
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	cyclin D1	Homo sapiens	39-48
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	cyclin A2	Homo sapiens	53-61
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	heat shock protein family A (Hsp70) member 5	Homo sapiens	98-130
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
18228003-8	2008	Cyclin A was the most sensitive regulator to tunicamycin-triggered degradation mechanism.	Tunicamycin	45-56	cyclin A2	Homo sapiens	0-8
18228003-9	2008	The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin.	Tunicamycin	98-109	interferon alpha inducible protein 27	Homo sapiens	19-22
18228003-9	2008	The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin.	Tunicamycin	98-109	cyclin dependent kinase inhibitor 1B	Homo sapiens	23-27
18228003-9	2008	The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin.	Tunicamycin	98-109	proliferating cell nuclear antigen	Homo sapiens	34-40
18228003-9	2008	The association of p27(Kip1) with cyclin D1/cyclin-dependent kinase (Cdk) 4 was also increased by tunicamycin.	Tunicamycin	98-109	proliferating cell nuclear antigen	Homo sapiens	44-50
18228003-11	2008	The knockdown of GRP78 expression by the siRNA transfection technique moderately increased tunicamycin-induced apoptosis but not the antiproliferative effect by sulforhodamine B assay.	Tunicamycin	91-102	heat shock protein family A (Hsp70) member 5	Homo sapiens	17-22
18228003-12	2008	We suggest that tunicamycin induces G1 arrest through down-regulation of cyclins and Cdks, in which cyclin A is more susceptible to ER stress-triggered degradation mechanism in Hep3B cells.	Tunicamycin	16-27	cyclin dependent kinase 4	Homo sapiens	85-89
18228003-12	2008	We suggest that tunicamycin induces G1 arrest through down-regulation of cyclins and Cdks, in which cyclin A is more susceptible to ER stress-triggered degradation mechanism in Hep3B cells.	Tunicamycin	16-27	cyclin A2	Homo sapiens	100-108
18228003-13	2008	The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest.	Tunicamycin	82-93	interferon alpha inducible protein 27	Homo sapiens	29-32
18228003-13	2008	The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest.	Tunicamycin	82-93	cyclin dependent kinase inhibitor 1B	Homo sapiens	33-37
18228003-13	2008	The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest.	Tunicamycin	82-93	cyclin D1	Homo sapiens	44-53
18228003-13	2008	The increased association of p27(Kip1) with cyclin D1/Cdk4 may also contribute to tunicamycin-induced cell-cycle arrest.	Tunicamycin	82-93	cyclin dependent kinase 4	Homo sapiens	54-58
18160625-12	2008	In contrast, ER-Bcl-2 protected against apoptosis during tunicamycin-induced ER stress.	Tunicamycin	57-68	BCL2 apoptosis regulator	Homo sapiens	16-21
18211961-10	2008	The thyroid-specific and epithelial dedifferentiation by thapsigargin or tunicamycin were completely prevented by the PP2 inhibitor of Src-family kinases and by stable expression of a dominant-negative Src.	Tunicamycin	73-84	SRC proto-oncogene, non-receptor tyrosine kinase	Rattus norvegicus	202-205
18283338-6	2008	Cells of the ATL-1 line, which were derived from an Atm-/- mouse thymic lymphoma, were more sensitive to the ER stress inducer tunicamycin than were Atm+/+ thymic leukemia ASL-1 cells.	Tunicamycin	127-138	atlastin GTPase 1	Mus musculus	13-18
18065414-5	2008	We found that several well characterized stress inducers (tunicamycin, thapsigargin, and A23187) as well as homocysteine could increase Mthfr mRNA and protein in Neuro-2a cells.	Tunicamycin	58-69	methylenetetrahydrofolate reductase	Mus musculus	136-141
18094145-4	2008	ORP150 expression was found to be regulated by the anti-C/enhancer-binding protein homologous protein (CHOP)/GADD153 transcription factor and ORP150 levels increased in the mitochondria and ER of COS-7 cells after diverse stresses, including hypoxia, serum starvation, prolyl hydroxylase inhibition with dimethyloxaloylglycine, and exposure to tunicamycin, ethidium, bromide, and 2-deoxyglucose.	Tunicamycin	344-355	hypoxia up-regulated 1	Rattus norvegicus	0-6
18094145-4	2008	ORP150 expression was found to be regulated by the anti-C/enhancer-binding protein homologous protein (CHOP)/GADD153 transcription factor and ORP150 levels increased in the mitochondria and ER of COS-7 cells after diverse stresses, including hypoxia, serum starvation, prolyl hydroxylase inhibition with dimethyloxaloylglycine, and exposure to tunicamycin, ethidium, bromide, and 2-deoxyglucose.	Tunicamycin	344-355	DNA-damage inducible transcript 3	Rattus norvegicus	103-107
18094145-4	2008	ORP150 expression was found to be regulated by the anti-C/enhancer-binding protein homologous protein (CHOP)/GADD153 transcription factor and ORP150 levels increased in the mitochondria and ER of COS-7 cells after diverse stresses, including hypoxia, serum starvation, prolyl hydroxylase inhibition with dimethyloxaloylglycine, and exposure to tunicamycin, ethidium, bromide, and 2-deoxyglucose.	Tunicamycin	344-355	DNA-damage inducible transcript 3	Rattus norvegicus	109-116
18245485-2	2008	We report in this study that apoptosis was induced by the ER stress inducer thapsigargin or tunicamycin via a caspase-8-mediated pathway in the melanoma cell line Me1007, although the MEK/ERK pathway was activated in this cell line.	Tunicamycin	92-103	caspase 8	Homo sapiens	110-119
18167147-13	2008	In addition, GmPDIM associated with the alpha" subunit of beta-conglycinin, a seed-storage protein in the presence of tunicamycin.	Tunicamycin	118-129	protein disulfide isomerse like protein	Glycine max	13-19
18167147-13	2008	In addition, GmPDIM associated with the alpha" subunit of beta-conglycinin, a seed-storage protein in the presence of tunicamycin.	Tunicamycin	118-129	alpha subunit of beta conglycinin	Glycine max	40-74
18041764-2	2008	We found that overexpressing Par-4 by stable transfection sensitizes Caki cells to induction of apoptosis by TRAIL and drugs that induce endoplasmic reticulum (ER) stress [thapsigargin (TG), tunicamycin (TU) and etoposide].	Tunicamycin	191-202	pro-apoptotic WT1 regulator	Homo sapiens	29-34
18041764-2	2008	We found that overexpressing Par-4 by stable transfection sensitizes Caki cells to induction of apoptosis by TRAIL and drugs that induce endoplasmic reticulum (ER) stress [thapsigargin (TG), tunicamycin (TU) and etoposide].	Tunicamycin	204-206	pro-apoptotic WT1 regulator	Homo sapiens	29-34
18029041-2	2008	A time-dependent induction of ER chaperons, glucose regulated protein (GRP)78 and GRP94, was observed after treatment with tunicamycin (TM), and cell death was also induced concomitantly in both cells.	Tunicamycin	123-134	heat shock protein family A (Hsp70) member 5	Homo sapiens	71-77
17928398-9	2008	In addition, cell death is enhanced by approximately 35% in tunicamycin-treated cells expressing an S51A eIF2 alpha mutant that cannot be phosphorylated or in cells lacking PERK (protein kinase regulated by RNA/endoplasmic reticulum-like kinase).	Tunicamycin	60-71	eukaryotic translation initiation factor 2A	Rattus norvegicus	105-115
18089754-7	2008	Treatment of mCAT1/insG-expressing cells with tunicamycin, an N-linked glycosylation inhibitor, increased the transduction titre.	Tunicamycin	46-57	solute carrier family 7 (cationic amino acid transporter, y+ system), member 1	Mus musculus	13-18
17996891-11	2008	Treatment of HL-1 cells with tunicamycin reduced the relative mass of expressed corin.	Tunicamycin	29-40	corin, serine peptidase	Mus musculus	80-85
18029041-2	2008	A time-dependent induction of ER chaperons, glucose regulated protein (GRP)78 and GRP94, was observed after treatment with tunicamycin (TM), and cell death was also induced concomitantly in both cells.	Tunicamycin	123-134	heat shock protein 90 beta family member 1	Homo sapiens	82-87
17651753-3	2007	Here we show that in response to a UPR inducing reagent, tunicamycin, the expression of calreticulin (crt-1) is specifically up-regulated in Caenorhabditis elegans.	Tunicamycin	57-68	Calreticulin	Caenorhabditis elegans	88-100
18022401-8	2007	We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression.	Tunicamycin	75-86	heat shock protein family A (Hsp70) member 5	Homo sapiens	95-100
18022401-8	2007	We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression.	Tunicamycin	75-86	activating transcription factor 6	Homo sapiens	105-109
18022401-8	2007	We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression.	Tunicamycin	88-90	heat shock protein family A (Hsp70) member 5	Homo sapiens	95-100
18022401-8	2007	We investigated the effect of exogenous UPR inducers thapsigargin (Tg) and tunicamycin (Tu) on Grp78 and ATF6 expression.	Tunicamycin	88-90	activating transcription factor 6	Homo sapiens	105-109
18156219-4	2007	One of these factors, bZIP28, an ER-resident transcription factor, is activated in response to treatment by tunicamycin (TM), an agent that blocks N-linked protein glycosylation.	Tunicamycin	108-119	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	22-28
18156219-4	2007	One of these factors, bZIP28, an ER-resident transcription factor, is activated in response to treatment by tunicamycin (TM), an agent that blocks N-linked protein glycosylation.	Tunicamycin	121-123	Basic-leucine zipper (bZIP) transcription factor family protein	Arabidopsis thaliana	22-28
17914579-0	2007	Glycosylation modulates TRAIL-R1/death receptor 4 protein: different regulations of two pro-apoptotic receptors for TRAIL by tunicamycin.	Tunicamycin	125-136	TNF receptor superfamily member 10a	Homo sapiens	24-32
17914579-0	2007	Glycosylation modulates TRAIL-R1/death receptor 4 protein: different regulations of two pro-apoptotic receptors for TRAIL by tunicamycin.	Tunicamycin	125-136	TNF receptor superfamily member 10a	Homo sapiens	33-49
17914579-0	2007	Glycosylation modulates TRAIL-R1/death receptor 4 protein: different regulations of two pro-apoptotic receptors for TRAIL by tunicamycin.	Tunicamycin	125-136	TNF superfamily member 10	Homo sapiens	24-29
17914579-3	2007	Tunicamycin treatment, which is an inducer of endoplasmic reticulum (ER)-stress, generated a lower molecular-weight pattern of DR4, but not DR5 protein in prostate cancer DU145 and PC3 cells.	Tunicamycin	0-11	TNF receptor superfamily member 10a	Homo sapiens	127-130
17914579-10	2007	These results indicate that tunicamycin regulates DR4 protein size via inhibition of glycosylation.	Tunicamycin	28-39	TNF receptor superfamily member 10a	Homo sapiens	50-53
17681378-6	2007	Caspase-3 staining revealed that neuronal death is primarily due to apoptosis in tunicamycin-treated slice cultures.	Tunicamycin	81-92	caspase 3	Homo sapiens	0-9
17681378-9	2007	Tunicamycin treatment resulted in upregulation of GRP78/BiP in the neuronal cells.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	50-55
17681378-9	2007	Tunicamycin treatment resulted in upregulation of GRP78/BiP in the neuronal cells.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Homo sapiens	56-59
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	X-box binding protein 1	Homo sapiens	119-123
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	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	138-142
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
17525289-4	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	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	212-216
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	activating transcription factor 6	Homo sapiens	234-267
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	activating transcription factor 6	Homo sapiens	269-273
17660514-8	2007	Treatment of HEK 293 cells expressing rat corin with tunicamycin prevented corin activation and inhibited its pro-atrial natriuretic peptide processing activity.	Tunicamycin	53-64	corin, serine peptidase	Rattus norvegicus	42-47
17660514-8	2007	Treatment of HEK 293 cells expressing rat corin with tunicamycin prevented corin activation and inhibited its pro-atrial natriuretic peptide processing activity.	Tunicamycin	53-64	corin, serine peptidase	Rattus norvegicus	75-80
17660514-9	2007	Similar effects of tunicamycin on endogenous corin activity were found in HL-1 cells.	Tunicamycin	19-30	corin, serine peptidase	Homo sapiens	45-50
17823375-6	2007	Instead, CO prevented X-box binding protein 1 expression and activating transcription factor 6 cleavage induced by ER-stress inducers such as thapsigargin, tunicamycin and homocysteine.	Tunicamycin	156-167	X-box binding protein 1	Homo sapiens	22-45
17712038-6	2007	In LNCaP cells, AIbZIP was processed to its transcriptionally active form by drugs that deplete ER calcium stores (i.e., A23187 and caffeine), but it was unaffected by an inhibitor of protein glycosylation (tunicamycin).	Tunicamycin	207-218	cAMP responsive element binding protein 3 like 4	Homo sapiens	16-22
17655822-1	2007	Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release.	Tunicamycin	91-102	cytochrome c, somatic	Homo sapiens	184-196
17655822-1	2007	Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release.	Tunicamycin	91-102	BCL2 associated X, apoptosis regulator	Homo sapiens	238-241
17655822-1	2007	Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release.	Tunicamycin	91-102	cytochrome c, somatic	Homo sapiens	310-322
17942905-3	2007	Treatment with the ER stress inducer tunicamycin or thapsigargin did not induce significant apoptosis in the majority of melanoma cell lines, but resistance to these agents was reversed by the MEK inhibitor U0126 or MEK1 small interfering RNA (siRNA).	Tunicamycin	37-48	mitogen-activated protein kinase kinase 7	Homo sapiens	193-196
17942905-3	2007	Treatment with the ER stress inducer tunicamycin or thapsigargin did not induce significant apoptosis in the majority of melanoma cell lines, but resistance to these agents was reversed by the MEK inhibitor U0126 or MEK1 small interfering RNA (siRNA).	Tunicamycin	37-48	mitogen-activated protein kinase kinase 1	Homo sapiens	216-220
17942905-7	2007	Inhibition of MEK/ERK also resulted in down-regulation of GRP78, which was physically associated with caspase-4, before and after treatment with tunicamycin or thapsigargin.	Tunicamycin	145-156	mitogen-activated protein kinase kinase 7	Homo sapiens	14-17
17942905-7	2007	Inhibition of MEK/ERK also resulted in down-regulation of GRP78, which was physically associated with caspase-4, before and after treatment with tunicamycin or thapsigargin.	Tunicamycin	145-156	mitogen-activated protein kinase 1	Homo sapiens	18-21
17942905-7	2007	Inhibition of MEK/ERK also resulted in down-regulation of GRP78, which was physically associated with caspase-4, before and after treatment with tunicamycin or thapsigargin.	Tunicamycin	145-156	heat shock protein family A (Hsp70) member 5	Homo sapiens	58-63
17937618-7	2007	Tunicamycin and monensin induced the synthesis of truncated non-glycosylated and partially glycosylated forms of SeP, which were secreted in spite of their impaired glycosylation.	Tunicamycin	0-11	selenoprotein P	Homo sapiens	113-116
17635918-7	2007	Specifically, the effect of low concentration of GS-HCl (1 mM) or of tunicamycin (0.1 microg/ml) to produce the aglycosylated COX-2 was rescued by the proteasomal inhibitor MG132 but not by the lysosomal or caspase inhibitors.	Tunicamycin	69-80	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	126-131
17651753-3	2007	Here we show that in response to a UPR inducing reagent, tunicamycin, the expression of calreticulin (crt-1) is specifically up-regulated in Caenorhabditis elegans.	Tunicamycin	57-68	Calreticulin	Caenorhabditis elegans	102-107
17651753-4	2007	Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent.	Tunicamycin	0-11	Calreticulin	Caenorhabditis elegans	43-48
17651753-4	2007	Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent.	Tunicamycin	0-11	Endoribonuclease;Serine/threonine-protein kinase	Caenorhabditis elegans	58-63
17651753-4	2007	Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent.	Tunicamycin	0-11	BZIP domain-containing protein	Caenorhabditis elegans	68-73
17651753-4	2007	Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent.	Tunicamycin	0-11	BZIP domain-containing protein	Caenorhabditis elegans	81-86
17651753-4	2007	Tunicamycin (TM) induced expression of the crt-1 requires IRE-1 and XBP-1 but is ATF-6 and PEK-1 independent.	Tunicamycin	0-11	Eukaryotic translation initiation factor 2-alpha kinase pek-1	Caenorhabditis elegans	91-96
17301828-7	2007	Addition of tunicamycin resulted in the resistance of CD23 to Der p I mediated cleavage in CC but no change in TT transfectants.	Tunicamycin	12-23	Fc epsilon receptor II	Homo sapiens	54-58
17607300-12	2007	Tunicamycin caused dose-dependent decreases in hepatocyte CD1d, inhibited hepatocyte activation of CD1d-restricted T-cell responses, depleted liver populations of CD1d-reactive NKT cells and promoted Th-1 polarization of hepatic cytokine production.	Tunicamycin	0-11	CD1d1 antigen	Mus musculus	58-62
17607300-12	2007	Tunicamycin caused dose-dependent decreases in hepatocyte CD1d, inhibited hepatocyte activation of CD1d-restricted T-cell responses, depleted liver populations of CD1d-reactive NKT cells and promoted Th-1 polarization of hepatic cytokine production.	Tunicamycin	0-11	CD1d1 antigen	Mus musculus	99-103
17607300-12	2007	Tunicamycin caused dose-dependent decreases in hepatocyte CD1d, inhibited hepatocyte activation of CD1d-restricted T-cell responses, depleted liver populations of CD1d-reactive NKT cells and promoted Th-1 polarization of hepatic cytokine production.	Tunicamycin	0-11	CD1d1 antigen	Mus musculus	99-103
17379544-7	2007	When the HeLa cells stably expressing Bcl-2 were treated with tunicamycin, endogenous RTN3 increased in the cell microsomal fraction.	Tunicamycin	62-73	BCL2 apoptosis regulator	Homo sapiens	38-43
17379544-7	2007	When the HeLa cells stably expressing Bcl-2 were treated with tunicamycin, endogenous RTN3 increased in the cell microsomal fraction.	Tunicamycin	62-73	reticulon 3	Homo sapiens	86-90
17827659-2	2007	In eukaryotes, tunicamycins inhibit UDP-N-acetylglucosamine: dolichol phosphate GlcNAc-1-P transferase (GPT) that catalyzes the first step in protein glycosylation.	Tunicamycin	15-27	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	80-102
17827659-2	2007	In eukaryotes, tunicamycins inhibit UDP-N-acetylglucosamine: dolichol phosphate GlcNAc-1-P transferase (GPT) that catalyzes the first step in protein glycosylation.	Tunicamycin	15-27	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	104-107
17827659-4	2007	Tunicamycins are substrate analog of GPT and MraY, such that the alphabeta-1"",11"-linked GlcNAc residue of the tunicamycins mimics the transferred GlcNAc-1-phosphate.	Tunicamycin	0-12	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	37-40
17827659-4	2007	Tunicamycins are substrate analog of GPT and MraY, such that the alphabeta-1"",11"-linked GlcNAc residue of the tunicamycins mimics the transferred GlcNAc-1-phosphate.	Tunicamycin	112-124	dolichyl-phosphate N-acetylglucosaminephosphotransferase 1	Homo sapiens	37-40
16904232-6	2007	Moreover, under the tunicamycin treatment, transcripts of BiP, PDI and calnexin in transgenic tomato plants accumulated to a less level than those in non-transgenic tomato plants.	Tunicamycin	20-31	luminal-binding protein	Solanum lycopersicum	58-61
17456790-2	2007	Here, we examined the role of inhibin subunit glycosylation in the assembly and secretion of mature inhibin A and activin A. Inhibition of subunit glycosylation by tunicamycin treatment of alpha- and beta(A)-expressing CHO cell lines reduced inhibin but not activin secretion.	Tunicamycin	164-175	inhibin alpha chain	Cricetulus griseus	100-109
17438523-6	2007	RESULTS: Treatment with tunicamycin induced apoptotic cell death in RGC-5 and also induced production of ER stress-related proteins (BiP, the phosphorylated form of eIF2alpha, and CHOP protein).	Tunicamycin	24-35	heat shock protein 5	Mus musculus	133-136
17438523-6	2007	RESULTS: Treatment with tunicamycin induced apoptotic cell death in RGC-5 and also induced production of ER stress-related proteins (BiP, the phosphorylated form of eIF2alpha, and CHOP protein).	Tunicamycin	24-35	eukaryotic translation initiation factor 2A	Mus musculus	165-174
17438523-6	2007	RESULTS: Treatment with tunicamycin induced apoptotic cell death in RGC-5 and also induced production of ER stress-related proteins (BiP, the phosphorylated form of eIF2alpha, and CHOP protein).	Tunicamycin	24-35	DNA-damage inducible transcript 3	Mus musculus	180-184
17438523-8	2007	In flatmounted retinas of ERAI mice, the fluorescence intensity arising from the XBP-1-venus fusion protein, indicating ER-stress activation, was increased at 24 h after tunicamycin, NMDA, or IOP elevation.	Tunicamycin	170-181	X-box binding protein 1	Mus musculus	81-86
17588536-3	2007	In this study, we found that the levels of Niban/NIBAN mRNA and protein were induced by treatment with tunicamycin, an inducer of endoplasmic reticulum (ER) stress.	Tunicamycin	103-114	niban apoptosis regulator 1	Homo sapiens	43-48
17588536-3	2007	In this study, we found that the levels of Niban/NIBAN mRNA and protein were induced by treatment with tunicamycin, an inducer of endoplasmic reticulum (ER) stress.	Tunicamycin	103-114	niban apoptosis regulator 1	Homo sapiens	49-54
17586475-10	2007	The glycosylation inhibitor tunicamycin also partially suppresses EpoR surface expression.	Tunicamycin	28-39	erythropoietin receptor	Homo sapiens	66-70
17652745-8	2007	Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation.	Tunicamycin	36-47	heat shock protein 5	Mus musculus	71-74
17652745-8	2007	Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation.	Tunicamycin	36-47	activating transcription factor 4	Mus musculus	76-80
17652745-8	2007	Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation.	Tunicamycin	36-47	DNA-damage inducible transcript 3	Mus musculus	86-90
17652745-8	2007	Immunoblotting analysis showed that tunicamycin at 2 microg/mL induced BiP, ATF4, and CHOP protein production and PKR phosphorylation.	Tunicamycin	36-47	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	114-117
17652745-9	2007	Both the PKR inhibitor (0.03-1 microM) and the PKR knockdown (using siRNA) inhibited tunicamycin-induced RGC-5 cell death.	Tunicamycin	85-96	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	9-12
17652745-9	2007	Both the PKR inhibitor (0.03-1 microM) and the PKR knockdown (using siRNA) inhibited tunicamycin-induced RGC-5 cell death.	Tunicamycin	85-96	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	47-50
17652745-11	2007	The PKR inhibitor reduced the tunicamycin-induced increase in CHOP but not that in BiP protein production.	Tunicamycin	30-41	eukaryotic translation initiation factor 2-alpha kinase 2	Mus musculus	4-7
17652745-11	2007	The PKR inhibitor reduced the tunicamycin-induced increase in CHOP but not that in BiP protein production.	Tunicamycin	30-41	DNA-damage inducible transcript 3	Mus musculus	62-66
17416481-4	2007	ER stress inducers (tunicamycin, thapsigargin and oxidized dithiothreitol (DTTox)) resulted in a dose-dependent increase in GRP78 and GRP94 stress protein expression, but the magnitude of induction was cell line- and inducer-dependent.	Tunicamycin	20-31	heat shock protein family A (Hsp70) member 5	Sus scrofa	124-129
17416481-4	2007	ER stress inducers (tunicamycin, thapsigargin and oxidized dithiothreitol (DTTox)) resulted in a dose-dependent increase in GRP78 and GRP94 stress protein expression, but the magnitude of induction was cell line- and inducer-dependent.	Tunicamycin	20-31	heat shock protein 90 beta family member 1	Sus scrofa	134-139
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	X-box binding protein 1	Homo sapiens	92-96
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
17560726-3	2007	When amyloid-beta protein was combined with tunicamycin (Abeta+TM), cell death was more acute than with TM alone.	Tunicamycin	44-55	amyloid beta precursor protein	Rattus norvegicus	57-62
17356011-8	2007	Studies with PNGase F and tunicamycin reveal the Slc37a2 protein is posttranslationally modified by addition of N-linked glycans.	Tunicamycin	26-37	solute carrier family 37 (glycerol-3-phosphate transporter), member 2	Mus musculus	49-56
17404493-7	2007	In contrast, IRE1 is required for autophagy induced by ER stress-inducing agents such a tunicamycin or thapsigargin.	Tunicamycin	88-99	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	13-17
17575157-0	2007	Tunicamycin sensitizes human melanoma cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis by up-regulation of TRAIL-R2 via the unfolded protein response.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	141-149
17575157-3	2007	We show in this study that the endoplasmic reticulum (ER) stress inducer, tunicamycin, selectively up-regulated the cell surface expression of TRAIL-R2, but not other members of the TNF receptor family, and enhanced TRAIL-induced apoptosis in cultured melanoma cells and fresh melanoma isolates.	Tunicamycin	74-85	TNF receptor superfamily member 10b	Homo sapiens	143-151
17575157-3	2007	We show in this study that the endoplasmic reticulum (ER) stress inducer, tunicamycin, selectively up-regulated the cell surface expression of TRAIL-R2, but not other members of the TNF receptor family, and enhanced TRAIL-induced apoptosis in cultured melanoma cells and fresh melanoma isolates.	Tunicamycin	74-85	TNF superfamily member 10	Homo sapiens	143-148
17575157-4	2007	Tunicamycin-mediated sensitization of melanoma cells to TRAIL-induced apoptosis was associated with increased activation of the caspase cascade and reduction in mitochondrial membrane potential and was inhibited by a recombinant TRAIL-R2/Fc chimeric protein.	Tunicamycin	0-11	TNF superfamily member 10	Homo sapiens	56-61
17575157-4	2007	Tunicamycin-mediated sensitization of melanoma cells to TRAIL-induced apoptosis was associated with increased activation of the caspase cascade and reduction in mitochondrial membrane potential and was inhibited by a recombinant TRAIL-R2/Fc chimeric protein.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	229-237
17575157-9	2007	Moreover, the transcription factor CCAAT/enhancer-binding protein homologous protein seemed to be involved in the up-regulation of TRAIL-R2 by tunicamycin, but its role varied between different melanoma lines.	Tunicamycin	143-154	TNF receptor superfamily member 10b	Homo sapiens	131-139
17442667-11	2007	However, the subcellular localization of either a mutant (C236S/C244S) I-MBP, which lacks carbohydrate-binding activity, or the wild-type I-MBP in tunicamycin-treated cells shows an equally diffuse cytoplasmic distribution, suggesting that the unique accumulation of I-MBP in the ER and COPII vesicles is mediated by an N-glycan-lectin interaction.	Tunicamycin	147-158	myelin basic protein	Homo sapiens	140-143
17442667-11	2007	However, the subcellular localization of either a mutant (C236S/C244S) I-MBP, which lacks carbohydrate-binding activity, or the wild-type I-MBP in tunicamycin-treated cells shows an equally diffuse cytoplasmic distribution, suggesting that the unique accumulation of I-MBP in the ER and COPII vesicles is mediated by an N-glycan-lectin interaction.	Tunicamycin	147-158	myelin basic protein	Homo sapiens	140-143
17455306-7	2007	The function of these NMDARs as Ca2+ channels is repressed by tunicamycin, because of the inhibition of NR1, but no NR2A, synthesis.	Tunicamycin	62-73	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	104-107
17455306-8	2007	The regulation of NR1 is relevant to the central nervous system, in that a dramatic decrease in synthesis of this subunit and assembly of NMDARs is observed in cortical neurons treated with tunicamycin.	Tunicamycin	190-201	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	18-21
17455323-0	2007	Brain-derived neurotrophic factor suppresses tunicamycin-induced upregulation of CHOP in neurons.	Tunicamycin	45-56	brain derived neurotrophic factor	Homo sapiens	0-33
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
17347267-6	2007	TC-R delivery to both BLM and BBM was inhibited by Brefeldin A and tunicamycin, but not by wortmannin or leupeptin.	Tunicamycin	67-78	CD320 molecule	Homo sapiens	0-4
17418825-4	2007	ER stress, induced by Thapsigargin and tunicamycin, elevated a phosphorylated form of eIF2alpha and ATF4, but the cellular fate depended on treatment duration.	Tunicamycin	39-50	eukaryotic translation initiation factor 2A	Mus musculus	86-95
17418825-4	2007	ER stress, induced by Thapsigargin and tunicamycin, elevated a phosphorylated form of eIF2alpha and ATF4, but the cellular fate depended on treatment duration.	Tunicamycin	39-50	activating transcription factor 4	Mus musculus	100-104
17283057-4	2007	The requirement of the p85alpha regulatory subunit for JNK occurs independently of its role as a component of the PI3K heterodimer and occurs only in response to specific stimuli, namely, insulin and tunicamycin, a chemical that induces endoplasmic reticulum stress.	Tunicamycin	200-211	phosphoinositide-3-kinase regulatory subunit 1	Homo sapiens	23-31
17283057-4	2007	The requirement of the p85alpha regulatory subunit for JNK occurs independently of its role as a component of the PI3K heterodimer and occurs only in response to specific stimuli, namely, insulin and tunicamycin, a chemical that induces endoplasmic reticulum stress.	Tunicamycin	200-211	mitogen-activated protein kinase 8	Homo sapiens	55-58
17314395-2	2007	Yeast mutants lacking Pmr1 show growth sensitivity to multiple drugs (amiodarone, wortmannin, sulfometuron methyl, and tunicamycin) and ions (Mn2+ and Ca2+).	Tunicamycin	119-130	Ca(2+)/Mn(2+)-transporting P-type ATPase PMR1	Saccharomyces cerevisiae S288C	22-26
17187761-5	2007	We found that the deletion of EOS1 enhances tunicamycin tolerance and that in Delta eos1 the transcription level of KAR2, which is the ER stress-inducible gene, was much lower than that in the wild-type strain (BY4741) when exposed to tunicamycin.	Tunicamycin	44-55	Eos1p	Saccharomyces cerevisiae S288C	30-34
16858427-0	2007	Calnexin-dependent regulation of tunicamycin-induced apoptosis in breast carcinoma MCF-7 cells.	Tunicamycin	33-44	calnexin	Homo sapiens	0-8
16858427-4	2007	We show that the expression level of the ER chaperone calnexin can directly influence tunicamycin sensitivity in this cell line.	Tunicamycin	86-97	calnexin	Homo sapiens	54-62
16858427-5	2007	Interestingly, the expression of a calnexin lacking the chaperone domain (DeltaE) partially restores their sensitivity to tunicamycin-induced apoptosis.	Tunicamycin	122-133	calnexin	Homo sapiens	35-43
16858427-7	2007	Utilizing the ability of MCF-7 cells to resist tunicamycin-induced apoptosis, we have characterized a molecular mechanism by which calnexin regulates ER-stress-mediated apoptosis in a manner independent of its chaperone functions but dependent of its binding to Bap31.	Tunicamycin	47-58	calnexin	Homo sapiens	131-139
17167073-8	2007	Transient overexpression of wild-type Akt, but not kinase-dead Akt, in JEG-3 cells diminished tunicamycin-OGD reoxygenation-induced apoptosis.	Tunicamycin	94-105	AKT serine/threonine kinase 1	Homo sapiens	38-41
17187761-5	2007	We found that the deletion of EOS1 enhances tunicamycin tolerance and that in Delta eos1 the transcription level of KAR2, which is the ER stress-inducible gene, was much lower than that in the wild-type strain (BY4741) when exposed to tunicamycin.	Tunicamycin	235-246	Eos1p	Saccharomyces cerevisiae S288C	84-88
17187761-6	2007	The inhibition of the N-glycosylation of carboxypeptidase Y and invertase activity caused by the addition of tunicamycin was depressed in Delta eos1, suggesting that EOS1 may be involved in N-glycosylation of the cellular proteins.	Tunicamycin	109-120	Eos1p	Saccharomyces cerevisiae S288C	144-148
17187761-6	2007	The inhibition of the N-glycosylation of carboxypeptidase Y and invertase activity caused by the addition of tunicamycin was depressed in Delta eos1, suggesting that EOS1 may be involved in N-glycosylation of the cellular proteins.	Tunicamycin	109-120	Eos1p	Saccharomyces cerevisiae S288C	166-170
17346424-6	2007	In vitro cell viability experiments using Hepatocellular Carcinoma HuH7 cells treated with ERdj5 small interfering RNA showed that ERdj5 knockdown cells exhibited less resistance to Doxorubicin (chemotherapy drug), but more resistance to Tunicamycin (Endoplasmic Stress inducer), compared to control cells.	Tunicamycin	238-249	DnaJ heat shock protein family (Hsp40) member C10	Homo sapiens	131-136
17203246-3	2007	Here, we show that tunicamycin causes significant alteration of calnexin sub-cellular distribution in MCF-7 cells.	Tunicamycin	19-30	calnexin	Homo sapiens	64-72
17203246-4	2007	Interestingly, this correlates with the absence of both tunicamycin-induced calnexin phosphorylation as well as tunicamycin-induced cell death.	Tunicamycin	56-67	calnexin	Homo sapiens	76-84
17131418-0	2007	Role of p53 in neurotoxicity induced by the endoplasmic reticulum stress agent tunicamycin in organotypic slice cultures of rat spinal cord.	Tunicamycin	79-90	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	8-11
17101776-3	2007	Disulfide-bonded ATF6 is reduced upon treatment of cells with not only the reducing reagent dithiothreitol but also the glycosylation inhibitor tunicamycin, and the extent of reduction correlates with that of activation.	Tunicamycin	144-155	activating transcription factor 6	Homo sapiens	17-21
17101776-6	2007	ER stress-induced reduction is specific to ATF6 as the oligomeric status of a second ER membrane-bound transcription factor, LZIP/Luman, is not changed upon tunicamycin treatment and LZIP/Luman is well cleaved by S1P in the absence of ER stress.	Tunicamycin	157-168	activating transcription factor 6	Homo sapiens	43-47
17157811-6	2007	The results showed that ER stress-inducing agent tunicamycin significantly enhanced ERAD in cells that either express endogenous or overexpress gp78.	Tunicamycin	49-60	autocrine motility factor receptor	Homo sapiens	144-148
17157811-8	2007	Surprisingly, tunicamycin treatment stabilized gp78, an established ERAD E3 and an ERAD substrate as well, for up to 8h.	Tunicamycin	14-25	autocrine motility factor receptor	Homo sapiens	47-51
17112510-5	2007	We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin.	Tunicamycin	191-202	SH2 domain containing adaptor protein B	Homo sapiens	16-19
17112510-5	2007	We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin.	Tunicamycin	191-202	SH2 domain containing adaptor protein B	Homo sapiens	47-50
17112510-5	2007	We also show by Shb knockdown experiments that Shb regulates c-Abl activity and modulates cell death in response to the genotoxic agent cisplatin and the endoplasmic reticulum stress-inducer tunicamycin.	Tunicamycin	191-202	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	61-66
16987996-4	2007	Pharmacological methods such as proteasome inhibition and treatment with brefeldin A and tunicamycin were used to induce ER stress and activate the UPR as monitored by increased levels of spliced XBP1 and BiP mRNA.	Tunicamycin	89-100	X-box binding protein 1	Homo sapiens	196-200
16987996-4	2007	Pharmacological methods such as proteasome inhibition and treatment with brefeldin A and tunicamycin were used to induce ER stress and activate the UPR as monitored by increased levels of spliced XBP1 and BiP mRNA.	Tunicamycin	89-100	heat shock protein family A (Hsp70) member 5	Homo sapiens	205-208
17127020-0	2007	Toxicogenomics of endoplasmic reticulum stress inducer tunicamycin in the small intestine and liver of Nrf2 knockout and C57BL/6J mice.	Tunicamycin	55-66	nuclear factor, erythroid derived 2, like 2	Mus musculus	103-107
17127020-1	2007	This objective of this study was to investigate the toxicogenomics and the spatial regulation of global gene expression profiles elicited by endoplasmic reticulum (ER) stress inducer tunicamycin (TM) in mouse small intestine and liver as well as to identify TM-modulated nuclear factor-E2-related factor 2 (Nrf2)-dependent genes.	Tunicamycin	183-194	nuclear factor, erythroid derived 2, like 2	Mus musculus	307-311
16841181-8	2007	Moreover, MCF-7 cells stably transfected with CD38wt cDNA, also revealed the presence of cross-linked oligomers when treated with a N-linked glycosylation inhibitor tunicamycin (TM).	Tunicamycin	165-176	CD38 molecule	Homo sapiens	46-50
16841181-8	2007	Moreover, MCF-7 cells stably transfected with CD38wt cDNA, also revealed the presence of cross-linked oligomers when treated with a N-linked glycosylation inhibitor tunicamycin (TM).	Tunicamycin	178-180	CD38 molecule	Homo sapiens	46-50
16875701-9	2006	In addition, dithiothreitol and tunicamycin (ER stress inducers), which increased the expression of GRP78 and activated caspase-12, caused gastric mucosal injury and mucosal cell apoptosis in vitro.	Tunicamycin	32-43	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	100-105
17055645-5	2006	Treatment with tunicamycin at 2 microg/ml for 24 h induced apoptotic cell death accompanied by nuclear condensation and/or fragmentation, and these cells were positive for YO-PRO-1 (early-phase apoptosis and necrosis indicator).	Tunicamycin	15-26	lamin A/C	Homo sapiens	175-180
17055645-6	2006	Treatment with the PKR inhibitor at 0.1 or 0.3 microM led to a decrease in the number of apoptotic cells induced by tunicamycin.	Tunicamycin	116-127	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	19-22
17055645-7	2006	In the resazurin-reduction test, the PKR inhibitor (at 0.1 and 0.3 microM) concentration-dependently inhibited the tunicamycin-induced decrease in metabolic activity.	Tunicamycin	115-126	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	37-40
17031492-4	2006	Furthermore, we demonstrated that endogenous FADD was recruited by ER-bound endogenous RTN3 to the ER membrane under the tunicamycin stimulation.	Tunicamycin	121-132	Fas associated via death domain	Homo sapiens	45-49
17031492-4	2006	Furthermore, we demonstrated that endogenous FADD was recruited by ER-bound endogenous RTN3 to the ER membrane under the tunicamycin stimulation.	Tunicamycin	121-132	reticulon 3	Homo sapiens	87-91
16931790-5	2006	Using the UPR inducing agent tunicamycin and selective siRNA targeting of the ATF4 and XBP1 branches of the UPR, we demonstrate that these transcription factors are essential mediators of IL8, IL6, and MCP1 expression in human aortic ECs required for maximal inflammatory gene expression in the basal state and after oxPAPC treatment.	Tunicamycin	29-40	C-X-C motif chemokine ligand 8	Homo sapiens	188-191
16931790-5	2006	Using the UPR inducing agent tunicamycin and selective siRNA targeting of the ATF4 and XBP1 branches of the UPR, we demonstrate that these transcription factors are essential mediators of IL8, IL6, and MCP1 expression in human aortic ECs required for maximal inflammatory gene expression in the basal state and after oxPAPC treatment.	Tunicamycin	29-40	interleukin 6	Homo sapiens	193-196
16931790-5	2006	Using the UPR inducing agent tunicamycin and selective siRNA targeting of the ATF4 and XBP1 branches of the UPR, we demonstrate that these transcription factors are essential mediators of IL8, IL6, and MCP1 expression in human aortic ECs required for maximal inflammatory gene expression in the basal state and after oxPAPC treatment.	Tunicamycin	29-40	C-C motif chemokine ligand 2	Homo sapiens	202-206
17200012-7	2006	Tunicamycin, an inhibitor of N-terminal glycoprotein synthesis, was added into the culture fluid of the FGFR1-IIIb transfected TAKA-1 cells to observe the changes of the FGFR1 bands.	Tunicamycin	0-11	fibroblast growth factor receptor 1	Mesocricetus auratus	104-109
17200012-7	2006	Tunicamycin, an inhibitor of N-terminal glycoprotein synthesis, was added into the culture fluid of the FGFR1-IIIb transfected TAKA-1 cells to observe the changes of the FGFR1 bands.	Tunicamycin	0-11	fibroblast growth factor receptor 1	Mesocricetus auratus	170-175
16875701-9	2006	In addition, dithiothreitol and tunicamycin (ER stress inducers), which increased the expression of GRP78 and activated caspase-12, caused gastric mucosal injury and mucosal cell apoptosis in vitro.	Tunicamycin	32-43	caspase 12	Rattus norvegicus	120-130
16954146-9	2006	Furthermore, in the kidneys of Apaf-1-deficient mice, apoptosis induced by in vivo administration of tunicamycin was remarkably suppressed as compared with wild type mice.	Tunicamycin	101-112	apoptotic peptidase activating factor 1	Mus musculus	31-37
16781668-4	2006	Transcripts for beta-glucuronidase (GUS) driven by BiP promoter respond to tunicamycin and sugar, being similar with endogenous BiP transcripts in transgenic A. thaliana.	Tunicamycin	75-86	Heat shock protein 70 (Hsp 70) family protein	Arabidopsis thaliana	51-54
16673398-3	2006	Overexpression of Galpha(s-L) to a level twice that of the vector-transfected cells did not directly affect cell viability but significantly increased the sensitivity to induction of cell death by serum deprivation and other apoptotic stimuli, including staurosporine, H(2)O(2), and tunicamycin.	Tunicamycin	283-294	succinate-CoA ligase GDP/ADP-forming subunit alpha	Homo sapiens	18-28
16957393-4	2006	Overexpression of ER-sHSP enhanced the resistance of the transgenic plant to tunicamycin (Fig.	Tunicamycin	77-88	small heat shock protein	Solanum lycopersicum	18-25
16957393-6	2006	Tunicamycin treatment induced an increase in mRNA level of BiP and calnexin in plant cell, but mRNAs of these two genes in transgenic plants were accumulated to a much smaller extent than those in non-transgenic plants (Fig.	Tunicamycin	0-11	luminal-binding protein	Solanum lycopersicum	59-62
16723486-6	2006	Treatment with the N-glycosylation inhibitor tunicamycin induces an epithelioid phenotype in clone-YH, like time in culture but disrupts the hTERT-RPE1 phenotype.	Tunicamycin	45-56	telomerase reverse transcriptase	Homo sapiens	141-151
16456185-5	2006	Exposure to tunicamycin to inhibit SP1 glycosylation reduces ClC-2 expression.	Tunicamycin	12-23	chloride voltage-gated channel 2	Homo sapiens	61-66
16701639-3	2006	Here we show that brefeldin A and tunicamycin-mediated ER stress lead to caspase-dependent apoptosis involving caspase-2.	Tunicamycin	34-45	caspase 2	Homo sapiens	111-120
16687406-10	2006	Treatment with tunicamycin, an endoplasmic reticulum stress inducer, caused an accumulation of a smaller form of Nrf1 that correlated with detection of Nrf1 in the nucleus by biochemical fractionation and immunofluorescent analysis.	Tunicamycin	15-26	nuclear respiratory factor 1	Homo sapiens	113-117
16687406-10	2006	Treatment with tunicamycin, an endoplasmic reticulum stress inducer, caused an accumulation of a smaller form of Nrf1 that correlated with detection of Nrf1 in the nucleus by biochemical fractionation and immunofluorescent analysis.	Tunicamycin	15-26	nuclear respiratory factor 1	Homo sapiens	152-156
16792699-5	2006	To demonstrate N-glycosylation of wild-type Kv3.1 in Sf9 cells, cells were treated with tunicamycin.	Tunicamycin	88-99	potassium voltage-gated channel subfamily C member 1	Rattus norvegicus	44-49
16765953-0	2006	Novel potential of tunicamycin as an activator of the aryl hydrocarbon receptor -- dioxin responsive element signaling pathway.	Tunicamycin	19-30	aryl hydrocarbon receptor	Homo sapiens	54-79
16765953-2	2006	We found that tunicamycin induced expression of cytochrome P450 1A1 in a dose-dependent manner.	Tunicamycin	14-25	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	48-67
16765953-5	2006	Pharmacological and genetic inhibition of the aryl hydrocarbon receptor (AhR) significantly attenuated activation of DRE by tunicamycin.	Tunicamycin	124-135	aryl hydrocarbon receptor	Homo sapiens	46-71
16765953-5	2006	Pharmacological and genetic inhibition of the aryl hydrocarbon receptor (AhR) significantly attenuated activation of DRE by tunicamycin.	Tunicamycin	124-135	aryl hydrocarbon receptor	Homo sapiens	73-76
16765953-6	2006	These results elucidated the novel potential of tunicamycin as an activator of the AhR -- DRE signaling pathway.	Tunicamycin	48-59	aryl hydrocarbon receptor	Homo sapiens	83-86
16513638-8	2006	Treatment with tunicamycin, an inhibitor of N-linked glycosylation, induced the appearance of the unglycosylated 115-kDa CaR form, which was further increased by exposure to MG132, or upon transfection with a dorfin dominant negative construct, suggesting that dorfin-mediated proteasomal degradation of immature CaR occurs from the endoplasmic reticulum.	Tunicamycin	15-26	calcium sensing receptor	Homo sapiens	121-124
16291577-5	2006	Inhibition of glycosylation with tunicamycin in wild-type NKCC2-injected oocytes resulted in an 80% reduction of NKCC2 activity.	Tunicamycin	33-44	solute carrier family 12 member 1 L homeolog	Xenopus laevis	58-63
16291577-5	2006	Inhibition of glycosylation with tunicamycin in wild-type NKCC2-injected oocytes resulted in an 80% reduction of NKCC2 activity.	Tunicamycin	33-44	solute carrier family 12 member 1 L homeolog	Xenopus laevis	113-118
16513638-8	2006	Treatment with tunicamycin, an inhibitor of N-linked glycosylation, induced the appearance of the unglycosylated 115-kDa CaR form, which was further increased by exposure to MG132, or upon transfection with a dorfin dominant negative construct, suggesting that dorfin-mediated proteasomal degradation of immature CaR occurs from the endoplasmic reticulum.	Tunicamycin	15-26	calcium sensing receptor	Homo sapiens	313-316
16533755-7	2006	Cells treated with tunicamycin, an inhibitor of glycosylation, prevented TLR3-induced NF-kappaB activation, confirming that N-linked glycosylation is required for bioactivity of this receptor.	Tunicamycin	19-30	toll like receptor 3	Homo sapiens	73-77
16645094-3	2006	DKO mice responded abnormally to tunicamycin-induced ER stress in the liver, with extensive tissue damage and decreased expression of the IRE1 substrate X-box-binding protein 1 and its target genes.	Tunicamycin	33-44	endoplasmic reticulum (ER) to nucleus signalling 2	Mus musculus	138-142
16645094-3	2006	DKO mice responded abnormally to tunicamycin-induced ER stress in the liver, with extensive tissue damage and decreased expression of the IRE1 substrate X-box-binding protein 1 and its target genes.	Tunicamycin	33-44	X-box binding protein 1	Mus musculus	153-176
16316340-5	2005	METHODS: The expression of ER stress inducible proteins (ORP150, GRP78, or GRP94) in cultured podocytes treated with tunicamycin, A23187, SNAP, hypoxia, or hyperglycemia, and the renal tissues or isolated glomeruli from megsin transgenic rats was analyzed by Western blotting analysis, immunohistochemistry, or confocal microscopy.	Tunicamycin	117-128	hypoxia up-regulated 1	Rattus norvegicus	57-63
16541468-7	2006	We observed that ammonium chloride and tunicamycin blocked TNF-alpha-EGFP fusion protein delivery to secretory granules.	Tunicamycin	39-50	tumor necrosis factor	Homo sapiens	59-68
16564150-10	2006	ER stress inducers tunicamycin and thapsigargin down-regulate cell cycle proteins ppRb and cyclin D1 in differentiated neuroblastoma cells.	Tunicamycin	19-30	cyclin D1	Homo sapiens	91-100
16564150-11	2006	In contrast, protein levels of p27, a cyclin dependent kinase inhibitor, are increased after induction of ER-stress using tunicamycin.	Tunicamycin	122-133	dynactin subunit 6	Homo sapiens	31-34
16525726-4	2006	Tunicamycin reduces MUC1 concentration on the cellular surface more than benzylglycoside, and greatly reduces glycosylation of glycoproteins, causing an increase in cell adhesion in both types of cancer cells.	Tunicamycin	0-11	mucin 1, cell surface associated	Homo sapiens	20-24
16754299-5	2006	By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells.	Tunicamycin	18-29	basigin	Mus musculus	96-101
16754299-5	2006	By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells.	Tunicamycin	18-29	basigin	Mus musculus	123-128
16754299-5	2006	By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells.	Tunicamycin	31-33	basigin	Mus musculus	96-101
16754299-5	2006	By treatment with tunicamycin (TM), an inhibitor of N-glycosylation, the expression level of HG-CD147 decreased and the LG-CD147 disappeared completely in HcaF cells.	Tunicamycin	31-33	basigin	Mus musculus	123-128
16581801-2	2006	Here, we use tunicamycin (Tn) to investigate ER stress-triggered changes in the translation of cytochrome c, a pivotal regulator of apoptosis.	Tunicamycin	13-24	cytochrome c, somatic	Homo sapiens	95-107
16388830-10	2006	Thapsigargin and tunicamycin each significantly activated caspase-3, -9, and -2 in the intrinsic apoptotic pathway in SH-SY5Y cells.	Tunicamycin	17-28	caspase 3	Homo sapiens	58-79
16526095-3	2006	Tat expression also resulted in protection from Tunicamycin-induced apoptosis as determined by DNA staining and TUNEL assays.	Tunicamycin	48-59	tyrosine aminotransferase	Homo sapiens	0-3
16332684-8	2006	Unexpectedly, we found that one of the mutants activates transcription of both Xbp-1-specific and non-Xbp-1-dependent UPR targets in response to tunicamycin treatment, even more potently than does wild type Xbp-1.	Tunicamycin	145-156	X-box binding protein 1	Homo sapiens	79-84
16332684-8	2006	Unexpectedly, we found that one of the mutants activates transcription of both Xbp-1-specific and non-Xbp-1-dependent UPR targets in response to tunicamycin treatment, even more potently than does wild type Xbp-1.	Tunicamycin	145-156	X-box binding protein 1	Homo sapiens	102-107
16332684-8	2006	Unexpectedly, we found that one of the mutants activates transcription of both Xbp-1-specific and non-Xbp-1-dependent UPR targets in response to tunicamycin treatment, even more potently than does wild type Xbp-1.	Tunicamycin	145-156	X-box binding protein 1	Homo sapiens	102-107
16316999-10	2006	Induction of the endoplasmic reticulum stress response by anoxia/recovery or tunicamycin (monitored by induction of Bip or Grp94 expression, phosphorylation of eukaryotic translation initiation factor 2alpha subunit, expression of CHOP, and activation of caspase-12) was attenuated in cells that overexpress SLK.	Tunicamycin	77-88	heat shock protein family A (Hsp70) member 5	Homo sapiens	116-119
16375864-4	2006	Treatment with tunicamycin or thapsigargin, ER stress inducers, caused dephosphorylation of Akt from 12 to 24 h and induced cell death.	Tunicamycin	15-26	AKT serine/threonine kinase 1	Homo sapiens	92-95
16271832-11	2006	Indeed, tunicamycin, known to inhibit N-linked glycosylation in the ER, was found to induce a similar inverse correlation between GRP78 overexpression and HSP72/73 under-expression.	Tunicamycin	8-19	heat shock protein family A (Hsp70) member 5	Homo sapiens	130-135
16271832-11	2006	Indeed, tunicamycin, known to inhibit N-linked glycosylation in the ER, was found to induce a similar inverse correlation between GRP78 overexpression and HSP72/73 under-expression.	Tunicamycin	8-19	heat shock protein family A (Hsp70) member 1A	Homo sapiens	155-160
16357177-4	2005	Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism.	Tunicamycin	90-101	mitogen-activated protein kinase 8	Homo sapiens	126-153
16357177-4	2005	Here, we show that bortezomib promotes apoptosis triggered by classic ER stress inducers (tunicamycin and thapsigargin) via a c-Jun NH(2)-terminal kinase (JNK)-dependent mechanism.	Tunicamycin	90-101	mitogen-activated protein kinase 8	Homo sapiens	155-158
16316340-5	2005	METHODS: The expression of ER stress inducible proteins (ORP150, GRP78, or GRP94) in cultured podocytes treated with tunicamycin, A23187, SNAP, hypoxia, or hyperglycemia, and the renal tissues or isolated glomeruli from megsin transgenic rats was analyzed by Western blotting analysis, immunohistochemistry, or confocal microscopy.	Tunicamycin	117-128	heat shock protein 90 beta family member 1	Rattus norvegicus	75-80
16014566-2	2005	In COS-7 cells transiently transfected with GPVI, deglycosylation with peptide-N-glycosidase F (PNGase F; specific for complex N-linked glycans) or tunicamycin decreases the molecular weight of GPVI and reduces transfected COS-7 cell binding to both CRP and CVX.	Tunicamycin	148-159	glycoprotein VI platelet	Homo sapiens	44-48
16118201-5	2005	Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function.	Tunicamycin	93-104	FG-nucleoporin NUP1	Saccharomyces cerevisiae S288C	12-16
16118201-5	2005	Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function.	Tunicamycin	93-104	linker nucleoporin NUP82	Saccharomyces cerevisiae S288C	21-26
16118201-5	2005	Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function.	Tunicamycin	159-170	linker nucleoporin NIC96	Saccharomyces cerevisiae S288C	112-117
16118201-5	2005	Conditional nup1 and nup82 mutations are partially suppressed by the glycosylation inhibitor tunicamycin, while nic96 and nup116 alleles are hypersensitive to tunicamycin treatment, further implicating glycosylation in NPC function.	Tunicamycin	159-170	FG-nucleoporin NUP116	Saccharomyces cerevisiae S288C	122-128
16014566-2	2005	In COS-7 cells transiently transfected with GPVI, deglycosylation with peptide-N-glycosidase F (PNGase F; specific for complex N-linked glycans) or tunicamycin decreases the molecular weight of GPVI and reduces transfected COS-7 cell binding to both CRP and CVX.	Tunicamycin	148-159	glycoprotein VI platelet	Homo sapiens	194-198
16014566-2	2005	In COS-7 cells transiently transfected with GPVI, deglycosylation with peptide-N-glycosidase F (PNGase F; specific for complex N-linked glycans) or tunicamycin decreases the molecular weight of GPVI and reduces transfected COS-7 cell binding to both CRP and CVX.	Tunicamycin	148-159	C-reactive protein	Homo sapiens	250-253
15925308-3	2005	In the present study, rns4 (VPS32/SNF7) gene mutation was identified by complementation of tunicamycin sensitivity.	Tunicamycin	91-102	ESCRT-III subunit protein SNF7	Saccharomyces cerevisiae S288C	28-33
16107336-6	2005	Conversely, the UPR induced by tunicamycin substantially suppresses TNFalpha-induced ROS accumulation and cell death by inhibiting reduction of cellular glutathione levels.	Tunicamycin	31-42	tumor necrosis factor	Mus musculus	68-76
16166642-3	2005	Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis.	Tunicamycin	44-55	JNK1/MAPK8 associated membrane protein	Homo sapiens	23-27
16166642-3	2005	Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis.	Tunicamycin	44-55	mitogen-activated protein kinase 8	Homo sapiens	87-90
16166642-3	2005	Elevated expression of JAMP following UV or tunicamycin treatment results in sustained JNK activity and a higher level of JNK-dependent apoptosis.	Tunicamycin	44-55	mitogen-activated protein kinase 8	Homo sapiens	122-125
16180102-5	2005	TGF-beta1 increases the binding of laminin gamma1 to WGA-agarose and the binding is abolished by tunicamycin suggesting that laminin gamma1 is modified by N-linked glycosylation.	Tunicamycin	97-108	transforming growth factor, beta 1	Mus musculus	0-9
16180102-5	2005	TGF-beta1 increases the binding of laminin gamma1 to WGA-agarose and the binding is abolished by tunicamycin suggesting that laminin gamma1 is modified by N-linked glycosylation.	Tunicamycin	97-108	laminin, gamma 1	Mus musculus	35-49
16180102-5	2005	TGF-beta1 increases the binding of laminin gamma1 to WGA-agarose and the binding is abolished by tunicamycin suggesting that laminin gamma1 is modified by N-linked glycosylation.	Tunicamycin	97-108	laminin, gamma 1	Mus musculus	125-139
16091421-8	2005	Treatment of rat islets with both chronic high glucose and two ER stress inducers, thapsigargin and tunicamycin, enhanced SREBP-1 binding to the human IRS2 promoter.	Tunicamycin	100-111	sterol regulatory element binding transcription factor 1	Rattus norvegicus	122-129
16091421-8	2005	Treatment of rat islets with both chronic high glucose and two ER stress inducers, thapsigargin and tunicamycin, enhanced SREBP-1 binding to the human IRS2 promoter.	Tunicamycin	100-111	insulin receptor substrate 2	Homo sapiens	151-155
16081652-8	2005	The results showed that various ER stressors (thapsigargin, A23187, tunicamycin, brefeldin A, and cisplatin) provoked a dramatic change in the localization of PSP from outside of the nucleus to inside the nucleus within 3 h. Moreover, the ER stressors induced PSP expression.	Tunicamycin	68-79	reactive intermediate imine deaminase A homolog	Homo sapiens	159-162
16081652-8	2005	The results showed that various ER stressors (thapsigargin, A23187, tunicamycin, brefeldin A, and cisplatin) provoked a dramatic change in the localization of PSP from outside of the nucleus to inside the nucleus within 3 h. Moreover, the ER stressors induced PSP expression.	Tunicamycin	68-79	reactive intermediate imine deaminase A homolog	Homo sapiens	260-263
15864808-3	2005	Treatment targeting the ER with tunicamycin or thapsigargin induced the phosphorylation of Hsp27 but not of alphaB-crystallin in U373 MG cells, increase being observed after 2-10 h and decline at 24 h. Similar phosphorylation of Hsp27 by ER stress was also observed with U251 MG and HeLa but not in COS cells and could be blocked using SB203580, an inhibitor of p38 MAP kinase.	Tunicamycin	32-43	heat shock protein family B (small) member 1	Homo sapiens	91-96
15864808-3	2005	Treatment targeting the ER with tunicamycin or thapsigargin induced the phosphorylation of Hsp27 but not of alphaB-crystallin in U373 MG cells, increase being observed after 2-10 h and decline at 24 h. Similar phosphorylation of Hsp27 by ER stress was also observed with U251 MG and HeLa but not in COS cells and could be blocked using SB203580, an inhibitor of p38 MAP kinase.	Tunicamycin	32-43	heat shock protein family B (small) member 1	Homo sapiens	229-234
15864808-3	2005	Treatment targeting the ER with tunicamycin or thapsigargin induced the phosphorylation of Hsp27 but not of alphaB-crystallin in U373 MG cells, increase being observed after 2-10 h and decline at 24 h. Similar phosphorylation of Hsp27 by ER stress was also observed with U251 MG and HeLa but not in COS cells and could be blocked using SB203580, an inhibitor of p38 MAP kinase.	Tunicamycin	32-43	mitogen-activated protein kinase 14	Homo sapiens	362-365
15864808-5	2005	Prolonged treatment with tunicamycin but not thapsigargin for 48 h caused the second induction of the phosphorylation of Hsp27 in U251 MG cells.	Tunicamycin	25-36	heat shock protein family B (small) member 1	Homo sapiens	121-126
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
15925308-3	2005	In the present study, rns4 (VPS32/SNF7) gene mutation was identified by complementation of tunicamycin sensitivity.	Tunicamycin	91-102	ESCRT-III subunit protein SNF7	Saccharomyces cerevisiae S288C	22-26
15626688-7	2005	Antioxidants superoxide dismutase and catalase prevented the downregulation of NET proteins and induction of ER stress signals produced by NE but not by tunicamycin or thapsigargin.	Tunicamycin	153-164	catalase	Rattus norvegicus	38-46
16061483-8	2005	Tunicamycin treatment of HeLa cells induced a slow accumulation of calnexin dimers, the appearance of which correlated with enhanced calnexin binding to deglycosylated MHC class I heavy chains.	Tunicamycin	0-11	calnexin	Homo sapiens	67-75
16061483-8	2005	Tunicamycin treatment of HeLa cells induced a slow accumulation of calnexin dimers, the appearance of which correlated with enhanced calnexin binding to deglycosylated MHC class I heavy chains.	Tunicamycin	0-11	calnexin	Homo sapiens	133-141
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
15845869-9	2005	Agents that perturb the synthesis and/or activity of ER chaperones such as tunicamycin and calcium ionophore A23187, have different effects on the solubility and degradation of alpha1-AT Z as well as on its residual secretion.	Tunicamycin	75-86	serpin family A member 1	Homo sapiens	177-186
16024639-2	2005	In this study, we showed that tunicamycin, a naturally occurring antibiotic, is a potent enhancer of TRAIL-induced apoptosis through up-regulation of DR5 expression.	Tunicamycin	30-41	TNF superfamily member 10	Homo sapiens	101-106
16024639-2	2005	In this study, we showed that tunicamycin, a naturally occurring antibiotic, is a potent enhancer of TRAIL-induced apoptosis through up-regulation of DR5 expression.	Tunicamycin	30-41	TNF receptor superfamily member 10b	Homo sapiens	150-153
16024639-3	2005	Tunicamycin significantly sensitized PC-3, androgen-independent human prostate cancer cells, to TRAIL-induced apoptosis.	Tunicamycin	0-11	TNF superfamily member 10	Homo sapiens	96-101
16024639-4	2005	The tunicamycin-mediated enhancement of TRAIL-induced apoptosis was markedly blocked by a recombinant human DR5/Fc chimeric protein.	Tunicamycin	4-15	TNF superfamily member 10	Homo sapiens	40-45
16024639-4	2005	The tunicamycin-mediated enhancement of TRAIL-induced apoptosis was markedly blocked by a recombinant human DR5/Fc chimeric protein.	Tunicamycin	4-15	TNF receptor superfamily member 10b	Homo sapiens	108-111
16024639-5	2005	Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera.	Tunicamycin	0-11	caspase 8	Homo sapiens	46-72
16024639-5	2005	Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera.	Tunicamycin	0-11	BH3 interacting domain death agonist	Homo sapiens	77-80
16024639-5	2005	Tunicamycin and TRAIL cooperatively activated caspase-8, -10, -9, and -3 and Bid cleavage and this activation was also blocked in the presence of the DR5/Fc chimera.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	150-153
16024639-6	2005	Tunicamycin up-regulated DR5 expression at the mRNA and protein levels in a dose-dependent manner.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	25-28
16024639-7	2005	Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression.	Tunicamycin	17-28	TNF superfamily member 10	Homo sapiens	55-60
16024639-7	2005	Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression.	Tunicamycin	17-28	TNF receptor superfamily member 10b	Homo sapiens	88-91
16024639-7	2005	Furthermore, the tunicamycin-mediated sensitization to TRAIL was efficiently reduced by DR5 small interfering RNA, suggesting that the sensitization was mediated through induction of DR5 expression.	Tunicamycin	17-28	TNF receptor superfamily member 10b	Homo sapiens	183-186
16024639-8	2005	Tunicamycin increased DR5 promoter activity and this enhanced activity was diminished by mutation of a CHOP-binding site.	Tunicamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	22-25
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
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
16024639-9	2005	In addition, suppression of CHOP expression by small interfering RNA reduced the tunicamycin-mediated induction of DR5.	Tunicamycin	81-92	TNF receptor superfamily member 10b	Homo sapiens	115-118
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
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	TNF receptor superfamily member 10b	Homo sapiens	52-55
15994758-13	2005	Treatment of fibroblasts and MIN6 cells with thapsigargin or tunicamycin increased WFS1 mRNA.	Tunicamycin	61-72	wolframin ER transmembrane glycoprotein	Mus musculus	83-87
15978049-9	2005	Phosphorylation of initiation factor-2alpha, which was inhibited by P58(IPK), was decreased in tunicamycin-treated plantlets.	Tunicamycin	95-106	DnaJ P58IPK-like protein	Arabidopsis thaliana	72-75
15857611-6	2005	Although transcription of the SNK gene was also regulated by tunicamycin, etoposide, or staurosporine, FK506 did not show any effects on these regulations.	Tunicamycin	61-72	polo like kinase 2	Homo sapiens	30-33
15760841-5	2005	Sp proteins are constitutively bound to the ERSE; however, activation of GRP78 protein (or reporter gene) by thapsigargin or tunicamycin is inhibited after cotransfection with small inhibitory RNAs for Sp1, Sp3, and Sp4.	Tunicamycin	125-136	heat shock protein family A (Hsp70) member 5	Homo sapiens	73-78
15760841-5	2005	Sp proteins are constitutively bound to the ERSE; however, activation of GRP78 protein (or reporter gene) by thapsigargin or tunicamycin is inhibited after cotransfection with small inhibitory RNAs for Sp1, Sp3, and Sp4.	Tunicamycin	125-136	Sp3 transcription factor	Homo sapiens	207-210
15760841-5	2005	Sp proteins are constitutively bound to the ERSE; however, activation of GRP78 protein (or reporter gene) by thapsigargin or tunicamycin is inhibited after cotransfection with small inhibitory RNAs for Sp1, Sp3, and Sp4.	Tunicamycin	125-136	Sp4 transcription factor	Homo sapiens	216-219
15823038-3	2005	Treatment of cells with a glycosylation inhibitor tunicamycin significantly impaired LRP folding, although binding to receptor-associated protein (RAP), a specialized chaperone for LRP, was not affected.	Tunicamycin	50-61	LDL receptor related protein 1	Homo sapiens	85-88
15823038-4	2005	The effects of tunicamycin on LRP folding were not due to an inhibition of RAP glycosylation since a mutant RAP that harbors a mutation at its sole glycosylation site was still capable of promoting LRP folding.	Tunicamycin	15-26	LDL receptor related protein 1	Homo sapiens	30-33
15823038-4	2005	The effects of tunicamycin on LRP folding were not due to an inhibition of RAP glycosylation since a mutant RAP that harbors a mutation at its sole glycosylation site was still capable of promoting LRP folding.	Tunicamycin	15-26	LDL receptor related protein associated protein 1	Homo sapiens	108-111
15823038-4	2005	The effects of tunicamycin on LRP folding were not due to an inhibition of RAP glycosylation since a mutant RAP that harbors a mutation at its sole glycosylation site was still capable of promoting LRP folding.	Tunicamycin	15-26	LDL receptor related protein 1	Homo sapiens	198-201
15823039-5	2005	The presence of N-glycans was first suggested by sensibility of the 113-kDa nucleolin isoform to tunicamycin treatment.	Tunicamycin	97-108	nucleolin	Homo sapiens	76-85
15781873-1	2005	Analysis of transcripts of 75 genes encoding putative basic leucine zipper (bZIP) transcription factors in the Arabidopsis genome identified AtbZIP60, which was induced by tunicamycin.	Tunicamycin	172-183	basic region/leucine zipper motif 60	Arabidopsis thaliana	141-149
15794758-9	2005	Glycosylation of Hu-K4 as shown by treatment with peptide N-glycosidase F or tunicamycin indicates that Hu-K4 has a type 2 transmembrane topology.	Tunicamycin	77-88	phospholipase D family member 3	Homo sapiens	17-22
15794758-9	2005	Glycosylation of Hu-K4 as shown by treatment with peptide N-glycosidase F or tunicamycin indicates that Hu-K4 has a type 2 transmembrane topology.	Tunicamycin	77-88	phospholipase D family member 3	Homo sapiens	104-109
15925308-3	2005	In the present study, rns4 (VPS32/SNF7) gene mutation was identified by complementation of tunicamycin sensitivity.	Tunicamycin	91-102	ESCRT-III subunit protein SNF7	Saccharomyces cerevisiae S288C	34-38
15662046-8	2005	Tunicamycin, an inhibitor of glycosylation, decreased the molecular mass and simultaneously impaired the trafficking of Mrp2 to the canalicular membrane.	Tunicamycin	0-11	ATP binding cassette subfamily C member 2	Rattus norvegicus	120-124
15655246-10	2005	By the use of tunicamycin and endoglycosidase, NAAA was found to be a glycoprotein.	Tunicamycin	14-25	N-acylethanolamine acid amidase	Homo sapiens	47-51
15775988-5	2005	Tunicamycin treatment enhanced the TRB3 promoter activity, while dominant-negative forms of CHOP suppressed the tunicamycin-induced activation.	Tunicamycin	0-11	tribbles pseudokinase 3	Homo sapiens	35-39
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	tribbles pseudokinase 3	Homo sapiens	52-56
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
15775988-6	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	activating transcription factor 4	Homo sapiens	152-156
15775988-7	2005	Knockdown of endogenous ATF4 or CHOP expression dramatically repressed tunicamycin-induced TRB3 induction.	Tunicamycin	71-82	activating transcription factor 4	Homo sapiens	24-28
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
15775988-7	2005	Knockdown of endogenous ATF4 or CHOP expression dramatically repressed tunicamycin-induced TRB3 induction.	Tunicamycin	71-82	tribbles pseudokinase 3	Homo sapiens	91-95
15320871-12	2005	Tunicamycin inhibited the expression of the 50 and 37 kDa CD83 forms, and also blocked CD83 surface expression on DCs and macrophages.	Tunicamycin	0-11	CD83 molecule	Homo sapiens	58-62
15576633-3	2005	We showed that both the disruption of the glycosylation sites by mutagenesis and the inhibition of glycosylation by tunicamycin treatment resulted in a nonglycosylated hOAT4, which was unable to target to the cell surface.	Tunicamycin	116-127	solute carrier family 22 member 11	Homo sapiens	168-173
15458386-5	2005	Treating alk-SMase cDNA-transfected COS-7 cells with tunicamycin rendered the expressed enzyme completely inactive.	Tunicamycin	53-64	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	9-18
15557337-9	2005	By contrast, HIF-1alpha-VP16-expressing HT22 cells were more resistant to DNA damage (induced by camptothecin) or endoplasmic reticulum stress (induced by thapsigargin and tunicamycin) than were VP16-expressing cells, and suppression of HIF-1alpha expression using RNA interference rendered HT22 cells more sensitive to death induced by DNA damage or endoplasmic reticulum stress.	Tunicamycin	172-183	hypoxia inducible factor 1, alpha subunit	Mus musculus	13-23
15320871-12	2005	Tunicamycin inhibited the expression of the 50 and 37 kDa CD83 forms, and also blocked CD83 surface expression on DCs and macrophages.	Tunicamycin	0-11	CD83 molecule	Homo sapiens	87-91
15733745-10	2005	Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum.	Tunicamycin	43-54	insulin receptor	Homo sapiens	24-26
15733745-10	2005	Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum.	Tunicamycin	43-54	protein tyrosine phosphatase non-receptor type 1	Homo sapiens	95-100
15733745-10	2005	Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum.	Tunicamycin	43-54	insulin receptor	Homo sapiens	106-108
15733745-10	2005	Moreover, inhibition of IR processing with tunicamycin indicated that the basal interaction of PTP1B with IR occurred during biosynthesis of the IR precursor in the endoplasmic reticulum.	Tunicamycin	43-54	insulin receptor	Homo sapiens	106-108
15488943-6	2005	mTSLPR produced in presence of tunicamycin migrated with a molecular weight around 40 kDa.	Tunicamycin	31-42	cytokine receptor-like factor 2	Mus musculus	0-6
15492001-9	2004	Because the cell surface expression of functional DAT requires its oligomerization, misfolded DAT, induced either by the protein glycosylation inhibitor tunicamycin or by its C-terminal truncation, significantly attenuated cell surface expression of native DAT and reduced dopamine uptake.	Tunicamycin	153-164	solute carrier family 6 member 3	Homo sapiens	50-53
15492001-9	2004	Because the cell surface expression of functional DAT requires its oligomerization, misfolded DAT, induced either by the protein glycosylation inhibitor tunicamycin or by its C-terminal truncation, significantly attenuated cell surface expression of native DAT and reduced dopamine uptake.	Tunicamycin	153-164	solute carrier family 6 member 3	Homo sapiens	94-97
15492001-9	2004	Because the cell surface expression of functional DAT requires its oligomerization, misfolded DAT, induced either by the protein glycosylation inhibitor tunicamycin or by its C-terminal truncation, significantly attenuated cell surface expression of native DAT and reduced dopamine uptake.	Tunicamycin	153-164	solute carrier family 6 member 3	Homo sapiens	94-97
15601821-6	2004	Furthermore, mice lacking GADD34-directed eIF2alpha dephosphorylation, like CHOP(-/-) mice, are resistant to renal toxicity of the ER stress-inducing drug tunicamycin.	Tunicamycin	155-166	protein phosphatase 1, regulatory subunit 15A	Mus musculus	26-32
15601821-6	2004	Furthermore, mice lacking GADD34-directed eIF2alpha dephosphorylation, like CHOP(-/-) mice, are resistant to renal toxicity of the ER stress-inducing drug tunicamycin.	Tunicamycin	155-166	eukaryotic translation initiation factor 2A	Mus musculus	42-51
15601821-6	2004	Furthermore, mice lacking GADD34-directed eIF2alpha dephosphorylation, like CHOP(-/-) mice, are resistant to renal toxicity of the ER stress-inducing drug tunicamycin.	Tunicamycin	155-166	DNA-damage inducible transcript 3	Mus musculus	76-80
15648788-3	2004	Expression of GRP78 at both protein and mRNA levels was markedly increased in cardiomyocytes pretreated with tunicamycin, when compared to non-treatment controls.	Tunicamycin	109-120	heat shock protein family A (Hsp70) member 5	Homo sapiens	14-19
15522226-4	2004	Another ER-stress inducer, the N-glycosylation inhibitor tunicamycin, also raised WFS1 mRNA but not protein levels.	Tunicamycin	57-68	wolframin ER transmembrane glycoprotein	Mus musculus	82-86
15522226-7	2004	Consistent with this, the WFS1 protein was more rapidly degraded in the presence of tunicamycin.	Tunicamycin	84-95	wolframin ER transmembrane glycoprotein	Mus musculus	26-30
15527836-8	2004	Tunicamycin, an N-glycosylation inhibitor, increased transduction titer in the wild-type rCAT1-expressing cells, but did not do so in the cells expressing either the mCAT1 or rCAT1 mutation 1.	Tunicamycin	0-11	solute carrier family 7 member 1	Rattus norvegicus	89-94
15465829-5	2004	More specifically, JNK activation, XBP-1 splicing, and EDEM (ER degradation-enhancing alpha-mannosidase-like protein) gene induction, as well as ER stress-induced apoptosis, were attenuated in PTP-1B knock-out mouse embryonic fibroblasts in response to two ER stressors, tunicamycin and azetidine-2 carboxylic acid.	Tunicamycin	271-282	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	193-199
15339911-3	2004	Here, we have shown that endogenous Akt and ERK are rapidly activated and act as downstream effectors of phosphatidylinositol 3-kinase in thapsigargin- or tunicamycin-induced ER stress.	Tunicamycin	155-166	AKT serine/threonine kinase 1	Homo sapiens	36-39
15339911-3	2004	Here, we have shown that endogenous Akt and ERK are rapidly activated and act as downstream effectors of phosphatidylinositol 3-kinase in thapsigargin- or tunicamycin-induced ER stress.	Tunicamycin	155-166	mitogen-activated protein kinase 1	Homo sapiens	44-47
15342690-2	2004	Reduction in molecular mass of EL after treatment with glycosidases and after treatment of EL-expressing cells with the glycosylation inhibitor tunicamycin demonstrated that EL is a glycosylated protein.	Tunicamycin	144-155	lipase G, endothelial type	Homo sapiens	91-93
15342690-2	2004	Reduction in molecular mass of EL after treatment with glycosidases and after treatment of EL-expressing cells with the glycosylation inhibitor tunicamycin demonstrated that EL is a glycosylated protein.	Tunicamycin	144-155	lipase G, endothelial type	Homo sapiens	91-93
15485913-3	2004	Expression of STC2 gene is rapidly upregulated in cultured cells after exposure to tunicamycin and thapsigargin, by ATF4 after activation of the ER-resident kinase PERK.	Tunicamycin	83-94	stanniocalcin 2	Homo sapiens	14-18
15485913-3	2004	Expression of STC2 gene is rapidly upregulated in cultured cells after exposure to tunicamycin and thapsigargin, by ATF4 after activation of the ER-resident kinase PERK.	Tunicamycin	83-94	activating transcription factor 4	Homo sapiens	116-120
15572843-9	2004	The tunicamycin-induced up-regulation of GRP78 and GRP94 and phosphorylation of PERK was suppressed by treatment with 4-PBA, indicating that 4-PBA suppresses ER stress responses by decreasing unfolded protein.	Tunicamycin	4-15	heat shock protein family A (Hsp70) member 5	Homo sapiens	41-46
15572843-9	2004	The tunicamycin-induced up-regulation of GRP78 and GRP94 and phosphorylation of PERK was suppressed by treatment with 4-PBA, indicating that 4-PBA suppresses ER stress responses by decreasing unfolded protein.	Tunicamycin	4-15	heat shock protein 90 beta family member 1	Homo sapiens	51-56
15572843-9	2004	The tunicamycin-induced up-regulation of GRP78 and GRP94 and phosphorylation of PERK was suppressed by treatment with 4-PBA, indicating that 4-PBA suppresses ER stress responses by decreasing unfolded protein.	Tunicamycin	4-15	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	80-84
15518647-5	2004	Here, we report that BDNF suppressed the ER stress-mediated cell death in tunicamycin (Tm)-treated cerebral cortical neurons.	Tunicamycin	74-85	brain-derived neurotrophic factor	Rattus norvegicus	21-25
15518647-5	2004	Here, we report that BDNF suppressed the ER stress-mediated cell death in tunicamycin (Tm)-treated cerebral cortical neurons.	Tunicamycin	87-89	brain-derived neurotrophic factor	Rattus norvegicus	21-25
15319438-4	2004	Tunicamycin and brefeldin A, two ER stress inducers, increased the expression of COX-2 in ML-1 or MCF-7 cells.	Tunicamycin	0-11	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	81-86
15319438-4	2004	Tunicamycin and brefeldin A, two ER stress inducers, increased the expression of COX-2 in ML-1 or MCF-7 cells.	Tunicamycin	0-11	interleukin 17F	Homo sapiens	90-94
15519674-8	2004	In addition, the levels of mHRD1 mRNA were markedly elevated in glial cells exposed to treatment with tunicamycin (Tm, an ER stress inducer).	Tunicamycin	102-113	synovial apoptosis inhibitor 1, synoviolin	Mus musculus	27-32
15178695-5	2004	In mouse primary cultured glial cells, edaravone attenuated ER stress as evidenced by inhibition of the induction of glucose regulated protein 78 and CHOP and XBP-1 splicing under treatment with tunicamycin (Tm), which induces ER stress.	Tunicamycin	195-206	X-box binding protein 1	Mus musculus	159-164
15178695-5	2004	In mouse primary cultured glial cells, edaravone attenuated ER stress as evidenced by inhibition of the induction of glucose regulated protein 78 and CHOP and XBP-1 splicing under treatment with tunicamycin (Tm), which induces ER stress.	Tunicamycin	208-210	DNA-damage inducible transcript 3	Mus musculus	150-154
15178695-5	2004	In mouse primary cultured glial cells, edaravone attenuated ER stress as evidenced by inhibition of the induction of glucose regulated protein 78 and CHOP and XBP-1 splicing under treatment with tunicamycin (Tm), which induces ER stress.	Tunicamycin	208-210	X-box binding protein 1	Mus musculus	159-164
15294089-5	2004	Analysis of glycosylation status of the J-chain in the transfectant was examined by tunicamycin treatment, endoglycosidase H digestion, and also by treatment with brefeldin A.	Tunicamycin	84-95	joining chain of multimeric IgA and IgM	Homo sapiens	40-47
15383281-5	2004	In cells, calreticulin oligomerization intermediates accumulate in response to conditions that induce protein misfolding (heat shock and tunicamycin treatments), and upon calcium depletion.	Tunicamycin	137-148	calreticulin	Homo sapiens	10-22
15313195-2	2004	Tunicamycin pretreatment of Madin-Darby canine kidney cells not only preserved E-cadherin staining at the plasma membrane, but also inhibited ATP-depletion-mediated E-cadherin degradation.	Tunicamycin	0-11	cadherin 1	Canis lupus familiaris	79-89
15313195-2	2004	Tunicamycin pretreatment of Madin-Darby canine kidney cells not only preserved E-cadherin staining at the plasma membrane, but also inhibited ATP-depletion-mediated E-cadherin degradation.	Tunicamycin	0-11	cadherin 1	Canis lupus familiaris	165-175
15313195-3	2004	Electron microscopic analysis, together with the preservation of the staining patterns of the tight junction marker ZO-1, the apical/microvillar marker gp135, and basolateral marker Na/K-ATPase suggested that tunicamycin preserved the junctional complex and the polarized epithelial cell phenotype.	Tunicamycin	209-220	podocalyxin like	Canis lupus familiaris	152-157
15341532-7	2004	This effect was prevented by pretreatment with tunicamycin or brefeldin, suggesting that donepezil affects trafficking and/or maturation of ADAM 10; additionally, this pretreatment significantly decreased sAPPalpha levels.	Tunicamycin	47-58	ADAM metallopeptidase domain 10	Homo sapiens	140-147
15155747-11	2004	Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5.	Tunicamycin	67-78	TNF receptor superfamily member 10b	Homo sapiens	144-154
15155747-12	2004	Our data suggest that tumor cells may become resistant to TRAIL through regulation of the death receptor cell surface transport and that resistance to TRAIL may be overcome by the glycosylation inhibitor/endoplasmic reticulum stress-inducing agent tunicamycin.	Tunicamycin	248-259	TNF superfamily member 10	Homo sapiens	151-156
15201339-2	2004	We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms.	Tunicamycin	80-91	mitogen activated protein kinase 3	Rattus norvegicus	178-181
15201339-2	2004	We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms.	Tunicamycin	80-91	mitogen activated protein kinase 3	Rattus norvegicus	188-227
15201339-2	2004	We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms.	Tunicamycin	80-91	mitogen activated protein kinase 3	Rattus norvegicus	229-234
15201339-2	2004	We demonstrate that the misfolding agents azetidine-2-carboxylic acid (Azc) and tunicamycin initiate signaling from the ER, resulting in the activation of Jun-N-terminal kinase, p44(MAPK)/extracellular signal-regulated kinase-1 (ERK-1), and p38(MAPK) through IRE1alpha-dependent mechanisms.	Tunicamycin	80-91	mitogen activated protein kinase 14	Rattus norvegicus	241-244
15155747-11	2004	Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5.	Tunicamycin	67-78	TNF superfamily member 10	Homo sapiens	15-20
15155747-11	2004	Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5.	Tunicamycin	67-78	TNF superfamily member 10	Homo sapiens	58-63
15155747-11	2004	Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5.	Tunicamycin	67-78	TNF receptor superfamily member 10a	Homo sapiens	136-139
15304216-3	2004	Cells from BI-1-deficient mice, including fibroblasts, hepatocytes, and neurons, display selective hypersensitivity to apoptosis induced by ER stress agents (thapsigargin, tunicamycin, brefeldin A), but not to stimulators of mitochondrial or TNF/Fas-death receptor apoptosis pathways.	Tunicamycin	172-183	transmembrane BAX inhibitor motif containing 6	Mus musculus	11-15
15304216-7	2004	In vivo, bi-1(-/-) mice exhibit increased sensitivity to tissue damage induced by stimuli that trigger ER stress, including stroke and tunicamycin injection.	Tunicamycin	135-146	transmembrane BAX inhibitor motif containing 6	Mus musculus	9-13
15102854-2	2004	The data in the present study document that transcription from the human C/EBPbeta gene is induced in response to endoplasmic reticulum stress, such as glucose deprivation, or treatment of cells with tunicamycin or thapsigargin.	Tunicamycin	200-211	CCAAT enhancer binding protein beta	Homo sapiens	73-82
15063746-3	2004	Glucose deprivation and the ER stress inducers tunicamycin and thapsigargin increased SelS gene expression and protein content several-fold in parallel with glucose-regulated protein 78.	Tunicamycin	47-58	selenoprotein S	Homo sapiens	86-90
14973138-1	2004	The endoplasmic reticulum (ER) transmembrane proteins, ATF6alpha and ATF6beta, are cleaved in response to ER stress, which can be induced by tunicamycin.	Tunicamycin	141-152	activating transcription factor 6	Homo sapiens	55-64
14973138-1	2004	The endoplasmic reticulum (ER) transmembrane proteins, ATF6alpha and ATF6beta, are cleaved in response to ER stress, which can be induced by tunicamycin.	Tunicamycin	141-152	activating transcription factor 6 beta	Homo sapiens	69-77
14990584-6	2004	Here we show that eIF4E rescued cells from the ER stressors brefeldin A, tunicamycin, thapsigargin, and the Ca(2+) ionophore A23187.	Tunicamycin	73-84	eukaryotic translation initiation factor 4E	Homo sapiens	18-23
14749323-4	2004	274, 1519-1524) that tunicamycin, an inhibitor of asparagine-linked glycosylation, significantly inhibited organic anion transport in COS-7 cells expressing a mouse organic anion transporter (mOAT1), suggesting an important role of glycosylation in mOAT1 function.	Tunicamycin	21-32	solute carrier family 22 (organic anion transporter), member 6	Mus musculus	192-197
14749323-4	2004	274, 1519-1524) that tunicamycin, an inhibitor of asparagine-linked glycosylation, significantly inhibited organic anion transport in COS-7 cells expressing a mouse organic anion transporter (mOAT1), suggesting an important role of glycosylation in mOAT1 function.	Tunicamycin	21-32	solute carrier family 22 (organic anion transporter), member 6	Mus musculus	249-254
15102851-6	2004	The transcript of uda-1 but not those of two other C. elegans ENTPDase mRNAs (ntp-1 and mig-23) was induced up to 3.5-fold by high temperature, tunicamycin, and ethanol.	Tunicamycin	144-155	Nucleoside-diphosphatase uda-1	Caenorhabditis elegans	18-23
14744598-9	2004	FR167653 also inhibited the transactivation of calreticulin stimulated by two other endoplasmic reticulum stress inducers, tunicamycin and A23187.	Tunicamycin	123-134	calreticulin	Homo sapiens	47-59
14676213-3	2004	Overexpression of Nck-1 enhances protein translation, whereas it abrogates eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation and inhibition of translation in response to tunicamycin or thapsigargin treatment.	Tunicamycin	184-195	non-catalytic region of tyrosine kinase adaptor protein 1	Mus musculus	18-23
15113843-2	2004	Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity.	Tunicamycin	93-104	nerve growth factor	Rattus norvegicus	20-39
15113843-2	2004	Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity.	Tunicamycin	93-104	nerve growth factor	Rattus norvegicus	41-44
15113843-2	2004	Here we report that nerve growth factor (NGF) suppressed the ER stress-mediated apoptosis in tunicamycin-treated PC12 cells through an extensive decrease of the caspase-3/-9/-12 activity.	Tunicamycin	93-104	caspase 3	Rattus norvegicus	161-173
15006708-0	2004	Fibroblasts from FAD-linked presenilin 1 mutations display a normal unfolded protein response but overproduce Abeta42 in response to tunicamycin.	Tunicamycin	133-144	presenilin 1	Homo sapiens	28-40
15006708-5	2004	In contrast, tunicamycin, which allowed exit of APP from the ER, increased secreted Abeta42 only in PS1 mutant fibroblasts.	Tunicamycin	13-24	presenilin 1	Homo sapiens	100-103
14765129-5	2004	The level of nuclear PKR was elevated, but the level of cytoplasmic PKR barely changed in tunicamycin-treated SK-N-SH cells.	Tunicamycin	90-101	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	68-71
14765129-6	2004	Furthermore, tunicamycin also raised levels of phosphorylated PKR in the nucleus.	Tunicamycin	13-24	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	62-65
14724446-8	2004	Tunicamycin and endoglycosidase treatments determined the extent of rNKp30 glycosylation.	Tunicamycin	0-11	natural cytotoxicity triggering receptor 3	Rattus norvegicus	68-74
14738568-8	2004	RESULTS: We found that glutamine deprivation and treatment with a chemical inducer of ER stress (tunicamycin) caused a marked induction of the secretion of both VEGF and IL-8 protein by a human breast adenocarcinoma cell line (TSE cells).	Tunicamycin	97-108	vascular endothelial growth factor A	Homo sapiens	161-165
14738568-8	2004	RESULTS: We found that glutamine deprivation and treatment with a chemical inducer of ER stress (tunicamycin) caused a marked induction of the secretion of both VEGF and IL-8 protein by a human breast adenocarcinoma cell line (TSE cells).	Tunicamycin	97-108	C-X-C motif chemokine ligand 8	Homo sapiens	170-174
15611953-2	2004	CHOP deficient (chop - / - ) mouse embryonic fibroblasts (MEFs) exposed to ER stresses such as tunicamycin exhibit decreased apoptosis and reduced toxicity when compared to chop + / + control cells.	Tunicamycin	95-106	DNA-damage inducible transcript 3	Mus musculus	16-20
15611953-2	2004	CHOP deficient (chop - / - ) mouse embryonic fibroblasts (MEFs) exposed to ER stresses such as tunicamycin exhibit decreased apoptosis and reduced toxicity when compared to chop + / + control cells.	Tunicamycin	95-106	DNA-damage inducible transcript 3	Mus musculus	173-177
15611953-8	2004	Enhanced apoptosis and toxicity were observed in chop + / + cells following exposure to tunicamycin or PH mediated PDT when compared to identical treatments in chop - / - cells.	Tunicamycin	88-99	DNA-damage inducible transcript 3	Mus musculus	49-53
14690445-3	2003	In contrast, tunicamycin, A23187, and low concentrations of cycloheximide promoted eIF2alpha phosphorylation in Sf9 cells but without apoptosis.	Tunicamycin	13-24	eukaryotic translation initiation factor 2A	Homo sapiens	83-92
12736248-7	2003	Furthermore, we demonstrated that dig2 is a novel stress response gene, as its mRNA is induced in response to a variety of cellular stressors including thapsigargin, tunicamycin, and heat shock.	Tunicamycin	166-177	DNA-damage-inducible transcript 4	Mus musculus	34-38
12805451-7	2003	The R(+) Env protein induced syncytia in XC cells expressing a mutant mCAT1 lacking both of two N glycosylation sites, and tunicamycin treatment suppressed syncytium formation by R(+) Env in those cells.	Tunicamycin	123-134	solute carrier family 7 (cationic amino acid transporter, y+ system), member 1	Mus musculus	70-75
14632661-11	2003	In addition, preincubation of WT-CD16-transfected cells with Tunicamycin (an inhibitor of N-glycosylation) resulted in an increased binding of monomeric IgG whereas N163Q-CD16-transfected cells remained unaffected.	Tunicamycin	61-72	Fc gamma receptor IIIa	Homo sapiens	33-37
14632661-11	2003	In addition, preincubation of WT-CD16-transfected cells with Tunicamycin (an inhibitor of N-glycosylation) resulted in an increased binding of monomeric IgG whereas N163Q-CD16-transfected cells remained unaffected.	Tunicamycin	61-72	Fc gamma receptor IIIa	Homo sapiens	171-175
12928435-8	2003	Tunicamycin, an inhibitor of N-linked glycosylation, blocked surface membrane expression of HCN2.	Tunicamycin	0-11	hyperpolarization activated cyclic nucleotide gated potassium and sodium channel 2	Homo sapiens	92-96
14530330-6	2003	Treatment of Ag-pulsed OT-1 CTL with agents that alter cell surface charge, including trypsin, papain, tunicamycin, neuraminidase, and polybrene, allowed Ag-specific TCR capping.	Tunicamycin	103-114	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	166-169
12969271-3	2003	Tunicamycin, an inhibitor of N-glycosylation, rapidly induced the expression of the ER-resident chaperone Bip/grp78, a known target gene of the unfolded protein response.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	106-109
12969271-3	2003	Tunicamycin, an inhibitor of N-glycosylation, rapidly induced the expression of the ER-resident chaperone Bip/grp78, a known target gene of the unfolded protein response.	Tunicamycin	0-11	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	110-115
14517337-4	2003	ER stress generated in response to miconazole, tunicamycin, or other inhibitors also triggered a transient G2/M arrest that depended upon the Swe1 protein kinase.	Tunicamycin	47-58	tyrosine protein kinase SWE1	Saccharomyces cerevisiae S288C	142-146
12950021-6	2003	Tunicamycin diminished the antigenicity of NCR-G3 cells.	Tunicamycin	0-11	Neutrophil migration (granulocyte glycoprotein)	Homo sapiens	43-46
12913114-4	2003	Microarray analysis of gene expression changes during tunicamycin-induced apoptosis revealed that the Bcl-2 homology domain 3-only family member, Bcl-2 binding component 3/p53 upregulated modulator of apoptosis (Bbc3/PUMA), was the most strongly induced pro-apoptotic gene.	Tunicamycin	54-65	BCL2 binding component 3	Homo sapiens	212-216
12738777-5	2003	TDAG51 expression was attenuated in homozygous A/A mutant eukaryotic translation initiation factor 2 alpha mouse embryonic fibroblasts treated with homocysteine or tunicamycin, suggesting that ER stress-induced phosphorylation of eukaryotic translation initiation factor 2 alpha is required for TDAG51 transcriptional activation.	Tunicamycin	164-175	pleckstrin homology like domain, family A, member 1	Mus musculus	0-6
12824288-6	2003	The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells.	Tunicamycin	190-201	eukaryotic translation initiation factor 2A	Mus musculus	23-71
12824288-6	2003	The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells.	Tunicamycin	190-201	eukaryotic translation initiation factor 2A	Mus musculus	73-82
12824288-6	2003	The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells.	Tunicamycin	190-201	protein phosphatase 1, regulatory subunit 15A	Mus musculus	141-147
12824288-6	2003	The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells.	Tunicamycin	190-201	eukaryotic translation initiation factor 2A	Mus musculus	207-216
12824288-6	2003	The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells.	Tunicamycin	190-201	protein phosphatase 1, regulatory subunit 15A	Mus musculus	264-270
12824288-6	2003	The phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2alpha) at Ser51 induced by thapsigargin or DTT was prolonged in GADD34-/- MEF, although following treatment with tunicamycin, the eIF2alpha phosphorylation level did not change in either GADD34+/+ or GADD34-/- cells.	Tunicamycin	190-201	protein phosphatase 1, regulatory subunit 15A	Mus musculus	264-270
12843613-5	2003	NF-kappaB was activated by ER stress-inducing agents, thapsigargin and tunicamycin.	Tunicamycin	71-82	nuclear factor kappa B subunit 1	Homo sapiens	0-9
12770613-2	2003	GRP78/Bip is expressed following ER stress induced by thapsigargin, tunicamycin or chemical factors.	Tunicamycin	68-79	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	0-5
12770613-2	2003	GRP78/Bip is expressed following ER stress induced by thapsigargin, tunicamycin or chemical factors.	Tunicamycin	68-79	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	6-9