PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16099428-1 2005 In 3T3-L1 adipocytes, insulin or anisomycin stimulated phosphorylation of IRS-1 at Ser(307) and Ser(636/639), both of which were partially reduced by the mTOR inhibitor, rapamycin, or the JNK inhibitor, SP600125, and were further inhibited by a combination of them. Anisomycin 33-43 mitogen-activated protein kinase 8 Homo sapiens 188-191 16099428-4 2005 These results indicate that mTOR and JNK play roles in phosphorylating IRS-1 serine residues, and that insulin and anisomycin are different in terms of the relationship of activation between mTOR and JNK, and the effects on IRS-1 localization and stability. Anisomycin 115-125 mitogen-activated protein kinase 8 Homo sapiens 200-203 15126504-7 2004 Activation of JNK1 by anisomycin further increased Tau phosphorylation, and SP600125 (a JNK inhibitor) and PD-98059 (an MEK1/2 inhibitor) blocked Tau phosphorylation and NFT formation in these WOX1 knock-down cells. Anisomycin 22-32 mitogen-activated protein kinase 8 Homo sapiens 14-18 16086581-12 2005 The stress-inducing agent, anisomycin, causes activation of JNK, raf, MEK, and ERK in this cell line; activation of JNK is not inhibitable by the MEK inhibitor, U0126, while activation of raf, MEK, and ERK are blocked by this agent. Anisomycin 27-37 mitogen-activated protein kinase 8 Homo sapiens 60-63 16086581-12 2005 The stress-inducing agent, anisomycin, causes activation of JNK, raf, MEK, and ERK in this cell line; activation of JNK is not inhibitable by the MEK inhibitor, U0126, while activation of raf, MEK, and ERK are blocked by this agent. Anisomycin 27-37 mitogen-activated protein kinase 8 Homo sapiens 116-119 15952059-5 2005 Whereas IGF-I phosphorylation of IRS(312) is PI (phosphatidylinositol) 3-kinase dependent, anisomycin stress treatment requires JNK activation to induce phosphorylation of IRS(312). Anisomycin 91-101 mitogen-activated protein kinase 8 Homo sapiens 128-131 15958059-4 2005 Anisomycin, a well-known inducer of ribotoxic stress that inhibits protein synthesis and activates both p38 kinase and JNK, also activated PAI-1 gene expression. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 119-122 15247770-7 2004 RESULTS: All cell lines treated with anisomycin resulted in a transient activation of JNK without inducing apoptosis. Anisomycin 37-47 mitogen-activated protein kinase 8 Homo sapiens 86-89 15247770-10 2004 Combined treatment of Caki-1 and KU 20-01 cells with anisomycin and Ro-318220 resulted in a decrease in MKP-1 expression concomitant with persistent JNK activation. Anisomycin 53-63 mitogen-activated protein kinase 8 Homo sapiens 149-152 15126504-7 2004 Activation of JNK1 by anisomycin further increased Tau phosphorylation, and SP600125 (a JNK inhibitor) and PD-98059 (an MEK1/2 inhibitor) blocked Tau phosphorylation and NFT formation in these WOX1 knock-down cells. Anisomycin 22-32 mitogen-activated protein kinase 8 Homo sapiens 14-17 12514174-8 2003 By stimulating cells with anisomycin or UV light, JNK1 became activated, and WOX1 was phosphorylated at Tyr(33). Anisomycin 26-36 mitogen-activated protein kinase 8 Homo sapiens 50-54 14614324-3 2003 HDI-mediated apoptosis was attenuated by pharmacologic JNK inhibitors and enhanced by the MEK1/2 inhibitor U0126 as well as by the JNK activator anisomycin. Anisomycin 145-155 mitogen-activated protein kinase 8 Homo sapiens 131-134 14555342-4 2003 The effect of a JNK activator anisomycin or c-Myc inhibitor peptides (Int-H1-S6A, F8A) on the amount of c-Myc protein and on the induction of apoptosis was investigated, respectively. Anisomycin 30-40 mitogen-activated protein kinase 8 Homo sapiens 16-19 14555342-7 2003 Anisomycin rapidly induced JNK activation and a subsequent decrease of c-Myc protein, causing cell death in MOLT-4 cells. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 27-30 14555342-8 2003 On the other hand, Rh-1a cells were more resistant to anisomycin than parental MOLT-4 cells, showing less JNK activation and a delayed decrease of c-Myc protein. Anisomycin 54-64 mitogen-activated protein kinase 8 Homo sapiens 106-109 15115662-5 2004 The JNK activator, anisomycin, inhibited iNOS expression and transcription in hepatocytes as well as AP-1 binding activity; and SP600125 reversed this effect of anisomycin. Anisomycin 19-29 mitogen-activated protein kinase 8 Homo sapiens 4-7 15115662-5 2004 The JNK activator, anisomycin, inhibited iNOS expression and transcription in hepatocytes as well as AP-1 binding activity; and SP600125 reversed this effect of anisomycin. Anisomycin 161-171 mitogen-activated protein kinase 8 Homo sapiens 4-7 14737674-0 2004 Synthetic anisomycin analogues activating the JNK/SAPK1 and p38/SAPK2 pathways. Anisomycin 10-20 mitogen-activated protein kinase 8 Homo sapiens 46-55 14737674-1 2004 The synthesis of C(4)H and C(4)Me analogues of the JNK/p38 pathway activator anisomycin, based upon an aldol or Claisen construction of the C(3)-C(4) bond, has been demonstrated. Anisomycin 77-87 mitogen-activated protein kinase 8 Homo sapiens 51-54 11707464-3 2002 Insulin inhibited the anisomycin-induced stimulation of both endogenous SEK1 and its substrate c-Jun N-terminal kinase (JNK), but not that of the upstream kinase MEKK1, in 293T cells. Anisomycin 22-32 mitogen-activated protein kinase 8 Homo sapiens 95-118 12593797-4 2003 The steady-state responses of JNK to sorbitol and anisomycin were found to be highly ultrasensitive in HeLa cells, HEK 293 cells, and Jurkat T cells. Anisomycin 50-60 mitogen-activated protein kinase 8 Homo sapiens 30-33 12220537-4 2002 All the cytocidal inhibitors induced cytochrome c release and caspases 9 activation within hours, but only anisomycin caused persistent JNK activation. Anisomycin 107-117 mitogen-activated protein kinase 8 Homo sapiens 136-139 12220537-5 2002 Although, the JNK inhibitor, SP600125, inhibited JNK-dependent anisomycin-induced c-Jun phosphorylation, it was ineffective in preventing anisomycin-induced caspase activation and cell death. Anisomycin 63-73 mitogen-activated protein kinase 8 Homo sapiens 14-17 12220537-5 2002 Although, the JNK inhibitor, SP600125, inhibited JNK-dependent anisomycin-induced c-Jun phosphorylation, it was ineffective in preventing anisomycin-induced caspase activation and cell death. Anisomycin 63-73 mitogen-activated protein kinase 8 Homo sapiens 49-52 12527329-4 2003 At a lower dose (10 microM), it also inhibited the ability of anisomycin to activate JNK, resulting in decreased c-jun phosphorylation, although it did not inhibit JNK activity directly. Anisomycin 62-72 mitogen-activated protein kinase 8 Homo sapiens 85-88 12499846-4 2002 When p-JNK, whose basic activity is very low and not enhanced by a cholinergic stimulation of the cells for up to 30 min, is activated in the presence of 50 microM anisomycin, both spontaneous and cholinergically induced lamellar protrusive activity is attenuated. Anisomycin 164-174 mitogen-activated protein kinase 8 Homo sapiens 7-10 12402161-0 2002 Anisomycin activates JNK and sensitises DU 145 prostate carcinoma cells to Fas mediated apoptosis. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 21-24 12402161-4 2002 Using anisomycin, a potent JNK agonist, we have demonstrated a role for JNK in Fas mediated apoptosis in DU 145 cells. Anisomycin 6-16 mitogen-activated protein kinase 8 Homo sapiens 27-30 12402161-4 2002 Using anisomycin, a potent JNK agonist, we have demonstrated a role for JNK in Fas mediated apoptosis in DU 145 cells. Anisomycin 6-16 mitogen-activated protein kinase 8 Homo sapiens 72-75 12077368-7 2002 We have rendered JNK and p38 activation in NIH 3T3 fibroblasts anchorage-independent either by treatment with anisomycin or by expression of upstream activators. Anisomycin 110-120 mitogen-activated protein kinase 8 Homo sapiens 17-20 11948422-4 2002 Both anisomycin and arsenite activate the JNK pathway and, in addition, inactivate the M3/6 phosphatase. Anisomycin 5-15 mitogen-activated protein kinase 8 Homo sapiens 42-45 11790785-4 2002 In 293(PED) cells, decreased apoptosis induced by anisomycin and H(2)O(2) was also accompanied by block of JNK1/2 and p38 phosphorylations, respectively. Anisomycin 50-60 mitogen-activated protein kinase 8 Homo sapiens 107-113 11790785-8 2002 Complete rescue of JNK and p38 functions in 293(PED) cells by overexpressing JNK1 or p38, respectively, enabled only partial recovery of apoptotic response to growth factor deprivation and anisomycin. Anisomycin 189-199 mitogen-activated protein kinase 8 Homo sapiens 19-22 11790785-8 2002 Complete rescue of JNK and p38 functions in 293(PED) cells by overexpressing JNK1 or p38, respectively, enabled only partial recovery of apoptotic response to growth factor deprivation and anisomycin. Anisomycin 189-199 mitogen-activated protein kinase 8 Homo sapiens 77-81 11707464-3 2002 Insulin inhibited the anisomycin-induced stimulation of both endogenous SEK1 and its substrate c-Jun N-terminal kinase (JNK), but not that of the upstream kinase MEKK1, in 293T cells. Anisomycin 22-32 mitogen-activated protein kinase 8 Homo sapiens 120-123 11795492-7 2001 These inhibitors also suppressed the motility stimulated by known JNK agonists such as TNFalpha and anisomycin. Anisomycin 100-110 mitogen-activated protein kinase 8 Homo sapiens 66-69 11734304-8 2002 These results suggest that mitoxantrone- and anisomycin-induced apoptosis is dependent on JNK/SAPK, but not p38, activity. Anisomycin 45-55 mitogen-activated protein kinase 8 Homo sapiens 90-98 11734304-0 2002 c-Jun N-terminal kinase/stress-activated protein kinase (JNK/SAPK) is required for mitoxantrone- and anisomycin-induced apoptosis in HL-60 cells. Anisomycin 101-111 mitogen-activated protein kinase 8 Homo sapiens 57-65 11734304-4 2002 Here, we found that mitoxantrone and anisomycin stimulated a dose- and time-dependent induction of JNK/SAPK activity, and to a lesser extent p38 activity, that preceded the appearance of apoptosis as measured by internucleosomal DNA fragmentation. Anisomycin 37-47 mitogen-activated protein kinase 8 Homo sapiens 99-102 11734304-7 2002 Additionally, direct inhibition of JNK/SAPK signaling through the use of dominant-negative MKK4/SEK1 (SEK-AL) inhibited mitoxantrone- and anisomycin-induced apoptosis. Anisomycin 138-148 mitogen-activated protein kinase 8 Homo sapiens 35-43 11323415-4 2001 Results indicate that anisomycin, a potent activator of the stress kinase JNK/SAPK, can induce Bcl2 phosphorylation at Ser(70) and that JNK1 can be latently activated following IL-3 withdrawal to mediate Bcl2 phosphorylation. Anisomycin 22-32 mitogen-activated protein kinase 8 Homo sapiens 74-82 11323415-4 2001 Results indicate that anisomycin, a potent activator of the stress kinase JNK/SAPK, can induce Bcl2 phosphorylation at Ser(70) and that JNK1 can be latently activated following IL-3 withdrawal to mediate Bcl2 phosphorylation. Anisomycin 22-32 mitogen-activated protein kinase 8 Homo sapiens 136-140 11323415-6 2001 Dominant-negative (DN)-JNK1 can block both anisomycin and latent IL-3 withdrawal-induced Bcl2 phosphorylation (>90%) and potently enhances cell death. Anisomycin 43-53 mitogen-activated protein kinase 8 Homo sapiens 23-27 11278395-11 2001 In addition, MLK2 is phosphorylated in vivo within several of the same C-terminal peptides phosphorylated by JNK2 in vitro, and this phosphorylation is increased by cotransfection of JNK2 and treatment with the JNK activator, anisomycin. Anisomycin 226-236 mitogen-activated protein kinase 8 Homo sapiens 109-112 11278395-12 2001 Cotransfection of dominant-negative JNK kinase inhibits phosphorylation of kinase-negative MLK2 by anisomycin-activated JNK. Anisomycin 99-109 mitogen-activated protein kinase 8 Homo sapiens 36-39 10318810-2 1999 Inhibitors of the peptidyltransferase reaction (e.g. anisomycin) can trigger a ribotoxic stress response that activates c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinases, components of a signaling cascade that regulates cell survival in response to stress. Anisomycin 53-63 mitogen-activated protein kinase 8 Homo sapiens 120-143 11527157-3 2001 Dose-response and time course studies of the effects of heat shock and anisomycin treatment showed a close correlation of the activation of JNK and hyperphosphorylation of HSF1. Anisomycin 71-81 mitogen-activated protein kinase 8 Homo sapiens 140-143 10849421-7 2000 This chimeric mRNA is also more stable in cells overexpressing p38/HOG and JNK that have been stimulated by anisomycin. Anisomycin 108-118 mitogen-activated protein kinase 8 Homo sapiens 75-78 10506143-6 1999 In HeLa cells, the JNKK2-JNK1 fusion protein showed significant JNK activity, which was comparable with that of JNK1 activated by many stimuli and activators, including EGF, TNF-alpha, anisomycin, UV irradiation, MEKK1, and small GTP binding proteins Rac1 and Cdc42Hs. Anisomycin 185-195 mitogen-activated protein kinase 8 Homo sapiens 25-29 10506143-6 1999 In HeLa cells, the JNKK2-JNK1 fusion protein showed significant JNK activity, which was comparable with that of JNK1 activated by many stimuli and activators, including EGF, TNF-alpha, anisomycin, UV irradiation, MEKK1, and small GTP binding proteins Rac1 and Cdc42Hs. Anisomycin 185-195 mitogen-activated protein kinase 8 Homo sapiens 19-22 10506143-6 1999 In HeLa cells, the JNKK2-JNK1 fusion protein showed significant JNK activity, which was comparable with that of JNK1 activated by many stimuli and activators, including EGF, TNF-alpha, anisomycin, UV irradiation, MEKK1, and small GTP binding proteins Rac1 and Cdc42Hs. Anisomycin 185-195 mitogen-activated protein kinase 8 Homo sapiens 112-116 10508211-1 1999 The protein synthesis inhibitor anisomycin activates stress-related mitogen-activated protein kinases (MAPKs), namely, c-jun NH(2)-terminal kinase (p46/54(JNK)) and p38(MAPK) in mammalian cells. Anisomycin 32-42 mitogen-activated protein kinase 8 Homo sapiens 148-160 10508211-2 1999 In this paper, we show that although exposure to anisomycin resulted in rapid and strong activation of p46/54(JNK) and p38(MAPK), with a delayed low level dual-phosphorylation of mitogen/extracellular protein kinase (p42/44(MAPK)), low density lipoprotein (LDL) receptor induction depends solely on the mild activation of p42/44(MAPK) signaling cascade in HepG2 cells. Anisomycin 49-59 mitogen-activated protein kinase 8 Homo sapiens 110-113 10967115-9 2000 FAK-independent stimulation of JNK with anisomycin treatment both in FAK(-)(/-) cells and in suspended FAK(+/+) cells confirmed that IRS-1 mRNA transcription can be partially regulated by JNK. Anisomycin 40-50 mitogen-activated protein kinase 8 Homo sapiens 188-191 10628325-2 1999 Activation of JNK by anisomycin, the inhibition of ERK activation by PD098059 or a blockage of the PI3-K/Akt pathway by wortmannin or LY294002 alone, was not sufficient for the induction of apoptosis. Anisomycin 21-31 mitogen-activated protein kinase 8 Homo sapiens 14-17 10318810-2 1999 Inhibitors of the peptidyltransferase reaction (e.g. anisomycin) can trigger a ribotoxic stress response that activates c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinases, components of a signaling cascade that regulates cell survival in response to stress. Anisomycin 53-63 mitogen-activated protein kinase 8 Homo sapiens 145-148 9886850-6 1999 In transfected 293T cells, PPARgamma1 is phosphorylated at Ser82 in response to known JNK activators such as UV irradiation and anisomycin treatment. Anisomycin 128-138 mitogen-activated protein kinase 8 Homo sapiens 86-89 9886850-8 1999 Finally, in transient transfection reporter assays, activation of JNK by anisomycin or by overexpression of MKK4 (the upstream JNK kinase) decreased ligand-dependent PPARgamma1 transcriptional activity. Anisomycin 73-83 mitogen-activated protein kinase 8 Homo sapiens 66-69 9528756-1 1998 Anisomycin, a translational inhibitor secreted by Streptomyces spp., strongly activates the stress-activated mitogen-activated protein (MAP) kinases JNK/SAPK (c-Jun NH2-terminal kinase/stress-activated protein kinase) and p38/RK in mammalian cells, resulting in rapid induction of immediate-early (IE) genes in the nucleus. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 149-157 9535820-5 1998 We report the use of 12-O-tetradecanoylphorbol-13-acetate (TPA) in the inhibition of apoptosis in HL-60 cells stimulated with the JNK/SAPK activator anisomycin. Anisomycin 149-159 mitogen-activated protein kinase 8 Homo sapiens 130-138 9748273-4 1998 In all cell types, endogenous or transfected JNK activity was strongly stimulated by anisomycin or tumor necrosis factor-alpha, and 10 nM IGF-I pretreatment suppressed the induced JNK activity. Anisomycin 85-95 mitogen-activated protein kinase 8 Homo sapiens 45-48 9743209-4 1998 The regulation of TNF-R2 expression in activated T cells seems to involve the c-Jun amino terminal kinase (JNK) pathway, as activation of JNK with anisomycin down-regulates TNF-R2. Anisomycin 147-157 mitogen-activated protein kinase 8 Homo sapiens 107-110 9743209-4 1998 The regulation of TNF-R2 expression in activated T cells seems to involve the c-Jun amino terminal kinase (JNK) pathway, as activation of JNK with anisomycin down-regulates TNF-R2. Anisomycin 147-157 mitogen-activated protein kinase 8 Homo sapiens 138-141 9674701-3 1998 In this report, we show that curcumin inhibits JNK activation by various agonists including PMA plus ionomycin, anisomycin, UV-C, gamma radiation, TNF-alpha, and sodium orthovanadate. Anisomycin 112-122 mitogen-activated protein kinase 8 Homo sapiens 47-50 9535820-10 1998 Therefore, we conclude that TPA inhibits the induction of apoptosis in anisomycin-treated HL-60 cells through an ERK-dependent pathway and that this effect can be reversed by the attenuation of ERK activity accompanied with the stimulation of JNK/SAPK activity. Anisomycin 71-81 mitogen-activated protein kinase 8 Homo sapiens 243-246 9528756-5 1998 Further, we show that anisomycin-induced homologous desensitization is caused by the fact that anisomycin no longer activates the JNK/SAPK and p38/RK MAP kinase cascades in desensitized cells. Anisomycin 22-32 mitogen-activated protein kinase 8 Homo sapiens 130-133 9528756-5 1998 Further, we show that anisomycin-induced homologous desensitization is caused by the fact that anisomycin no longer activates the JNK/SAPK and p38/RK MAP kinase cascades in desensitized cells. Anisomycin 95-105 mitogen-activated protein kinase 8 Homo sapiens 130-133 9528756-6 1998 In anisomycin-desensitized cells, activation of JNK/SAPKs by UV radiation and hyperosmolarity is almost completely lost, and that of the p38/RK cascade is reduced to about 50% of the normal response. Anisomycin 3-13 mitogen-activated protein kinase 8 Homo sapiens 48-51 9154836-4 1997 We provide evidence that in order to activate SAPK/JNK1, anisomycin requires ribosomes that are translationally active at the time of contact with the drug, suggesting a ribosomal origin of the anisomycin-induced signaling to SAPK/JNK1. Anisomycin 57-67 mitogen-activated protein kinase 8 Homo sapiens 51-55 9551965-7 1998 In comparing the effect of different stress stimuli to DA-MEKK1, we found that UV, gamma irradiation, and anisomycin prolonged JNK activation in parallel with FasL expression and onset of cell death. Anisomycin 106-116 mitogen-activated protein kinase 8 Homo sapiens 127-130 9401960-7 1997 In contrast, stimulation by anisomycin, a potent Jun-NH2-terminal kinase (JNK) agonist, exhibited no lag phase. Anisomycin 28-38 mitogen-activated protein kinase 8 Homo sapiens 49-72 9401960-7 1997 In contrast, stimulation by anisomycin, a potent Jun-NH2-terminal kinase (JNK) agonist, exhibited no lag phase. Anisomycin 28-38 mitogen-activated protein kinase 8 Homo sapiens 74-77 9401960-11 1997 The stimulation of transport by a low concentration of anisomycin (0.3 microM) was transient, peaked at 30-60 min and it was inhibited (IC50 < 1 microM) by SB203580, which indicates that its mediator is not JNK, but the homologous p38(MAP kinase) (p38(MAPK)). Anisomycin 55-65 mitogen-activated protein kinase 8 Homo sapiens 210-213 9154836-4 1997 We provide evidence that in order to activate SAPK/JNK1, anisomycin requires ribosomes that are translationally active at the time of contact with the drug, suggesting a ribosomal origin of the anisomycin-induced signaling to SAPK/JNK1. Anisomycin 57-67 mitogen-activated protein kinase 8 Homo sapiens 231-235 9154836-4 1997 We provide evidence that in order to activate SAPK/JNK1, anisomycin requires ribosomes that are translationally active at the time of contact with the drug, suggesting a ribosomal origin of the anisomycin-induced signaling to SAPK/JNK1. Anisomycin 194-204 mitogen-activated protein kinase 8 Homo sapiens 51-55 9154836-4 1997 We provide evidence that in order to activate SAPK/JNK1, anisomycin requires ribosomes that are translationally active at the time of contact with the drug, suggesting a ribosomal origin of the anisomycin-induced signaling to SAPK/JNK1. Anisomycin 194-204 mitogen-activated protein kinase 8 Homo sapiens 231-235 9154836-5 1997 In support of this notion, we have found that aminohexose pyrimidine nucleoside antibiotics, which bind to the same region in the 28S rRNA that is the target site for anisomycin, are also potent activators of SAPK/JNK1. Anisomycin 167-177 mitogen-activated protein kinase 8 Homo sapiens 214-218 9154836-10 1997 As in the case of anisomycin, ribosomes that were active at the time of exposure to ricin A chain or alpha-sarcin were able to initiate signal transduction from the damaged 28S rRNA to SAPK/JNK1 while inactive ribosomes were not. Anisomycin 18-28 mitogen-activated protein kinase 8 Homo sapiens 190-194 8940056-9 1996 Activation of JNK by anisomycin in vivo mimics activation of glycogen synthase by insulin. Anisomycin 21-31 mitogen-activated protein kinase 8 Homo sapiens 14-17 8967341-7 1996 JNK was also stimulated by anisomycin and okadaic acid but not by phorbol 12-myristate 13-acetate. Anisomycin 27-37 mitogen-activated protein kinase 8 Homo sapiens 0-3 8805335-2 1996 Anisomycin and UV radiation have been suggested to induce c-fos and c-jun transcription via JNK/SAPK-mediated phosphorylation of TCF (ternary complex factor), for c-fos induction [6-8], and c-Jun and/or ATF-2 for c-jun induction [9-11] [12,13]. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 92-95 8805335-4 1996 By using the p38/RK inhibitor SB 203580 [20,21], we show that activation of p38/RK and/or its downstream effectors are essential for anisomycin- and UV-stimulated c-fos/c-jun induction and histone H3/HMG-14 phosphorylation, whereas JNK/SAPK activation and phosphorylation of c-Jun and ATF-2 are insufficient for these responses. Anisomycin 133-143 mitogen-activated protein kinase 8 Homo sapiens 232-235 8939945-10 1996 Finally, while some stress-dependent activators of the JNK pathway (NaCl and sorbitol) stimulated CADTK, others (anisomycin, UV, and TNFalpha) did not. Anisomycin 113-123 mitogen-activated protein kinase 8 Homo sapiens 55-58 8626428-3 1996 To examine the relative role of the mitogen-activated protein kinases in the feedback phosphorylation of SOS we determined the signaling specificity of insulin, osmotic shock, and anisomycin to activate the ERK (extracellular-signal regulated kinase) and JNK (c-Jun kinase) pathways. Anisomycin 180-190 mitogen-activated protein kinase 8 Homo sapiens 255-258 8626428-3 1996 To examine the relative role of the mitogen-activated protein kinases in the feedback phosphorylation of SOS we determined the signaling specificity of insulin, osmotic shock, and anisomycin to activate the ERK (extracellular-signal regulated kinase) and JNK (c-Jun kinase) pathways. Anisomycin 180-190 mitogen-activated protein kinase 8 Homo sapiens 260-272 33768099-9 2021 Treatment with the JNK agonist anisomycin can induce apoptosis, lead to increased p-JNK expression and decreased p-STAT3 expression. Anisomycin 31-41 mitogen-activated protein kinase 8 Homo sapiens 19-22 33588264-12 2021 Further studies in 16HBE showed that AVE0991 pre-treatment inhibited LPS-induced or anisomycin-induced CCL2 increase and THP-1 macrophages migration via JNK pathways. Anisomycin 84-94 mitogen-activated protein kinase 8 Homo sapiens 153-156 33768099-9 2021 Treatment with the JNK agonist anisomycin can induce apoptosis, lead to increased p-JNK expression and decreased p-STAT3 expression. Anisomycin 31-41 mitogen-activated protein kinase 8 Homo sapiens 84-87 35129807-9 2022 Additionally, we also investigated whether zinc protected against sorafenib-induced neuronal cells apoptosis via ROS/JNK pathway through treating SH-SY5Y cells with the NAC or the specific JNK activator anisomycin. Anisomycin 203-213 mitogen-activated protein kinase 8 Homo sapiens 189-192 34741589-7 2022 However, the inhibitory effect of tCQA on JNK and P38 levels activated by the JNK agonist anisomycin is not obvious; meanwhile, tCQA could inhibit the activation of JNK/P38 induced by H2 O2 , which suggests that tCQA might inhibit the JNK/P38 signaling pathway by reducing ROS. Anisomycin 90-100 mitogen-activated protein kinase 8 Homo sapiens 42-45 34741589-7 2022 However, the inhibitory effect of tCQA on JNK and P38 levels activated by the JNK agonist anisomycin is not obvious; meanwhile, tCQA could inhibit the activation of JNK/P38 induced by H2 O2 , which suggests that tCQA might inhibit the JNK/P38 signaling pathway by reducing ROS. Anisomycin 90-100 mitogen-activated protein kinase 8 Homo sapiens 78-81 34800541-7 2021 The adverse effects of IL-1beta on TJs were mimicked by anisomycin, which is an activator of p38 and JNK signalling, and were blocked by MEC pretreatment with a p38 inhibitor but not a JNK inhibitor. Anisomycin 56-66 mitogen-activated protein kinase 8 Homo sapiens 101-104 34151031-1 2021 Anisomycin is used as a chemical compound that possesses c-Jun N-terminal kinase (JNK)-activating effects. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 57-80 34151031-1 2021 Anisomycin is used as a chemical compound that possesses c-Jun N-terminal kinase (JNK)-activating effects. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 82-85 34151031-3 2021 In addition to its JNK-activating effects, anisomycin has been reported to affect gene expression in osteosarcoma, leukemia, hepatocellular carcinoma, ovarian cancer and other cancers. Anisomycin 43-53 mitogen-activated protein kinase 8 Homo sapiens 19-22 35129807-10 2022 The results indicated that NAC performed the same protective effects as zinc in sorafenib-challenged SH-SY5Y cells and activation of JNK by anisomycin partly abolished the protective effects of zinc. Anisomycin 140-150 mitogen-activated protein kinase 8 Homo sapiens 133-136 30878547-11 2019 Finally, pretreatment with JNK agonist, anisomycin, was done to observe the change in expressions of MKK4 and JNK. Anisomycin 40-50 mitogen-activated protein kinase 8 Homo sapiens 27-30 32241917-6 2020 In contrast, a JNK activator, anisomycin, partially abolished the effects of SP600125 on Prss14/epithin shedding. Anisomycin 30-40 mitogen-activated protein kinase 8 Homo sapiens 15-18 31836142-5 2020 Furthermore, treatment with the JNK agonist anisomycin enhanced the damage to the joint cartilage and increased the levels of IL-1beta, IL-6 and TNF-alpha. Anisomycin 44-54 mitogen-activated protein kinase 8 Homo sapiens 32-35 32662898-5 2020 Anisomycin (a JNK activator) with/without RBBP6 siRNA was used to treat PC3 cells for further investigating the ramification of the RBBP6-mediated JNK pathway in PCa. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 14-17 32226536-9 2020 The selective JNK activator anisomycin also inhibited melanin production through phosphoinhibition of CRTC3, while JNK inhibition enhanced melanogenesis by stimulating CRTC3 dephosphorylation and nuclear migration. Anisomycin 28-38 mitogen-activated protein kinase 8 Homo sapiens 14-17 32189173-3 2020 JNK signaling activation and inhibition in primary corneal fibroblasts were obtained by treatments with anisomycin and SP600125, respectively. Anisomycin 104-114 mitogen-activated protein kinase 8 Homo sapiens 0-3 30878547-15 2019 In addition, pretreatment with JNK agonist, anisomycin effectively suppressed TBTC-induced cytotoxicity in hypothalamic neuron. Anisomycin 44-54 mitogen-activated protein kinase 8 Homo sapiens 31-34 30594507-10 2019 Furthermore, anisomycin, a specific activator for JNK, reversed the effect of Gal-7 siRNA on cell apoptosis induced by TGF-beta1. Anisomycin 13-23 mitogen-activated protein kinase 8 Homo sapiens 50-53 29170390-7 2017 Specifically, the stress kinase pathways p38 and JNK were modified in latently infected cells, and activation of p38 and JNK signaling by anisomycin resulted in increased cell death independent of HIV reactivation. Anisomycin 138-148 mitogen-activated protein kinase 8 Homo sapiens 121-124 30662298-10 2019 Moreover, anisomycin, an activator of p38 and JNK, significantly abolished the anti-apoptotic effects of CK. Anisomycin 10-20 mitogen-activated protein kinase 8 Homo sapiens 46-49 29636680-6 2018 The inhibitory effect of CEP could be partly reversed by treatment with anisomycin (a JNK and p38 agonist) and/or SC79 (an AKT agonist) in vitro. Anisomycin 72-82 mitogen-activated protein kinase 8 Homo sapiens 86-89 28772243-8 2017 Activation of JNK by anisomycin reversed the effect of daphnoretin on daphnoretin-inhibited pJNK expression and dendrite formation of DCs. Anisomycin 21-31 mitogen-activated protein kinase 8 Homo sapiens 14-17 24906456-9 2014 Anisomycin, an activator of EGFR"s downstream kinases, p38 and JNK, caused DA contraction; conversely, oxygen-induced DA contraction was blocked by inhibitors of p38 mitogen-activated protein kinases (MAPK) (SB203580) or JNK (JNK inhibitor II). Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 63-66 28176854-6 2017 We also demonstrate that activation of JNK by subtoxic concentrations of anisomycin induced selective apoptotic killing of Mtb-infected human macrophages, which was completely blocked in the presence of a specific JNK inhibitor. Anisomycin 73-83 mitogen-activated protein kinase 8 Homo sapiens 39-42 28176854-6 2017 We also demonstrate that activation of JNK by subtoxic concentrations of anisomycin induced selective apoptotic killing of Mtb-infected human macrophages, which was completely blocked in the presence of a specific JNK inhibitor. Anisomycin 73-83 mitogen-activated protein kinase 8 Homo sapiens 214-217 27087117-0 2016 microRNA let-7c is essential for the anisomycin-elicited apoptosis in Jurkat T cells by linking JNK1/2 to AP-1/STAT1/STAT3 signaling. Anisomycin 37-47 mitogen-activated protein kinase 8 Homo sapiens 96-102 27087117-4 2016 microRNA let-7c (let-7c) contributed to the anisomycin-induced apoptosis, which could be abrogated by the inactivation of JNK signaling. Anisomycin 44-54 mitogen-activated protein kinase 8 Homo sapiens 122-125 27087117-8 2016 The findings indicate for the first time that miR let-7c is essential for the anisomycin-triggered apoptosis by linking JNK1/2 to AP-1/STAT1/STAT3/Bim/Bcl-xL/Bax/Bak signaling. Anisomycin 78-88 mitogen-activated protein kinase 8 Homo sapiens 120-126 24597985-0 2014 Low-dose anisomycin sensitizes glucocorticoid-resistant T-acute lymphoblastic leukemia CEM-C1 cells to dexamethasone-induced apoptosis through activation of glucocorticoid receptor and p38-MAPK/JNK. Anisomycin 9-19 mitogen-activated protein kinase 8 Homo sapiens 194-197 24597985-6 2014 We conclude that low-dose anisomycin sensitizes GC-resistant CEM-C1 cells to DEX and this effect is mediated, at least in part, by activation of the GR-p38-MAPK/JNK signaling pathway. Anisomycin 26-36 mitogen-activated protein kinase 8 Homo sapiens 161-164 28349059-11 2017 Pretreatment by IRE1 agonist tunicamycin or JNK agonist anisomycin attenuated the effect of psoralen on osteoporotic osteoblasts. Anisomycin 56-66 mitogen-activated protein kinase 8 Homo sapiens 44-47 27403417-7 2016 Metformin decreased hyperphosphorylated JNK induced by Abeta; however, the protection of metformin against Abeta was blocked when anisomycin, the activator of JNK, was added to the medium, indicating that metformin performed its protection against Abeta in a JNK-dependent way. Anisomycin 130-140 mitogen-activated protein kinase 8 Homo sapiens 159-162 27403417-7 2016 Metformin decreased hyperphosphorylated JNK induced by Abeta; however, the protection of metformin against Abeta was blocked when anisomycin, the activator of JNK, was added to the medium, indicating that metformin performed its protection against Abeta in a JNK-dependent way. Anisomycin 130-140 mitogen-activated protein kinase 8 Homo sapiens 159-162 25874865-3 2015 We found that both JNK and AMPK were phosphorylated at their activation sites by TNF-alpha, Anisomycin, H2O2 and sorbitol. Anisomycin 92-102 mitogen-activated protein kinase 8 Homo sapiens 19-22 24906456-9 2014 Anisomycin, an activator of EGFR"s downstream kinases, p38 and JNK, caused DA contraction; conversely, oxygen-induced DA contraction was blocked by inhibitors of p38 mitogen-activated protein kinases (MAPK) (SB203580) or JNK (JNK inhibitor II). Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 221-224 24906456-9 2014 Anisomycin, an activator of EGFR"s downstream kinases, p38 and JNK, caused DA contraction; conversely, oxygen-induced DA contraction was blocked by inhibitors of p38 mitogen-activated protein kinases (MAPK) (SB203580) or JNK (JNK inhibitor II). Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 221-224 23720056-10 2013 Finally, cisplatin resistance was partially overcome by ectopic TR3 overexpression and by treatment with the JNK activator anisomycin and Akt pathway inhibitor, wortmannin. Anisomycin 123-133 mitogen-activated protein kinase 8 Homo sapiens 109-112 24784707-9 2014 In addition, anisomycin, a JNK activator, increased caspase 3 activity and apoptosis as well as triglycerides accumulation and SREBP1 expression, and RvD1 treatment reversed these changes. Anisomycin 13-23 mitogen-activated protein kinase 8 Homo sapiens 27-30 23444236-4 2013 We found that p38 and JNK agonist anisomycin abolishes spontaneous cytoplasmic vacuolization of HepG2 cells through p38 activation, but not through JNK activation. Anisomycin 34-44 mitogen-activated protein kinase 8 Homo sapiens 22-25 24801387-7 2014 In contrast, both JNK activation with anisomycin and knockdown of the mTORC2 subunit rictor specifically stimulated phosphorylation of the Thr421/Ser424 sites, suggesting that mTORC2 represses JNK-mediated phosphorylation of these sites. Anisomycin 38-48 mitogen-activated protein kinase 8 Homo sapiens 18-21 22790444-7 2012 Finally, the effects of FRK on cell migration and invasion and JNK/c-Jun inhibition were abolished by anisomycin, a JNK specific activator. Anisomycin 102-112 mitogen-activated protein kinase 8 Homo sapiens 63-66 23067223-0 2013 Anisomycin induces apoptosis of glucocorticoid resistant acute lymphoblastic leukemia CEM-C1 cells via activation of mitogen-activated protein kinases p38 and JNK. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 159-162 23067223-7 2013 The rapid up-regulation of phosphorylated mitogen-activated protein kinases (MAPKs) p38 and Jun N-terminal kinase (JNK) were observed after CEM-C1 cells were incubated with anisomycin. Anisomycin 173-183 mitogen-activated protein kinase 8 Homo sapiens 92-113 23067223-7 2013 The rapid up-regulation of phosphorylated mitogen-activated protein kinases (MAPKs) p38 and Jun N-terminal kinase (JNK) were observed after CEM-C1 cells were incubated with anisomycin. Anisomycin 173-183 mitogen-activated protein kinase 8 Homo sapiens 115-118 23067223-9 2013 These results suggested that anisomycin induced apoptosis of CEM-C1 cells via activation of p38 and JNK, and might be an attractive new agent for treatment of GC-resistant ALL. Anisomycin 29-39 mitogen-activated protein kinase 8 Homo sapiens 100-103 22790444-7 2012 Finally, the effects of FRK on cell migration and invasion and JNK/c-Jun inhibition were abolished by anisomycin, a JNK specific activator. Anisomycin 102-112 mitogen-activated protein kinase 8 Homo sapiens 116-119 22695114-7 2012 Furthermore, it seems likely that the JNK activated by anisomycin may stimulate not only the nuclear export of GATA-6 through CRM1 but also the degradation of GATA-6 by cytoplasmic proteasomes. Anisomycin 55-65 mitogen-activated protein kinase 8 Homo sapiens 38-41 22695114-2 2012 We further examined the effects of SP600125 on the degradation of GATA-6 in detail, since an activator of JNK (anisomycin) is available. Anisomycin 111-121 mitogen-activated protein kinase 8 Homo sapiens 106-109 22695114-4 2012 Such an effect of anisomycin was inhibited by SP600125, indicating that the observed phenomenon might be linked to the JNK signaling pathway. Anisomycin 18-28 mitogen-activated protein kinase 8 Homo sapiens 119-122 22800348-7 2012 JNK signal was inhibited in FaDu or FaDu/T cells and the inhibited JNK was reactivated by taxol or anisomycin (an activator for MAPK signal transduction pathways). Anisomycin 99-109 mitogen-activated protein kinase 8 Homo sapiens 0-3 22684030-8 2012 In the two cell lines, anisomycin (4 mumol/L) activated p38 MAPK and JNK, and inactivated ERK1/2. Anisomycin 23-33 mitogen-activated protein kinase 8 Homo sapiens 69-72 22800348-7 2012 JNK signal was inhibited in FaDu or FaDu/T cells and the inhibited JNK was reactivated by taxol or anisomycin (an activator for MAPK signal transduction pathways). Anisomycin 99-109 mitogen-activated protein kinase 8 Homo sapiens 67-70 22800348-8 2012 Anisomycin down-regulated the expression of ABCB1 (F = 33.72, P < 0.05) and up-regulated the expression of ABCG2 (F = 220.16, P < 0.05) in FaDu/T cells, but not in FaDu/T cells pretreated by JNK inhibitor SP600125 (P > 0.05). Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 197-200 21909619-10 2012 Inhibition of c-Jun NH2-terminal kinase (JNK) with a specific inhibitor augmented this apoptosis, and anisomycin (an activator of JNK) attenuated this apoptosis. Anisomycin 102-112 mitogen-activated protein kinase 8 Homo sapiens 130-133 21946058-11 2012 The inhibitors of p38(MAPK) (sb202190) and JNK (sp600125) enhanced the inhibition induced by As2O3, which was counteracted by anisomycin, an activating agent of p38(MAPK) and JNK. Anisomycin 126-136 mitogen-activated protein kinase 8 Homo sapiens 43-46 21946058-11 2012 The inhibitors of p38(MAPK) (sb202190) and JNK (sp600125) enhanced the inhibition induced by As2O3, which was counteracted by anisomycin, an activating agent of p38(MAPK) and JNK. Anisomycin 126-136 mitogen-activated protein kinase 8 Homo sapiens 175-178 21272161-9 2011 Anisomycin, an activator of JNK, reduced RARalpha protein. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 28-31 21843603-5 2011 Human neuroblastoma SH-SY5Y cells were treated by anisomycin, an activator of stress-related MAPKs (JNK and p38 MAPK). Anisomycin 50-60 mitogen-activated protein kinase 8 Homo sapiens 100-103 21875572-5 2011 Activation of the non-canonical Wnt/JNK pathway by anisomycin enhanced osteoblast differentiation whereas its inhibition by SP600125 enhanced adipocyte differentiation of hMSC. Anisomycin 51-61 mitogen-activated protein kinase 8 Homo sapiens 36-39 21438496-4 2011 Examination of both peptides in HEK293 cells revealed a potent ability to inhibit the induction of both JNK activation and c-Jun phosphorylation in cells treated with anisomycin. Anisomycin 167-177 mitogen-activated protein kinase 8 Homo sapiens 104-107 21463260-3 2011 In the present paper we show that the JDP2 protein level is dramatically reduced in response to serum stimulation, anisomycin treatment, ultraviolet light irradiation and cycloheximide treatment, all of which activate the JNK pathway. Anisomycin 115-125 mitogen-activated protein kinase 8 Homo sapiens 222-225 21454558-4 2011 We observed that inhibition of JNK activity and JNK silencing with siRNA reduced the level of reactive oxygen species (ROS) generated during anisomycin-induced stress in HeLa cells. Anisomycin 141-151 mitogen-activated protein kinase 8 Homo sapiens 31-34 21454558-4 2011 We observed that inhibition of JNK activity and JNK silencing with siRNA reduced the level of reactive oxygen species (ROS) generated during anisomycin-induced stress in HeLa cells. Anisomycin 141-151 mitogen-activated protein kinase 8 Homo sapiens 48-51 21277902-8 2011 In addition, we observed that the effect of L-kynurenine was blocked by JNK agonist, anisomycin, suggesting the involvement of the JNK pathway in the signal transduction of L-kynurenine-reduced NKG2D expression. Anisomycin 85-95 mitogen-activated protein kinase 8 Homo sapiens 72-75 21277902-8 2011 In addition, we observed that the effect of L-kynurenine was blocked by JNK agonist, anisomycin, suggesting the involvement of the JNK pathway in the signal transduction of L-kynurenine-reduced NKG2D expression. Anisomycin 85-95 mitogen-activated protein kinase 8 Homo sapiens 131-134 20533305-2 2010 To investigate whether TRIC is regulated via a c-Jun N-terminal kinase (JNK) pathway, human pancreatic HPAC cells, highly expressed at tricellular contacts, were exposed to various stimuli such as the JNK activators anisomycin and 12-O-tetradecanoylphorbol 13-acetate (TPA), and the proinflammatory cytokines IL-1beta, TNFalpha, and IL-1alpha. Anisomycin 216-226 mitogen-activated protein kinase 8 Homo sapiens 201-204 20533305-3 2010 TRIC expression and the barrier function were moderated by treatment with the JNK activator anisomycin, and suppressed not only by inhibitors of JNK and PKC but also by siRNAs of TRIC. Anisomycin 92-102 mitogen-activated protein kinase 8 Homo sapiens 78-81 20533305-3 2010 TRIC expression and the barrier function were moderated by treatment with the JNK activator anisomycin, and suppressed not only by inhibitors of JNK and PKC but also by siRNAs of TRIC. Anisomycin 92-102 mitogen-activated protein kinase 8 Homo sapiens 145-148 20212108-4 2010 JNK activity was detected not only in the cytoplasm, but also in the nucleus, mitochondria, and plasma membrane with similar kinetics after induction of ribotoxic stress by anisomycin, suggesting relatively rapid signal propagation to the nuclear, mitochondrial, and plasma membrane compartments. Anisomycin 173-183 mitogen-activated protein kinase 8 Homo sapiens 0-3 20405237-8 2010 Moreover, pretreatment with anisomycin (AM), an activator of p38 and JNK, instead of LPS, the expression of COX-2 and iNOS is still inhibited by sulforaphane. Anisomycin 28-38 mitogen-activated protein kinase 8 Homo sapiens 69-72 20568119-9 2010 Direct activation of p38 MAPK and JNK by anisomycin in the absence of TSA increased myostatin mRNA by fourfold. Anisomycin 41-51 mitogen-activated protein kinase 8 Homo sapiens 34-37 20212108-5 2010 Furthermore, quantitative single-cell analysis revealed that anisomycin-induced JNK activity exhibited ultrasensitivity, sustainability, and bimodality, features that are consistent with behaviors of bistable systems. Anisomycin 61-71 mitogen-activated protein kinase 8 Homo sapiens 80-83 19502798-5 2009 The opposite process, TJ/AJ reassembly, was accelerated by JNK inhibition and suppressed by the JNK activator anisomycin. Anisomycin 110-120 mitogen-activated protein kinase 8 Homo sapiens 96-99 18241849-1 2008 Anisomycin is known as a potent apoptosis inducer by activating JNK/SAPK and inhibiting protein synthesis during translation. Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 64-67 18029162-8 2008 The involvement of the p38 and JNK pathways in the selective effects of anisomycin and cycloheximide on MMP/TIMP expression was supported by use of pharmacological inhibitors. Anisomycin 72-82 mitogen-activated protein kinase 8 Homo sapiens 31-34 18029162-7 2008 The extracellular signal-regulated kinases (ERKs)-1/2 were strongly activated by PMA, while anisomycin activated the c-Jun N-terminal kinase (JNK) and p38 pathways, and cycloheximide activated p38, but emetine had no effect on the stress-activated mitogen-activated protein kinase (MAPK) pathways. Anisomycin 92-102 mitogen-activated protein kinase 8 Homo sapiens 117-140 18029162-7 2008 The extracellular signal-regulated kinases (ERKs)-1/2 were strongly activated by PMA, while anisomycin activated the c-Jun N-terminal kinase (JNK) and p38 pathways, and cycloheximide activated p38, but emetine had no effect on the stress-activated mitogen-activated protein kinase (MAPK) pathways. Anisomycin 92-102 mitogen-activated protein kinase 8 Homo sapiens 142-145 17194804-12 2007 Finally, the protein synthesis inhibitors Stx1 and anisomycin triggered limited apoptosis and prolonged JNK and p38 MAPK activation, while macrophage-like cells treated with cycloheximide remained viable and showed transient activation of MAPKs. Anisomycin 51-61 mitogen-activated protein kinase 8 Homo sapiens 104-107 17699104-2 2007 In this study, we explored the possibility of modulating death receptor-induced cell death with the c-Jun-NH2-terminal kinase (JNK) activator anisomycin. Anisomycin 142-152 mitogen-activated protein kinase 8 Homo sapiens 100-125 17699104-2 2007 In this study, we explored the possibility of modulating death receptor-induced cell death with the c-Jun-NH2-terminal kinase (JNK) activator anisomycin. Anisomycin 142-152 mitogen-activated protein kinase 8 Homo sapiens 127-130 17699104-3 2007 Anisomycin activates JNK by inactivating the ribosome and inducing "ribotoxic stress." Anisomycin 0-10 mitogen-activated protein kinase 8 Homo sapiens 21-24 17699104-8 2007 The potentiation of death receptor-dependent cell death by anisomycin was specific because emetine, another ribosome inhibitor that does not induce ribotoxic stress or activate JNK, did not have a similar effect. Anisomycin 59-69 mitogen-activated protein kinase 8 Homo sapiens 177-180 17699104-11 2007 JNK was activated 10- to 22-fold by anisomycin+CH-11 in U87 cells. Anisomycin 36-46 mitogen-activated protein kinase 8 Homo sapiens 0-3 17699104-12 2007 Inhibiting JNK activation with pharmacologic inhibitors of JNKK and JNK or with dominant negative mitogen-activated protein kinase (MAPK) kinase kinase 2 (MEKK2) significantly prevented cell death induced by the combination of anisomycin+CH-11. Anisomycin 227-237 mitogen-activated protein kinase 8 Homo sapiens 11-14 17699104-12 2007 Inhibiting JNK activation with pharmacologic inhibitors of JNKK and JNK or with dominant negative mitogen-activated protein kinase (MAPK) kinase kinase 2 (MEKK2) significantly prevented cell death induced by the combination of anisomycin+CH-11. Anisomycin 227-237 mitogen-activated protein kinase 8 Homo sapiens 59-62 17699104-14 2007 Simultaneously inhibiting Bim expression and JNK activation additively desensitized U87 cells to anisomycin+CH-11. Anisomycin 97-107 mitogen-activated protein kinase 8 Homo sapiens 45-48 17699104-15 2007 These findings show that anisomycin-induced ribotoxic stress sensitizes glioblastoma cells to death receptor-induced apoptosis via a specific mechanism requiring both JNK activation and Bim induction. Anisomycin 25-35 mitogen-activated protein kinase 8 Homo sapiens 167-170 17023523-4 2007 Here we showed that JNK activator anisomycin induced TR3 phosphorylation through JNK1 rather than p38 and ERK signals, which is mediated by its upstream factors MAPK kinase 4 and MAPK kinase 7. Anisomycin 34-44 mitogen-activated protein kinase 8 Homo sapiens 20-23 17023523-4 2007 Here we showed that JNK activator anisomycin induced TR3 phosphorylation through JNK1 rather than p38 and ERK signals, which is mediated by its upstream factors MAPK kinase 4 and MAPK kinase 7. Anisomycin 34-44 mitogen-activated protein kinase 8 Homo sapiens 81-85 16815888-4 2006 To establish a relationship between JNK and Sp1, we show that JNK activator anisomycin increases Sp1 phosphorylation, and JNK inhibitors as well as dominant-negative JNK1 attenuate H(2)O(2)-induced Sp1 phosphorylation. Anisomycin 76-86 mitogen-activated protein kinase 8 Homo sapiens 36-39 16815888-4 2006 To establish a relationship between JNK and Sp1, we show that JNK activator anisomycin increases Sp1 phosphorylation, and JNK inhibitors as well as dominant-negative JNK1 attenuate H(2)O(2)-induced Sp1 phosphorylation. Anisomycin 76-86 mitogen-activated protein kinase 8 Homo sapiens 62-65 16815888-4 2006 To establish a relationship between JNK and Sp1, we show that JNK activator anisomycin increases Sp1 phosphorylation, and JNK inhibitors as well as dominant-negative JNK1 attenuate H(2)O(2)-induced Sp1 phosphorylation. Anisomycin 76-86 mitogen-activated protein kinase 8 Homo sapiens 62-65 16672691-4 2006 Activation of JNK by anisomycin was sufficient to induce expression of both MMP-2 and MT1-MMP mRNA in quiescent cells. Anisomycin 21-31 mitogen-activated protein kinase 8 Homo sapiens 14-17 16672691-5 2006 Downregulation of c-Jun, a downstream target of JNK, with small interference (si)RNA inhibited MMP-2 expression in response to anisomycin. Anisomycin 127-137 mitogen-activated protein kinase 8 Homo sapiens 48-51 16802349-9 2006 RESULTS: IL-1beta-induced JNK phosphorylation was dependent on MKK-7 but not on MKK-4; however, anisomycin-activated JNK required both kinases. Anisomycin 96-106 mitogen-activated protein kinase 8 Homo sapiens 117-120 16802349-10 2006 In vitro kinase assay demonstrated that IL-1beta-or TNFalpha induced JNK activity was only MKK-7 dependent, while anisomycin-activated JNK was both MKK-4 and MKK-7 dependent. Anisomycin 114-124 mitogen-activated protein kinase 8 Homo sapiens 135-138 16734734-9 2006 Combined treatment with ATO and anisomycin induced sustained activation of JNK and apoptosis in the ATO-insensitive MM line, XG-7. Anisomycin 32-42 mitogen-activated protein kinase 8 Homo sapiens 75-78 16434970-6 2006 In addition, several JNK upstream activators, including the phorbol ester TPA, anisomycin and MAPK kinase kinase-1 (MEKK1), phosphorylated Nur77 and induced its nuclear export. Anisomycin 79-89 mitogen-activated protein kinase 8 Homo sapiens 21-24 16124869-7 2006 However, activation of JNK and p38 MAPK by non-ER stress stimuli including UV irradiation, anisomycin, and TNF-alpha (tumour necrosis factor-alpha) was found to be independent of PERK. Anisomycin 91-101 mitogen-activated protein kinase 8 Homo sapiens 23-26