PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 19429262-0 2009 NADPH oxidase and ERK1/2 are involved in cadmium induced-STAT3 activation in HepG2 cells. Cadmium 41-48 mitogen-activated protein kinase 3 Homo sapiens 18-24 19429262-12 2009 MAPK promotes STAT3 phosphorylation that could induce a protective mechanism against Cd toxicity. Cadmium 85-87 mitogen-activated protein kinase 3 Homo sapiens 0-4 19041697-4 2009 However, Cd stimulated phosphorylation of ERK1/2 MAPK, detectable following 10 min and 18 h of treatment. Cadmium 9-11 mitogen-activated protein kinase 3 Homo sapiens 42-48 19028507-5 2009 Inhibition of ERKs by prior treatment of cells with 10muM U0126 relieves cadmium-mediated inhibition of apoptosis/bax induction/caspase-9 activation. Cadmium 73-80 mitogen-activated protein kinase 3 Homo sapiens 14-18 19041697-5 2009 The sustained Cd-induced ERK1/2 phosphorylation was inhibited by the ER antagonist ICI 182,780, suggesting the involvement of ER. Cadmium 14-16 mitogen-activated protein kinase 3 Homo sapiens 25-31 19041697-9 2009 The sustained ERK1/2 phosphorylation may contribute to the Cd-induced enhancement of DNA synthesis and pS2 mRNA in mixture with low-concentration E2. Cadmium 59-61 mitogen-activated protein kinase 3 Homo sapiens 14-20 18703135-0 2008 Cadmium activates the mitogen-activated protein kinase (MAPK) pathway via induction of reactive oxygen species and inhibition of protein phosphatases 2A and 5. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 56-60 18703135-7 2008 Overexpression of PP2A or PP5 partially prevented Cd-induced activation of Erk1/2 and JNK, as well as cell death. Cadmium 50-52 mitogen-activated protein kinase 3 Homo sapiens 75-81 18703135-9 2008 Pretreatment with inhibitors of JNK (SP600125) and Erk1/2 (U0126) partially blocked Cd-induced cleavage of caspase-3 and prevented cell death. Cadmium 84-86 mitogen-activated protein kinase 3 Homo sapiens 51-57 18703135-11 2008 The results indicate that Cd induction of ROS inhibits PP2A and PP5, leading to activation of JNK and Erk1/2 pathways, and consequently resulting in caspase-dependent and -independent apoptosis of neuronal cells. Cadmium 26-28 mitogen-activated protein kinase 3 Homo sapiens 102-108 18703135-12 2008 The findings strongly suggest that the inhibitors of JNK, Erk1/2, or antioxidants may be exploited for prevention of Cd-induced neurodegenerative diseases. Cadmium 117-119 mitogen-activated protein kinase 3 Homo sapiens 58-64 18703135-2 2008 Recently we have demonstrated that Cd may induce neuronal apoptosis in part through activation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase 1/2 (Erk1/2) pathways. Cadmium 35-37 mitogen-activated protein kinase 3 Homo sapiens 175-181 18703135-6 2008 Furthermore, we found that Cd-induced ROS inhibited serine/threonine protein phosphatases 2A (PP2A) and 5 (PP5), leading to activation of Erk1/2 and JNK, which was abrogated by NAC. Cadmium 27-29 mitogen-activated protein kinase 3 Homo sapiens 138-144 18275979-0 2008 Rapid activation of ERK1/2 and AKT in human breast cancer cells by cadmium. Cadmium 67-74 mitogen-activated protein kinase 3 Homo sapiens 20-26 18571719-7 2008 At 30 microM Cd, stimulations of about 300%, 550% and 250% were observed for ERK1/2, JNK1/2, and p38MAPK, respectively. Cadmium 13-15 mitogen-activated protein kinase 3 Homo sapiens 77-83 18571719-8 2008 Phosphorylation of ERK1/2 and JNK1/2 was significantly induced after a 1-h exposure to 30 microM Cd, while that of p38MAPK occurred only after 8h. Cadmium 97-99 mitogen-activated protein kinase 3 Homo sapiens 19-25 18571719-11 2008 In conclusion, Cd triggers different stress responses in trophoblast cells involving HSP70 and SAPK, and also enhances ERK1/2 phosphorylation. Cadmium 15-17 mitogen-activated protein kinase 3 Homo sapiens 119-125 18275979-1 2008 Cadmium (Cd), an endocrine disruptor, can induce a variety of signaling events including the activation of ERK1/2 and AKT. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 107-113 18275979-1 2008 Cadmium (Cd), an endocrine disruptor, can induce a variety of signaling events including the activation of ERK1/2 and AKT. Cadmium 9-11 mitogen-activated protein kinase 3 Homo sapiens 107-113 18275979-4 2008 Specifically, treatment of MCF-7 cells, that express ER alpha, ER beta and GPR30, to 0.5-10 microM Cd for only 2.5 min resulted in transient phosphorylation of ERK1/2. Cadmium 99-101 mitogen-activated protein kinase 3 Homo sapiens 160-166 18275979-6 2008 In SK-BR-3 cells, that express only GPR30, Cd also caused a transient activation of ERK1/2, but not of AKT. Cadmium 43-45 mitogen-activated protein kinase 3 Homo sapiens 84-90 18275979-9 2008 While the estrogen receptor antagonist, ICI 182,780, did not prevent the effect of Cd on these signals, specific siRNA against hER alpha significantly reduced Cd-induced activation of ERK1/2 and completely blocked the activation of AKT. Cadmium 159-161 mitogen-activated protein kinase 3 Homo sapiens 184-190 18275979-10 2008 It is concluded that Cd, like estradiol, can cause rapid activation of ERK1/2 and AKT and that these signaling events are mediated by possible interaction with membrane ER alpha and GPR30, but not ER beta. Cadmium 21-23 mitogen-activated protein kinase 3 Homo sapiens 71-77 18021293-4 2008 Cd rapidly activated the mitogen-activated protein kinases (MAPK) including extracellular signal-regulated kinase 1/2 (Erk1/2), c-Jun N-terminal kinase (JNK) and p38. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 119-125 18021293-5 2008 Inhibition of Erk1/2 and JNK, but not p38, partially protected the cells from Cd-induced apoptosis. Cadmium 78-80 mitogen-activated protein kinase 3 Homo sapiens 14-20 18021293-6 2008 Consistently, over-expression of dominant negative c-Jun or down-regulation of Erk1/2, but not p38 MAPK, partially prevented Cd-induced apoptosis. Cadmium 125-127 mitogen-activated protein kinase 3 Homo sapiens 79-85 17637928-5 2007 Signal-regulated mitogen-activated protein kinases, extracellular signal-regulated kinases 1 and 2, c-Jun N-terminal kinases (JNK1 and JNK2), and p38 were phosphorylated in a cadmium concentration-dependent fashion in CTPE and control cells. Cadmium 175-182 mitogen-activated protein kinase 3 Homo sapiens 52-98 17485079-3 2007 Cadmium exposure stimulated intracellular calcium and the phosphorylation of ERK1/2. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 77-83 25343777-7 2015 However, in both cells types, Cd (0.1 muM and 10 muM) activated p44/42 MAPK (ERK1/2), and a MAPK inhibitor (PD98059) abrogated Cd-induced cell proliferation. Cadmium 30-32 mitogen-activated protein kinase 3 Homo sapiens 77-83 17125913-5 2007 Purpose of our study was to evaluate whether Cd regulates MCF-7 cell proliferation by activating ERK1/2, Akt and PDGFRalpha kinases. Cadmium 45-47 mitogen-activated protein kinase 3 Homo sapiens 97-103 17125913-9 2007 Cd also increased ERK1/2, Akt and PDGFRalpha phosphorylation while ICI blocked it. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 18-24 17125913-13 2007 In conclusion, our results indicate that Cd increases BC cell proliferation in vitro by stimulating Akt, ERK1/2 and PDGFRalpha kinases activity likely by activating c-fos, c-jun and PDGFA by an ERalpha-dependent mechanism. Cadmium 41-43 mitogen-activated protein kinase 3 Homo sapiens 105-111 12508112-6 2003 Cadmium-induced release of proteins from ND10 could be blocked by inhibiting activation of p38 MAPK or ERK1/2. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 103-109 11709198-0 2001 Potentiation of cadmium-induced cytotoxicity by sulfur amino acid deprivation through activation of extracellular signal-regulated kinase1/2 (ERK1/2) in conjunction with p38 kinase or c-jun N-terminal kinase (JNK). Cadmium 16-23 mitogen-activated protein kinase 3 Homo sapiens 142-148 10874022-6 2000 Conversely, the activities of ERK1 and ERK2 were decreased by low cytotoxic doses of Cd (</=80 microM) and moderately activated by high Cd doses. Cadmium 85-87 mitogen-activated protein kinase 3 Homo sapiens 30-34 10874022-6 2000 Conversely, the activities of ERK1 and ERK2 were decreased by low cytotoxic doses of Cd (</=80 microM) and moderately activated by high Cd doses. Cadmium 139-141 mitogen-activated protein kinase 3 Homo sapiens 30-34 34580807-3 2021 We have previously shown that Cd induces ERK1/2 activation in differentiated but not proliferative human enterocytic-like Caco-2 cells. Cadmium 30-32 mitogen-activated protein kinase 3 Homo sapiens 41-47 34580807-4 2021 As autophagy is a dynamic process that plays a critical role in intestinal mucosa, we aimed the present study 1) to investigate the role of p-ERK1/2 in constitutive autophagy in proliferative Caco-2 cells and 2) to investigate whether Cd-induced activation of ERK1/2 modifies autophagic activity in postconfluent Caco-2 cell monolayers. Cadmium 235-237 mitogen-activated protein kinase 3 Homo sapiens 142-148 34580807-4 2021 As autophagy is a dynamic process that plays a critical role in intestinal mucosa, we aimed the present study 1) to investigate the role of p-ERK1/2 in constitutive autophagy in proliferative Caco-2 cells and 2) to investigate whether Cd-induced activation of ERK1/2 modifies autophagic activity in postconfluent Caco-2 cell monolayers. Cadmium 235-237 mitogen-activated protein kinase 3 Homo sapiens 260-266 34580807-7 2021 In the latter condition, serum and glucose deprivation triggered autophagy via a transient phosphorylation of ERK1/2, whereas Cd-modified autophagy via a ROS-dependent sustained activation of ERK1/2. Cadmium 126-128 mitogen-activated protein kinase 3 Homo sapiens 192-198 34580807-8 2021 Basal autophagy flux in proliferative cells and Cd-induced increases in autophagic markers in postconfluent cells both involved p-ERK1/2. Cadmium 48-50 mitogen-activated protein kinase 3 Homo sapiens 130-136 34580807-10 2021 Our results prompt further studies investigating the consequences that Cd-induced ERK1/2 activation and the related effect on autophagy may have on the intestinal cells, which may accumulate and trap high levels of Cd under some nutritional conditions. Cadmium 71-73 mitogen-activated protein kinase 3 Homo sapiens 82-88 34580807-10 2021 Our results prompt further studies investigating the consequences that Cd-induced ERK1/2 activation and the related effect on autophagy may have on the intestinal cells, which may accumulate and trap high levels of Cd under some nutritional conditions. Cadmium 215-217 mitogen-activated protein kinase 3 Homo sapiens 82-88 35524288-4 2022 Cd toxicity also stimulated the activity of cellular kinases (MAPK-ERK1/2 and Akt) and NFkB transcription factor, and cJun expression. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 62-66 35524288-4 2022 Cd toxicity also stimulated the activity of cellular kinases (MAPK-ERK1/2 and Akt) and NFkB transcription factor, and cJun expression. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 67-73 35524288-7 2022 An upregulation of CAT and MAPK-ERK1/2 activity was associated with these effects at 5 muM Cd, whereas glutathione biosynthesis and efflux were involved at 10 muM Cd together with an increased expression of the cystine transporter xCT and marked upregulation of Akt and NFkB activity, and cJun expression. Cadmium 91-93 mitogen-activated protein kinase 3 Homo sapiens 27-31 35524288-7 2022 An upregulation of CAT and MAPK-ERK1/2 activity was associated with these effects at 5 muM Cd, whereas glutathione biosynthesis and efflux were involved at 10 muM Cd together with an increased expression of the cystine transporter xCT and marked upregulation of Akt and NFkB activity, and cJun expression. Cadmium 91-93 mitogen-activated protein kinase 3 Homo sapiens 32-38 35524288-7 2022 An upregulation of CAT and MAPK-ERK1/2 activity was associated with these effects at 5 muM Cd, whereas glutathione biosynthesis and efflux were involved at 10 muM Cd together with an increased expression of the cystine transporter xCT and marked upregulation of Akt and NFkB activity, and cJun expression. Cadmium 163-165 mitogen-activated protein kinase 3 Homo sapiens 27-31 35524288-7 2022 An upregulation of CAT and MAPK-ERK1/2 activity was associated with these effects at 5 muM Cd, whereas glutathione biosynthesis and efflux were involved at 10 muM Cd together with an increased expression of the cystine transporter xCT and marked upregulation of Akt and NFkB activity, and cJun expression. Cadmium 163-165 mitogen-activated protein kinase 3 Homo sapiens 32-38 33075233-5 2020 The results showed that after exposure of the U-87 MG cells to CdCl2 at 1 and 10 microM, there was an up-regulation of CCL2 mRNA expression after 3 h of exposure and increased CCL2 secretion after 6 and 24 h. The study also found that inhibition of MAPK pathways, including ERK1/2, p38, and JNK by U0126, SB203580 and SP600125, respectively, reduced Cd-induced CCL2 secretion by the cells. Cadmium 63-65 mitogen-activated protein kinase 3 Homo sapiens 274-280 32512071-12 2020 An increase in phosphorylation of the Erk1/2 and Mek1/2 was observed in Cd-RWPE1 and Cd-PWR1E cells compared to parental cells, confirming that Cd-exposure induces activation of the Erk/MAPK pathway. Cadmium 72-74 mitogen-activated protein kinase 3 Homo sapiens 38-44 31562949-8 2019 Western blotting revealed that cadmium and carvacrol co-exposure alleviated the cadmium-induced down-regulations of mammalian target of rapamycin (mTOR), protein kinase B (Akt), nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB), extracellular signal-regulated kinase-1 (ERK-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) expressions. Cadmium 31-38 mitogen-activated protein kinase 3 Homo sapiens 249-288 31860779-3 2020 Using human enterocytic-like Caco-2 cells, we have previously shown that Cd may induce a concentration and time-dependent increase in 3-(4,5-dimethyl-2-thiazol-2-yl)-2,5-diphenyltetrazolium bromide assay (MTT)-reducing activity in differentiated cultures with correlation to ERK1/2 activation. Cadmium 73-75 mitogen-activated protein kinase 3 Homo sapiens 275-281 31860779-4 2020 The present study shows that (a) Zn prevents the Cd-induced hormesis effect on MTT reduction in a concentration-dependent manner, without inhibiting Cd-induced ERK1/2 activation; (b) Zn also induces similar hormetic stimulation of MTT-reducing activity but without ERK1/2 activation. Cadmium 49-51 mitogen-activated protein kinase 3 Homo sapiens 265-271 31860779-6 2020 There is evidence for the involvement of reactive oxygen species (ROS) in Cd-induced ERK1/2 activation. Cadmium 74-76 mitogen-activated protein kinase 3 Homo sapiens 85-91 31860779-8 2020 Steps downstream ERK1/2 activation by Cd does not involve eIF4E which is rather downregulated by Cd. Cadmium 38-40 mitogen-activated protein kinase 3 Homo sapiens 17-23 31860779-8 2020 Steps downstream ERK1/2 activation by Cd does not involve eIF4E which is rather downregulated by Cd. Cadmium 97-99 mitogen-activated protein kinase 3 Homo sapiens 17-23 31562949-8 2019 Western blotting revealed that cadmium and carvacrol co-exposure alleviated the cadmium-induced down-regulations of mammalian target of rapamycin (mTOR), protein kinase B (Akt), nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB), extracellular signal-regulated kinase-1 (ERK-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) expressions. Cadmium 31-38 mitogen-activated protein kinase 3 Homo sapiens 290-295 31562949-8 2019 Western blotting revealed that cadmium and carvacrol co-exposure alleviated the cadmium-induced down-regulations of mammalian target of rapamycin (mTOR), protein kinase B (Akt), nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB), extracellular signal-regulated kinase-1 (ERK-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) expressions. Cadmium 80-87 mitogen-activated protein kinase 3 Homo sapiens 249-288 31562949-8 2019 Western blotting revealed that cadmium and carvacrol co-exposure alleviated the cadmium-induced down-regulations of mammalian target of rapamycin (mTOR), protein kinase B (Akt), nuclear factor kappa-light-chain-enhancer of activated B cells (NFKB), extracellular signal-regulated kinase-1 (ERK-1) and nuclear factor erythroid 2-related factor 2 (Nrf2) expressions. Cadmium 80-87 mitogen-activated protein kinase 3 Homo sapiens 290-295 31252067-0 2019 Cadmium exposure induces interleukin-6 production via ROS-dependent activation of the ERK1/2 but independent of JNK signaling pathway in human placental JEG-3 trophoblast cells. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 86-92 31252067-8 2019 Cd exposure induced IL-6 production and increased ERK1/2, JNK, and c-Jun phosphorylation. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 50-56 31252067-9 2019 NAC and the inhibition of ERK1/2 significantly reduced Cd-induced IL-6 production. Cadmium 55-57 mitogen-activated protein kinase 3 Homo sapiens 26-32 31252067-10 2019 These data indicate that Cd induces IL-6 production in trophoblast cells through a ROS-dependent activation of ERK1/2. Cadmium 25-27 mitogen-activated protein kinase 3 Homo sapiens 111-117 31190890-9 2019 Furthermore, the proliferation and migration abilities evidently facilitated by pcDNA3.1(+) expression vector containing full-length CDS of NSD3 (pcDNA3.1(+)-NSD3, or NSD3) were partially decreased after incubation with ERK1/2 signaling pathway inhibitor (PD98059) and/or specific siRNA against CAPG (siCAPG) in SW480 and HT-29 CRC cells. Cadmium 133-136 mitogen-activated protein kinase 3 Homo sapiens 220-226 30682495-11 2019 Cd exposure induced activation of p-ERK1/2 in these cells. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 36-42 30682495-13 2019 Taken together, the current work suggests that Cd induces ovarian cancer cell proliferation in an ER-dependent mechanism induced ERK1/2 activation pathway. Cadmium 47-49 mitogen-activated protein kinase 3 Homo sapiens 129-135 28288823-11 2017 Acute exposure to cadmium increased phosphorylation of ERK1/2, p38 MAPK, and p65 NF-kappaB. Cadmium 18-25 mitogen-activated protein kinase 3 Homo sapiens 55-61 27108949-9 2016 However, cadmium accumulation in the liver was accompanied with activation of EGFR and MAPK-ERK1/2 in line with our earlier CdCl2 studies. Cadmium 9-16 mitogen-activated protein kinase 3 Homo sapiens 87-91 30023612-9 2017 Moreover, increased m-RNA expression of CD44, ALDH1, and CD133 and protein expression of p-Ras, p-Raf-1, p-MEK-1, and p-ERK-1 were observed in the cadmium-treated MCF-7 and HepG2 cells. Cadmium 147-154 mitogen-activated protein kinase 3 Homo sapiens 120-125 27108949-9 2016 However, cadmium accumulation in the liver was accompanied with activation of EGFR and MAPK-ERK1/2 in line with our earlier CdCl2 studies. Cadmium 9-16 mitogen-activated protein kinase 3 Homo sapiens 92-98 26782637-0 2016 Cadmium induces mucin 8 expression via Toll-like receptor 4-mediated extracellular signal related kinase 1/2 and p38 mitogen-activated protein kinase in human airway epithelial cells. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 69-108 26782637-10 2016 CONCLUSION: The results of this study suggest for the first time that cadmium induces MUC8 expression via TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells. Cadmium 70-77 mitogen-activated protein kinase 3 Homo sapiens 120-126 26782637-7 2016 Cadmium significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 51-90 26782637-10 2016 CONCLUSION: The results of this study suggest for the first time that cadmium induces MUC8 expression via TLR4-mediated ERK1/2 and p38 MAPK signaling pathway in human airway epithelial cells. Cadmium 70-77 mitogen-activated protein kinase 3 Homo sapiens 135-139 26782637-7 2016 Cadmium significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 92-98 26782637-7 2016 Cadmium significantly activated phosphorylation of extracellular signal related kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) and p38 MAPK. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 134-138 26782637-8 2016 ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, TLR4 siRNA, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked cadmium-induced MUC8 mRNA expression. Cadmium 115-122 mitogen-activated protein kinase 3 Homo sapiens 0-6 26782637-8 2016 ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, TLR4 siRNA, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked cadmium-induced MUC8 mRNA expression. Cadmium 115-122 mitogen-activated protein kinase 3 Homo sapiens 55-61 26782637-8 2016 ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, TLR4 siRNA, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked cadmium-induced MUC8 mRNA expression. Cadmium 115-122 mitogen-activated protein kinase 3 Homo sapiens 7-11 26782637-8 2016 ERK1/2 MAPK inhibitor, p38 MAPK inhibitor, TLR4 siRNA, ERK1/2 MAPK siRNA, and p38 MAPK siRNA significantly blocked cadmium-induced MUC8 mRNA expression. Cadmium 115-122 mitogen-activated protein kinase 3 Homo sapiens 27-31 26782637-9 2016 TLR4 siRNA significantly blocked cadmium-activated phosphorylation of ERK1/2 MAPK and p38 MAPK. Cadmium 33-40 mitogen-activated protein kinase 3 Homo sapiens 70-76 26782637-9 2016 TLR4 siRNA significantly blocked cadmium-activated phosphorylation of ERK1/2 MAPK and p38 MAPK. Cadmium 33-40 mitogen-activated protein kinase 3 Homo sapiens 77-81 26716417-5 2016 Cd potently stimulates the phosphorylations of p38alpha (MAPK14), JNK1/2 (MAPK8/9), and JUN; while the phosphorylations of Akt1, ERK1/2 (MAPK3/1), GSK3beta, and mTOR were suppressed. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 129-135 26716417-5 2016 Cd potently stimulates the phosphorylations of p38alpha (MAPK14), JNK1/2 (MAPK8/9), and JUN; while the phosphorylations of Akt1, ERK1/2 (MAPK3/1), GSK3beta, and mTOR were suppressed. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 137-145 26716417-7 2016 Pretreatment of cells with the thiol antioxidant glutathione or p38 MAPK/JNK inhibitors before Cd treatment effectively abrogated ROS activation of p38 MAPK/JNK pathways and apoptosis-related proteins. Cadmium 95-97 mitogen-activated protein kinase 3 Homo sapiens 68-72 26716417-7 2016 Pretreatment of cells with the thiol antioxidant glutathione or p38 MAPK/JNK inhibitors before Cd treatment effectively abrogated ROS activation of p38 MAPK/JNK pathways and apoptosis-related proteins. Cadmium 95-97 mitogen-activated protein kinase 3 Homo sapiens 152-156 26716417-8 2016 Taken together, our results demonstrate that Cd causes oxidative stress-induced apoptosis; and the p38 MAPK/JNK and mitochondrial pathways are more importantly participated for signal transduction and the induction of apoptosis in Cd-exposed human lung cells. Cadmium 231-233 mitogen-activated protein kinase 3 Homo sapiens 103-107 26514923-6 2015 Cd also activated the phosphorylation of EGFR, Akt, Erk1/2, and JNK1/2 in addition to promoting NF-kB and AP-1 binding activities. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 52-58 26514923-7 2015 Specific inhibitor and mutagenesis studies showed that EGFR, Akt, Erk1/2, JNK1/2 and transcription factors NF-kappaB and AP-1 were related to Cd-induced MMP-9 expression in endothelial cells. Cadmium 142-144 mitogen-activated protein kinase 3 Homo sapiens 66-72 26248512-0 2015 Calcium Signaling Involvement in Cadmium-Induced Astrocyte Cytotoxicity and Cell Death Through Activation of MAPK and PI3K/Akt Signaling Pathways. Cadmium 33-40 mitogen-activated protein kinase 3 Homo sapiens 109-113 26514923-9 2015 In addition, N-acetyl-l-cystein (NAC), diphenyleneiodonium chloride (DPI) and apocynin (APO) inhibited the Cd-induced activation of EGFR, Akt, Erk1/2, JNK1/2, and p38 MAPK, indicating that ROS production by NADPH oxidase is the furthest upstream signal in MMP-9 expression. Cadmium 107-109 mitogen-activated protein kinase 3 Homo sapiens 143-149 26514923-11 2015 These results demonstrated that Cd induces MMP-9 expression via ROS-dependent EGFR->Erk1/2, JNK1/2->AP-1 and EGFR->Akt->NF-kappaB signaling pathways and, in turn, stimulates invasiveness in human endothelial cells. Cadmium 32-34 mitogen-activated protein kinase 3 Homo sapiens 87-93 26146868-0 2015 Resveratrol prevents cadmium activation of Erk1/2 and JNK pathways from neuronal cell death via protein phosphatases 2A and 5. Cadmium 21-28 mitogen-activated protein kinase 3 Homo sapiens 43-49 26146868-7 2015 Over-expression of PP2A or PP5 strengthened the inhibitory effects of resveratrol on Cd-induced activation of Erk1/2 and/or JNK, as well as cell death. Cadmium 85-87 mitogen-activated protein kinase 3 Homo sapiens 110-116 26146868-8 2015 The results indicate that resveratrol prevents Cd-induced activation of Erk1/2 and JNK pathways and neuronal cell death in part via activating PP2A and PP5. Cadmium 47-49 mitogen-activated protein kinase 3 Homo sapiens 72-78 26248512-6 2015 Further studies demonstrated that acute and chronic Cd treatment phosphorylated JNK, p38 and Akt to different degrees, while ERK1/2 was only phosphorylated under low doses of Cd (10 muM) exposure. Cadmium 175-177 mitogen-activated protein kinase 3 Homo sapiens 125-131 26248512-8 2015 Moreover, Cd also induced a strong calcium signal, while BAPTA, a specific intracellular calcium (Ca(2+)) chelator, prevented Cd-induced intracellular increase of calcium levels in astrocytes; inhibited the Cd-induced activation of ERK1/2, JNK, p38 and Akt; and also significantly reduced astrocyte cell death. Cadmium 10-12 mitogen-activated protein kinase 3 Homo sapiens 232-238 26248512-8 2015 Moreover, Cd also induced a strong calcium signal, while BAPTA, a specific intracellular calcium (Ca(2+)) chelator, prevented Cd-induced intracellular increase of calcium levels in astrocytes; inhibited the Cd-induced activation of ERK1/2, JNK, p38 and Akt; and also significantly reduced astrocyte cell death. Cadmium 126-128 mitogen-activated protein kinase 3 Homo sapiens 232-238 26248512-8 2015 Moreover, Cd also induced a strong calcium signal, while BAPTA, a specific intracellular calcium (Ca(2+)) chelator, prevented Cd-induced intracellular increase of calcium levels in astrocytes; inhibited the Cd-induced activation of ERK1/2, JNK, p38 and Akt; and also significantly reduced astrocyte cell death. Cadmium 126-128 mitogen-activated protein kinase 3 Homo sapiens 232-238 26248512-9 2015 All of these results suggested that the Cd-Ca(2+)-MAPK and PI3K/Akt signaling pathways were involved in Cd-induced toxicity in astrocytes. Cadmium 40-42 mitogen-activated protein kinase 3 Homo sapiens 50-54 26046303-0 2015 Rapamycin inhibits Erk1/2-mediated neuronal apoptosis caused by cadmium. Cadmium 64-71 mitogen-activated protein kinase 3 Homo sapiens 19-25 26046303-3 2015 Here we found that rapamycin exerted its prevention against Cd-induced neuronal cell death also partially via blocking Erk1/2 pathway. Cadmium 60-62 mitogen-activated protein kinase 3 Homo sapiens 119-125 26046303-4 2015 Inhibiting Erk1/2 with PD98059 or silencing Erk1/2 potentiated rapamycin"s inhibition of Cd-induced phosphorylation of Erk1/2 and apoptosis in neuronal cells. Cadmium 89-91 mitogen-activated protein kinase 3 Homo sapiens 11-17 26046303-4 2015 Inhibiting Erk1/2 with PD98059 or silencing Erk1/2 potentiated rapamycin"s inhibition of Cd-induced phosphorylation of Erk1/2 and apoptosis in neuronal cells. Cadmium 89-91 mitogen-activated protein kinase 3 Homo sapiens 44-50 26046303-4 2015 Inhibiting Erk1/2 with PD98059 or silencing Erk1/2 potentiated rapamycin"s inhibition of Cd-induced phosphorylation of Erk1/2 and apoptosis in neuronal cells. Cadmium 89-91 mitogen-activated protein kinase 3 Homo sapiens 44-50 26046303-5 2015 Both PP2A and PTEN/Akt were involved in the regulation of Erk1/2 activation and cell death triggered by Cd. Cadmium 104-106 mitogen-activated protein kinase 3 Homo sapiens 58-64 26046303-6 2015 Inhibition of PP2A with okadaic acid or ectopic expression of dominant negative PP2A attenuated rapamycin"s inhibition of Cd-induced phospho-Erk1/2 and apoptosis, whereas over-expression of wild-type PP2A enhanced rapamycin"s effects; Over-expression of wild-type PTEN or dominant negative Akt, or inhibition of Akt with Akt inhibitor X strengthened rapamycin"s inhibition of Cd-induced phospho-Erk1/2 and cell death. Cadmium 122-124 mitogen-activated protein kinase 3 Homo sapiens 141-147 26046303-6 2015 Inhibition of PP2A with okadaic acid or ectopic expression of dominant negative PP2A attenuated rapamycin"s inhibition of Cd-induced phospho-Erk1/2 and apoptosis, whereas over-expression of wild-type PP2A enhanced rapamycin"s effects; Over-expression of wild-type PTEN or dominant negative Akt, or inhibition of Akt with Akt inhibitor X strengthened rapamycin"s inhibition of Cd-induced phospho-Erk1/2 and cell death. Cadmium 122-124 mitogen-activated protein kinase 3 Homo sapiens 395-401 26046303-7 2015 Furthermore, expression of a rapamycin-resistant and kinase-active mTOR (mTOR-T) blocked rapamycin"s inhibitory effects on Cd-induced inhibition of PP2A, down-regulation of PTEN, and activation of Akt, leading to Erk1/2 activation and cell death, whereas silencing mTOR mimicked rapamycin"s effects. Cadmium 123-125 mitogen-activated protein kinase 3 Homo sapiens 213-219 26046303-8 2015 The results uncover that rapamycin inhibits Cd activation of Erk1/2-mediated neuronal apoptosis through intervening mTOR-PP2A/PTEN signaling network. Cadmium 44-46 mitogen-activated protein kinase 3 Homo sapiens 61-67 26006730-0 2015 Requirement of ERalpha and basal activities of EGFR and Src kinase in Cd-induced activation of MAPK/ERK pathway in human breast cancer MCF-7 cells. Cadmium 70-72 mitogen-activated protein kinase 3 Homo sapiens 95-99 26006730-15 2015 Based on these results, it is concluded that not only ERalpha, but also basal activities of EGFR and Src kinase are essential for Cd-induced signal transduction and activation of MAPK/ERK pathway for breast cancer cell proliferation. Cadmium 130-132 mitogen-activated protein kinase 3 Homo sapiens 179-183 26006730-5 2015 This study explores the mechanism of Cd-induced activation of MAPK/ERK pathway. Cadmium 37-39 mitogen-activated protein kinase 3 Homo sapiens 62-66 26006730-9 2015 Cd treatment increased both the SRE reporter activity and ERK1/2 phosphorylation in a concentration-dependent manner. Cadmium 0-2 mitogen-activated protein kinase 3 Homo sapiens 58-64 25744307-0 2015 Cadmium at nanomolar concentrations activates Raf-MEK-ERK1/2 MAPKs signaling via EGFR in human cancer cell lines. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 54-60 25744307-7 2015 Here we investigate further the ERK1/2 MAPK signaling activation by Cd in vitro by using nanomolar concentrations of cadmium chloride (CdCl2) in three different human carcinoma cell lines: HepG2, MCF-7, and ECC-1. Cadmium 68-70 mitogen-activated protein kinase 3 Homo sapiens 32-38 25744307-7 2015 Here we investigate further the ERK1/2 MAPK signaling activation by Cd in vitro by using nanomolar concentrations of cadmium chloride (CdCl2) in three different human carcinoma cell lines: HepG2, MCF-7, and ECC-1. Cadmium 68-70 mitogen-activated protein kinase 3 Homo sapiens 39-43 23966319-9 2013 In addition, given that we previously showed that cadmium reduced placental 11beta-HSD2 expression via a transcriptional mechanism, but the signal transduction pathways involved remain unclear, we also addressed this question and found that treatment of trophoblast cells with cadmium led to rapid activation of ERK1/2. Cadmium 277-284 mitogen-activated protein kinase 3 Homo sapiens 312-318 25998312-0 2015 Cadmium Induced Apoptosis in MG63 Cells by Increasing ROS, Activation of p38 MAPK and Inhibition of ERK 1/2 Pathways. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 100-107 25998312-6 2015 Additionally, the inhibition of the phosphorylation of p38 MAPK by SB202190 protected MG63 cells from Cd-induced apoptosis. Cadmium 102-104 mitogen-activated protein kinase 3 Homo sapiens 59-63 25998312-10 2015 CONCLUSION: Our results suggested that Cd induced apoptosis in MG63 cells by increasing ROS, activation of p38 MAPK and inhibition of ERK1/2 pathways. Cadmium 39-41 mitogen-activated protein kinase 3 Homo sapiens 134-140 25069788-0 2014 Cadmium induces urokinase-type plasminogen activator receptor expression and the cell invasiveness of human gastric cancer cells via the ERK-1/2, NF-kappaB, and AP-1 signaling pathways. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 137-144 25069788-5 2014 Additionally, cadmium induced the activation of extracellular signal regulated kinase-1/2 (ERK-1/2), p38 mitogen-activated protein kinase (MAPK), and the activation of c-Jun amino terminal kinase (JNK). Cadmium 14-21 mitogen-activated protein kinase 3 Homo sapiens 139-143 24973647-10 2014 Moreover, the increased DUSP4 expression can redox-regulate the p38 and ERK1/2 pathways from hyperactivation, providing a survival mechanism against the toxicity of Cd(2+). Cadmium 165-167 mitogen-activated protein kinase 3 Homo sapiens 72-78 23966319-11 2013 Taken together, the present study not only identifies the ERK1/2 signaling pathway as a potent negative regulator of placental 11beta-HSD2 but also demonstrates that this pathway mediates cadmium repression of placental 11beta-HSD2. Cadmium 188-195 mitogen-activated protein kinase 3 Homo sapiens 58-64 23405080-7 2013 Furthermore, exposure to Cd induced the phosphorylations of c-jun N-terminal kinases (JNK), extracellular signal-regulated kinases (ERK)1/2, and p38-mitogen-activated protein kinase (MAPK), which was prevented by NAC. Cadmium 25-27 mitogen-activated protein kinase 3 Homo sapiens 92-139 22659318-0 2012 Cadmium-induced apoptosis in the BJAB human B cell line: involvement of PKC/ERK1/2/JNK signaling pathways in HO-1 expression. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 76-82 21697648-11 2012 In conclusion, at least 2 pathways appear activated by cadmium in osteoblasts: a direct induction of caspase-8 followed by activation of caspase-3 and an indirect induction by phosphorylation of ERK1/2, p38, and JNK MAPK triggering activation of caspase-8 and -3. Cadmium 55-62 mitogen-activated protein kinase 3 Homo sapiens 195-201 22094458-0 2012 An NF-kappaB-independent and Erk1/2-dependent mechanism controls CXCL8/IL-8 responses of airway epithelial cells to cadmium. Cadmium 116-123 mitogen-activated protein kinase 3 Homo sapiens 29-35 22094458-8 2012 Cadmium could activate the main MAPKs (i.e., p38, JNK, and Erk1/2) in human airway epithelial cells. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 59-65 22094458-9 2012 However, only pharmacological inhibition of Erk1/2 pathway or knockdown of the expression of Erk1 and Erk2 using small interfering RNAs suppressed secretion of IL-8 induced by cadmium. Cadmium 176-183 mitogen-activated protein kinase 3 Homo sapiens 44-50 22094458-9 2012 However, only pharmacological inhibition of Erk1/2 pathway or knockdown of the expression of Erk1 and Erk2 using small interfering RNAs suppressed secretion of IL-8 induced by cadmium. Cadmium 176-183 mitogen-activated protein kinase 3 Homo sapiens 44-48 22142850-4 2012 We also determined that two distinct pathways controlled secretion of these proinflammatory cytokines by human airway epithelial cells as cadmium-induced IL-6 secretion occurs via an NF-kappaB dependent pathway, whereas IL-8 secretion involves the Erk1/2 signaling pathway. Cadmium 138-145 mitogen-activated protein kinase 3 Homo sapiens 248-254 22011313-4 2012 RESULTS & DISCUSSION: Our findings demonstrate that in vitro cadmium-containing QDs induce cellular proliferation, estrogen receptor alpha activation, and biphasic phosphorylation of AKT and ERK1/2, comparable with 17beta-estradiol. Cadmium 65-72 mitogen-activated protein kinase 3 Homo sapiens 195-201 21933187-6 2011 Inhibiting CaMKII with KN93 or silencing CaMKII attenuated Cd activation of MAPK/mTOR pathways and cell death. Cadmium 59-61 mitogen-activated protein kinase 3 Homo sapiens 76-80 21933187-7 2011 Furthermore, inhibitors of mTOR (rapamycin), c-Jun N-terminal kinase (SP600125) and extracellular signal-regulated kinase 1/2 (U0126), but not of p38 (PD169316), prevented Cd-induced neuronal cell death in part through inhibition of [Ca(2+) ](i) elevation and CaMKII phosphorylation. Cadmium 172-174 mitogen-activated protein kinase 3 Homo sapiens 84-125 21933187-8 2011 The results indicate that Cd activates MAPK/mTOR network triggering neuronal cell death, by stimulating CaMKII. Cadmium 26-28 mitogen-activated protein kinase 3 Homo sapiens 39-43 20153348-3 2010 We have previously published that Cd promotes activation of the extracellular regulated kinases, erk-1 and -2 in both ER-positive and ER-negative human breast cancer cells, suggesting that this estrogen-like effect of Cd is not associated with the ER. Cadmium 34-36 mitogen-activated protein kinase 3 Homo sapiens 97-109 21933187-0 2011 CaMKII is involved in cadmium activation of MAPK and mTOR pathways leading to neuronal cell death. Cadmium 22-29 mitogen-activated protein kinase 3 Homo sapiens 44-48 21933187-2 2011 Recently, we have shown that Cd elevates intracellular free calcium ion ([Ca(2+) ](i) ) level, leading to neuronal apoptosis partly by activating mitogen-activated protein kinases (MAPK) and mammalian target of rapamycin (mTOR) pathways. Cadmium 29-31 mitogen-activated protein kinase 3 Homo sapiens 181-185 21933187-4 2011 In this study, we show that the effects of Cd-elevated [Ca(2+) ](i) on MAPK and mTOR network as well as neuronal cell death are through stimulating phosphorylation of calcium/calmodulin-dependent protein kinase II (CaMKII). Cadmium 43-45 mitogen-activated protein kinase 3 Homo sapiens 71-75 21544200-10 2011 Our findings indicate that Cd elevates [Ca2+](i), which induces ROS and activates MAPK and mTOR pathways, leading to neuronal apoptosis. Cadmium 27-29 mitogen-activated protein kinase 3 Homo sapiens 82-86 21544200-0 2011 Calcium signaling is involved in cadmium-induced neuronal apoptosis via induction of reactive oxygen species and activation of MAPK/mTOR network. Cadmium 33-40 mitogen-activated protein kinase 3 Homo sapiens 127-131 21544200-2 2011 Recently we have demonstrated that Cd induces neuronal apoptosis in part by activation of the mitogen-activated protein kineses (MAPK) and mammalian target of rapamycin (mTOR) pathways. Cadmium 35-37 mitogen-activated protein kinase 3 Homo sapiens 129-133 21544200-5 2011 BAPTA/AM, an intracellular Ca2+ chelator, abolished Cd-induced [Ca2+](i) elevation, and blocked Cd activation of MAKPs including extracellular signal-regulated kinase 1/2 (Erk1/2), c-Jun N-terminal kinase (JNK) and p38, and mTOR-mediated signaling pathways, as well as cell death. Cadmium 52-54 mitogen-activated protein kinase 3 Homo sapiens 172-178 21544200-6 2011 Pretreatment with the extracellular Ca2+ chelator EGTA also prevented Cd-induced [Ca2+](i) elevation, MAPK/mTOR activation, as well as cell death, suggesting that Cd-induced extracellular Ca2+ influx plays a critical role in contributing to neuronal apoptosis. Cadmium 70-72 mitogen-activated protein kinase 3 Homo sapiens 102-106 21544200-6 2011 Pretreatment with the extracellular Ca2+ chelator EGTA also prevented Cd-induced [Ca2+](i) elevation, MAPK/mTOR activation, as well as cell death, suggesting that Cd-induced extracellular Ca2+ influx plays a critical role in contributing to neuronal apoptosis. Cadmium 163-165 mitogen-activated protein kinase 3 Homo sapiens 102-106 21544200-7 2011 In addition, calmodulin (CaM) antagonist trifluoperazine (TFP) or silencing CaM attenuated the effects of Cd on MAPK/mTOR activation and cell death. Cadmium 106-108 mitogen-activated protein kinase 3 Homo sapiens 112-116 20868229-9 2010 Notably, cadmium induced ERK1/2 phosphorylation in HL-60 cells. Cadmium 9-16 mitogen-activated protein kinase 3 Homo sapiens 25-31 20868229-10 2010 Furthermore, U0126, which inhibits ERK1/2 phosphorylation by upstream MAPK/ERK kinases (MEK)1/2, reduced VD3-mediated differentiation and abrogated the effects of cadmium. Cadmium 163-170 mitogen-activated protein kinase 3 Homo sapiens 35-41 20868229-10 2010 Furthermore, U0126, which inhibits ERK1/2 phosphorylation by upstream MAPK/ERK kinases (MEK)1/2, reduced VD3-mediated differentiation and abrogated the effects of cadmium. Cadmium 163-170 mitogen-activated protein kinase 3 Homo sapiens 70-74 20868229-11 2010 In conclusion, cadmium can augment monocytic differentiation by activating ERK1/2 signaling, leading to increased generation of functional monocytes. Cadmium 15-22 mitogen-activated protein kinase 3 Homo sapiens 75-81 20232314-6 2010 However, Cd-induced increase in MTT activity was inhibited by cycloheximine as well as by inhibitors of ERK1/2 and p38, but not by that of JNK. Cadmium 9-11 mitogen-activated protein kinase 3 Homo sapiens 104-110 20232314-7 2010 Consistently, Cd increased the levels of ERK1/2 and p38 phosphorylation. Cadmium 14-16 mitogen-activated protein kinase 3 Homo sapiens 41-47 20153348-3 2010 We have previously published that Cd promotes activation of the extracellular regulated kinases, erk-1 and -2 in both ER-positive and ER-negative human breast cancer cells, suggesting that this estrogen-like effect of Cd is not associated with the ER. Cadmium 218-220 mitogen-activated protein kinase 3 Homo sapiens 97-109 20153348-8 2010 Furthermore, Cd treatment rapidly activated (within 2.5 min) raf-1, mitogen-activated protein kinase kinase, mek-1, extracellular signal regulated kinases, erk-1/2, ribosomal S6 kinase, rsk, and E-26 like protein kinase, elk, about 4-fold in vector transfectants. Cadmium 13-15 mitogen-activated protein kinase 3 Homo sapiens 156-163 19573589-3 2009 The present study was to investigate the relationship between the hormesis effect of cadmium (Cd) and activation of ERK1/2, JNK and p38 pathways in human embryo lung fibroblast cells. Cadmium 85-92 mitogen-activated protein kinase 3 Homo sapiens 116-122 19524565-0 2009 Cadmium-induced apoptotic death of human retinal pigment epithelial cells is mediated by MAPK pathway. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 89-93 19524565-5 2009 Cadmium also caused reactive oxygen species (ROS) generation and activation of mitogen-activated protein kinases (MAPKs) pathway including c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (Erk1/2), and p38 in ARPE-19 cells. Cadmium 0-7 mitogen-activated protein kinase 3 Homo sapiens 213-219 19524565-7 2009 These results indicate that elevated ROS-induced activation of the MAPK signaling pathway could be associated with Cd-induced RPE cell apoptosis, one of the major contributing factors in AMD. Cadmium 115-117 mitogen-activated protein kinase 3 Homo sapiens 67-71 19573589-3 2009 The present study was to investigate the relationship between the hormesis effect of cadmium (Cd) and activation of ERK1/2, JNK and p38 pathways in human embryo lung fibroblast cells. Cadmium 94-96 mitogen-activated protein kinase 3 Homo sapiens 116-122 19573589-5 2009 Our data indicated that cell proliferation promoted by low concentrations of Cd was blocked obviously by ERK1/2 inhibitor PD98059 and partly by JNK inhibitor SP600125; while the decreases of cell proliferation induced by high concentrations of Cd were significantly restored by p38 inhibitor SB203580. Cadmium 77-79 mitogen-activated protein kinase 3 Homo sapiens 105-111 19573589-6 2009 Further analysis showed that phospho-ERK1/2 and phospho-JNK activities were increased with different concentrations of Cd, whereas phospho-p38 activity was markedly increased at high concentrations. Cadmium 119-121 mitogen-activated protein kinase 3 Homo sapiens 37-43 19573589-7 2009 Our findings suggested that low concentration of Cd induces the ERK and JNK pathways and promotes cell proliferation; while high concentration of Cd induces p38 pathway and inhibits cell proliferation. Cadmium 49-51 mitogen-activated protein kinase 3 Homo sapiens 64-67 19573589-8 2009 Activation of the ERK1/2 pathways seems to play a more important role than the JNK pathway in the biphasic effect of Cd on cell proliferation. Cadmium 117-119 mitogen-activated protein kinase 3 Homo sapiens 18-24