| Name | p38 |
|---|---|
| Synonyms | AIMP 2; p38; AIMP2; JTV 1; JTV1; JTV1 gene; JTV1 protein; Multisynthetase complex auxiliary component p38… |
| Name | rotenone |
|---|---|
| CAS |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 14976342 | Newhouse K, Hsuan SL, Chang SH, Cai B, Wang Y, Xia Z: Rotenone-induced apoptosis is mediated by p38 and JNK MAP kinases in human dopaminergic SH-SY5Y cells. Toxicol Sci. 2004 May;79(1):137-46. Epub 2004 Feb 19. |
274(3,4,4,4) | Details |
| 20157567 | Hsieh CC, Papaconstantinou J: Dermal fibroblasts from long-lived Ames dwarf mice maintain their in vivo resistance to mitochondrial generated reactive oxygen species (ROS). Aging (Albany NY). 2009 Jul 31;1(9):784-802. In these studies we demonstrate that dermal fibroblasts from these long-lived mice exhibit (a) higher levels of (SH)(2) Trx-ASK1 that correlate with their resistance to ROS generated by inhibitors of electron transport chain complexes CI (rotenone), CII (3-nitropropionic acid), CIII, (antimycin A), and H (2) O (2)-mediated activation of p38 MAPK, and (b) maintain their in vivo resistance to ROS generated by 3NPA. |
83(1,1,1,3) | Details |
| 19539006 | Kim HJ, Park HJ, Park HK, Chung JH: Tranexamic acid protects against rotenone-induced apoptosis in human neuroblastoma SH-SY5Y cells. Toxicology. 2009 Aug 3;262(2):171-4. Epub 2009 Jun 16. TA blocked the rotenone-induced phosphorylation of JNK and P38, the downregulation of BCL2 and the upregulation of BAX. |
81(1,1,1,1) | Details |
| 15650392 | Bundy RE, Hoare GS, Kite A, Beach J, Yacoub M, Marczin N: Redox regulation of p38 MAPK activation and expression of ICAM-1 and heme oxygenase-1 in human alveolar epithelial (A549) cells. Antioxid Redox Signal. 2005 Jan-Feb;7(1-2):14-24. The mitochondrial complex I and III inhibitors, rotenone and antimycin A, and allopurinol partially inhibited H2O2- but not TNFalpha-induced p38 activation. |
5(0,0,0,5) | Details |
| 18840762 | Eley HL, Russell ST, Tisdale MJ: Mechanism of attenuation of muscle protein degradation induced by tumor necrosis factor-alpha and angiotensin II by Am J Physiol Endocrinol Metab. 2008 Dec;295(6):E1417-26. Epub 2008 Oct 7. Formation of ROS was attenuated by rotenone, an inhibitor of the mitochondrial electron transport chain, nitro- methyl ester, an inhibitor of synthase, and SB 203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), which also attenuated total protein degradation. Formation of ROS was attenuated by rotenone, an inhibitor of the mitochondrial electron transport chain, nitro- methyl ester, an inhibitor of synthase, and SB 203580, a specific inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), which also attenuated total protein degradation. |
3(0,0,0,3) | Details |
| 16571865 | Li Z, Hyseni X, Carter JD, Soukup JM, Dailey LA, Huang YC: Pollutant particles enhanced H2O2 production from NAD (P) H oxidase and mitochondria in human pulmonary artery endothelial cells. Am J Physiol Cell Physiol. 2006 Aug;291(2):C357-65. Epub 2006 Mar 29. We measured the production of extracellular H2O2, activation of extracellular signal-regulated kinases1/2 (ERK1/2) and p38 MAPKs in human pulmonary artery endothelial cells (HPAEC) treated with urban particles (UP; SRM1648), and assessed the effects of H2O2 on vasoconstriction in pulmonary artery ring and isolated perfused lung. Inhibitors of other H2O2-producing enzymes, including Nomega-methyl-L-argnine, indomethacin, allopurinol, cimetidine, rotenone, and antimycin, had no effects. |
2(0,0,0,2) | Details |
| 19371610 | Mo Y, Wan R, Chien S, Tollerud DJ, Zhang Q: Activation of endothelial cells after exposure to ambient ultrafine particles: the role of oxidase. Toxicol Appl Pharmacol. 2009 Apr 15;236(2):183-93. Epub 2009 Feb 5. Our results showed that exposure of MPMVEC to UFPs caused increased phosphorylation of p38 and ERK1/2 MAPKs that was blocked by pre-treatment with DPI or p67 (phox) siRNA. Our results showed that UFPs, at a non-toxic dose, induced reactive species (ROS) generation in mouse pulmonary microvascular endothelial cells (MPMVEC) that was inhibited by pre-treatment with the ROS scavengers or inhibitors, but not with the mitochondrial inhibitor, rotenone. |
2(0,0,0,2) | Details |
| 17635749 | Ho C, Lee PH, Huang WJ, Hsu YC, Lin CL, Wang JY: -induced fibronectin gene expression through Ras-mediated oxidase activation in renal mesangial cells. Nephrology. 2007 Aug;12(4):348-56. High MGO rapidly enhanced Ras activation in 1 h and progressively increased cytosolic p38 activation. METHODS: Rat kidney mesangial cells with or without pretreatment with inhibitors, including superoxide dismutase, catalase, L-NAME, diphenylene iodonium, rotenone, allopurinol, PD98059, SB203580 and SP600125 were cultured in medium containing 100 microM MGO. |
2(0,0,0,2) | Details |
| 19723537 | Park HJ, Kim HJ, Park HK, Chung JH: Protective effect of histamine H2 receptor antagonist against rotenone-induced apoptosis. Neurotoxicology. 2009 Nov;30(6):1114-9. Epub 2009 Aug 31. These results indicate that protects against rotenone-induced apoptosis, inhibiting phosphorylation of JNK and P38, and activation of CASPs in human dopaminergic SH-SY5Y cells. |
81(1,1,1,1) | Details |
| 19885011 | Kim HJ, Song JY, Park HJ, Park HK, Yun DH, Chung JH: Protects against Rotenone-induced Apoptosis in Human Neuroblastoma SH-SY5Y Cells. Korean J Physiol Pharmacol. 2009 Aug;13(4):281-5. Epub 2009 Aug 31. also blocked rotenone-induced phosphorylation of Jun NH2-terminal protein kinase (JNK) and P38, and prevented changes in B-cell CLL/lymphoma 2 (BCL2) and BCL2-associated X protein (BAX) expression levels. |
81(1,1,1,1) | Details |
| 15778391 | Sim S, Yong TS, Park SJ, Im KI, Kong Y, Ryu JS, Min DY, Shin MH: oxidase-derived reactive species-mediated activation of ERK1/2 is required for apoptosis of human neutrophils induced by Entamoeba histolytica. J Immunol. 2005 Apr 1;174(7):4279-88. However, a mitochondrial inhibitor rotenone did not attenuate the Entamoeba-induced ROS generation and apoptosis. Although E. histolytica strongly induced activation of ERK1/2 and p38 MAPK in neutrophils, the activation of ERK1/2 was closely associated with ROS-mediated apoptosis. |
1(0,0,0,1) | Details |
| 19074146 | Ren Y, Jiang H, Yang F, Nakaso K, Feng J: Parkin protects dopaminergic neurons against microtubule-depolymerizing toxins by attenuating microtubule-associated protein kinase activation. J Biol Chem. 2009 Feb 6;284(6):4009-17. Epub 2008 Dec 11. Here we report that microtubule-depolymerizing agents such as colchicine or nocodazole induced strong activation of MAP kinases including JNK, ERK, and p38. Such mutations produced truncated parkin proteins lacking any microtubule binding domain and prevented parkin from protecting midbrain dopaminergic neurons against microtubule-depolymerizing toxins such as rotenone or colchicine. |
1(0,0,0,1) | Details |
| 16449798 | Hsieh CC, Papaconstantinou J: Thioredoxin-ASK1 complex levels regulate ROS-mediated p38 MAPK pathway activity in livers of aged and long-lived Snell dwarf mice. FASEB J. 2006 Feb;20(2):259-68. We have proposed that the age-associated increase of reactive species (ROS) by electron transport chain (ETC) dysfunction may cause the elevated basal level of p38 MAPK stress response pathway activity. Here we propose that activation of the p38 MAPK pathway by complex I (CI) generated ROS, in response to rotenone (ROT) treatment, is based on the ability of reduced Trx to bind to and inhibit ASK 1 and its release from the complex upon oxidation. |
1(0,0,0,1) | Details |
| 15806174 | Lee YJ, Lee DH, Cho CK, Chung HY, Bae S, Jhon GJ, Soh JW, Jeoung DI, Lee SJ, Lee YS: HSP25 inhibits radiation-induced apoptosis through reduction of PKCdelta-mediated ROS production. Oncogene. 2005 May 26;24(23):3715-25. In the present study, radiation-induced cytochrome c release from mitochondria and activation of caspases accompanied by a decrease of mitochondrial membrane potential in Jurkat T cells were shown to be inhibited by mitochondrial complex I inhibitor rotenone, suggesting that mitochondrial ROS might be important in radiation-induced caspase-dependent apoptosis. Furthermore, activation of p38 MAP kinase by radiation was associated with radiation-induced cell death and ROS production and PKCdelta was an upstream molecule for p38 MAP kinase activation, ROS generation and subsequent caspase-dependent apoptotic events. |
1(0,0,0,1) | Details |
| 16572112 | Lin CL, Wang FS, Kuo YR, Huang YT, Huang HC, Sun YC, Kuo YH: Ras modulation of activates ERK-dependent fibronectin expression in diabetes-induced renal injuries. Kidney Int. 2006 May;69(9):1593-600. Transforming growth factor (TGF)-beta1, fibronectin expression, Ras, ERK, p38, and c-Jun activation of glomerular mesangial cells or urinary albumin secretion were assessed. Pretreatment with diphenyliodonium, not allopurinol or rotenone, reduced high- and AGE augmentation of synthesis and fibronection expression. |
1(0,0,0,1) | Details |
| 12388366 | Parinandi NL, Kleinberg MA, Usatyuk PV, Cummings RJ, Pennathur A, Cardounel AJ, Zweier JL, Garcia JG, Natarajan V: Hyperoxia-induced NAD (P) H oxidase activation and regulation by MAP kinases in human lung endothelial cells. Am J Physiol Lung Cell Mol Physiol. 2003 Jan;284(1):L26-38. Epub 2002 Jul 26. Exposure of HPAECs to hyperoxia for 1, 3, and 12 h increased the generation of which was blocked by diphenyleneiodonium but not by rotenone or Exposure of HPAECs to hyperoxia activated p38 MAPK and ERK, and inhibition of p38 MAPK and MEK1/2 attenuated the hyperoxia-induced ROS generation. |
1(0,0,0,1) | Details |
| 18242171 | Chen S, Zhang X, Yang D, Du Y, Li L, Li X, Ming M, Le W: D2/D3 receptor agonist ropinirole protects dopaminergic cell line against rotenone-induced apoptosis through inhibition of caspase- and JNK-dependent pathways. FEBS Lett. 2008 Mar 5;582(5):603-10. Epub 2008 Jan 31. We found that ropinirole can block the rotenone-induced phosphorylation of JNK, P38 and p-c-Jun, but promote the phosphorylation of ERK1/2. |
81(1,1,1,1) | Details |
| 17324951 | Klintworth H, Newhouse K, Li T, Choi WS, Faigle R, Xia Z: Activation of c-Jun N-terminal protein kinase is a common mechanism underlying paraquat- and rotenone-induced dopaminergic cell apoptosis. Toxicol Sci. 2007 May;97(1):149-62. Epub 2007 Feb 25. The selective ability of paraquat and rotenone to induce apoptosis in different cell lines correlates with their ability to activate c-Jun N-terminal protein kinase (JNK) and p38 mitogen-activated protein kinases. |
37(0,1,2,2) | Details |
| 15557194 | Woo CH, Lim JH, Kim JH: Lipopolysaccharide induces matrix metalloproteinase-9 expression via a mitochondrial reactive species-p38 kinase-activator protein-1 pathway in Raw 264.7 cells. J Immunol. 2004 Dec 1;173(11):6973-80. LPS-induced MMP-9 expression and p38 kinase phosphorylation were also inhibited by rotenone, a specific inhibitor of mitochondrial complex I, supporting the role of mitochondrial ROS in LPS signaling to MMP-9. |
35(0,1,1,5) | Details |
| 17356569 | Zhou F, Wu JY, Sun XL, Yao HH, Ding JH, Hu G: Iptakalim alleviates rotenone-induced degeneration of dopaminergic neurons through inhibiting microglia-mediated neuroinflammation. Neuropsychopharmacology. 2007 Dec;32(12):2570-80. Epub 2007 Mar 14. Furthermore, pretreatment with IPT prevented rotenone-induced mitochondrial membrane potential loss and p38/c-jun N-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) activation in microglia, which might in turn regulate microglial activation and subsequent production of TNF-alpha and PGE (2). |
31(0,1,1,1) | Details |
| 16413574 | Zhang C, Hein TW, Wang W, Ren Y, Shipley RD, Kuo L: Activation of JNK and xanthine oxidase by TNF-alpha impairs -mediated dilation of coronary arterioles. J Mol Cell Cardiol. 2006 Feb;40(2):247-57. Epub 2006 Jan 18. Conversely, the effects of TNF were insensitive to inhibitors of p38 (SB203580), ERK (PD98059), NAD (P) H oxidase (apocynin), or mitochondrial respiratory chain (rotenone). |
31(0,1,1,1) | Details |
| 16004991 | Wang G, Qi C, Fan GH, Zhou HY, Chen SD: PACAP protects neuronal differentiated PC12 cells against the neurotoxicity induced by a mitochondrial complex I inhibitor, rotenone. FEBS Lett. 2005 Jul 18;579(18):4005-11. The effects of PACAP27 on rotenone-induced cell death were mimicked by dibutyryl-cAMP (db-cAMP), forskolin and prevented by the PKA inhibitor H89, the ERK inhibitor PD98059 and the p38 inhibitor SB203580. |
31(0,1,1,1) | Details |
| 17029596 | Hirata Y, Meguro T, Kiuchi K: Differential effect of nerve growth factor on dopaminergic neurotoxin-induced apoptosis. J Neurochem. 2006 Oct;99(2):416-25. There were distinct differences in intracellular mechanisms between rotenone- and -induced apoptosis such as the production of reactive species, the response to antioxidants, and the activation of the c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). |
31(0,1,1,1) | Details |
| 12003789 | Kulisz A, Chen N, Chandel NS, Shao Z, Schumacker PT: Mitochondrial ROS initiate phosphorylation of p38 MAP kinase during hypoxia in cardiomyocytes. Am J Physiol Lung Cell Mol Physiol. 2002 Jun;282(6):L1324-9. This response was inhibited by rotenone, thenoyltrifluoroacetone, and myxothiazol, inhibitors of mitochondrial complexes I, II, and III, respectively. |
6(0,0,0,6) | Details |
| 15170659 | Morazzani M, de Carvalho DD, Kovacic H, Smida-Rezgui S, Briand C, Penel C: Monolayer versus aggregate balance in survival process for EGF-induced apoptosis in A431 carcinoma cells: Implication of ROS-P38 MAPK-integrin alpha2beta1 pathway. Int J Cancer. 2004 Jul 20;110(6):788-99. EGF-induced dose-dependent ROS production was inhibited by the oxidase inhibitor, diphenylene iodonium (DPI), in these cells while rotenone was ineffective. |
3(0,0,0,3) | Details |
| 15749729 | Simoncini S, Sapet C, Camoin-Jau L, Bardin N, Harle JR, Sampol J, Dignat-George F, Anfosso F: Role of reactive species and p38 MAPK in the induction of the pro-adhesive endothelial state mediated by IgG from patients with anti-phospholipid syndrome. Int Immunol. 2005 Apr;17(4):489-500. Epub 2005 Mar 4. ROS inhibition observed in the presence of diphenylene iodonium and rotenone indicated an involvement of a membrane-bound oxidase and the mitochondrial transport chain as sources of ROS. |
2(0,0,0,2) | Details |
| 16024921 | Yang T, Zhang A, Honeggar M, Kohan DE, Mizel D, Sanders K, Hoidal JR, Briggs JP, Schnermann JB: Hypertonic induction of COX-2 in collecting duct cells by reactive species of mitochondrial origin. J Biol Chem. 2005 Oct 14;280(41):34966-73. Epub 2005 Jul 17. The increases in phosphorylation of ERK1/2 and p38 were detected 20 min following the hypertonic treatment and were both prevented by N-acetyl- The increases in ROSs in response to hypertonic treatment were completely blocked by any one of the mitochondrial inhibitors tested, such as rotenone, thenoyltrifluoroacetone, or carbonyl m-chlorophenylhydrazone, associated with remarkable inhibition of COX-2 expression. |
1(0,0,0,1) | Details |
| 15328001 | Alba G, El Bekay R, Alvarez-Maqueda M, Chacon P, Vega A, Monteseirin J, Santa Maria C, Pintado E, Bedoya FJ, Bartrons R, Sobrino F: Stimulators of AMP-activated protein kinase inhibit the respiratory burst in human neutrophils. FEBS Lett. 2004 Aug 27;573(1-3):219-25. Furthermore, also strongly reduced PMA-dependent H2O2 release, and induced the phosphorylation of c-jun N-terminal kinase 1 (p46), p38 mitogen-activated protein kinase and extracellular signal-regulated kinase. |
1(0,0,0,1) | Details |
| 18563357 | Han M, Im DS: Effects of mitochondrial inhibitors on cell viability in U937 monocytes under deprivation. Arch Pharm Res. 2008 Jun;31(6):749-57. Epub 2008 Jun 19. Mitochondrial inhibitors such as rotenone, TTFA, antimycin A, azide, oligomycin, and valinomycin were used in this study. Activities of Akt and p38 MAPK, however, were decreased by the inhibitors under deprivation condition except TTFA. |
1(0,0,0,1) | Details |
| 16573651 | Casarejos MJ, Menendez J, Solano RM, Rodriguez-Navarro JA, Garcia de Yebenes J, Mena MA: Susceptibility to rotenone is increased in neurons from parkin null mice and is reduced by minocycline. J Neurochem. 2006 May;97(4):934-46. Epub 2006 Mar 29. The roles of p38 MAPK and extracellular signal-regulated kinase signaling pathways were tested by treatment with SB20358 and PD98059, respectively. |
1(0,0,0,1) | Details |
| 19012619 | Zhou F, Yao HH, Wu JY, Ding JH, Sun T, Hu G: Opening of microglial K (ATP) channels inhibits rotenone-induced neuroinflammation. J Cell Mol Med. 2008 Sep-Oct;12(5A):1559-70. Moreover, the underlying mechanisms involved the stabilization of mitochodrial membrane potential and inhibition of p38/c-Jun-N-terminal kinase (JNK) activation in microglia. |
1(0,0,0,1) | Details |
| 18201823 | Nakaso K, Ito S, Nakashima K: activates the PI3K/Akt pathway and prevents apoptotic cell death in a Parkinson's disease model of SH-SY5Y cells. Neurosci Lett. 2008 Feb 20;432(2):146-50. Epub 2007 Dec 23. prevented the apoptotic cell death induced by serum/ (RA) deprivation, MPP+, rotenone, and 6-OHDA in SH-SY5Y cells in a dose dependent manner. |
0(0,0,0,0) | Details |
| 17389326 | Chen YH, Lin SJ, Lin FY, Wu TC, Tsao CR, Huang PH, Liu PL, Chen YL, Chen JW: High glucose impairs early and late endothelial progenitor cells by modifying -related but not oxidative stress-mediated mechanisms. Diabetes. 2007 Jun;56(6):1559-68. Epub 2007 Mar 26. Antioxidants including -and polyethylene glycol (PEG)-conjugated superoxide dismutase, and PEG-catalase had no effects, whereas pyrrolidine dithiocarbamate, diphenyleneiodonium, apocynin, and rotenone even deteriorated the downregulation of both EPCs. |
0(0,0,0,0) | Details |
| 16819171 | Zhao FL, Hu JH, Zhu XZ: Monocyte-mediated rotenone neurotoxicity towards human neuroblastoma SH-SY5Y: role of mitogen-activated protein kinases. Biol Pharm Bull. 2006 Jul;29(7):1372-7. |
0(0,0,0,0) | Details |
| 19900598 | Kwak HB, Lee BK, Oh J, Yeon JT, Choi SW, Cho HJ, Lee MS, Kim JJ, Bae JM, Kim SH, Kim HS: Inhibition of osteoclast differentiation and bone resorption by rotenone, through down-regulation of RANKL-induced c-Fos and NFATc1 expression. Bone. 2010 Mar;46(3):724-31. Epub 2009 Nov 6. |
0(0,0,0,0) | Details |
| 19777565 | Deng YT, Huang HC, Lin JK: Rotenone induces apoptosis in MCF-7 human breast cancer cell-mediated ROS through JNK and p38 signaling. Mol Carcinog. 2010 Feb;49(2):141-51. |
224(2,4,4,4) | Details |
| 18705696 | Liu WH, Chang LS: Reactive species and p38 mitogen-activated protein kinase induce apoptotic death of U937 cells in response to Naja nigricollis toxin gamma. J Cell Mol Med. 2008 Aug 14. Noticeably, pretreatment with or rotenone eliminated markedly ROS accompanied with reduction in p38 MAPK activation. |
85(1,1,1,5) | Details |
| 20187293 | Liu WH, Chang LS: Reactive species and p38 mitogen-activated protein kinase induce apoptotic death of U937 cells in response to Naja nigricollis toxin-gamma. J Cell Mol Med. 2009 Aug;13(8B):1695-705. Noticeably, pre-treatment with or rotenone eliminated markedly ROS accompanied with reduction in p38 MAPK activation. |
85(1,1,1,5) | Details |
| 18832435 | Hu LF, Lu M, Wu ZY, Wong PT, Bian JS: inhibits rotenone-induced apoptosis via preservation of mitochondrial function. Mol Pharmacol. 2009 Jan;75(1):27-34. Epub 2008 Oct 2. NaHS also prevented rotenone-induced p38- and c-Jun NH (2)-terminal kinase (JNK)-mitogen-activated protein kinase (MAPK) phosphorylation and rotenone-mediated changes in Bcl-2/Bax levels, mitochondrial membrane potential (DeltaPsi (m)) dissipation, cytochrome c release, caspase-9/3 activation and poly (ADP- polymerase cleavage. |
62(0,2,2,2) | Details |
| 15677311 | Rhyu DY, Yang Y, Ha H, Lee GT, Song JS, Uh ST, Lee HB: Role of reactive species in TGF-beta1-induced mitogen-activated protein kinase activation and epithelial-mesenchymal transition in renal tubular epithelial cells. J Am Soc Nephrol. 2005 Mar;16(3):667-75. Epub 2005 Jan 26. Growth-arrested and synchronized NRK-52E cells were stimulated with TGF-beta1 (0.2 to 20 ng/ml) or H (2) O (2) (1 to 500 microM) in the presence or absence of antioxidants or catalase), inhibitors of oxidase (diphenyleneiodonium and apocynin), mitochondrial electron transfer chain subunit I (rotenone), and MAPK (PD 98059, an MEK [MAP kinase/ERK kinase] inhibitor, or p38 MAPK inhibitor) for up to 96 h. |
32(0,1,1,2) | Details |
| 12130563 | Hsieh TJ, Zhang SL, Filep JG, Tang SS, Ingelfinger JR, Chan JS: High glucose stimulates angiotensinogen gene expression via reactive species generation in rat kidney proximal tubular cells. Endocrinology. 2002 Aug;143(8):2975-85. The present studies investigated whether the effect of high levels on angiotensinogen (ANG) gene expression in kidney proximal tubular cells is mediated via reactive species (ROS) generation and p38 MAPK activation. These effects of high were blocked by antioxidants and tiron), inhibitors of mitochondrial electron transport chain complex I (rotenone) and II (thenoyltrifluoroacetone), an inhibitor of glycolysis-derived transport into mitochondria (alpha-cyano- an uncoupler of oxidative phosphorylation (carbonyl m-chlorophenylhydrazone), a manganese superoxide dismutase mimetic, catalase, and a specific inhibitor of p38 MAPK (SB 203580), but were not affected by an inhibitor of the - shuttle (aminooxyacetate acid). |
5(0,0,0,5) | Details |