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.0309 Mitophagy - animal TFE3, PINK1 0.0365 Inflammatory bowel disease (IBD) IL4R, TGFB3 0.0386 Protein processing in endoplasmic reticulum SEC13, SEC24C, SAR1A 0.0393 Renal cell carcinoma TFE3, TGFB3 0.0417 MAPK signaling
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Activin has previously been shown to act as a nerve cell survival factor and to have neurotrophic effects on neurons. However, the role of activin in regulating neurotransmitter expression in the central nervous system and the exact mechanisms involved in this process are poorly understood. In the present study, we report that activin A and basic fibroblast growth factor (bFGF) synergistically increased the protein level of tyrosine hydroxylase (TH), and also greatly increased the TH mRNA level, in both mouse E14 striatal primary cell cultures and the hippocampal neuronal cell line HT22. Activin A and bFGF cooperatively stimulated nuclear translocation of Smad3 and specifically activated ERK1/2, but not p38 or JNK. Interestingly, a specific inhibitor for MEK, U0126, efficiently blocked the induction of TH promoter activity by activin A and bFGF, indicating that activin A collaborated with bFGF signaling to induce the TH gene through selective activation of ERK-type MAP kinase in mouse striatal and HT22 cells. These data suggest that activin A may act in concert with bFGF for the development of TH-positive neurons.
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study of E2 replacement in ovarian insufficiency is crucial for a better understanding of the E2 mechanisms. In this context, the goal of the present study was to test the hypotheses that PKC and p38 MAPK signaling are involved in fluid intake (mainly
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, 8 activation was not affected in the presence of E 2 (100 nM). It was of note that treatment with E 2 (100 nM) significantly activated MAPK phosphorylation including ERK1/ERK2 and SAPK/JNK but not p38-MAPK signaling ( Fig. 6 A). BMP-2 and BMP-4
Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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Graduate School of the Chinese Academy of Sciences, 19 Yu-quan Road, Beijing 10009, China
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participates in the transactivation of LRH-1 promoter in GCs ( Falender et al. 2003 ). Based on the descriptions above, we hypothesize that an FSH-activated p38 MAPK signaling cascade is involved in the regulation of GC steroidogenesis, and start out
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-terminal kinase and p38 MAPK signalling pathways ( Freshney et al . 1994 ). Extracellular signal-regulated kinases 1 and 2 (ERK1/2), albeit mostly activated by mitogenic factors, are also activated by IL1α in selective cases ( Bird et al . 1991 , Waterfield et
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). These data reveal that PGF 2 α upregulates the expression of Slit2 and Robo1 in a dose-dependent and time-dependent manner. PGF 2 α specifically increases Slit2/Robo1 expression through PKC-dependent ERK1/2 and P38 MAPK signaling
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and cyclin D1 production, which suggests that integrin β1 receives laminin as a signal on FS cells and that its signaling activates MAPK signaling cascades, leading to cyclin D1 transcription and contributing to cell cycle progression. However, there
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assays respectively. Data are presented as means± s.e.m . ( n =4). * P <0.05 vs vehicle-treated control group and # P <0.05 vs the group not treated with BIM23127. NMB-induced osteoblast proliferation via ERK1/2 activation ERK1/2 MAPK signaling is
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that PS triggered activation of PKA and PKC, followed by MAPK signaling, enhanced PRL synthesis and secretion, and enhanced the proliferation of GH3 cells. The effects of PS were further evidenced in vivo based on the increased expression of PRL and
