| Identifier | HPI071976 |
| Interaction | TGF-beta <==> p53 |
| Role & State | --- |
| Interaction Type | IT:0000316,induce; IT:0000114,activation; IT:0000068,transcription; |
| Biological Process | BP:0031099,regeneration; |
| Biological Function | --- |
| Subcelluar Location | SCL:0000002,intracellular; SCL:0000001,extracellular; |
| Detection Method | --- |
| Reference | 18212064_6, We propose that activation of TGF-beta signaling restores a dynamic interplay between p53 and TGF-beta effectors that cooperate to effectively target mSin3A to tumor marker AFP and reestablish transcription repression.
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| Reference | 20583212_15, CONCLUSION: TGF-beta induces p53-independent and p16(Ink4a)-independent, but Nox4-dependent, p21(Cip1)-dependent, p15(Ink4b)-dependent, and ROS-dependent senescence arrest in well-differentiated HCC cells.
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| Reference | 8666158_3, It has provided insights into the concerted action of extracellular (HGF/SF, TGF-alpha, EGF, TGF-beta) and intracellular factors (c-myc, c-fos, c-jun, p53, c-met, and others) in liver regeneration.
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| Reference | 9721329_3, The cytokines TNF-alpha, IL-1beta, and INF-gamma synergistically activate iNOS expression in the liver, and the human iNOS gene was first cloned from cytokine-stimulated hepatocytes. iNOS expression requires the transcription factor NF-kappaB and is down-regulated by steroids, TGF-beta, the heat shock response, p53, and nitric oxide (NO) itself.
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