8/30/2023 0 Comments Jnk1 regulate jun protein turnoverSphingosylphosphocholine (SPC) is a deacylated derivative of sphingomyelin known to accumulate in Niemann-Pick disease type A ( 257200). They presented experimental evidence that activation of the JNK (see 601158)/JUN pathway and increased expression of BIM ( 603827) are key events required for cytochrome c release and apoptosis following NGF withdrawal. (2001) noted that apoptosis induced in rat sympathetic neurons by nerve growth factor (NGF see 162030) withdrawal can be blocked by inhibitors of RNA and protein synthesis. Cells lacking Jun exhibited prolonged p21 induction, whereas constitutive Jun inhibited UV-mediated p21 induction. This function of Jun was exerted through negative regulation of p53 ( 191170) association with the p21 ( 116899) promoter. Cells lacking Jun underwent prolonged cell cycle arrest but resisted apoptosis, whereas cells that expressed Jun constitutively did not arrest and undergo apoptosis. (2000) found that in mouse fibroblasts, Jun was necessary for cell cycle reentry of ultraviolet (UV)-irradiated cells but did not participate in the response to ionizing radiation. Marx (1988) reviewed information indicating that the protein encoded by the JUN gene acts directly to activate gene transcription in response to cell stimulation that the product of the FOS oncogene cooperates with the JUN product in fostering gene transcription that there is a structural and functional similarity between JUN and GCN4, which induces the activity of a large set of genes needed for amino acid synthesis in yeast that specifically both have a DNA-binding domain on the carboxyl end essential for the activation of genes that the JUN and FOS proteins are held together in a complex by a leucine zipper and that there are other JUN genes in addition to the original one. (1988) investigated regulation of murine c-jun gene transcription and found that both serum and phorbol-ester TPA induced c-jun gene expression.
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