IndraLab

Statements

COPS5 activates TGFB. 7 / 7
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"It is possible that overexpression of Jab1 and CSN5 during the tumorigenic process results in enhanced TGF-beta signaling that contributes to the progression of the disease."
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"Moreover, CSN5 silencing inhibited the secretion of TGF-beta, IL-1beta and IL-6 and the transcriptional activity of transcription factor NF-kappaB and Twist in human colorectal cancer cells."
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"Kim et al. (2004) showed that Jab1/CSN5 enhances TGF-β1 signaling by binding to Smad7 and promoting its degradation in human carcinoma cells ( Kim et al., 2004 )."
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"It is questionable whether Jab1/CSN5 mediates TGF-β1 signaling via Smad7 dependence or if there is another mechanism which are not dependent on the Smad proteins in CRS.On the other hand, we have foun[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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"Over-expression of ANGPTL2 weakened the JAB1 silence-induced decrease of IL-6, TNF-α, MCP-1, IL-1β, TGF-β1, collagen I, collagen IV, and fibronectin."
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"Csn5 and Jab1 can modulate TGF-beta superfamily signaling that is mediated by TGF-beta and BMP through direct interaction with various Smads."
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"Together, these data establish Jab1 as an ubiquitination target for the CUL4B ubiquitin ligase complex.In addition to its role in deneddylation [32,33], Jab1 and CSN5 has been shown to bind to Smad7, [MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"
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