IndraLab

Statements

COPS6 binds FOXO4. 12 / 12
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"Results showed that FOXO4 bound to the C‐terminus of CSN6 (aa 185‐327 containing) but not to the N‐terminus (aa 1‐184, containing the MPN domain; Figure  xref )."
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"Significantly, as the CSN6–FOXO4 axis is crucial in regulating gene expression of Glut1 and SGOC genes, these genes were reduced in CSN6 knockdown tumors (Figure S17E, Supporting Information)."
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"Together, the regulatory circuit of CSN6‐FOXO4 axis could be recapitulated in mouse xenograft cancer model, and level of FOXO4 deregulation plays roles in affecting the outcome of tumorigenicity."
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"These data suggested that CSN6‐FOXO4 axis deregulation could exist in many types of cancer."
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"CSN6‐FOXO4 Axis Is Critical for Tumorigenicity in Xenograft Mouse Model."
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"Deregulation of CSN6‐FOXO4 Axis Rewires Metabolic Programming via Enhancing Glucose Uptake and Promotes the Expression of SGOC Genes."
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"We further confirmed that CSN6‐FOXO4 link could affect cell proliferation."
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"As CSN6‐FOXO4 axis impacts on the expression of Glut1, biochemical assays that quantitates the glucose uptake (consumption) by assessing uptake of (2‐( N ‐(7‐nitrobenz‐2‐oxa‐1,3‐diazol‐4‐yl)amino)‐2‐deoxyglucose (2‐NBDG)), a green fluorescent glucose analog, additionally demonstrated that CSN6 knockdown inhibited 2‐NBDG uptake (Figure  xref ), while FOXO4 knockdown increased 2‐NBDG uptake (Figure  xref )."
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"Mechanistic studies show that CSN6 binds and regulates FOXO4 stability through enhancing the E3 ligase activity of COP1, and that COP1 directly interacts with FOXO4 through a VP motif on FOXO4 and accelerates the ubiquitin-mediated degradation of FOXO4."
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biogrid
No evidence text available
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biogrid
No evidence text available
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sparser
"Thus, these data suggest a link of CSN6‐FOXO4 axis and ser/gly metabolism."
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