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Studies elucidated the inhibitory mechanism in which mTORC1 phosphorylates the autophagy regulatory complex containing unc-51-like kinase 1 (ULK1), the mammalian Atg13 protein, and focal adhesion kinase interacting protein of 200 kD (FIP200). |
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Nuclear RB1CC1 directly activates the RB1 promoter to enhance RB1 expression associated with breast cancer. |
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The ULK-Atg13-FIP200 complexes are direct targets of mTOR and important regulators of autophagy in response to mTOR signaling. |
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ATG13 and ULK1 are phosphorylated by the mTOR pathway in a nutrient starvation-regulated manner, indicating that the ULK1.ATG13.FIP200 complex acts as a node for integrating incoming autophagy signals into autophagosome biogenesis. |
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Nuclear RB1CC1 directly activates the RB1 promoter to enhance RB1 expression in cancer cells. |
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Observational study of gene-disease association. (HuGE Navigator) |
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These results suggest that FIP200 is a novel mammalian autophagy factor that functions together with ULKs. |
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Cellular functions of FIP200 and its interacting proteins, and the emerging roles of FIP200 in embryogenesis and cancer development. Review. |
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provide the first evidence for the existence of a close-spatially controlled-mode of regulation of FIP200 and PIASy nucleocytoplasmic functions |
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RB1CC1 insufficiency causes neuronal atrophy through mTOR signaling alteration and involved in the pathology of Alzheimer's diseases. |
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RB1CC1 and PACE4 genes might be the DNA targets of sodium arsenite treatment in human lymphoblastoid cells. |
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RB1CC1 gene preferentially expressed and contributed to the maturation of human embryonic musculoskeletal cells, and may regulate the proliferative activity and maturation of tumor cells derived from these tissues. |
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RB1CC1 induces the expression of RB1, especially of underphosphorylated forms, then suppresses cell cycle progression in human neoplastic cells |
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FIP200 regulates of cell size by interaction with the TSC1-TSC2 complex. |
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RB1CC1 is frequently mutated in breast cancer and shows characteristics of a classical tumor-suppressor gene. |
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expression and promoter activities of RB1CC1 in developing murine and human tissues; RB1CC1 expression is controlled more stringently by modification at intron 1 in humans than in mice |
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FIP200 increases p21 protein levels via stabilization of its upstream regulator p53 and decreases cyclin D1 protein. Both effects are critical for FIP200-induced G1 arrest and may contribute to the antitumor activities of FIP200 in breast cancer. |
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Rb1cc1 expression is a prerequisite for the induction of RB1 and myosin heavy chain. Rb1cc1 plays a crucial role in muscular differentiation and function. |