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The protein encoded by RB1CC1 interacts with signaling pathways to coordinately regulate cell growth, cell proliferation, apoptosis, autophagy, and cell migration. Additionally we are shipping RB1CC1 Antibodies (63) and and many more products for this protein.
MiR (show MLXIP ELISA Kits)-20a and miR (show MLXIP ELISA Kits)-20b negatively regulate autophagy by targeting RB1CC1/FIP200 in breast cancer cells
RB1CC1 has been implicated in cell cycle progression, cell growth, cell proliferation, cell survival, cell spreading/migration and neurodegeneration.
miR (show MLXIP ELISA Kits)-133b targeted and downregulated RB1CC1 in prostate cancer cells.
RB1CC1 knockdown in PC3 (show PCSK1 ELISA Kits) cells enhances clonal growth in vitro and tumor growth in vivo.
Liver-specific deficiency of FIP200 leads to chronic liver injury associated with fibrosis and inflammation.
The APC (show APC ELISA Kits)-independent beta-catenin (show CTNNB1 ELISA Kits) degradation by FIP200 suggests a role for FIP200 in tumor suppression in the presence of APC (show APC ELISA Kits) dysfunction.
Interaction between FIP200 and ATG16L1 (show ATG16L1 ELISA Kits) distinguishes ULK1 (show ULK1 ELISA Kits) complex-dependent and -independent autophagy.
Nuclear expression of RB1CC1 predicts a better clinical outcome and is useful in the follow-up of salivary gland cancers.
analysis of preparation of the monoclonal antibody for RB1CC1
RB1CC1 protein suppresses type II collagen (show COL2A1 ELISA Kits) synthesis in chondrocytes and causes dwarfism
residues 582-585 (LQFL) in FIP200 are required for interaction with Atg13 (show ATG13 ELISA Kits), and mutation of these residues to AAAA (designated the FIP200-4A mutant) abolished its canonical autophagy function in vitro.
Deletion of autophagy inducer RB1CC1 results in degeneration of the retinal pigment epithelium
Data indicate that fip200 protein deficiency was responsible for high mobility group (show SSRP1 ELISA Kits) protein HMGB1 (show HMGB1 ELISA Kits) translocation in alveolar macrophage MH-S cells.
these data identify FIP200 as an important regulator of bone development.
Fip200 regulates Atg16L1 (show ATG16L1 ELISA Kits) membrane targeting via direct interaction with Atg16L1 (show ATG16L1 ELISA Kits).
The data of this study revealed that FIP200-mediated autophagy contributes to the maintenance and functions of NSCs through regulation of oxidative state.
these results identify a new function for FIP200 in the regulation of DNA damage response and cell survival through its activity in autophagy
RB1CC1 thus appears to play a unique role as a modulator of TGF-beta (show TGFB1 ELISA Kits) signaling by restricting substrate specificity of Arkadia (show RNF111 ELISA Kits).
Deletion of FIP200 resulted in multiple autophagy defects including accumulation of ubiquitinated protein aggregates and p62/SQSTM1 (show SQSTM1 ELISA Kits), deficient LC3 (show MAP1LC3A ELISA Kits) conversion, and increased number of mitochondria with abnormal morphology in tumor cells
The protein encoded by this gene interacts with signaling pathways to coordinately regulate cell growth, cell proliferation, apoptosis, autophagy, and cell migration. This tumor suppressor also enhances retinoblastoma 1 gene expression in cancer cells. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
RB1-inducible coiled-coil 1
, Rb1-inducible coiled coil protein 1
, Rb1-inducible coiled coil protein 1-like
, RB1-inducible coiled-coil protein 1-like
, 200 kDa FAK family kinase-interacting protein
, FAK family kinase-interacting protein of 200 kDa
, RB1-inducible coiled-coil protein 1
, coiled coil forming protein 1
, coiled-coil-forming protein 1