Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all species
Show all synonyms
Select your species and application
anti-Human RB1CC1 Antibodies:
anti-Mouse (Murine) RB1CC1 Antibodies:
anti-Rat (Rattus) RB1CC1 Antibodies:
Go to our pre-filtered search.
Human Polyclonal RB1CC1 Primary Antibody for IP, WB - ABIN262229
Jung, Jun, Ro, Kim, Otto, Cao, Kundu, Kim: ULK-Atg13-FIP200 complexes mediate mTOR signaling to the autophagy machinery. in Molecular biology of the cell 2009
Show all 3 Pubmed References
Human Polyclonal RB1CC1 Primary Antibody for IF (p), IHC (p) - ABIN872758
Xue, Xue, Zhang, Li, Jiang: miR-130b-3p/301b-3p negatively regulated Rb1cc1 expression on myogenic differentiation of chicken primary myoblasts. in Biotechnology letters 2017
RB1CC1 was shown to target ZBTB38 to initiate autophagy in spinal cord injury.
These findings suggested that PHF8 played an oncogenic role in facilitating FIP200-dependent autophagic degradation of E-cadherin, EMT and metastasis in hepatocellular carcinoma (HCC). PHF8 might be a promising target for prevention, treatment and prognostic prediction of HCC.
miR-224-3p regulates autophagy in hrHPV-induced cervical cancer cells through targeting FIP200 expression.
Data suggest that, in patients with diabetic kidney disease, urinary excretion of mRNAs for MAP1LC3A, WIPI2, and RB1CC1 is down-regulated as compared to healthy control subjects; these transcripts may serve as urinary autophagy biomarkers. (MAP1LC3A = microtubule associated protein 1 light chain 3; WIPI2 = WD repeat domain phosphoinositide-interacting protein 2; RB1CC1 = RB1 inducible coiled-coil 1)
This is the first report demonstrating that polymorphisms in the autophagy-related FIP200 gene may predict hypertension in patients with mCRC treated with FOLFIRI and bevacizumab.
MiR-20a and miR-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-133b targeted and downregulated RB1CC1 in prostate cancer cells.
RB1CC1 knockdown in PC3 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-independent beta-catenin degradation by FIP200 suggests a role for FIP200 in tumor suppression in the presence of APC dysfunction.
Interaction between FIP200 and ATG16L1 distinguishes ULK1 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 synthesis in chondrocytes and causes dwarfism
p53 regulates autophagy through a direct molecular interaction with RB1CC1/FIP200, a protein that is essential for the very apical step of autophagy initiation.
RB1CC1 activates the expression of p16 (also called INK4a/CDKN2a) through the activation of its promoter. RB1CC1 essentially requires binding with hSNF5 to activate the p16 promoter.
RB1CC1 thus appears to play a unique role as a modulator of TGF-beta signaling by restricting substrate specificity of Arkadia.
downregulation of FIP200 protein in glioblastoma tumor cells, astrocytes, and brain microvessel endothelial cells promotes apoptosis, most likely due to the removal of a direct interaction of FIP200 with Pyk2 that inhibits Pyk2 activation
RB1CC1, RB1 and p53 have prognostic roles in breast cancer in Japanese patients
Genetic FIP200 protein deletion impairs autophagy induction and causes T cell apoptosis.
Suggest that autophagy gene FIP200 plays a crucial role in regulating neurogenesis and restricting local immune response in postnatal neural stem cells through non-cell autonomous mechanisms.
residues 582-585 (LQFL) in FIP200 are required for interaction with Atg13, 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 protein HMGB1 translocation in alveolar macrophage MH-S cells.
these data identify FIP200 as an important regulator of bone development.
Fip200 regulates Atg16L1 membrane targeting via direct interaction with Atg16L1.
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
Deletion of FIP200 resulted in multiple autophagy defects including accumulation of ubiquitinated protein aggregates and p62/SQSTM1, deficient LC3 conversion, and increased number of mitochondria with abnormal morphology in tumor cells
data identify FIP200 as a key intrinsic regulator of fetal hematopoietic stem cells
FIP200 has a role in the regulation of neuronal homeostasis through its function in autophagy in vivo
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
FIP200 (Rb1cc1, RB1CC1) is shown to interact with the TSC1-TSC2 complex and this interaction leads to increased S6K activity and cell growth.
FIP200 functions as a regulatory node to couple two important signaling pathways to regulate cell growth and survival during mouse embryogenesis.
RB1CC1 insufficiency causes neuronal atrophy through mTOR signaling alteration.
Rb1cc1 is a target gene of ERRalpha, driven by a novel type of recognition sequence.
provide the first evidence for the existence of a close-spatially controlled-mode of regulation of FIP200 and PIASy nucleocytoplasmic functions
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