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Transcriptional regulation of NOX genes expression in human breast adenocarcinoma cells is modulated by adaptor protein CIN85.
The multiple Src (show SRC Antibodies) homology 3 (SH3) domains of trimeric CIN85 molecules associated with multiple SLP-65 (show BLNK Antibodies) molecules, which recruited further CIN85 trimers, thereby perpetuating the oligomerization process.
these data support a role for the novel PP2Ac (show PPP2CA Antibodies)-CIN85 complex in supporting integrin-dependent platelet function by dampening the phosphatase activity.
CIN85 promotes recycling of TGF-beta (show TGFB1 Antibodies) receptors and thereby positively regulates TGF-beta (show TGFB1 Antibodies) signaling.
we demonstrate that SEPT9 (show SEPT9 Antibodies) negatively regulates EGFR (show EGFR Antibodies) degradation by preventing the association of the ubiquitin ligase Cbl (show CBL Antibodies) with CIN85, resulting in reduced EGFR (show EGFR Antibodies) ubiquitylation
Results support the model that Cbl (show CBL Antibodies)-CIN85-endophilin complex is not required for efficient internalization of EGFR (show EGFR Antibodies), a prototype RTK.
Multiple molecular forms of adaptor protein Ruk/CIN85 specifically associate with different subcellular compartments in human breast adenocarcinoma cell line.
LOX (show LOX Antibodies)-PP interacts with CIN85 via a novel SH3-binding motif and this association reduces CIN85-promoted invasion by breast cancer cells.
an FRS2beta (show FRS3 Antibodies)-CIN85/CD2AP (show Cd2ap Antibodies)-Cbl (show CBL Antibodies) axis for downregulation of ErbB2 (show ERBB2 Antibodies) may regulate ErbB2 (show ERBB2 Antibodies) protein levels in physiological and pathological settings
Data show that EGFR (show EGFR Antibodies) activation leads to a pronounced src (show SRC Antibodies)-mediated tyrosine phosphorylation of CIN85 that subsequently influences EGFR (show EGFR Antibodies) ubiquitination.
Cin85-deficient mother mice had reduced pituitary hormone (show CGA Antibodies) prolactin (show PRL Antibodies) secretion as a result of excessive dopamine signaling in the brain. Their offspring matured normally and produced their own pups; however, nurturing behaviors such as pup retrieval and nursing were strongly inhibited.
competitive analytical gel-filtration chromatography and isothermal titration calorimetry (ITC) results showed that ARAP1 (show ARAP1 Antibodies) could compete with Cbl (show CBL Antibodies) for CIN85 binding, which provides a biochemical basis for the regulatory roles of ARAP1 (show ARAP1 Antibodies) in the CIN85-mediated EGFR (show EGFR Antibodies) internalizing process.
CIN85/RukL is involved in endocytosis of nephrin (show NPHS1 Antibodies) in podocytes under diabetic conditions, causing podocyte depletion and promoting proteinuria. CIN85/RukL expression therefore shows potential to be a novel target for antiproteinuric therapy in diabetes.
Dab1 (show DAB1 Antibodies) mediated the association of CIN85 with ApoER2 (show LRP8 Antibodies) or VLDLR (show VLDLR Antibodies) in neurons.
Data suggest that Ser587 Cin85 phosphomimetic mutant protein shows dramatically reduced binding to Dab1 (show DAB1 Antibodies) (disabled protein 1) (without affecting binding to CapZ (show CAPZA1 Antibodies)).
Sh3kbp1 is SUMOylated by SUMO-1 (show SUMO1 Antibodies), -2, and -3 and that SUMOylation is enhanced in the presence of Cd2ap (show Cd2ap Antibodies).
the interaction between SHIP-1 (show INPP5D Antibodies) and CIN85 might synergistically facilitate the down-regulation of phosphatidylinositol-3,4,5-trisphosphate levels.
Live cell imaging and co-immunoprecipitation experiments confirmed that both SLP65 (show BLNK Antibodies) and CIN85 are both required for the onset and progression phases of B-cell antigen receptor signal transduction.
a B cell-specific deletion of CIN85 led to impaired T cell-independent type II antibody responses in vivo and diminished IKK-beta (show IKBKB Antibodies) activation and cellular responses to B (show TDO2 Antibodies) cell receptor cross-linking in vitro
Coexpression of CIN85/Ruk(L) with CD2AP (show Cd2ap Antibodies) led to a decreased binding of CIN85/Ruk(L) to nephrin (show NPHS1 Antibodies) and podocin, which indicates a functional competition between CD2AP (show Cd2ap Antibodies) and CIN85/Ruk(L).
This gene encodes an adapter protein that contains three N-terminal Src homology domains, a proline rich region and a C-terminal coiled-coil domain. The encoded protein facilitates protein-protein interactions and has been implicated in numerous cellular processes including apoptosis, cytoskeletal rearrangement, cell adhesion and in the regulation of clathrin-dependent endocytosis. Alternate splicing results in multiple transcript variants.
SH3-domain kinase binding protein 1
, SH3 domain-containing kinase-binding protein 1-like
, CD2-binding protein 3
, SH3 domain-containing kinase-binding protein 1
, Src family kinase-binding protein 1
, c-Cbl-interacting protein
, cbl-interacting protein of 85 kDa
, human Src family kinase-binding protein 1
, migration-inducing gene 18
, src-related kinase binding protein-1
, SH3-containing, expressed in tumorigenic astrocytes
, Sh3 containing, expressed in astrocytes
, regulator of ubiquitous kinase
, SH3 domain-containing adapter protein