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Rho family GTPases use the I-BAR proteins, IRSp53 (show BAIAP2 Antibodies) (also known as BAIAP2 (show BAIAP2 Antibodies)), IRTKS and Pinkbar (show BAIAP2L2 Antibodies), as a central mechanism to modulate cell morphology.
IRTKS promoted serum-induced cell migration along with enhanced phosphorylation of mitogen activated kinases Erk1/2 and p38 (show CRK Antibodies), and activation of small GTPases Rac1 (show RAC1 Antibodies) and Cdc42 (show CDC42 Antibodies). In addition, cells overexpressing IRTKS exhibited an increased polarity characterized by elongated cytoplasm and extensive lamellipodia at leading edges.
Upregulation of BAIAP2L1 is associated with ovarian cancer.
Lacking the Bin-Amphiphysin (show AMPH Antibodies)-Rvs (BAR) dimerization domain of BAIAP2L1.
IRTKS can interact with epidermal growth factor receptor (EGFR (show EGFR Antibodies)), results in the phosphorylation of extracellular signal-regulated kinase
Identification of a novel oncogenic FGFR3 (show FGFR3 Antibodies)-BAIAP2L1 fusion protein in bladder cancer.
These data suggest that IRTKS is a novel regulator of p53 (show TP53 Antibodies), modulating low level of MDM2 (show MDM2 Antibodies)-mediated p53 (show TP53 Antibodies) ubiquitination in unstressed cells.
data suggest Src (show SRC Antibodies)-stimulated IRTKS phosphorylation is essential for its function in cell motility
Results describe the NMR structure of insulin receptor tyrosine kinase substrate (IRTKS) SH3 domain (show ITSN1 Antibodies) in complex with a repeat from Escherichia coli-secreted protein F-like protein encoded on prophage U (EspF(U)).
Study characterised IRTKS, which has widespread tissue distribution, is a substrate for the insulin receptor and binds Rac, and expression of IRTKS induces clusters of short actin bundles rather than filopodia-like protrusions.
double knockout of IRSp53 (show BAIAP2 Antibodies) and its closest family member, IRTKS, resulted in exacerbated placental abnormalities, particularly in spongiotrophoblast differentiation and development, giving rise to complete embryonic lethality.
The IRTKS, as an adaptor of the insulin receptor (IR (show INSR Antibodies)), modulates IR-IRS1 (show IRS1 Antibodies)-PI3K-AKT (show AKT1 Antibodies) signaling via regulating the phosphorylation of IR.
IRTKS functions as a negative modulator of excessive inflammation in viral infections.
This gene encodes a member of the IMD (IRSp53/MIM homology domain) family. Members of this family can be subdivided in two groups, the IRSp53-like and MIM-like, based on the presence or absence of the SH3 (Src homology 3) domain. The protein encoded by this gene contains a conserved IMD, also known as F-actin bundling domain, at the N-terminus, and a canonical SH3 domain near the C-terminus, so it belongs to the IRSp53-like group. This protein is the substrate for insulin receptor tyrosine kinase and binds to the small GTPase Rac. It is involved in signal transduction pathways that link deformation of the plasma membrane and remodeling of the actin cytoskeleton. It also promotes actin assembly and membrane protrusions when overexpressed in mammalian cells, and is essential to the formation of a potent actin assembly complex during EHEC (Enterohemorrhagic Escherichia coli) pedestal formation.
BAI1-associated protein 2-like 1
, insulin receptor tyrosine kinase substrate homolog
, insulin receptor tyrosine kinase substrate
, brain-specific angiogenesis inhibitor 1-associated protein 2-like protein 1-like
, BAI1-associated protein 2-like protein 1
, brain-specific angiogenesis inhibitor 1-associated protein 2-like protein 1