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The protein encoded by BAIAP2 has been identified as a brain-specific angiogenesis inhibitor (BAI1)-binding protein. Additionally we are shipping BAIAP2 Antibodies (125) and BAIAP2 Proteins (11) and many more products for this protein.
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Overexpression of LIN7 (show LIN7A ELISA Kits) or IRSp53 did not prevent the formation of hyperfused mitochondria in cells coexpressing the Drp1 (show CRMP1 ELISA Kits) K38A mutant, thus suggesting that LIN7 (show LIN7A ELISA Kits)-IRSp53 complex requires functional Drp1 (show CRMP1 ELISA Kits) to regulate mitochondrial morphology.
Results suggest the hypothesis that defective actin/membrane modulation in IRSp53-deficient dendritic spines may lead to social and cognitive deficits through N-methyl-d-aspartate receptor (show GRIN1 ELISA Kits) dysfunction.
determined the alpha-synuclein (show SNCA ELISA Kits)-binding domain of beta-III tubulin (show TUBB ELISA Kits) and demonstrated that a short fragment containing this domain can suppress alpha-synuclein (show SNCA ELISA Kits) accumulation in the primary cultured cells
BAIAP2 is related to emotional modulation of human memory strength.
These above results indicated the possible involvement of BAIAP2 in the etiology of attention deficit disorder with hyperactivity, especially ADHD-I.
IRSp53 adopts a closed inactive conformation that opens synergistically with the binding of human Cdc42 (show CDC42 ELISA Kits) to the CRIB (show SCRIB ELISA Kits)-PR and effector proteins, such as the tumor-promoting factor Eps8 (show EPS8 ELISA Kits), to the SH3 domain (show ITSN1 ELISA Kits).
LIN7 (show LIN7A ELISA Kits) is a novel regulator of IRSp53.
mDia1 and WAVE2 (show WASF2 ELISA Kits) are important Src (show SRC ELISA Kits) homology 3 domain partners of IRSp53 in forming filopodia.
Structural basis for complex formation between human IRSp53 and the translocated intimin receptor Tir of enterohemorrhagic E. coli
Studied generation of filopodia with regards to the dynamic interaction established by Eps8, IRSp53 and VASP with actin filaments.
CDC42 activation inhibits this activity and promotes IRSp53-dependent recruitment and clustering of VASP to drive actin assembly.
VASP (show VASP ELISA Kits) physically interacted with IRSp53 in NIH-Src (show SRC ELISA Kits) cells and was essential for podosome formation.
propose that IRSp53 is a negative regulator of myogenic differentiation which correlates with the observed down regulation of IRSp53 expression during myoblast differentiation to myotubes
IRSp53, through its interaction with Eps8 (show EPS8 ELISA Kits), not only affects cell migration but also dictates cellular growth in cancer cells.
IRSp53 and spinophilin (show PPP1R9B ELISA Kits) regulate localized Rac (show AKT1 ELISA Kits) activation by T-lymphocyte invasion and metastasis protein 1
In cells spread well on a laminin substrate, IRSp53 was localised at the tips of both lamellipodia and filopodia and in in living cells during protrusion.
Rac1, along with IRSp53 and Abi1 (show ABI1 ELISA Kits), is involved in a more complex and tight regulation of WAVE2 (show WASF2 ELISA Kits) than one operating solely through membrane localization.
Consistent with altered synaptic plasticity, IRSp53-deficient mice exhibit cognitive deficits in the contextual fear-conditioning paradigm
Formation of filopodia is dependent on the Rho family GTPase Cdc42 (show CDC42 ELISA Kits) and the Cdc42 effector (show FNBP1L ELISA Kits) IRSp53 (Baiap2).
The protein encoded by this gene has been identified as a brain-specific angiogenesis inhibitor (BAI1)-binding protein. This adaptor protein links membrane bound G-proteins to cytoplasmic effector proteins. This protein functions as an insulin receptor tyrosine kinase substrate and suggests a role for insulin in the central nervous system. It also associates with a downstream effector of Rho small G proteins, which is associated with the formation of stress fibers and cytokinesis. This protein is involved in lamellipodia and filopodia formation in motile cells and may affect neuronal growth-cone guidance. This protein has also been identified as interacting with the dentatorubral-pallidoluysian atrophy gene, which is associated with an autosomal dominant neurodegenerative disease. Alternative splicing results in multiple transcript variants encoding distinct isoforms.
BAI1-associated protein 2
, brain-specific angiogenesis inhibitor 1-associated protein 2-like
, brain-specific angiogenesis inhibitor 1-associated protein 2
, fas ligand-associated factor 3
, insulin receptor substrate p53/p58
, insulin receptor substrate protein of 53 kDa
, BAI-associated protein 2
, insulin receptor substrate 53
, insulin receptor substrate p53
, insulin receptor tyrosine kinase substrate protein p53
, insulin recptor substrate p53
, insulin receptor tyrosine kinase 53 kDa substrate