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The protein encoded by BAIAP2 has been identified as a brain-specific angiogenesis inhibitor (BAI1)-binding protein. De plus, nous expédions BAIAP2 Protéines (9) et beaucoup plus de produits pour cette protéine.
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Human Polyclonal BAIAP2 Primary Antibody pour EIA, IHC (p) - ABIN360705
Fujiwara, Mammoto, Kim, Takai: Rho small G-protein-dependent binding of mDia to an Src homology 3 domain-containing IRSp53/BAIAP2. dans Biochemical and biophysical research communications 2000
Show all 4 references for ABIN360705
Human Polyclonal BAIAP2 Primary Antibody pour IHC (p), WB - ABIN392809
Abbott, Wells, Fallon: The insulin receptor tyrosine kinase substrate p58/53 and the insulin receptor are components of CNS synapses. dans The Journal of neuroscience : the official journal of the Society for Neuroscience 1999
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Human Monoclonal BAIAP2 Primary Antibody pour WB - ABIN1882211
Miyahara, Okamura-Oho, Miyashita, Hoshika, Yamada: Genomic structure and alternative splicing of the insulin receptor tyrosine kinase substrate of 53-kDa protein. dans Journal of human genetics 2003
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Human Polyclonal BAIAP2 Primary Antibody pour WB - ABIN374113
Oda, Shiratsuchi, Nishimori, Inazawa, Yoshikawa, Taketani, Nakamura, Tokino: Identification of BAIAP2 (BAI-associated protein 2), a novel human homologue of hamster IRSp53, whose SH3 domain interacts with the cytoplasmic domain of BAI1. dans Cytogenetics and cell genetics 1999
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 (Montrer GRIN1 Anticorps) dysfunction.
determined the alpha-synuclein (Montrer SNCA Anticorps)-binding domain of beta-III tubulin (Montrer TUBB Anticorps) and demonstrated that a short fragment containing this domain can suppress alpha-synuclein (Montrer SNCA Anticorps) 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 (Montrer CDC42 Anticorps) to the CRIB (Montrer SCRIB Anticorps)-PR and effector proteins, such as the tumor-promoting factor Eps8 (Montrer EPS8 Anticorps), to the SH3 domain (Montrer ITSN1 Anticorps).
LIN7 is a novel regulator of IRSp53.
mDia1 and WAVE2 (Montrer WASF2 Anticorps) are important Src (Montrer SRC Anticorps) 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.
A molecular dynamics study of the interaction between domain I-BAR of the IRSp53 protein and negatively charged membranes
CDC42 activation inhibits this activity and promotes IRSp53-dependent recruitment and clustering of VASP to drive actin assembly.
VASP (Montrer VASP Anticorps) physically interacted with IRSp53 in NIH-Src (Montrer SRC Anticorps) 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 (Montrer EPS8 Anticorps), not only affects cell migration but also dictates cellular growth in cancer cells.
IRSp53 and spinophilin (Montrer PPP1R9B Anticorps) regulate localized Rac (Montrer AKT1 Anticorps) 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 (Montrer ABI1 Anticorps), is involved in a more complex and tight regulation of WAVE2 (Montrer WASF2 Anticorps) 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 (Montrer CDC42 Anticorps) and the Cdc42 effector (Montrer FNBP1L Anticorps) 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