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GTPase-activating protein for RAC1 and perhaps Cdc42, but not for RhoA small GTPase. Zusätzlich bieten wir Ihnen SRGAP3 Antikörper (30) und und viele weitere Produktgruppen zu diesem Protein an.
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SrGAP3 plays a role in neurodevelopmental disorders.
This study found a more than 15-fold enlargement of the lateral ventricles of homozygous SrGAP3-deficient mice.
SrGAP3 dynamically regulates neuronal cytoskeletal reorganization through inhibition of the Rho GTPase Rac1 and interaction with actin remodeling proteins.
The inverse F-BAR domain protein srGAP2 acts through srGAP3 to modulate neuronal differentiation and neurite outgrowth of mouse neuroblastoma cells.
Disruption of wave-associated Rac GTPase-activating protein (Wrp) leads to abnormal adult neural progenitor migration associated with hydrocephalus
These results show neurodevelopmental aberration in Srgap3(-/-) mice, with many of the observed phenotypes matching several schizophrenia-related intermediate phenotypes. Mutations of SRGAP3 may thus contribute to various neurodevelopmental disorders.
Following sciatic nerve transection, srGAP3 in neurons is significantly increased in the ipsilateral relative to contralateral dorsal root ganglions, which peak at day 7 to day 14.
srGAP3 is an inhibitor of actin dynamics and lamellipodia formation in primary fibroblasts. srGAP3 influences focal adhesion formation through the downregulation of Rac1.
Data suggest a role for srGAP3 in the lateral positioning of post crossing axons within the ventrolateral funiculus.
srGAP3 could regulate neuronal differentiation in a Rac1-dependent manner.
Results from these studies confirm that loss of WRP is linked to impaired learning and memory.
Both Slit and Netrin-1 contribute to floor plate-derived chemorepulsion of cranial motor axons.
WRP anchoring to WAVE-1 is a homeostatic mechanism that contributes to neuronal development and the fidelity of synaptic connectivity.
Expression of Robo/Slit and Semaphorin/Plexin/Neuropilin family members in the developing hypothalamic paraventricular and supraoptic nuclei.
Data show that compared to srGAP2 and srGAP3, the onset of srGAP1 expression is later in most CNS tissues in mouse.
A single PXXP motif in the C-terminal region of srGAP3 mediates binding to multiple SH3 domains.
Nuclear-localized srGAP3 interacts with Brg1. This interaction is mediated by the C-terminal of srGAP3 and the ATPase motif of Brg1.
deletion of SRGAP3 provides the most convincing explanation for our patient's phenotype, and our observations lend further weight to a causative role of SRGAP3 haploinsufficiency in mental retardation.
conclude that srGAP3 has tumor suppressor-like activity in HMECs, likely through its activity as a negative regulator of Rac1
putative role in severe mental retardation
Data suggest that MEGAP negatively regulates cell migration by perturbing the actin and microtubule cytoskeleton and by hindering the formation of focal complexes.
We found no association between SRGAP3/MEGAP haploinsufficiency and mental retardation.
Current evidence suggests that SRGAP3 is the major determinant of mental retardation in distal 3p deletions.
FNBP2, ARHGAP13, ARHGAP14 and ARHGAP4 constitute the FNBP2 family characterized by FCH, RhoGAP and SH3 domains.
GTPase-activating protein for RAC1 and perhaps Cdc42, but not for RhoA small GTPase. May attenuate RAC1 signaling in neurons.
SLIT-ROBO Rho GTPase activating protein 2
, SLIT-ROBO Rho GTPase-activating protein 3
, WAVE-associated Rac GTPase-activating protein
, brain stress early protein Gbi
, rho GTPase activating protein 14
, rho GTPase-activating protein 14
, WAVE-associated Rac GTPase activating protein
, mental disorder-associated GAP
, SLIT-ROBO Rho GTPase activating protein 2 L homeolog