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RICS is a neuron-associated GTPase-activating protein that may regulate dendritic spine morphology and strength by modulating Rho GTPase (see RHOA\; MIM 165390) activity (Okabe et al., 2003 [PubMed 12531901]).[supplied by OMIM, Mar 2008].. Additionally we are shipping and many more products for this protein.
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Cdh1-APC together with the RhoA regulators p250GAP and Smurf1 controls axon growth in the mammalian brain
the p250GAP gene might be a new candidate gene for susceptibility to schizophrenia.
The PX-RICS-14-3-3zeta/theta complex couples N-cadherin-beta-catenin with dynein-dynactin to mediate its export from the endoplasmic reticulum.
These results suggest that Grit, a novel TrkA-interacting protein, regulates neurite outgrowth by modulating the Rho family of small GTPases.
involvement in the regulation of neurite outgrowth by exerting its RhoGAP activity and that its cellular activity may be regulated through interaction with Src-like tyrosine kinases
This article analyzes Rac activation during live neutrophil chemotaxis.
RICS may regulate dendritic spine morphology and strength by modulating Rho GTPases
is phosphorylated by Fyn in oligodendrocytes
GC-GAP may play a role in dendritic morphogenesis and also possibly in neural/glial cell proliferation
p250GAP may be involved in NMDA receptor activity-dependent actin reorganization in dendritic spines
Results suggest that a splice variant of RICS, PX-RICS, is involved in early brain development including extension of axons and dendrites, and postnatal remodeling and fine-tuning of neural circuits.
Results suggest that PX-RICS ensures the efficient entry of the N-cadherin/beta-catenin complex into the secretory pathway, and thereby regulates the amount of N-cadherin available for cell adhesion and FGFR4-mediated signaling.
miR132-p250GAP pathway plays a key role in activity-dependent structural and functional plasticity.
Our results suggest that PX-RICS-mediated GABAAR trafficking is a key target for GABAergic plasticity and its dysfunction leads to atypical emotional processing underlying autism.
PX-RICS-deficient mice exhibit ASD-like social behaviours and ASD-related comorbidities. PX-RICS-deficient neurons show reduced surface gamma-aminobutyric acid type A receptor (GABAAR) levels and impaired GABAAR-mediated synaptic transmission.
leptin stimulates the MAPK pathways and CREB dependent transcription. This then leads to an increase in miR132 that suppresses expression of the Rac1 inhibitor p250GAP, thus activating Rac1 and promoting synaptogenesis.
Overexpression of p250GAP abolishes brain-derived neurotrophic factor (BDNF)-induced branching.
RICS may regulate dendritic spine morphology and strength by modulating Rho GTPases [RICS]
RICS plays an important role in neurite extension
p200 RhoGAP can mediate cross-talks between Ras- and Rho-regulated signaling pathways in cell growth regulation
These results suggest that PX-RICS is involved in early brain development including extension of axons and dendrites, and postnatal remodeling and fine-tuning of neural circuits.
p250GAP plays an important role in NMDA receptor-mediated regulation of RhoA activity leading to spine morphological plasticity.
RICS is a neuron-associated GTPase-activating protein that may regulate dendritic spine morphology and strength by modulating Rho GTPase (see RHOA\; MIM 165390) activity (Okabe et al., 2003
GAB-associated CDC42 , GAB-associated Cdc42/Rac GTPase-activating protein , GTPase regulator interacting with TrkA , GTPase-activating protein for Cdc42 and Rac1 , RhoGAP involved in the -catenin-N-cadherin and NMDA receptor signaling , brain-specific Rho GTP-ase-activating protein , brain-specific Rho GTPase-activating protein , rac GTPase activating protein , rho GTPase-activating protein 32 , rho-type GTPase-activating protein 32 , rho/Cdc42/Rac GTPase-activating protein RICS , rhoGAP involved in the beta-catenin-N-cadherin and NMDA receptor signaling , Rho GTPase activating protein 33 pseudogene , Rho GTPase-activating protein