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RAS p21 protein activator

GAP, GTPase-activating protein, RasGAP
The protein encoded by this gene is located in the cytoplasm and is part of the GAP1 family of GTPase-activating proteins. The gene product stimulates the GTPase activity of normal RAS p21 but not its oncogenic counterpart. Acting as a suppressor of RAS function, the protein enhances the weak intrinsic GTPase activity of RAS proteins resulting in the inactive GDP-bound form of RAS, thereby allowing control of cellular proliferation and differentiation. Mutations leading to changes in the binding sites of either protein are associated with basal cell carcinomas. Mutations also have been associated with hereditary capillary malformations (CM) with or without arteriovenous malformations (AVM) and Parkes Weber syndrome. Alternative splicing results in two isoforms where the shorter isoform, lacking the N-terminal hydrophobic region but retaining the same activity, appears to be abundantly expressed in placental but not adult tissues. [provided by RefSeq, May 2012] (from NCBI)
Top mentioned proteins: GAP-43, Rhodopsin, CAN, V1a, Actin
Papers using GAP antibodies
The neurite outgrowth multiadaptor RhoGAP, NOMA-GAP, regulates neurite extension through SHP2 and Cdc42
Birchmeier Walter et al., In The Journal of Cell Biology, 2002
... International); anti-Myc (A14), anti-SHP2 (C18), and anti-Trk (C14) antibodies from Santa Cruz Biotechnology, Inc.; Fast-Track anti-NOMA-GAP antibody (AbCam); anti-GFP antibody (Invitrogen); anti-Shc ...
Novel p62dok family members, dok-4 and dok-5, are substrates of the c-Ret receptor tyrosine kinase and mediate neuronal differentiation
Birchmeier Walter et al., In The Journal of Cell Biology, 1999
... Antibodies used were anti-Ret C-19 and anti-rasGAP B4F8 (Santa Cruz Biotechnology, Inc.), anti-Nck and anti-PY ...
Microtubule growth activates Rac1 to promote lamellipodial protrusion in fibroblasts
Pawson Tony et al., In The Journal of Cell Biology, 1998
... ) resulting in pMSCV-GAP or the pCDNA3 vector (Clontech).
A dynamically regulated 14-3-3, Slob, and Slowpoke potassium channel complex in Drosophila presynaptic nerve terminals
Nguyen Trung P. et al., In Journal of Neuroimmune Pharmacology, 1998
... GAP43 (GAP-7B10)Sigma Aldrich ...
Papers on GAP
Defects in autophagy caused by glaucoma-associated mutations in optineurin.
Swarup et al., Hyderābād, India. In Exp Eye Res, Mar 2016
E50K-OPTN-induced block in autophagy is dependent on a GTPase activating protein, TBC1D17.
Constitutive expression and anticancer potency of a novel immunotoxin onconase-DV3.
Sun et al., Changchun, China. In Oncol Rep, Feb 2016
In the present study, we constructed a constitutive expression vector for onconase-(DV3)2 (Onc-DV3) production in yeast Pichia pastoris with the GAP promoter, in which the Onc-DV3 gene is inserted downstream of the truncated Saccharomyces cerevisiae α-mating factor-pre (α-MF-pre) secretion signal.
Expression of aurora kinase A correlates with the Wnt-modulator RACGAP1 in gastric cancer.
Malfertheiner et al., Magdeburg, Germany. In Cancer Med, Feb 2016
There was a direct association of AURKA with Rac GTPase-activating protein 1 (RACGAP1), as well as with CTNBB1 (β-catenin) and CDKN1A as second-order interactors.
Mapping the functional versatility and fragility of Ras GTPase signaling circuits through in vitro network reconstitution.
Lim et al., San Francisco, United States. In Elife, Feb 2016
Distortion by oncogenic Ras alleles was dependent on the balance of positive (GEF) and negative (GAP) regulators in the system.
Simulation and Experimental on the Solvation Interaction between GAP Matrix and Insensitive Energetic Plasticizers in Solid Propellants.
Liu et al., In J Phys Chem A, Feb 2016
UNASSIGNED: Multi-methods of simulation and experimental have been performed to investigate the interaction between glycidyl azide polymer (GAP) matrix and insensitive energetic plasticizers N-butyl-N-(2-nitroxy-ethyl)nitramine (Bu-NENA) and bis(2,2-dinitropropyl)formal/acetal(BDNPF/A).
Multiple copy number variants in a pediatric patient with Hb H disease and intellectual disability.
Varela et al., Buenos Aires, Argentina. In Am J Med Genet A, Feb 2016
PCR-GAP, MLPA and FISH analyses established the cause of the α-thalassemia.
Recurrent inactivating RASA2 mutations in melanoma.
Samuels et al., Israel. In Nat Genet, Dec 2015
Analysis of 501 melanoma exomes identified RASA2, encoding a RasGAP, as a tumor-suppressor gene mutated in 5% of melanomas.
The complexity of the Nrf2 pathway: beyond the antioxidant response.
Kong et al., United States. In J Nutr Biochem, Dec 2015
The stability and cellular distribution of Nrf2 is tightly controlled by its inhibitory binding protein Kelch-like ECH-associated protein 1. Nrf2 signalling is also regulated by posttranslational, transcriptional, translational and epigenetic mechanisms, as well as by other protein partners, including p62, p21 and IQ motif-containing GTPase activating protein 1.
Regulating G protein activity by lipase-independent functions of phospholipase C.
Litosch, Miami, United States. In Life Sci, Oct 2015
It is not known whether GAP/GEF activity is coupled to the lipase activity of PLC, nor is it clear whether or how lipid factors may contribute to this synergistic interaction.
MicroRNA-Based Therapeutic Strategies for Targeting Mutant and Wild Type RAS in Cancer.
Ruppert et al., Morgantown, United States. In Drug Dev Res, Sep 2015
To this end, we discuss the potential for miR-based therapies focused on three prominent miRs including the pan-RAS regulator let-7 and the GAP regulator comprised of miR-206 and miR-21 (miR-206/21).
Epigenetic activation of a cryptic TBC1D16 transcript enhances melanoma progression by targeting EGFR.
Esteller et al., Barcelona, Spain. In Nat Med, Jul 2015
We found a hypomethylation event that reactivates a cryptic transcript of the Rab GTPase activating protein TBC1D16 (TBC1D16-47 kDa; referred to hereafter as TBC1D16-47KD) to be a characteristic feature of the metastatic cascade.
YAP is essential for tissue tension to ensure vertebrate 3D body shape.
Furutani-Seiki et al., Tokyo, Japan. In Nature, Jun 2015
By analysing YAP function in 3D spheroids of human cells, we identify the Rho GTPase activating protein ARHGAP18 as an effector of YAP in controlling tissue tension.
A RASopathy gene commonly mutated in cancer: the neurofibromatosis type 1 tumour suppressor.
Miller et al., Cincinnati, United States. In Nat Rev Cancer, May 2015
The NF1 gene encodes a RAS GTPase-activating protein called neurofibromin and is one of several genes that (when mutant) affect RAS-MAPK signalling, causing related diseases collectively known as RASopathies.
The Rho GTPase Rnd1 suppresses mammary tumorigenesis and EMT by restraining Ras-MAPK signalling.
Giancotti et al., New York City, United States. In Nat Cell Biol, 2015
Rap1 inhibition in turn led to derepression of p120 Ras-GAP, which was able to inhibit Ras.
Physiology of RGS10 in Neurons and Immune Cells.
Tansey et al., Atlanta, United States. In Prog Mol Biol Transl Sci, 2014
Regulator of G protein signaling-10 (RGS10), a GTPase-activating protein (GAP) for Gαi3, Gαq, and Gαz, belongs to the D/R12 subfamily based on the homology within the RGS domain and is one of the smallest RGS proteins, outside the RGS box.
Phenotypic variability in a family with capillary malformations caused by a mutation in the RASA1 gene.
van der Horst et al., Amsterdam, Netherlands. In Eur J Med Genet, 2012
An update of the associated phenotype variability in a family with hereditary capillary malformations caused by a mutation in the RASA1 gene.
Regulator of G protein signaling 6 (RGS6) protein ensures coordination of motor movement by modulating GABAB receptor signaling.
Fisher et al., Iowa City, United States. In J Biol Chem, 2012
establish RGS6 as a key component of GABA(B)R signaling
RASA1 analysis: clinical and molecular findings in a series of consecutive cases.
Bayrak-Toydemir et al., Salt Lake City, United States. In Eur J Med Genet, 2012
multifocal capillary malformations is the key clinical finding to suggest a RASA1 mutation
RASA1 maintains the lymphatic vasculature in a quiescent functional state in mice.
King et al., Ann Arbor, United States. In J Clin Invest, 2012
Data reveal a role for RASA1 as a physiological negative regulator of lymphatic endothelial cell growth that maintains the lymphatic vasculature in a quiescent functional state through its ability to inhibit Ras signal transduction.
Revisiting G3BP1 as a RasGAP binding protein: sensitization of tumor cells to chemotherapy by the RasGAP 317-326 sequence does not involve G3BP1.
Widmann et al., Lausanne, Switzerland. In Plos One, 2010
arguments against G3BP1 being a genuine RasGAP-binding partner
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