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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

G protein-coupled receptor kinase interacting ArfGAP 1

mediates beta2-adrenergic receptor endocytosis [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: paxillin, p16, CAN, Akt, V1a
Papers using GIT1 antibodies
A GIT1/PIX/Rac/PAK signaling module regulates spine morphogenesis and synapse formation through MLC
Curtis Ivan de et al., In Biology of the Cell, 2004
... sequences corresponding to the following DNA sequences: 5′-CAACAGGAATGACAATCAC-3′ for rat βPIX and 5′-GCACTCAGCAACCGGCTCT-3′ for rat GIT1 (MWG-Biotech AG) (Zhang et al., 2005); 5′-CTGAGTACTCCTCGACACGAA-3′ for rat GIT2 (Qiagen); 5′-CAUCACGTACGCGGAATAC-3′ for luciferase (Invitrogen) ...
ProFound: an expert system for protein identification using mass spectrometric peptide mapping information.
Parsons Maddy, In PLoS ONE, 1999
... Polyclonal antibodies (pAb) anti-FLAG and anti-actin (Sigma-Aldrich); anti-FAK and anti-GIT1 (Santa Cruz Biotechnology, Santa Cruz, CA); pAbs ...
Papers on GIT1
Cyclic Nucleotide-dependent Protein Kinases Target ARHGAP17 and ARHGEF6 Complexes in Platelets.
Smolenski et al., Dublin, Ireland. In J Biol Chem, Jan 2016
Furthermore, we show that ARHGEF6 is constitutively linked to GIT1, a GAP of Arf family small G proteins, and that ARHGEF6 phosphorylation enables binding of the 14-3-3 adaptor protein to the ARHGEF6/GIT1 complex.
Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse.
Young et al., Jupiter, United States. In Neuron, Jan 2016
Here, we demonstrate that presynaptic deletion of the two G protein-coupled receptor kinase-interacting proteins (GITs), GIT1 and GIT2, at the mouse calyx of Held leads to a large increase in AP-evoked release with no change in the readily releasable pool size.
GIT1 promotes lung cancer cell metastasis through modulating Rac1/Cdc42 activity and is associated with poor prognosis.
Hsiao et al., Taipei, Taiwan. In Oncotarget, Dec 2015
G-protein-coupled receptor kinase interacting protein 1 (GIT1) is participated in cell movement activation, which is a fundamental process during tissue development and cancer progression.
MiR-138 inhibits cell proliferation and reverses epithelial-mesenchymal transition in non-small cell lung cancer cells by targeting GIT1 and SEMA4C.
Tang et al., Guangzhou, China. In J Cell Mol Med, Sep 2015
Then the targeting connections of miR-138 with G-protein-coupled receptor kinase-interacting protein 1 (GIT1) and semaphorin 4C (SEMA4C) were confirmed by dual luciferase reporter assays.
Inhibiting the Recruitment of PLCγ1 to Kaposi's Sarcoma Herpesvirus K15 Protein Reduces the Invasiveness and Angiogenesis of Infected Endothelial Cells.
Schulz et al., Hannover, Germany. In Plos Pathog, Aug 2015
We identified βPIX, GIT1 and cdc42, downstream effectors of PLCγ1 in cell migration, as K15 interacting partners and as contributors to KSHV-triggered invasiveness.
The molecular genetic architecture of attention deficit hyperactivity disorder.
Bellgrove et al., Melbourne, Australia. In Mol Psychiatry, Mar 2015
Candidate gene associations of minor effect size have been replicated across a number of genes including SLC6A3, DRD5, DRD4, SLC6A4, LPHN3, SNAP-25, HTR1B, NOS1 and GIT1.
Tyrosyl phosphorylated serine-threonine kinase PAK1 is a novel regulator of prolactin-dependent breast cancer cell motility and invasion.
Diakonova et al., Toledo, United States. In Adv Exp Med Biol, 2014
Tyrosyl phosphorylated PAK1 facilitates PRL-dependent motility via at least two mechanisms: formation of paxillin/GIT1/βPIX/pTyr-PAK1 complexes resulting in increased adhesion turnover and phosphorylation of actin-binding protein filamin A. Increased adhesion turnover is the basis for cell migration and phosphorylated filamin A stimulates the kinase activity of PAK1 and increases actin-regulating activity to facilitate cell motility.
GIT1 is a novel prognostic biomarker and facilitates tumor progression via activating ERK/MMP9 signaling in hepatocellular carcinoma.
Zheng et al., Shanghai, China. In Onco Targets Ther, 2014
AIM: Multiple studies have revealed that G-protein-coupled receptor kinase-interacting protein 1 (GIT1) is overexpressed in many cancers and facilitates tumor progression.
Role of G protein-coupled receptor kinases in cell migration.
Mayor et al., Madrid, Spain. In Curr Opin Cell Biol, 2014
In addition to its well-established role in the desensitization of G protein-coupled receptors involved in chemotaxis, GRK2 can play an effector role in the organization of actin and microtubule networks and in adhesion dynamics, by means of novel substrates and transient interacting partners, such as the GIT1 scaffold or the cytoplasmic α-tubulin deacetylase histone deacetylase 6 (HDAC6).
The adaptor protein and Arf GTPase-activating protein Cat-1/Git-1 is required for cellular transformation.
Cerione et al., Ithaca, United States. In J Biol Chem, 2012
novel roles for Cat-1 and its interactions with the Arf GTPases and paxillin in oncogenic transformation.
Phosphorylation of GIT1 tyrosine 321 is required for association with FAK at focal adhesions and for PDGF-activated migration of osteoblasts.
Yin et al., Nanjing, China. In Mol Cell Biochem, 2012
Phosphorylation of tyrosine 321 of GIT1 is necessary for PDGF-induced association with FAK, FAK activation in focal adhesions, and for osteoblastic cell migration.
G-protein-coupled receptor kinase interactor-1 (GIT1) is a new endothelial nitric-oxide synthase (eNOS) interactor with functional effects on vascular homeostasis.
Rockey et al., Dallas, United States. In J Biol Chem, 2012
We have identified a novel eNOS interactor, G-protein-coupled receptor (GPCR) kinase interactor-1 (GIT1), which plays an unexpected role in GPCR stimulated nitric oxide signaling.
G protein coupled receptor kinase 2 interacting protein 1 (GIT1) is a novel regulator of mitochondrial biogenesis in heart.
Berk et al., Rochester, United States. In J Mol Cell Cardiol, 2011
G protein coupled receptor kinase 2 interacting protein 1 (GIT1) is a novel regulator of mitochondrial biogenesis in heart.
GIT1 is associated with ADHD in humans and ADHD-like behaviors in mice.
Kim et al., Taejŏn, South Korea. In Nat Med, 2011
Git1-deficient mice show ADHD-like phenotypes, with traits including hyperactivity, enhanced electroencephalogram theta rhythms and impaired learning and memory.
Robo4-dependent Slit signaling stabilizes the vasculature during pathologic angiogenesis and cytokine storm.
Li et al., Salt Lake City, United States. In Curr Opin Hematol, 2011
Upon Robo4 activation by Slit, paxillin is recruited to the cytoplasmic domain along with an ArfGAP known as GIT1.
Slit2-Robo4 signalling promotes vascular stability by blocking Arf6 activity.
Li et al., Salt Lake City, United States. In Nat Cell Biol, 2009
Formation of a Robo4-paxillin complex at the cell surface blocks activation of the small GTPase Arf6 and, consequently, Rac by recruitment of Arf-GAPs (ADP-ribosylation factor- directed GTPase-activating proteins) such as GIT1.
Transport and metabolism of glycerophosphodiesters produced through phospholipid deacylation.
Patton-Vogt, Pittsburgh, United States. In Biochim Biophys Acta, 2007
A permease encoded by the GIT1 gene imports extracellular glycerophosphodiesters across the plasma membrane, where their hydrolytic products can provide crucial nutrients such as inositol, choline, and phosphate to the cell.
Dynamic recruitment of PAK1 to the immunological synapse is mediated by PIX independently of SLP-76 and Vav1.
Weiss et al., San Francisco, United States. In Nat Immunol, 2005
In addition, PAK1, PIX and GIT1 were recruited to the T cell-antigen-presenting cell contact site independently of SLP-76 and Vav1.
p95-APP1 links membrane transport to Rac-mediated reorganization of actin.
de Curtis et al., Milano, Italy. In Nat Cell Biol, 2000
Here we show that p95-APP1 (ArfGAP-putative, Pix-interacting, paxillin-interacting protein 1), a member of the GIT1/PKL family, is part of a complex that interacts with Rac.
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