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FLASH GENE
Symbol ARHGAP1 contributors: mct/npt - updated : 30-09-2009
HGNC name Rho GTPase activating protein 1
HGNC id 673
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • a proline-rich, Src homology 3 (SH3) binding domain
  • three consensus box regions characteristic of Rho GAP
    • HOMOLOGY
    Homologene
    FAMILY
    CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm
    basic FUNCTION
  • regulating the basal apoptosis of cells through the JNK pathway
  • promotes inactivation of CDC42, a small GTPase whose activation at the leading edge by guanine nucleotide exchange factors is critical for cell migration (Shen 2008)
  • inhibitor of active-state small Rho GTPases and counter-regulatory mediator for tubule formation
  • implicated in the regulation of cell motility, adhesion, proliferation, and apoptosis (Li 2009)
  • regulates the vimentin network through the CDC42-PAK pathway in smooth muscle cells during 5-hydroxytryptamine stimulation (Li 2009)
    • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • interacting with NDL1 (NDLl and ARHGAP1 exhibit leading-edge localization in migrating cells)(Shen 2008)
  • binds NDEL1 to modulate CDC42 activity at the leading edge of migrating cells (Shen 2008))
    • cell & other
    REGULATION
    Other its activity is regulated upon contractile activation, which is mediated by intracellular ROS (Li 2009)
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --low  
    in tubular microvascular endothelial cells
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    ANIMAL & CELL MODELS
    Cdc42GAP-/- mouse embryonic fibroblasts and/or tissues display reduced population doubling, significantly dampened DNA damage repair activity after DNA-damaging agent treatment, accumulated genomic abnormalities, and induction of p53, p16Ink4a, p21Cip1, and senescence-associated beta-galactosidase expressions (Wang 2007)