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FLASH GENE
Symbol RASD2 contributors: mct/npt - updated : 03-06-2015
HGNC name RASD family, member 2
HGNC id 18229
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
3 - 3047 - 266 - 2004 14724584
EXPRESSION
Type
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Nervousbrainforebraincerebral cortex   Homo sapiens
 brainbasal nucleistriatum highly Homo sapiens
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Connectivecartilage   
cells
SystemCellPubmedSpeciesStageRna symbol
Nervousneuron Homo sapiens
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
  • an extended variable domain in the C-terminal region (Vargiu 2004)
  • mono polymer monomer
    HOMOLOGY
    interspecies homolog to murine Rasd2 (95.1pc)
    homolog to rattus Rasd2 (95.1pc)
    Homologene
    FAMILY
  • small GTPase superfamily
  • ras family
  • RasD family
  • CATEGORY regulatory
    SUBCELLULAR LOCALIZATION     plasma membrane
    basic FUNCTION
  • may be playing a role in mediating signal transduction
  • GTPase activity
  • may be involved in mediating the insulin secretory response to efaroxan
  • impairs the activation of the cAMP/PKA pathway by thyroid-stimulating hormone, and by an activated beta2 adrenergic receptor by a mechanism that suggests uncoupling of the receptor to its cognate heterotrimeric complex (Vargiu 2004)
  • involvement of Rhes in cAMP/PKA signalling pathway, at a level proximal to the activation of heterotrimeric G-protein complex
  • is an important modulator of dopaminergic transmission in the striatum
  • small monomeric G protein which functions in a variety of cellular processes, including attenuation of G protein-coupled receptor (GPCR) signalling (Hill 2009)
  • is likely a novel striatal regulator of the AKT-mediated pathway in the striatum
  • acts as an E3 ligase for attachment of SUMO (small ubiquitin-like modifier)
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • with RASD1, RASD2 define a new group of Ras-like monomeric G proteins (Thapliyal 2008)
  • INTERACTION
    DNA
    RNA
    small molecule nucleotide,
  • GTP binding
  • protein
  • binding to mHtt (mutant Huntingtin) and induces sumoylation leading to the cytotoxicity (Subramaniam 2009)
  • binds to and activates PI3K (Vargiu 2004)
  • binds selectively to GNB1, GNB2 and GNB3 subunits (Hill 2009)
  • RASD1 with RASD2 modulate Ca(2+) influx through Ca(V)2.2 channels under more physiological conditions and thereby influence Ca(2+)-dependent events such as neurosecretion (Thapliyal 2008)
  • binds directly to both E1 and UBE2I, enhancing cross-sumoylation as well as thioester transfer from E1 to UBE2I
  • also binds and activates MTOR, enhancing its influence on protein synthesis, and may be the principal determinant of striatal MTOR activation
  • exerts some of its effects by interacting with G(alpha) i
  • striatal-specific protein, binding to and activates MTOR
  • interacts with PIK3R1, the regulatory subunit of PI3K
  • may be a co-factor with mutant huntingtin in cell death
  • robustly binds the autophagy regulator BECN1, decreasing its inhibitory interaction with BCL2 independent of MAPK8 signaling
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    neurologyneurodegenerativehuntington chorea
    drugs that block or inhibit the actions of RASD2 may be useful as the first treatments for Huntington disease
    ANIMAL & CELL MODELS
  • Rhes -/- mice weighed less than wild type mice and displayed minor behavioral abnormalities (Spano 2004)
  • Rhes(-/-) mice showed reduced striatal MTOR signaling and diminished dyskinesia, but maintained motor improvement on L-DOPA treatment
  • Rhes-deleted mice are dramatically protected from neurodegeneration and motor dysfunction in mouse models of Huntington disease