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FLASH GENE
Symbol RRAD contributors: mct - updated : 23-12-2011
HGNC name Ras-related associated with diabetes
HGNC id 10446
Location 16q22.1      Physical location : 66.955.581 - 66.959.439
Synonym name RAS (RAD and GEM) like GTP binding 3
Synonym symbol(s) RAD, RAD1, REM3
DNA
TYPE functioning gene
STRUCTURE 3.86 kb     5 Exon(s)
10 Kb 5' upstream gene genomic sequence study
regulatory sequence Promoter
Binding site
text structure
  • direct binding of EGR1 to the RRAD promoter region (
  • MAPPING cloned Y linked Y status provisional
    RNA
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    5 - 1467 - 308 - 1996 8781531
    5 - 1476 - 308 - 1996 8781531
    EXPRESSION
    Type widely
       expressed in (based on citations)
    organ(s)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Cardiovascularheart   highly Homo sapiens
    Respiratorylung   highly Homo sapiens
    Visualeye   highly
    tissue
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    Muscularstriatumcardiac highly Homo sapiens
    Muscularstriatumskeletal highly Homo sapiens
    cell lineage
    cell lines
    fluid/secretion
    at STAGE
    PROTEIN
    PHYSICAL PROPERTIES
    STRUCTURE
    motifs/domains
    HOMOLOGY
    intraspecies homolog to GEM, highly
    Homologene
    FAMILY
  • Ras-GTPase activating protein family member
  • k1 Ras oncogene superfamily member
  • RGK (Rem, Rem2, Rad, Gem/Kir) family of monomeric G proteins
  • CATEGORY protooncogene
    SUBCELLULAR LOCALIZATION     plasma membrane
        intracellular
    intracellular,cytoplasm,organelle,mitochondria
    basic FUNCTION
  • may act as an oncogenic protein in breast tissues
  • mediator that inhibits cardiac hypertrophy through the CAMK2B pathway
  • Ras-related GTPase that promotes cell growth by accelerating cell cycle transitions
  • may promote carcinogenesis at least in part by inhibiting CCNDBP1-mediated tumor suppression
  • necessary for trigger cardiomyocyte apoptosis
  • its expression is essential in maintaining normal cardiac function
  • is not only sufficient but also essential for serum deprivation induced apoptosis
  • inhibits vascular lesion formation by reducing the attachment and migration of vascular smooth muscle cells (VSMCs)
  • regulates ventricular action potential duration and excitation-contraction (EC) coupling gain through its ability to inhibit cardiac L-type channel activity
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling signal transduction
  • MAPK14 pathway is the main component in RRAD-mediated apoptosis
  • a component
    INTERACTION
    DNA
    RNA
    small molecule
    protein
  • GTP-binding protein
  • interacting with calmodulin preferentially to the inactive, GDP-form
  • interacts with calmodulin and calmodulin-dependent protein kinase II, leading to inhibition to their downstream signal
  • interaction with NME1 may regulate growth and tumorigenicity of breast cancer
  • CCNDBP1 is a cell cycle-inhibitory molecule, and a binding partner of RRAD (RRAD translocates CCNDBP1 from the nucleus to the cytoplasm, thereby inhibiting the tumor suppressor activity of CCNDBP1, which occurs in the nucleus)
  • inhibits CTGF expression through binding with CEBPD, thus regulating ECM (extracellular matrix) production in the heart
  • cell & other
    REGULATION
    Other its repression leads to QT prolongation and causes ventricular arrhythmias via modulation of CACNB2 in the heart
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --over  
    in non-insulin dependent diabetes mellitus (increasing insulin resistant)
    tumoral     --low  
    in breast cancer cell line with high tumorigenic and metastatic potential
    constitutional     --over  
    in skeletal muscle in a subset of patients with type II diabetes
    constitutional     --over  
    in cardiomyocytes induces cell apoptosis by activation of MAPK14 and inhibition of BCL2L1 expression
    constitutional     --low  
    in failing hearts and plays an important role in attenuating cardiac hypertrophy, and can lead to cardiac fibrosis
    tumoral     --low  
    by epigenetic silencing that is a frequent event in lung and breast cancers
    constitutional germinal mutation      
    RRAD Q66P, a less common variant identified in a cohort of congestive heart failure patients, inhibits Ca2+ currents conducted by cardiac L-type channels (CACNA1C, CACNA1D) as effectively as wild-type RRAD
    Susceptibility to congestive heart failure
    Variant & Polymorphism other RRAD Q66P contributes to cardiomyopathy and congestive heart failure
    Candidate gene
    Marker
    Therapy target
  • mice lacking Rad are more susceptible to the development of hypertrophy in response to thoracic transverse aortic constriction than wild-type mice
  • ANIMAL & CELL MODELS