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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
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
    Physical map
    LOC390736 16 similar to Spermatogenesis associated protein 2 (Spermatogenesis associated protein PD1) TK2 16q22 thymidine kinase 2, mitochondrial FLJ20006 16q22.1 hypothetical protein FLJ20006 CKLF 16q22.1 chemokine-like factor CKLFSF1 16q22.1 chemokine-like factor super family 1 CKLFSF2 16q22.1 chemokine-like factor super family 2 CKLFSF3 16q22.1 chemokine-like factor super family 3 CKLFSF4 16q22.1 chemokine-like factor super family 4 DNCLI2 16q22.1 dynein, cytoplasmic, light intermediate polypeptide 2 FLJ35894 16q22.1 hypothetical protein FLJ35894 APPBP1 16q22 amyloid beta precursor protein binding protein 1, 59kDa CA7 16q22.1 carbonic anhydrase VII KIAA1348 CDH16 16q22.1 cadherin 16, KSP-cadherin RRAD 16q22 Ras-related associated with diabetes CGI-128 16q22.1-q22.3 CGI-128 protein CES2 16q22.1 carboxylesterase 2 (intestine, liver) FLJ21736 16q22.1 esterase 31 FLJ37464 16q22.1 hypothetical protein FLJ37464 CBFB 16q22.1 core-binding factor, beta subunit Lin10 16q22.1 lin-10 protein homolog MGC4655 16q22.1 hypothetical protein MGC4655 TRADD 16q22 TNFRSF1A-associated via death domain FBXL8 16q23.1 F-box and leucine-rich repeat protein 8 HSF4 16q21 heat shock transcription factor 4 NOL3 16qp21-q23 nucleolar protein 3 (apoptosis repressor with CARD domain) LOC283849 16q22.1 hypothetical protein LOC283849 E2F4 16q22.1 E2F transcription factor 4, p107/p130-binding ELMO3 16q23.1 engulfment and cell motility 3 (ced-12 homolog, C. elegans) FBXL9 16q23-q31 F-box and leucine-rich repeat protein 9 HSPC171 16q22.1 HSPC171 protein FHOD1 16q22 formin homology 2 domain containing 1 SLC9A5 16q22.1 solute carrier family 9 (sodium/hydrogen exchanger), isoform 5 DKFZP434I216 16q22.1 DKFZP434I216 protein FLJ40162 16q22.1 FLJ40162 protein FLJ11004 16q22.1 hypothetical protein FLJ11004
    TRANSCRIPTS type messenger
    identificationnb exonstypebpproduct
    ProteinkDaAAspecific expressionYearPubmed
    5 - 1467 - 308 - 1996 8781531
    5 - 1476 - 308 - 1996 8781531
    Type widely
       expressed in (based on citations)
    SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
    Cardiovascularheart   highly Homo sapiens
    Respiratorylung   highly Homo sapiens
    Visualeye   highly
    SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
    Muscularstriatumcardiac highly Homo sapiens
    Muscularstriatumskeletal highly Homo sapiens
    cell lineage
    cell lines
    at STAGE
    intraspecies homolog to GEM, highly
  • 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
    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
    signaling signal transduction
  • MAPK14 pathway is the main component in RRAD-mediated apoptosis
  • a component
    small molecule
  • 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
    Other its repression leads to QT prolongation and causes ventricular arrhythmias via modulation of CACNB2 in the heart
    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
    Therapy target
  • mice lacking Rad are more susceptible to the development of hypertrophy in response to thoracic transverse aortic constriction than wild-type mice