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FLASH GENE
Symbol CREG1 contributors: mct - updated : 20-11-2019
HGNC name cellular repressor of E1A-stimulated genes
HGNC id 2351
RNA
TRANSCRIPTS type messenger
identificationnb exonstypebpproduct
ProteinkDaAAspecific expressionYearPubmed
4 - 2048 - 220 - 2011 21263217
EXPRESSION
Type ubiquitous
   expressed in (based on citations)
organ(s)
SystemOrgan level 1Organ level 2Organ level 3Organ level 4LevelPubmedSpeciesStageRna symbol
Cardiovascularheart     Homo sapiensAdult
 heart     Homo sapiensFetal
Endocrinepancreas    
Respiratorylung    
Urinarykidney    
tissue
SystemTissueTissue level 1Tissue level 2LevelPubmedSpeciesStageRna symbol
Blood / Hematopoieticbone marrow   
cell lineage
cell lines
fluid/secretion
at STAGE
PROTEIN
PHYSICAL PROPERTIES
STRUCTURE
motifs/domains
conjugated GlycoP
HOMOLOGY
interspecies homolog to murine Creg
Homologene
FAMILY
CATEGORY transcription factor
SUBCELLULAR LOCALIZATION extracellular
    intracellular
intracellular,cytoplasm,organelle,lysosome
text
  • intracellular protein localized in the endocytic-lysosomal compartment
  • basic FUNCTION
  • antagonizing transcriptional activation and cellular transformation by adenovirus E1a
  • contributing to the transcription control of cell growth and differentiation
  • acts as a ligand that enhances differentiation and/or reduces cell proliferation
  • improves cardiac functions and inhibits cardiac hypertrophy, inflammation and fibrosis through blocking MEK-ERK1/2-dependent signalling
  • plays a critical role in the inhibition of smooth muscle cells migration
  • novel and potent survival factor for mesenchymal stem cells
  • glycoprotein inhibiting transcription activation, on the regulation of vascular smooth muscle cell apoptosis (VSMCs)
  • plays a key role in modulating VSMC apoptosis through the MAPK14 and JNK signal transduction pathways
  • coexpression of CREG1 and CDKN2A, has a greater effect than either CREG1 and CDKN2A alone to reduce cell growth, induce cell cycle arrest and cellular senescence
  • enhances CDKN2A -induced senescence by transcriptional repression of cell cycle-regulated genes
  • CREG1 is a novel adventitial fibroblasts (AFs) phenotypic modulator in a MAPK14-dependent manner
  • can inhibit NFKB1 activation, TNF-induced inflammatory responses and the hyperpermeability of endothelial cells
  • CREG1 participates in the regulation of apoptosis, inflammation and wound healing of vascular endothelial cells 8)
  • promotes angiogenesis and neovascularization
  • involved in maintaining cellular differentiation and endothelial homeostasis
  • is a conserved lysosomal protein, and an important new factor in regulating tissues homeostasis that has been shown to antagonize injury of tissues or cells
  • CREG1-induced autophagy is required to maintain heart function in the face of stress-induced myocardiac damage
  • protects heart against myocardial ischemia/reperfusion (MI/R) injury-induced cardiomyocytes apoptosis by activating lysosomal autophagy
  • CREG1 plays an important role on the regulation of UCP1 expression and brown adipogenesis
  • essential role for CREG1 in development
  • CELLULAR PROCESS
    PHYSIOLOGICAL PROCESS
    PATHWAY
    metabolism
    signaling
    a component
  • forms a tight homodimeric complex, and CREG monomers display a beta-barrel fold
  • INTERACTION
    DNA
    RNA
    small molecule
    protein
  • is a novel factor in regulating endothelial differentiation and vasculogenesis via VEGFA/PIK3CA/AKT1 pathway
  • CREG1 directly interacts with EXOC4 of the exocyst complex, which tethers vesicles to the plasma membrane
  • CREG1 binding to EXOC4 enhances the assembly of intercellular junctions and promotes cardiomyogenesis
  • CREG1 interacts with EXOC4 to promote cardiomyogenic differentiation and cell-cell adhesion
  • CREG1 binds to retinoid X receptor alpha, which interacts with thyroid hormone receptor for brown adipogenesis
  • cell & other
    REGULATION
    ASSOCIATED DISORDERS
    corresponding disease(s)
    Other morbid association(s)
    TypeGene ModificationChromosome rearrangementProtein expressionProtein Function
    constitutional     --low  
    dramatically downregulated in atherosclerotic lesions
    Susceptibility
    Variant & Polymorphism
    Candidate gene
    Marker
    Therapy target
    SystemTypeDisorderPubmed
    cardiovascularatheromacardiac
    may be a useful therapeutic adjunct for transplanting MSCs into damaged heart after myocardial infarction
    cardiovascularaquired 
    autophagy activation via CREG1 may be a viable therapeutic strategy autophagy for improving cardiac performance under pathologic conditions
    ANIMAL & CELL MODELS
  • in mice, global deletion of the Creg1 gene leads to early embryonic death
  • Creg1+/- mice exhibited a more prominent obesity phenotype with no change in food intake compared with WT controls when challenged with high fat diet (HFD)