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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
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)