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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Cellular repressor of E1A-stimulated genes 1

CREG, cellular repressor of E1A-stimulated genes
The adenovirus E1A protein both activates and represses gene expression to promote cellular proliferation and inhibit differentiation. The protein encoded by this gene antagonizes transcriptional activation and cellular transformation by E1A. This protein shares limited sequence similarity with E1A and binds both the general transcription factor TBP and the tumor suppressor pRb in vitro. This gene may contribute to the transcriptional control of cell growth and differentiation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: E1A, CD45, V1a, CAN, HLA-B
Papers on CREG
Glycoproteomic Approach Identifies KRAS as a Positive Regulator of CREG1 in Non-small Cell Lung Cancer Cells.
New
Mao et al., Baltimore, United States. In Theranostics, Dec 2015
Further investigation of a panel of NSCLC cell lines found that Cellular repressor of E1A-stimulated genes (CREG1) overexpression was closely correlated with KRAS mutation status in NSCLC cells and could be down-regulated by inhibition of KRAS expression.
Cellular repressor of E1A-stimulated genes inhibits inflammation to decrease atherosclerosis in ApoE(-/-) mice.
New
Han et al., Xi'an, China. In J Mol Cell Cardiol, Sep 2015
We investigated the role and mechanism of cellular repressor of E1A-stimulated genes (CREG) in regulating TNF-α induced inflammation response in macrophages and explore whether CREG might be a therapeutic target for atherosclerosis.
Cellular repressor of E1A-stimulated gene overexpression in bone mesenchymal stem cells protects against rat myocardial infarction.
New
Han et al., Xi'an, China. In Int J Cardiol, Apr 2015
Cellular repressor of E1A-stimulated genes (CREG) can prevent BMSCs from apoptosis in vitro; however, the effects of CREG-modified BMSCs on ischemic heart disease and the related mechanism remain undefined.
Drosophila melanogaster cellular repressor of E1A-stimulated genes is a lysosomal protein essential for fly development.
Mach et al., Vienna, Austria. In Biochim Biophys Acta, 2014
Mammalian cellular repressor of E1A-stimulated genes is a lysosomal glycoprotein implicated in cellular growth and differentiation.
CREG promotes vasculogenesis by activation of VEGF/PI3K/Akt pathway.
Han et al., Shenyang, China. In Front Biosci, 2013
The cellular repressor of E1A-stimulated gene (CREG) has been reported to be involved in maintaining cellular differentiation and endothelial homeostasis, thus we hypothesize that CREG may be a novel factor regulating vasculogenesis.
CREG1 promotes angiogenesis and neovascularization.
Han et al., In Front Biosci, 2013
It has been reported that cellular repressor of E1A-stimulated genes (CREG1) promotes human umbilical vein endothelial cell (HUVEC) proliferation, migration, and protects endothelial cell (EC) from apoptosis.
Cellular repressor of E1A stimulated genes enhances endothelial monolayer integrity.
Han et al., Shenyang, China. In Mol Biol Rep, 2013
Cellular repressor of E1A stimulated genes (CREG) is a novel modulator that maintains the homeostasis of vascular cells.
MicroRNA-31 controls phenotypic modulation of human vascular smooth muscle cells by regulating its target gene cellular repressor of E1A-stimulated genes.
Han et al., Xi'an, China. In Exp Cell Res, 2013
The cellular repressor of E1A-stimulated genes (CREG) has been shown to play an important role in phenotypic modulation of VSMCs.
CREG: a possible candidate for both prevention and treatment of proliferative vascular disease.
Review
Han et al., Shenyang, China. In Curr Mol Med, 2012
Cellular repressor of E1A-stimulated genes (CREG), a novel cellular protein, was discovered in 1998.
CREG promotes the proliferation of human umbilical vein endothelial cells through the ERK/cyclin E signaling pathway.
Han et al., Chongqing, China. In Int J Mol Sci, 2012
Cellular repressor of E1A-stimulated genes (CREG) is a recently discovered secreted glycoprotein involved in homeostatic modulation.
Cellular repressor E1A-stimulated genes controls phenotypic switching of adventitial fibroblasts by blocking p38MAPK activation.
Han et al., Chongqing, China. In Atherosclerosis, 2012
The current study aimed to identify the role of cellular repressor E1A-stimulated genes (CREG), a critical mediator in the maintenance of vascular homeostasis, in AF phenotypic modulation and adventitial remodeling.
Gene-expression profiles and transcriptional regulatory pathways that underlie the identity and diversity of mouse tissue macrophages.
Impact
Immunological Genome Consortium et al., New York City, United States. In Nat Immunol, 2012
TCEF3, C/EBP-α, Bach1 and CREG-1 were among the transcriptional regulators predicted to regulate these core macrophage-associated genes.
CREG mediated adventitial fibroblast phenotype modulation: a possible therapeutic target for proliferative vascular disease.
Han et al., Shenyang, China. In Med Hypotheses, 2012
Our previous studies have demonstrated that cellular repressor of E1A-stimulated genes (CREG) plays critical roles in reducing neointimal hyperplasia by promoting vascular smooth muscle cell (VSMC) differentiation and grow arrest and inhibiting migration.
Cellular repressor of E1A-stimulated genes regulates vascular endothelial cell migration by the ILK/AKT/mTOR/VEGF(165) signaling pathway.
GeneRIF
Li et al., Shenyang, China. In Exp Cell Res, 2012
Upregulation of CREG expression induced HUVEC migration.
Diminished expression of complement regulatory proteins on peripheral blood cells from systemic lupus erythematosus patients.
Xavier et al., Porto Alegre, Brazil. In Clin Dev Immunol, 2011
CD55, CD59, CD46, and CD35 are proteins with complement regulatory (Creg) properties that ensure cell and tissue integrity when this system is activated.
Overexpression of CREG attenuates atherosclerotic endothelium apoptosis via VEGF/PI3K/AKT pathway.
GeneRIF
Yan et al., Shenyang, China. In Atherosclerosis, 2011
CREG plays a critical role in protecting the vascular endothelium from apoptosis, and the protective effort of CREG against ECs apoptosis is through the activation of the VEGF/PI3K/AKT signaling pathway
Pregnancy-associated plasma protein-A2 (PAPP-A2): tissue expression and biological consequences of gene knockout in mice.
GeneRIF
Powell et al., Rochester, United States. In Endocrinology, 2011
investigation of biological role of PAPP-A2 using knockout mice, heterozygotes, primary fibroblasts: The most striking phenotype of PAPP-A2 KO mice was postnatal growth retardation. PAPP-A2 KO mice were fertile, but exhibited compromised fecundity.
Overexpression of cellular repressor of E1A-stimulated genes inhibits TNF-α-induced apoptosis via NF-κB in mesenchymal stem cells.
GeneRIF
Jie-Li et al., Xi'an, China. In Biochem Biophys Res Commun, 2011
The results of this study indicate that CREG acts as a novel and potent survival factor in mesenchymal stem cells.
CREG1 enhances p16(INK4a) -induced cellular senescence.
GeneRIF
Tainsky et al., Detroit, United States. In Cell Cycle, 2011
Cooperation of CREG1 and p16 (INK4a) inhibits the expression of cyclin A and cyclin B by inhibiting promoter activity thereby decreasing mRNA and protein levels; these proteins are required for S-phase entry and G2/M transition.
Histological and direct evidence for the role of complement in the neuroinflammation of AD.
Review
Veerhuis, Amsterdam, Netherlands. In Curr Alzheimer Res, 2011
Also C regulatory proteins (Creg) and Crec can be found in the brain parenchyma and are upregulated, especially under acute inflammatory conditions, such as meningitis.
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