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The adenovirus E1A protein both activates and represses gene expression to promote cellular proliferation and inhibit differentiation. Additionally we are shipping CREG1 Antibodies (99) and CREG1 Proteins (13) and many more products for this protein.
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These results indicate that CREG1 is a down-stream effector of KRAS in a sub-type of non-small cell lung cancer cells and a novel candidate biomarker or therapeutic target for KRAS mutant non-small cell lung cancer.
Results indicate that cellular repressor of E1A (show BCKDHA ELISA Kits)-stimulated gene 1 protein (CREG1) increases endothelial cell (EC) filopodia formation.
The results suggest a novel role of CREG to promote HUVEC proliferation through the ERK (show EPHB2 ELISA Kits)/cyclin E (show CCNE1 ELISA Kits) signaling pathway.
CREG can inhibit NF-kappaB (show NFKB1 ELISA Kits) activation, TNF-alpha (show TNF ELISA Kits)-induced inflammatory responses and the hyperpermeability of endothelial cells.
miR (show MLXIP ELISA Kits)-31 not only directly binds to its target gene CREG and modulates the vascular smooth muscle cells(VSMC) phenotype through this interaction, but also can be an important biomarker in diseases involving VSMC phenotypic modulation.
Suggest that CREG is a novel adventitial fibroblast phenotypic modulator in a p38MAPK (show MAPK14 ELISA Kits)-dependent manner.
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 (show VEGFA ELISA Kits)/PI3K (show PIK3CA ELISA Kits)/AKT (show AKT1 ELISA Kits) signaling pathway
Upregulation of CREG expression induced HUVEC migration.
Cooperation of CREG1 and p16 (INK4a) inhibits the expression of cyclin A (show CCNA2 ELISA Kits) 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.
Data suggest that soluble CREG protein can exert its biological function via glycosylation-independent binding to the extracellular domains 11-13 of cell surface M6P/IGF2R (show IGF2R ELISA Kits), modulating SMC (show DYM ELISA Kits) phenotypic switching from contractile to proliferative.
Study demonstrated that haplodeficiency of Creg1 exacerbated high fat diet-induced obesity, insulin (show INS ELISA Kits) resistance and dyslipidemia. In addition, Creg1+/- mice showed increased systemic and adipose tissue inflammation, possibly through activation of the NF-kappaB (show NFKB1 ELISA Kits) pathway.
CREG is a novel mediator of vascular remodeling in response to Ang II (show AGT ELISA Kits).
CREG inhibits inflammation and promotes autophagy mediated by lysosome formation; it might be a potential therapeutic target in atherosclerosis.
CREG1 deficiency influenced the maturation of lysosomes and reduced the espression of Rab7 (show RAB7A ELISA Kits), which might be involved in CREG1-induced cardiomyocyte autophagy.
Data indicate cellular repressor of E1A (show BCKDHA ELISA Kits)-stimulated gene (CREG) as a factor in regulating endothelial differentiation and vasculogenesis via VEGF (show VEGFA ELISA Kits)/PI3K/Akt (show AKT1 ELISA Kits) pathway.
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 (show VEGFA ELISA Kits)/PI3K/AKT (show AKT1 ELISA Kits) signaling pathway
These results indicate that CREG is expressed during mouse embryogenesis and might participate in the differentiation of these organs during embryogenesis.
Results show that CREG is a lysosomal protein that undergoes proteolytic maturation during biosynthesis, carries the mannose 6-phosphate recognition marker and depends on the interaction with M-6-P receptors for efficient delivery to lysosomes.
Secreted Creg inhibits cell proliferation mediated by mannose-6-phosphate/insulin-like growth factor II receptor (show IGF2R ELISA Kits) in NIH 3T3 fibroblasts.
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.
cellular repressor of E1A-stimulated genes 1
, protein CREG1
, Protein CREG1
, hypothetical protein