anti-Cellular Repressor of E1A-Stimulated Genes 1 (CREG1) Anticorps

Human Cellular Repressor of E1A-Stimulated Genes 1 (CREG1) interaction partners

1. Studies demonstrated that CREG may modulate homeostasis of vascular wall cells and inhibit inflammation of vascular tissue cells and macrophages. Mechanistically, CREG behaves like a typical soluble lysosomal protein that regulates the formation and maturation of lysosomes by modulating the small GTPase protein Rab7, to mediate autophagy in vascular vascular tissue cells. [review]

2. 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.

3. Results indicate that cellular repressor of E1A-stimulated gene 1 protein (CREG1) increases endothelial cell (EC) filopodia formation.

4. The results suggest a novel role of CREG to promote HUVEC proliferation through the ERK/cyclin E signaling pathway.

5. CREG can inhibit NF-kappaB activation, TNF-alpha-induced inflammatory responses and the hyperpermeability of endothelial cells.

6. miR-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.

7. Suggest that CREG is a novel adventitial fibroblast phenotypic modulator in a p38MAPK-dependent manner.

8. 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

9. Upregulation of CREG expression induced HUVEC migration.

10. 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.

11. 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, modulating SMC phenotypic switching from contractile to proliferative.

12. no ssociation between common variants of CREG and coronary artery disease in the northern Chinese Han population

13. CREG plays a key role in modulating VSMC apoptosis through the p38 and JNK signal transduction pathways, both in vitro and in s

14. CREG plays a critical role in the inhibition of SMC migration, as well as maintaining SMCs in a mature phenotype

15. putative flavin mononucleotide-binding pocket in CREG is sterically blocked by a loop and several key bulky residues

16. CREG promotes a mature smooth muscle cell phenotype and reduces neointimal formation in balloon-injured rat carotid artery.

17. We demonstrate that CREG is expressed in the vascular endothelium; data suggests that CREG differentially regulates the growth of the denuded artery wall and smooth vascular muscle cell.

18. The expression of CREG improves cardiac functions and inhibits cardiac hypertrophy, inflammation and fibrosis through blocking MEK-ERK1/2-dependent signalling.

Mouse (Murine) Cellular Repressor of E1A-Stimulated Genes 1 (CREG1) interaction partners

1. effect of CREG1 on Ucp1 promoter activity was also stimulated by retinoic acid. These results strongly suggest that CREG1 plays an important role on the regulation of UCP1 expression and brown adipogenesis

2. Transplantation of CREG-modified embryonic stem cells exhibits a favorable survival pattern in infarcted hearts, which translates into a substantial preservation of cardiac function after acute myocardial infarction.

3. CREG protects heart against MI/R injury-induced cardiomyocytes apoptosis by activating lysosomal autophagy.

4. CREG1 interacts with Sec8 to promote cardiomyogenic differentiation and cell-cell adhesion.

5. Study demonstrated that haplodeficiency of Creg1 exacerbated high fat diet-induced obesity, insulin resistance and dyslipidemia. In addition, Creg1+/- mice showed increased systemic and adipose tissue inflammation, possibly through activation of the NF-kappaB pathway.

6. CREG is a novel mediator of vascular remodeling in response to Ang II.

7. CREG inhibits inflammation and promotes autophagy mediated by lysosome formation; it might be a potential therapeutic target in atherosclerosis.

8. CREG1 deficiency influenced the maturation of lysosomes and reduced the espression of Rab7, which might be involved in CREG1-induced cardiomyocyte autophagy.

9. Data indicate cellular repressor of E1A-stimulated gene (CREG) as a factor in regulating endothelial differentiation and vasculogenesis via VEGF/PI3K/Akt pathway.

10. Suggest that CREG is a novel adventitial fibroblast phenotypic modulator in a p38MAPK-dependent manner.

11. 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

12. These results indicate that CREG is expressed during mouse embryogenesis and might participate in the differentiation of these organs during embryogenesis.

13. 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.

14. Secreted Creg inhibits cell proliferation mediated by mannose-6-phosphate/insulin-like growth factor II receptor in NIH 3T3 fibroblasts.