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C13orf15 is thought to regulate cell cycle progression. Additionally we are shipping Chromosome 13 Open Reading Frame 15 Antibodies (20) and Chromosome 13 Open Reading Frame 15 Kits (3) and many more products for this protein.
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This study demonstrated the up-regulation of RGC-32 contributed to the imbalance of Treg/Th17 cells in patients with Dilated Cardiomyopathy. [RGC-32]
RGC-32 mediates human aortic endothelial cell migration through the regulation of RhoA (show RHOA Proteins) and ROCK1 (show ROCK1 Proteins) expression.
RGCC may be a candidate cell cycle target for neuroprotection during the onset of Alzheimer's disease.
RGC-32 expression on M2-polarized and tumor-associated macrophages is M-CSF (show CSF1 Proteins)-dependent and enhanced by tumor-derived IL-4 (show IL4 Proteins).
Data suggest that expression of RGC32 is down-regulated in placental trophoblasts in women with pre-eclampsia as compared to women with normal term pregnancies; silencing RGC32 expression by RNA interference inhibits trophoblast migration/invasion.
Suggest that RGC32 is involved in tumorigenesis of human lung cancer, inducing apoptosis and inhibiting cell growth, migration, and invasion.
In conclusion, the present study indicates that C5a may promote the proliferation of breast cancer cells through Akt1 (show AKT1 Proteins) activation of the RGC-32 gene.
results demonstrate for the first time that RGC-32 is a novel membrane regulator for macrophage phagocytosis.
RGC32 promotes cell migration and invasion and induces epithelial-mesenchymal transition in lung cancer cells via the NF-kappaB (show NFKB1 Proteins) signaling pathway.
data suggest RGC-32 plays a dual role in multiple sclerosis, both as a regulator of T-cells mediated apoptosis and as a promoter of TGF-beta (show TGFB1 Proteins)-mediated profibrotic effects in astrocytes
results identify RGC-32 as a novel regulator of Th17 cell differentiation in vitro and in vivo and suggest that RGC-32 is a potential therapeutic target in multiple sclerosis and other Th17-mediated autoimmune diseases
results demonstrate that RGC-32 contributes to the development of hepatic steatosis by facilitating de novo lipogenesis through activating liver X receptor, leading to the induction of SREBP-1c (show SREBF1 Proteins) and its target genes
RGC-32 is involved in controlling the cell cycle of T cells in vivo, and this effect is mediated by IL-2 (show IL2 Proteins) in a PI3K-dependent fashion.
RGC32 plays an important role in diet-induced obesity and insulin (show INS Proteins) resistance, and thus it may serve as a potential novel drug target for developing therapeutics to treat obesity and metabolic disorders.
knockdown of RGC-32 by shRNA inhibited VEGF (show VEGFA Proteins)-induced endothelial cell proliferation, migration, and tube formation while blocking VEGFR2 (show KDR Proteins) expression.
RGC-32 as a novel fibrogenic factor contributing to the pathogenesis of renal fibrosis through fibroblast activation.
Smad2 (show SMAD2 Proteins) and PEA3 (show ETV4 Proteins) regulate RGC-32 transcription which is essential for smooth muscle cell differentiation from neural crest cells.
This gene is thought to regulate cell cycle progression. It is induced by p53 in response to DNA damage, or by sublytic levels of complement system proteins that result in activation of the cell cycle. The encoded protein localizes to the cytoplasm during interphase and to centrosomes during mitosis. The protein forms a complex with polo-like kinase 1. The protein also translocates to the nucleus in response to treatment with complement system proteins, and can associate with and increase the kinase activity of cell division cycle 2 protein. In different assays and cell types, overexpression of this protein has been shown to activate or suppress cell cycle progression.
regulator of cell cycle RGCC
, response gene to complement 32 protein