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C13orf15 is thought to regulate cell cycle progression. Zusätzlich bieten wir Ihnen Chromosome 13 Open Reading Frame 15 Antikörper (23) und Chromosome 13 Open Reading Frame 15 Kits (3) und viele weitere Produktgruppen zu diesem Protein an.
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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 (zeige RHOA Proteine) and ROCK1 (zeige ROCK1 Proteine) 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 (zeige CSF1 Proteine)-dependent and enhanced by tumor-derived IL-4 (zeige IL4 Proteine).
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 (zeige AKT1 Proteine) 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 (zeige NFKB1 Proteine) 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 (zeige TGFB1 Proteine)-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 (zeige SREBF1 Proteine) 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 (zeige IL2 Proteine) in a PI3K-dependent fashion.
RGC32 plays an important role in diet-induced obesity and insulin (zeige INS Proteine) 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 (zeige VEGFA Proteine)-induced endothelial cell proliferation, migration, and tube formation while blocking VEGFR2 (zeige KDR Proteine) expression.
RGC-32 as a novel fibrogenic factor contributing to the pathogenesis of renal fibrosis through fibroblast activation.
Smad2 (zeige SMAD2 Proteine) and PEA3 (zeige ETV4 Proteine) 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