Disease relevance of C13orf15

• RGC32 expression levels showed the greatest difference between the two groups, and were significantly elevated in HIES compared with those in severe atopic dermatitis or healthy controls using real-time PCR [1].
• Overexpression of RGC-32 increased DNA synthesis in OLGxC6 glioma cell hybrids [2].
• Overexpression of RGC-32 in colon cancer and other tumors [3].
• On the other hand, an increased RGC-32 protein was found in 70% of colon adenocarcinoma samples tested [3].
• In colon carcinomas, two major patterns of RGC-32 immunoreactivity were seen: staining of malignant epithelial cells only in some tumors and RGC-32 reactivity of both malignant epithelia as well as cells in the interstitium in others [3].

High impact information on C13orf15

• RGC-32 appears to be a cell cycle regulatory factor that mediates cell proliferation, both as an activator and substrate of p34CDC2 [4].
• Sublytic complement activation enhanced RGC-32 mRNA expression in human aortic smooth muscle cells and induced nuclear translocation of the protein [4].
• RGC-32 is a novel protein that may promote cell cycle progression in response to complement activation [4].
• Overexpression of RGC-32 induced quiescent aortic smooth muscle cells to enter S-phase [4].
• Human RGC-32 maps to chromosome 13 and is expressed in most tissues [4].

Biological context of C13orf15

• The distinct patterns of gene expression profiles and RGC32 expression levels will be useful for understanding the pathophysiology and for diagnosis of HIES, respectively [1].
• These results suggest that RGC-32 may play a role in cell cycle activation [2].
• We cloned human RGC-32 cDNA from a human fetal brain cDNA library [4].
• Mutation of RGC-32 protein at Thr-91 prevented the p34CDC2-mediated phosphorylation and resulted in loss of p34CDC2 kinase enhancing activity [4].

Anatomical context of C13orf15

• Molecular cloning and characterization of RGC-32, a novel gene induced by complement activation in oligodendrocytes [2].
• RGC-32 expression was present in the same malignant epithelial cells that also expressed the proliferation marker Ki-67 [3].
• Colonic epithelium obtained from normal individuals was consistently negative for RGC-32 protein [3].
• Overexpression of RGC-32 protein was found in other tumors including prostate, bladder, breast, lung, and other digestive tract tumors [3].

Associations of C13orf15 with chemical compounds

• Finally, knockdown of Runx1 mRNA by small interfering RNA decreased progesterone secretion and reduced levels of mRNA for Cyp11a1, Hapln1, Mt1a, and Rgc32 [5].

Physical interactions of C13orf15

• RGC-32 protein was localized in the cytoplasm and co-immunoprecipitated with cdc2 kinase [2].

Other interactions of C13orf15

• RGC-32 increases p34CDC2 kinase activity and entry of aortic smooth muscle cells into S-phase [4].
• Functionally, RGC-32 appears to mediate TGF-beta-induced EMT of HPTCs [6].

References