Disease relevance of Sfrs10

• Cloning of a novel RNA binding polypeptide (RA301) induced by hypoxia/reoxygenation [1].
• To elucidate the role of astrocytes in the stress response of the central nervous system to ischemia, early gene expression was examined in rat cultured astrocytes after the exposure to hypoxia/reoxygenation, and we have previously cloned a novel RNA binding protein, RA301, from the reoxygenated astrocytes [2].

High impact information on Sfrs10

• RA301/Tra2beta, a sequence-specific RNA-binding protein, was first cloned as a stress molecule in re-oxygenated astrocytes [3].
• Consistent with a link between RA301/Tra2beta and cell proliferation, platelet-derived growth factor also induced expression of RA301/Tra2beta in cultured VSMCS: These data suggest a possible role for RA301/Tra2beta in the regulation of VSMC proliferation, especially in the setting of hypoxia/re-oxygenation-induced cell stress [3].
• Balloon injury to the rat carotid artery induced RA301/Tra2beta transcripts followed by expression of the antigen, which was detected in medial and neointimal vascular smooth muscle cells (VSMCs) [3].
• In human vascular tissues, we have found enhanced RA301/Tra2beta expression in coronary artery with intimal thickening, and atherosclerotic aorta [3].
• Expression of a novel RNA-splicing factor, RA301/Tra2beta, in vascular lesions and its role in smooth muscle cell proliferation [3].

Biological context of Sfrs10

• Using a differential display method, a novel putative RNA binding protein, RA301, was cloned from reoxygenated astrocytes [1].

Associations of Sfrs10 with chemical compounds

• Induction of RA301 mRNA was mediated, in large part, by endogenously generated reactive oxygen species, as shown by diphenyl iodonium, an inhibitor of neutrophil-type nicotinamide adenine dinucleotide phosphate oxidase which blocks oxygen-free radical formation by astrocytes [1].

Other interactions of Sfrs10

• Similarly, increased expression of RA301 in supporting a neurotrophic function of astrocytes was suggested by inhibition of interleukin-6 elaboration, a neuroprotective cytokine, in the presence of antisense oligonucleotide for RA301 [1].

References