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Cold-inducible RNA-binding protein (CIRBP) is an evolutionarily conserved RNA-binding protein that responds to various cellular stressors, such as hypothermia, hypoxia, and UV radiation. It exerts its effects through RNA-binding motifs (RRM and RGG), regulating mRNA stability and translation for a wide range of target genes involved in cell survival, redox homeostasis, DNA repair, apoptosis, and circadian rhythm. CIRBP participates in several key signaling pathways, including MAPK and NF-κB, and is implicated in angiogenesis, cellular proliferation, and organismal adaptation to stress. Depending on context, CIRBP can act as an oncogene or tumor suppressor and is involved in the progression of diseases such as cancer, neurodegeneration, cardiovascular disorders, and inflammatory syndromes. There are no currently approved therapeutics directly targeting CIRBP, but its modulation is a subject of ongoing research as a potential disease biomarker and therapeutic target[1][4][5][6][7].
Not directly targeted by approved drugs; no small molecule inhibitors or biologics are in clinical use targeting CIRBP as of now. Potential for modulation of CIRBP expression or function (e.g., by gene therapy, antisense, or small molecules designed to alter RNA-binding).
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