NF90 regulates cell cycle exit and terminal myogenic differentiation by direct binding to the 3 '-untranslated region of MyoD and p21(WAF1/CIP1) mRNAs JOURNAL OF BIOLOGICAL CHEMISTRY Shi, L. F., Zhao, G. H., Qiu, D. M., Godfrey, W. R., Vogel, H., Rando, T. A., Hu, H., Kao, P. N. 2005; 280 (19): 18981-18989


NF90 and splice variant NF110/ILF3/NFAR are double-stranded RNA-binding proteins that regulate gene expression. Mice with targeted disruption of NF90 were engineered. NF90(-/-) mice were born small and weak and succumbed to perinatal death within 12 h because of neuromuscular respiratory failure. Lung inflation and morphology were normal in NF90(-/-) mice. The diaphragm and other skeletal muscles in NF90(-/-) mice demonstrated disorganized arrangement and paucity of myofibers, evidence of myocyte degeneration and increased apoptosis. The expression of myogenic regulators, MyoD, myogenin, and p21WAF1/CIP1, was severely decreased in NF90(-/-) mice. These myogenic transcription factors and cell cycle inhibitors are regulated in part through post-transcriptional mRNA stabilization. Northwestern blotting revealed that NF90 is the principal and specific p21WAF1/CIP1 and MyoD 3'-untranslated region RNA-binding protein in developing skeletal muscles. NF90 regulates transcription factors and a cell cycle inhibitor essential for skeletal muscle differentiation and for survival.

View details for DOI 10.1074/jbc.M411034200

View details for Web of Science ID 000228932300052

View details for PubMedID 15746098