NF90 regulates cell cycle exit and terminal myogenic differentiation by direct binding to the 3'-untranslated region of MyoD and p21WAF1/CIP1 mRNAs. Export

@article{citeulike:305672, abstract = {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.}, address = {Division of Pulmonary and Critical Care Medicine, Stanford University Medical Center, Stanford, California 94305-5236, USA.}, author = {Shi, L. and Zhao, G. and Qiu, D. and Godfrey, W. R. and Vogel, H. and Rando, T. A. and Hu, H. and Kao, P. N.}, citeulike-article-id = {305672}, citeulike-linkout-0 = {http://dx.doi.org/10.1074/jbc.M411034200}, citeulike-linkout-1 = {http://www.jbc.org/cgi/content/abstract/280/19/18981}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/15746098}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=15746098}, day = {13}, doi = {10.1074/jbc.M411034200}, issn = {0021-9258}, journal = {J Biol Chem}, keywords = {alt, muscle, splicing}, month = {May}, number = {19}, pages = {18981--18989}, posted-at = {2005-08-27 13:59:57}, priority = {2}, title = {NF90 regulates cell cycle exit and terminal myogenic differentiation by direct binding to the 3'-untranslated region of MyoD and p21WAF1/CIP1 mRNAs.}, url = {http://dx.doi.org/10.1074/jbc.M411034200}, volume = {280}, year = {2005} }

TY - JOUR ID - citeulike:305672 L3 - citeulike-article-id:305672 N2 - 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. IS - 19 JF - J Biol Chem SN - 0021-9258 AD - Division of Pulmonary and Critical Care Medicine, Stanford University Medical Center, Stanford, California 94305-5236, USA. EP - 18989 TI - NF90 regulates cell cycle exit and terminal myogenic differentiation by direct binding to the 3'-untranslated region of MyoD and p21WAF1/CIP1 mRNAs. VL - 280 SP - 18981 KW - alt KW - muscle KW - splicing AU - Shi, L AU - Zhao, G AU - Qiu, D AU - Godfrey, WR AU - Vogel, H AU - Rando, TA AU - Hu, H AU - Kao, PN PY - 2005/05/13/ UR - http://dx.doi.org/10.1074/jbc.M411034200 ER -