期刊
CELLULAR SIGNALLING
卷 20, 期 9, 页码 1579-1591出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cellsig.2008.02.003
关键词
TGF-beta; smad; tumor suppressors; PPM1A; signaling; transcription; post-translational modifications; kinases; Phosphatases; phosphorylation; SUMOylation; ubiquitination
类别
资金
- NATIONAL CANCER INSTITUTE [R01CA108454] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [P50HL083794] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [R01AR053591] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [R01DK073932, P50DK064233] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM063773] Funding Source: NIH RePORTER
- NCI NIH HHS [R01 CA108454-05, R01 CA108454] Funding Source: Medline
- NHLBI NIH HHS [P50 HL083794, P50 HL083794-030001, P50HL083794] Funding Source: Medline
- NIAMS NIH HHS [R01 AR053591] Funding Source: Medline
- NIDDK NIH HHS [R01 DK073932, P50 DK064233-050009, R01DK073932, P50 DK064233, P50DK064233] Funding Source: Medline
- NIGMS NIH HHS [R01 GM063773-05, R01 GM063773, R01 GM063773-05S1, R01 GM63773] Funding Source: Medline
Smad proteins are key signal transducers for the TGF-beta superfamily and are frequently inactivated in human cancers, yet the molecular basis of how their levels and activities are regulated remains unclear. Recent progress, discussed herein, illustrates the critical roles of Smad post-translational modifications in the cellular outcome to TGF-beta signaling. (C) 2008 Elsevier Inc. All rights reserved.
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