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Specificity, diversity, and regulation in TGF-β superfamily signaling
被引:700
作者:
Piek, E
[1
]
Heldin, CH
[1
]
Ten Dijke, P
[1
]
机构:
[1] Ludwig Inst Canc Res, S-75124 Uppsala, Sweden
关键词:
activin;
bone;
morphogenetic protein;
signal transduction;
Smad;
transforming growth factor-beta;
D O I:
10.1096/fasebj.13.15.2105
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Transforming growth factor-beta (TGF-beta) superfamily members are multifunctional cell-cell signaling proteins that play pivotal roles in tissue homeostasis and development of multicellular animals, They mediate their pleiotropic effects from membrane to nucleus through distinct combinations of type I and type II serine/threonine kinase receptors and their downstream effecters, known as Smad proteins. Certain Smads, termed receptor-regulated Smads, become phosphorylated by activated type I receptors and form heteromeric complexes with a common-partner Smad4, which translocates into the nucleus to control gene transcription, In addition to these signal transducing Smads, inhibitory Smads have been identified that inhibit the activation of receptor-regulated Smads, In contrast to the still growing TGF-beta superfamily (with similar to 30 members in mammals), relatively few type I and type II receptors as well as Smads have been identified. We will focus on recent insights into the molecular mechanisms by which signaling specificity between different TGF-beta superfamily members is achieved and regulated, and how a single family member can elicit a broad scala of biological responses.
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页码:2105 / 2124
页数:20
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