BMP signalling: agony and antagony in the family

被引:262
作者
Brazil, Derek P. [1 ]
Church, Rachel H. [1 ]
Surae, Satnam [2 ]
Godson, Catherine [2 ]
Martin, Finian [2 ]
机构
[1] Queens Univ Belfast, Ctr Med Expt, Belfast BT12 6BA, Antrim, North Ireland
[2] Univ Coll Dublin, Conway Inst, Dublin 4, Ireland
基金
英国生物技术与生命科学研究理事会; 爱尔兰科学基金会;
关键词
bone morphogenetic proteins; antagonist; miRNA; Gremlin; disease; BONE MORPHOGENETIC PROTEIN; GROWTH-FACTOR-BETA; TO-MESENCHYMAL TRANSITION; SKELETAL-MUSCLE DIFFERENTIATION; KIELIN/CHORDIN-LIKE PROTEIN; GREMLIN-MEDIATED DECREASE; TGF-BETA; RENAL FIBROSIS; CELL-PROLIFERATION; EPITHELIAL-CELLS;
D O I
10.1016/j.tcb.2014.12.004
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Bone morphogenetic proteins (BMPs) are secreted extracellular matrix (ECM)-associated proteins that regulate a wide range of developmental processes, including limb and kidney formation. A critical element of BMP regulation is the presence of secreted antagonists that bind and inhibit BMP binding to their cognate Ser/Thr kinase receptors at the plasma membrane. Antagonists such as Noggin, Chordin, Gremlin (Grem1), and twisted gastrulation-1 (Twsg1) have been shown to inhibit BMP action in a range of different cell types and developmental stage-specific contexts. Here we review new developments in the field of BMP and BMP antagonist biology during mammalian development and suggest strategies for targeting these proteins in human disease.
引用
收藏
页码:249 / 264
页数:16
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