描述：
BMP-10, along with BMP-9, GDF-5, -6, and -7, belongs to a subgroup of TGF-β superfamily
proteins that signal through heterodimeric complexes composed of type I and type II BMP
receptors. Proteolytic removal of the propeptide from the 60 kDa proprotein yields a 12 kDa
mature BMP-10 which forms disulfidelinked nonglycosylated homodimers. Mature human
BMP-10 shares 98% amino acid sequence identity with mouse and rat BMP-10 and 49%- 63%
with human BMP-9, GDF-5, -6, and -7. BMP-10 is critical for the proper development of the
heart but is not expressed until after cardiac patterning or looping are completed. BMP-10
production appears at the onset of trabeculation and chamber formation and is restricted to
the right atrium in the adult heart. Homozygous BMP-10 knock out mice die in utero due to
arrested cardiac development. BMP-10 is required for the expression of the cardiogenic
transcription factors NKX2.5 and MEF2C in developing myocardium and the growth of
embryonic cardiomyocytes. NKX2.5 itself negatively regulates BMP10 expression in cardiac
myocytes. Multiple human congenital heart defects result from mutations in NKX2.5 and
require BMP-10 expression. In mice, genetic knockout of ErbB leads to a similar phenotype
but appears not to involve BMP-10, and knockout of the calcium channel subunit FKBP12
induces BMP-10 overexpression. BMP-10 in the postnatal heart promotes increased
cardiomyocyte and heart size. BMP-10 has been shown to signal through ALK-1, BMPR-IA,
BMPR-IB, and BMPR-II in transfectants and noncardiac cell lines. A functional BMP-10 receptor
in the heart has not yet been identified, although deletion of BMPR-IA causes similar cardiac
morphogenetic abnormalities. In dermal endothelial cells, BMP-10 induces migration,
proliferation, and gene expression typically associated with ALK-1.
原厂资料：
BMP-10, along with BMP-9, GDF-5, -6, and -7, belongs to a subgroup of TGF-β superfamily
proteins that signal through heterodimeric complexes composed of type I and type II BMP
receptors. Proteolytic removal of the propeptide from the 60 kDa proprotein yields a 12 kDa
mature BMP-10 which forms disulfidelinked nonglycosylated homodimers. Mature human
BMP-10 shares 98% amino acid sequence identity with mouse and rat BMP-10 and 49%- 63%
with human BMP-9, GDF-5, -6, and -7. BMP-10 is critical for the proper development of the
heart but is not expressed until after cardiac patterning or looping are completed. BMP-10
production appears at the onset of trabeculation and chamber formation and is restricted to
the right atrium in the adult heart. Homozygous BMP-10 knock out mice die in utero due to
arrested cardiac development. BMP-10 is required for the expression of the cardiogenic
transcription factors NKX2.5 and MEF2C in developing myocardium and the growth of
embryonic cardiomyocytes. NKX2.5 itself negatively regulates BMP10 expression in cardiac
myocytes. Multiple human congenital heart defects result from mutations in NKX2.5 and
require BMP-10 expression. In mice, genetic knockout of ErbB leads to a similar phenotype
but appears not to involve BMP-10, and knockout of the calcium channel subunit FKBP12
induces BMP-10 overexpression. BMP-10 in the postnatal heart promotes increased
cardiomyocyte and heart size. BMP-10 has been shown to signal through ALK-1, BMPR-IA,
BMPR-IB, and BMPR-II in transfectants and noncardiac cell lines. A functional BMP-10 receptor
in the heart has not yet been identified, although deletion of BMPR-IA causes similar cardiac
morphogenetic abnormalities. In dermal endothelial cells, BMP-10 induces migration,
proliferation, and gene expression typically associated with ALK-1.
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