Abstract:
:T box (Tbx) genes are a large family of transcription regulators that play critical roles in invertebrate and vertebrate development. Mutations in Tbx5 gene have been found to cause Holt-Oram syndrome (HOS) in humans. Partial dysfunction of TBX5 in mouse also causes HOS phenotype. Little is known about its molecular and cellular mechanism. Here, we report that ectopic expression of TBX5 inhibited colony formation, induced apoptosis, and decreased the growth rate of cells. The two point mutations in T domain and a truncated mutation in C-terminal found in human HOS patients produced TBX5 mutant proteins with a significantly reduction of colony suppression activity. Deletion of the DNA-binding domain, however, nearly completely abrogated its ability to suppress colony formation. These results reveal TBX5 as a new regulator of apoptosis and cell growth, suggesting a possible mechanism for Holt-Oram syndrome, and a potential reagent for controlling tumor growth.
journal_name
Biochem Biophys Res Communjournal_title
Biochemical and biophysical research communicationsauthors
He ML,Chen Y,Peng Y,Jin D,Du D,Wu J,Lu P,Lin MC,Kung HFdoi
10.1016/s0006-291x(02)02142-3subject
Has Abstractpub_date
2002-09-20 00:00:00pages
185-92issue
2eissn
0006-291Xissn
1090-2104pii
S0006291X02021423journal_volume
297pub_type
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