B-Myb represses trans-activation of the Col5A2 collagen promoter indirectly via inhibition of binding of factors interacting with positive elements within the first exon.
B-Myb represses trans-activation of the Col5A2 collagen promoter indirectly via inhibition of binding of factors interacting with positive elements within the first exon.
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B-Myb 通过抑制与第一个外显子内的阳性元件相互作用的因子的结合，间接抑制 Col5A2 胶原蛋白启动子的反式激活。
DOI：
10.1016/s0945-053x(99)00023-2
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发表时间：
1999
期刊：
影响因子：
--
通讯作者：
Sonenshein,GE
中科院分区：
文献类型：
--
作者：
Kypreos,KE;Marhamati,DJ;Sonenshein,GE
B-myb, a member of the myb gene family, was originally isolated based on its high homology with c-myb in the DNA-binding domain. Previously we showed that B-myb is expressed in bovine vascular smooth muscle cells (SMCs) in a cell cycle-dependent fashion, and inhibits type I collagen gene promoter activity. Here, we have explored its role in regulation of another fibrillar collagen gene, Col5A2, encoding the α2 chain of type V collagen. Ectopic expression of B-Myb decreased α2(V) promoter activity and endogenous α2(V) collagen mRNA levels. The responsive region of the α2(V) collagen gene was localized to a fragment including 100 bp of basal promoter and 150 bp of exon 1 sequences, which contained two CRE-like elements. Binding to these elements increased upon deprivation of serum-growth factors, when expression of the Col5A2 gene is elevated, leading us to test their role despite the failure of excess unlabelled CRE oligonucleotide from the somatostatin gene to successfully compete for binding. Mutation of the elements significantly decreased the basal level of α2(V) collagen promoter activity and ablated inhibition by B-Myb. Furthermore, addition of B-Myb-glutathionine S-transferase fusion protein inhibited complex formation. Thus, these results confirm a major role for B-Myb in mediating intracellular signals controlling collagen gene expression in vascular SMCs. A model of indirect repression of the Col5A2 gene by B-Myb, via interaction with a positively-acting matrix regulatory factor, termed MRF-V, is discussed.
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DOI：
10.1073/pnas.83.18.6682
发表时间：
1986-09-01
影响因子：
11.1
作者：
MONTMINY, MR;SEVARINO, KA;GOODMAN, RH
通讯作者：
GOODMAN, RH
牛血管平滑肌细胞中 α 1(XI) 和 α 2(V) 胶原蛋白 mRNA 的协同调节。
DOI：
--
发表时间：
1991
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Brown,KE;Lawrence,R;Sonenshein,GE
通讯作者：
Sonenshein,GE
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DOI：
10.1074/jbc.272.40.24921
发表时间：
1997
期刊：
The Journal of Biological Chemistry
影响因子：
--
作者：
G. Ying;M. Arsura;M. Introna;J. Golay
通讯作者：
J. Golay
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影响因子：
8
作者：
S. Tashiro;Y. Takemoto;H. Handa;S. Ishii
通讯作者：
S. Ishii
nih 3T3 细胞的多效性突变体，I 型胶原蛋白和纤连蛋白的表达调节发生改变
影响因子：
64.5
作者：
C. Setoyama;G. Liau;B. Crombrugghe
通讯作者：
B. Crombrugghe