Alternative splicing within the TGF‐β type I receptor gene (ALK‐5) generates two major functional isoforms in vascular smooth muscle cells

Alternative splicing within the TGF‐β type I receptor gene (ALK‐5) generates two major functional isoforms in vascular smooth muscle cells
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TGF-β I 型受体基因 (ALK-5) 内的选择性剪接在血管平滑肌细胞中产生两种主要的功能亚型

DOI:
10.1016/s0014-5793(00)01132-7
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发表时间:
2000
期刊:
影响因子:
3.5
通讯作者:
A. Bobik
A. Bobik
中科院分区:
生物学3区
文献类型:
--
作者:
A. Agrotis;M. Condron;A. Bobik

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我们在大鼠血管平滑肌细胞(SMCs)中发现了两种TGF - β I型受体(ALK - 5) cdna的同时表达,这是由位于内含子-外显子连接处的12个核苷酸分离的AG剪接受体基序交替使用的结果。翻译后得到的全长蛋白彼此之间的区别仅在于其跨膜结构域附近是否存在Gly - Pro - Phe - Ser残基。在ALK‐5缺陷细胞中,这些替代的ALK‐5亚型的稳定表达表明,它们都能信号传导TGF‐β诱导的生长抑制和基因转录,但具有明显不同的效力。我们的数据表明,ALK‐5基因内的交替剪接是SMCs调节其对TGF‐β反应的重要机制。
We have identified in rat vascular smooth muscle cells (SMCs) the simultaneous expression of two TGF‐β type I receptor (ALK‐5) cDNAs, occurring as a consequence of alternate usage of AG splice acceptor motifs separated by 12 nucleotides located at an intron‐exon junction. When translated the resultant full length proteins differ from each other only by the in‐frame presence or absence of Gly‐Pro‐Phe‐Ser residues adjacent to their transmembrane domain. Stable expression of these alternate ALK‐5 isoforms in ALK‐5‐deficient cells demonstrated that both were competent in signaling TGF‐β‐induced growth inhibition and gene transcription, but with an apparently distinct potency. Our data suggest that alternate splicing within the ALK‐5 gene is an important mechanism whereby SMCs may regulate their response to TGF‐β.
人类转化生长因子-β I 型受体基因的克隆和基因组组织。
DOI: 10.1006/geno.1997.5023
发表时间: 1997
期刊: Genomics
影响因子: 4.4
作者:
Vellucci,VF;Reiss,M
通讯作者: Reiss,M
通过 TGF-β 受体 I 和 II 缺陷的细胞之间的基因互补,恢复对转化生长因子-β (TGF-β) 的反应性。
DOI: --
发表时间: 1991
期刊: The Journal of biological chemistry
影响因子: --
作者:
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DOI: --
发表时间: 1998-07
期刊: Cancer research
影响因子: 11.2
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DOI: --
发表时间: 1994-02
期刊: The American journal of pathology
影响因子: --
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通讯作者: M. Botney;Lila Bahadori;Goldt
DOI: --
发表时间: 1989-02
期刊: The Journal of biological chemistry
影响因子: --
作者:
Frederick T. Boyd;J. Massagué
通讯作者: Frederick T. Boyd;J. Massagué