Alternative splicing of T-box transcription factor genes

被引：17

作者：

DeBenedittis, Paige ^{[1
]}

Jiao, Kai ^{[1
]}

机构：

[1] Univ Alabama Birmingham, Dept Genet, Birmingham, AL 35294 USA

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2011年 / 412卷 / 04期

关键词：

Alternative splicing; T-box; TBX3; TBX5; TBX20; ULNAR-MAMMARY SYNDROME; CELL-PROLIFERATION; EPITHELIAL-CELLS; HUMAN TBX3; MUTATIONS; EXPRESSION; MUSKELIN; LIMB; SPECIFICATION; COMPLEX;

D O I：

10.1016/j.bbrc.2011.08.010

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

T-box (TBX) transcription factors are an ancient gene family with critical roles in embryogenesis. Currently, TBX3, TBX5, and TBX20 are TBX genes defined to have multiple protein isoforms created by alternative splicing and characterized by expression and functional studies. These proteins are important for development as mutations lead to severe developmental disorders in humans and mice. Cumulative studies suggest that alternative splicing of these genes can regulate TBX activities during multiple biological processes including cardiogenesis, limb development, and cancer mechanisms. This mini-review focuses on how alternative splicing adds complexity to transcriptional regulation of target genes controlled by TBX transcription factors. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：513 / 517

页数：5

共 46 条

[1] Muskelin, a novel intracellular mediator of cell adhesive and cytoskeletal responses to thrombospondin-1
Adams, JC
Seed, B
Lawler, J
[J]. EMBO JOURNAL, 1998, 17 (17) : 4964 - 4974
[2] Agulnik SI, 1996, GENETICS, V144, P249
[3] Transcription factor Tbx3 is required for the specification of the atrioventricular conduction system
Bakker, Martijn L.
Boukens, Bastiaan J.
Mommersteeg, Mathilda T. M.
Brons, Janynke F.
Wakker, Vincent
Moorman, Antoon F. M.
Christoffels, Vincent M.
[J]. CIRCULATION RESEARCH, 2008, 102 (11) : 1340 - 1349
[4] Mutations in human TBX3 alter limb, apocrine and genital development in ulnar-mammary syndrome
Bamshad, M
Lin, RC
Law, DJ
Watkins, WS
Krakowiak, PA
Moore, ME
Franceschini, P
Lala, R
Holmes, LB
Gebuhr, TC
Bruneau, BG
Schinzel, A
Seidman, JG
Seidman, CE
Jorde, LB
[J]. NATURE GENETICS, 1997, 16 (03) : 311 - 315
[5] The spectrum of mutations in TBX3:: Genotype phenotype relationship in ulnar-mammary syndrome
Bamshad, M
Le, T
Watkins, WS
Dixon, ME
Kramer, BE
Roeder, AD
Carey, JC
Root, S
Schinzel, A
Van Maldergem, L
Gardner, RJM
Lin, RC
Seidman, CE
Seidman, JG
Wallerstein, R
Moran, E
Sutphen, R
Campbell, CE
Jorde, LB
[J]. AMERICAN JOURNAL OF HUMAN GENETICS, 1999, 64 (06) : 1550 - 1562
[6] Mutations in human cause limb and cardiac malformation in Holt-Oram syndrome
Basson, CT
Bachinsky, DR
Lin, RC
Levi, T
Elkins, JA
Soults, J
Grayzel, D
Kroumpouzou, E
Traill, TA
LeblancStraceski, J
Renault, B
Kucherlapati, R
Seidman, JG
Seidman, CE
[J]. NATURE GENETICS, 1997, 15 (01) : 30 - 35
[7] Mechanisms of alternative pre-messenger RNA splicing
Black, DL
[J]. ANNUAL REVIEW OF BIOCHEMISTRY, 2003, 72 : 291 - 336
[8] TBX-3, the gene mutated in ulnar-mammary syndrome, is a negative regulator of p19ARF and inhibits senescence
Brummelkamp, TR
Kortlever, RM
Lingbeek, M
Trettel, F
MacDonald, ME
van Lohuizen, M
Bernards, R
[J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (08) : 6567 - 6572
[9] T-box genes coordinate regional rates of proliferation and regional specification during cardiogenesis
Cai, CL
Zhou, WL
Yang, L
Bu, L
Qyang, YB
Zhang, XX
Li, XD
Rosenfeld, MG
Chen, J
Evans, S
[J]. DEVELOPMENT, 2005, 132 (10): : 2475 - 2487
[10] A dominant repression domain in Tbx3 mediates transcriptional repression and cell immortalization: relevance to mutations in Tbx3 that cause ulnar-mammary syndrome
Carlson, H
Ota, S
Campbell, CE
Hurlin, PJ
[J]. HUMAN MOLECULAR GENETICS, 2001, 10 (21) : 2403 - 2413

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