Role of transforming growth factor-β superfamily signaling pathways in human disease

被引:578
作者
Gordon, Kelly J. [1 ]
Blobe, Gerard C. [1 ,2 ]
机构
[1] Duke Univ, Dept Pharmacol & Canc Biol, Durham, NC USA
[2] Duke Univ, Dept Med, Durham, NC USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2008年 / 1782卷 / 04期
关键词
TGF-beta superfamily; hereditary disease; sporadic disease;
D O I
10.1016/j.bbadis.2008.01.006
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
Transforming growth factor (TGF-beta) superfamily signaling pathways are ubiquitous and essential regulators of cellular processes including proliferation, differentiation, migration, and survival, as well as physiological processes, including embryonic development, angiogenesis, and wound healing. Alterations in these pathways, including either germ-line or somatic mutations or alterations in the expression of members of these signaling pathways often result in human disease. Appropriate regulation of these pathways is required at all levels, particularly at the ligand level, with either a deficiency or an excess of specific TGF-beta superfamily ligands resulting in human disease. TGF-beta superfamily ligands and members of these TGF-beta superfamily signaling pathways also have emerging roles as diagnostic, prognostic or predictive markers for human disease. Ongoing studies will enable targeting of TGF-beta superfamily signaling pathways for the chemoprevention and treatment of human disease. (C) 2008 Elsevier B.V. All rights reserved.
引用
收藏
页码:197 / 228
页数:32
相关论文
共 394 条
[111]   Role of transforming growth factor beta in human cancer [J].
Elliott, RL ;
Blobe, GC .
JOURNAL OF CLINICAL ONCOLOGY, 2005, 23 (09) :2078-2093
[112]  
Ewart-Toland A, 2004, CANCER EPIDEM BIOMAR, V13, P759
[113]   Mutant isoforms of the anti-Mullerian hormone type II receptor are not expressed at the cell membrane [J].
Faure, E ;
Gouedard, L ;
Imbeaud, S ;
Cate, R ;
Picard, JY ;
Josso, N ;
diClemente, N .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (48) :30571-30575
[114]   Blood outgrowth endothelial cells from hereditary haemorrhagic telangiectasia patients reveal abnormalities compatible with vascular lesions [J].
Fernandez-L, A ;
Sanz-Rodriguez, F ;
Zarrabeitia, R ;
Pérez-Molino, A ;
Hebbel, RP ;
Nguyen, J ;
Bernabéu, C ;
Botella, LM .
CARDIOVASCULAR RESEARCH, 2005, 68 (02) :235-248
[115]   Therapeutic action of tranexamic acid in hereditary haemorrhagic telangiectasia (HHT):: Regulation of ALK-I/endoglin pathway in endothelial cells [J].
Fernandez-L, Africa ;
Garrido-Martin, Eva M. ;
Sanz-Rodriguez, Francisco ;
Ramirez, Jose-Ramon ;
Morales-Angulo, Carmelo ;
Zarrabeitia, Roberto ;
Perez-Molino, Alfonso ;
Bernabeu, Carmelo ;
Botella, Luisa-Mari .
THROMBOSIS AND HAEMOSTASIS, 2007, 97 (02) :254-262
[116]   Hereditary Hemorrhagic Telangiectasia, a Vascular Dysplasia Affecting the TGF-beta Signaling Pathway [J].
Fernandez-L, Africa ;
Sanz-Rodriguez, Francisco ;
Blanco, Francisco J. ;
Bernabeu, Carmelo ;
Botella, Luisa M. .
CLINICAL MEDICINE & RESEARCH, 2006, 4 (01) :66-78
[117]  
FINGER EC, IN PRESS CARCINOGENE
[118]   Dysregulation of the BMP-p38 MAPK signaling pathway in cells from patients with fibrodysplasia ossificans progressiva (FOP) [J].
Fiori, Jennifer L. ;
Billings, Paul C. ;
Serrano de la Pena, Lourdes ;
Kaplan, Frederick S. ;
Shore, Eileen M. .
JOURNAL OF BONE AND MINERAL RESEARCH, 2006, 21 (06) :902-909
[119]   Mice lacking Smad3 are protected against cutaneous injury induced by ionizing radiation [J].
Flanders, KC ;
Sullivan, CD ;
Fujii, M ;
Sowers, A ;
Anzano, MA ;
Arabshahi, A ;
Major, C ;
Deng, CX ;
Russo, A ;
Mitchell, JB ;
Roberts, AB .
AMERICAN JOURNAL OF PATHOLOGY, 2002, 160 (03) :1057-1068
[120]   Smad3 as a mediator of the fibrotic response [J].
Flanders, KC .
INTERNATIONAL JOURNAL OF EXPERIMENTAL PATHOLOGY, 2004, 85 (02) :47-64