Regulation of Cardiac Hypertrophic Remodeling by the USP15/SLIM1 Pathway
作者： Hiroto Nakajima
DOI: 10.1007/978-1-4614-5930-9_5
关键词: SMAD 、 Animal model 、 Proteasome 、 Interactor 、 Medicine 、 Cardiomyopathy 、 Skeletal muscle 、 Cell biology 、 Ubiquitin 、 Volume overload
摘要: Many lines of evidence support the important role ubiquitin (Ub)–proteasome system (UPS) in development heart diseases. Cardiomyopathy or cardiac responses to pressure volume overload are also accompanied by alterations UPS. At beginning this review, we provide an overview recent studies regarding features and roles UPS its components hypertrophic remodeling. Then, focus on our animal model remodeling, which was induced cardiac-targeted overexpression Ub-specific protease 15 (USP15) mice. Skeletal muscle LIM protein 1 (SLIM1), a direct interactor substrate USP15, increased remodeling model. We discuss possible mechanisms basis several novel findings USP15 SLIM1.
springer.com
sci-hub.st 参考文章(63)
A. Subramaniam, W.K. Jones, J. Gulick, S. Wert, J. Neumann, J. Robbins, Tissue-specific regulation of the alpha-myosin heavy chain gene promoter in transgenic mice. Journal of Biological Chemistry. ,vol. 266, pp. 24613- 24620 ,(1991) , 10.1016/S0021-9258(18)54273-3
Susan Wee, Rory K. Geyer, Takashi Toda, Dieter A. Wolf, CSN facilitates Cullin–RING ubiquitin ligase function by counteracting autocatalytic adapter instability Nature Cell Biology. ,vol. 7, pp. 387- 391 ,(2005) , 10.1038/NCB1241
Yoshitaka Isumi, Tsuyoshi Hirata, Hiroshi Saitoh, Tomoya Miyakawa, Kenji Murakami, Gen Kudoh, Hirofumi Doi, Kohtaro Ishibashi, Hiroto Nakajima, Transgenic overexpression of USP15 in the heart induces cardiac remodeling in mice. Biochemical and Biophysical Research Communications. ,vol. 405, pp. 216- 221 ,(2011) , 10.1016/J.BBRC.2011.01.012
Corinne Angelats, Xiao-Wen Wang, Lars S. Jermiin, Neal G. Copeland, Nancy A. Jenkins, Rohan T. Baker, Isolation and characterization of the mouse ubiquitin-specific protease Usp15 Mammalian Genome. ,vol. 14, pp. 31- 46 ,(2003) , 10.1007/S00335-002-3035-0
M.J. Morgan, A.J.A. Madgwick, Slim Defines a Novel Family of LIM-Proteins Expressed in Skeletal Muscle Biochemical and Biophysical Research Communications. ,vol. 225, pp. 632- 638 ,(1996) , 10.1006/BBRC.1996.1222
Susan Brown, Christine Biben, Lisa M. Ooms, Margaret Maimone, Meagan J. McGrath, Rajendra Gurung, Richard P. Harvey, Christina A. Mitchell, The Cardiac Expression of Striated Muscle LIM Protein 1 (SLIM1) is Restricted to the Outflow Tract of the Developing Heart Journal of Molecular and Cellular Cardiology. ,vol. 31, pp. 837- 843 ,(1999) , 10.1006/JMCC.1998.0922
Christophe Depre, Qian Wang, Lin Yan, Nadia Hedhli, Pallavi Peter, Li Chen, Chull Hong, Luc Hittinger, Bijan Ghaleh, Junichi Sadoshima, Dorothy E. Vatner, Stephen F. Vatner, Kiran Madura, Activation of the Cardiac Proteasome During Pressure Overload Promotes Ventricular Hypertrophy Circulation. ,vol. 114, pp. 1821- 1828 ,(2006) , 10.1161/CIRCULATIONAHA.106.637827
T BRAND, M SCHNEIDER, The TGFβ superfamily in myocardium: Ligands, receptors, transduction, and function Journal of Molecular and Cellular Cardiology. ,vol. 27, pp. 5- 18 ,(1995) , 10.1016/S0022-2828(08)80003-X
N. Hedhli, L. Wang, Q. Wang, E. Rashed, Y. Tian, X. Sui, K. Madura, C. Depre, Proteasome activation during cardiac hypertrophy by the chaperone H11 Kinase/Hsp22 Cardiovascular Research. ,vol. 77, pp. 497- 505 ,(2007) , 10.1093/CVR/CVM054
Belinda S. Cowling, Denny L. Cottle, Brendan R. Wilding, Colleen E. D’Arcy, Christina A. Mitchell, Meagan J. McGrath, Four and a half LIM protein 1 gene mutations cause four distinct human myopathies: a comprehensive review of the clinical, histological and pathological features. Neuromuscular Disorders. ,vol. 21, pp. 237- 251 ,(2011) , 10.1016/J.NMD.2011.01.001