Ubiquitin and Ubiquitin-like Proteins in Cardiac Disease and Protection

被引:20
作者
Li, Jie [1 ]
Johnson, John A. [2 ]
Su, Huabo [1 ,2 ]
机构
[1] Augusta Univ, Med Coll Georgia, Vasc Biol Ctr, Augusta, GA 30912 USA
[2] Augusta Univ, Dept Pharmacol & Toxicol, Med Coll Georgia, Augusta, GA 30912 USA
关键词
Ubiquitin; ubiquitin; like proteins; cardiomyopathies; proteasome; SUMO; NEDD8; RING FINGER 1; INTERFERON-STIMULATED GENE; RETICULUM STRESS-RESPONSE; PROTEASOME SYSTEM; ISCHEMIA/REPERFUSION INJURY; CARDIOMYOCYTE HYPERTROPHY; ISG15; MODIFICATION; COP9; SIGNALOSOME; QUALITY CONTROL; 26S PROTEASOME;
D O I
10.2174/1389450117666151209114608
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Post-translational modification represents an important mechanism to regulate protein function in cardiac cells. Ubiquitin (Ub) and ubiquitin-like proteins (UBLs) are a family of protein modifiers that share a certain extent of sequence and structure similarity. Conjugation of Ub or UBLs to target proteins is dynamically regulated by a set of UBL-specific enzymes and modulates the physical and physiological properties of protein substrates. Ub and UBLs control a strikingly wide spectrum of cellular processes and not surprisingly are involved in the development of multiple human diseases including cardiac diseases. Further identification of novel UBL targets will expand our understanding of the functional diversity of UBL pathways in physiology and pathology. Here we review recent findings on the mechanisms, proteome and functions of a subset of UBLs and highlight their potential impacts on the development and progression of various forms of cardiac diseases.
引用
收藏
页码:989 / 1002
页数:14
相关论文
共 140 条
  • [1] Small heat shock proteins target mutant cystic fibrosis transmembrane conductance regulator for degradation via a small ubiquitin-like modifier-dependent pathway
    Ahner, Annette
    Gong, Xiaoyan
    Schmidt, Bela Z.
    Peters, Kathryn W.
    Rabeh, Wael M.
    Thibodeau, Patrick H.
    Lukacs, Gergely L.
    Frizzell, Raymond A.
    [J]. MOLECULAR BIOLOGY OF THE CELL, 2013, 24 (02) : 74 - 84
  • [2] The proteomic analysis of endogenous FAT10 substrates identifies p62/SQSTM1 as a substrate of FAT10ylation
    Aichem, Annette
    Kalveram, Birte
    Spinnenhirn, Valentina
    Kluge, Kathrin
    Catone, Nicola
    Johansen, Terje
    Groettrup, Marcus
    [J]. JOURNAL OF CELL SCIENCE, 2012, 125 (19) : 4576 - 4585
  • [3] SUMO1 haploinsufficiency leads to cleft lip and palate
    Alkuraya, Fowzan S.
    Saadi, Irfan
    Lund, Jennifer J.
    Turbe-Doan, Annick
    Morton, Cynthia C.
    Maas, Richard L.
    [J]. SCIENCE, 2006, 313 (5794) : 1751 - 1751
  • [4] Muscle ring finger protein-1 inhibits PKCε activation and prevents cardiomyocyte hypertrophy
    Arya, R
    Kedar, V
    Hwang, JR
    McDonough, H
    Li, HH
    Taylor, J
    Patterson, C
    [J]. JOURNAL OF CELL BIOLOGY, 2004, 167 (06) : 1147 - 1159
  • [5] Activation of endoplasmic reticulum stress response during the development of ischemic heart disease
    Azfer, Asim
    Niu, Jianli
    Rogers, Linda M.
    Adamski, Frances M.
    Kolattukudy, Pappachan E.
    [J]. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 291 (03): : H1411 - H1420
  • [6] MAFbx/Atrogin-1 is required for atrophic remodeling of the unloaded heart
    Baskin, Kedryn K.
    Rodriguez, Meredith R.
    Kansara, Seema
    Chen, Wenhao
    Carranza, Sylvia
    Frazier, O. Howard
    Glass, David J.
    Taegtmeyer, Heinrich
    [J]. JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY, 2014, 72 : 168 - 176
  • [7] Ubiquitin-like protein conjugation and the ubiquitin-proteasome system as drug targets
    Bedford, Lynn
    Lowe, James
    Dick, Lawrence R.
    Mayer, R. John
    Brownell, James E.
    [J]. NATURE REVIEWS DRUG DISCOVERY, 2011, 10 (01) : 29 - 46
  • [8] Potentiation of Tbx5-mediated transactivation by SUMO conjugation and protein inhibitor of activated STAT 1 (PIAS1)
    Beketaev, Ilimbek
    Kim, Eun Young
    Zhang, Yi
    Yu, Wei
    Qian, Ling
    Wang, Jun
    [J]. INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY, 2014, 50 : 82 - 92
  • [9] Elevated p53 expression is associated with dysregulation of the ubiquitin-proteasome system in dilated cardiomyopathy
    Birks, Emma J.
    Latif, Najma
    Enesa, Karine
    Folkvang, Tonje
    Luong, Le Anh
    Sarathchandra, Padmini
    Khan, Mak
    Ovaa, Huib
    Terracciano, Cesare M.
    Barton, Paul J. R.
    Yacoub, Magdi H.
    Evans, Paul C.
    [J]. CARDIOVASCULAR RESEARCH, 2008, 79 (03) : 472 - 480
  • [10] Class I HDAC inhibition stimulates cardiac protein SUMOylation through a post-translational mechanism
    Blakeslee, Weston W.
    Wysoczynski, Christina L.
    Fritz, Kristofer S.
    Nyborg, Jennifer K.
    Churchill, Mair E. A.
    McKinsey, Timothy A.
    [J]. CELLULAR SIGNALLING, 2014, 26 (12) : 2912 - 2920