Zobrazeno 1 - 10
of 11
pro vyhledávání: '"Kritton Shay-Winkler"'
Autor:
Marianne E Emmert, Parul Aggarwal, Kritton Shay-Winkler, Se-Jin Lee, Qingnian Goh, Roger Cornwall
Publikováno v:
eLife, Vol 11 (2022)
Neonatal brachial plexus injury (NBPI) causes disabling and incurable muscle contractures that result from impaired longitudinal growth of denervated muscles. This deficit in muscle growth is driven by increased proteasome-mediated protein degradatio
Externí odkaz:
https://doaj.org/article/b389100cb389497bb75b7e3c45bcc659
Publikováno v:
Febs Letters
Neonatal brachial plexus injury (NBPI) causes disabling and incurable muscle contractures that are driven by impaired growth of denervated muscles. A rare form of NBPI, which maintains afferent muscle innervation despite motor denervation, does not c
Publikováno v:
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Neonatal brachial plexus injury (NBPI) causes disabling and incurable contractures, or limb stiffness, which result from proteasome-mediated protein degradation impairing the longitudinal growth of neonatally denervated muscles. We recently showed in
Autor:
Jeffrey Robbins, Katherine E. Yutzey, James Gulick, Yang Yu, Na Xu, Hanna Osinska, Kritton Shay-Winkler, Patrick M. McLendon
Publikováno v:
Circ Res
Rationale: Compromised protein quality control can result in proteotoxic intracellular protein aggregates in the heart, leading to cardiac disease and heart failure. Defining the participants and understanding the underlying mechanisms of cardiac pro
Publikováno v:
SSRN Electronic Journal.
Background: Neonatal brachial plexus injury (NBPI) causes disabling and incurable contractures, or limb stiffness, which result from proteasome-mediated protein degradation impairing the longitudinal growth of neonatally denervated muscles. We recent
Autor:
Keri Anne Drake, Prasad Devarajan, Brian J. Siroky, Kritton Shay-Winkler, Priyanka Parameswaran, LaTawnya Pleasant, Qing Ma, Jeffrey Robbins, Mahima Devarajan
Publikováno v:
American Journal of Physiology-Renal Physiology. 313:F699-F705
The early events that signal renal dysfunction in presymptomatic heart failure are unclear. We tested the hypothesis that functional and mechanistic changes occur in the kidney that precede the development of symptomatic heart failure. We employed a
Autor:
Shenuarin Bhuiyan, Iñigo Valiente-Alandi, Jeffrey Robbins, Burns C. Blaxall, Jeffery D. Molkentin, James Gulick, Qinghang Meng, Bidur Bhandary, Hanna Osinska, Kritton Shay-Winkler, Jeanne James
Publikováno v:
Circulation research. 123(12)
Rationale: Hypertrophic cardiomyopathy occurs with a frequency of about 1 in 500 people. Approximately 30% of those affected carry mutations within the gene encoding cMyBP-C (cardiac myosin binding protein C). Cardiac stress, as well as cMyBP-C mutat
Autor:
James Gulick, Jeffrey Robbins, Jeanne James, James W. McNamara, Md. Shenuarin Bhuiyan, Qinghang Meng, Bidur Bhandary, Kritton Shay-Winkler, Sakthivel Sadayappan, Hanna Osinska
Publikováno v:
Circulation Research. 123
Background: Mutations in cardiac myosin binding protein C ( MYBPC3 ) account for more than one third of identified hypertrophic cardiomyopathy (HCM). Data from both human patients and mouse models suggest that cardiac fibrosis preceeds hypertrophy an
Autor:
Cynthia Lander, Na Xu, Bidur Bhandary, Monte S. Willis, Jeffrey Robbins, James Gulick, Hanna Osinska, Jeanne James, Kritton Shay-Winkler, Qinghang Meng
Publikováno v:
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Background Cardiac stress can trigger production of a 40‐kDa peptide fragment derived from the amino terminus of the cardiac myosin‐binding protein C. Cardiac stress, as well as cMyBP ‐C mutations, can trigger production of 1 such truncated pro
Autor:
Qinghang Meng, Jeffrey Robbins, Monte S. Willis, Hanna Osinska, Kritton Shay-Winkler, Bidur Bhandary, Na Xu
Publikováno v:
Circulation Research. 121
Background: Hypertrophic cardiomyopathy is considered one of the most common genetic heart disorders, occurring with a frequency of about 1 in 200, with approximately 30% of those affected showing mutations within the cardiac myosin-binding protein C