K
Kirk U. Knowlton
Researcher at Intermountain Medical Center
Publications - 184
Citations - 9319
Kirk U. Knowlton is an academic researcher from Intermountain Medical Center. The author has contributed to research in topics: Medicine & Internal medicine. The author has an hindex of 42, co-authored 137 publications receiving 8623 citations. Previous affiliations of Kirk U. Knowlton include University of California & American Heart Association.
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Journal ArticleDOI
Regulation of cardiac gene expression during myocardial growth and hypertrophy: molecular studies of an adaptive physiologic response.
TL;DR: The development of a bona fide in vivo pressure overload model of hypertrophy in a small animal model that can be genetically manipulated should allow a rigorous analysis of the role of specific signaling mechanisms in the activation of the responses of cardiac genes during the hypertrophic process in vivo.
Journal ArticleDOI
Segregation of atrial-specific and inducible expression of an atrial natriuretic factor transgene in an in vivo murine model of cardiac hypertrophy
Howard A. Rockman,Robert S. Ross,Adrienne N. Harris,Kirk U. Knowlton,Mark E. Steinhelper,Loren J. Field,John Ross,Kenneth R. Chien +7 more
TL;DR: Evidence is provided that atrial-specific and inducible expression of the atrial natriuretic factor gene can be segregated, suggesting that a distinct set of regulatory cis sequences may mediate the up-regulation of the ANF gene during in vivo pressure overload hypertrophy.
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Endothelin induction of inositol phospholipid hydrolysis, sarcomere assembly, and cardiac gene expression in ventricular myocytes. A paracrine mechanism for myocardial cell hypertrophy.
H E Shubeita,Patrick M. McDonough,Adrienne N. Harris,Kirk U. Knowlton,C C Glembotski,Joan Heller Brown,Kenneth R. Chien +6 more
TL;DR: Iwaki et al. as mentioned in this paper examined the effects of endothelin-1 on phosphoinositide hydrolysis, diacylglycerol formation, and the induction of myocardial cell hypertrophy.
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Enteroviral protease 2A cleaves dystrophin: Evidence of cytoskeletal disruption in an acquired cardiomyopathy
Cornel Badorff,Gil-Hwan Lee,Barry J. Lamphear,Maryann E. Martone,Kevin P. Campbell,Robert E. Rhoads,Kirk U. Knowlton +6 more
TL;DR: It is demonstrated here that purified Coxsackievirus protease 2A cleaves dystrophin in vitro as predicted by computer analysis, suggesting a molecular mechanism through which enteroviral infection contributes to the pathogenesis of acquired forms of dilated cardiomyopathy.
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Cardiotrophin 1 (CT-1) Inhibition of Cardiac Myocyte Apoptosis via a Mitogen-activated Protein Kinase-dependent Pathway DIVERGENCE FROM DOWNSTREAM CT-1 SIGNALS FOR MYOCARDIAL CELL HYPERTROPHY
TL;DR: CT-1 promotes cardiac myocyte survival via the activation of an antiapoptotic signaling pathway that requires MAP kinases, whereas the hypertrophy induced by CT-1 may be mediated by alternative pathways, e.g. Janus kinase/STAT or MEK kinase /c-Jun NH2-terminal protein kinase.