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D-Index & Metrics

Biology and Biochemistry

D-Index
84
Citations
28409
World Ranking
3287
National Ranking
1665

Overview

Timothy A. McKinsey is affiliated with the University of Colorado Anschutz Medical Campus in the United States. Their research focuses primarily on medicine, with significant contributions in biochemistry, genetics, and molecular biology. The body of work spans key subfields including molecular biology, cardiology and cardiovascular medicine, oncology, surgery, and physiology.

The scientist's work covers several main topics, such as peptidase inhibition and analysis, cardiac fibrosis and remodeling, cardiovascular function and risk factors, histone deacetylase inhibitors research, signaling pathways in disease, tissue engineering and regenerative medicine, and adipose tissue and metabolism.

Timothy A. McKinsey has frequently published in venues including bioRxiv (Cold Spring Harbor Laboratory), Journal of Molecular and Cellular Cardiology, Circulation Research, Faculty Opinions - Post-Publication Peer Review of the Biomedical Literature, and Circulation.

Their notable recent papers include:

  • A transcriptional switch governs fibroblast activation in heart disease, 2021, Nature
  • HDAC Inhibition Reverses Preexisting Diastolic Dysfunction and Blocks Covert Extracellular Matrix Remodeling, 2021, Circulation
  • HDAC inhibition improves cardiopulmonary function in a feline model of diastolic dysfunction, 2020, Science Translational Medicine
  • Structural and in Vivo Characterization of Tubastatin A, a Widely Used Histone Deacetylase 6 Inhibitor, 2020, ACS Medicinal Chemistry Letters
  • Chromatin remodelling drives immune cell-fibroblast communication in heart failure, 2024, Nature

Frequently collaborating coauthors include Joshua G. Travers, Rushita A. Bagchi, Maria A. Cavasin, Steven R. Houser, and Kathleen C. Woulfe.

Best Publications

  • Signal-dependent nuclear export of a histone deacetylase regulates muscle differentiation

    Timothy A. McKinsey;Chun-Li Zhang;Jianrong Lu;Eric N. Olson

  • Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy

    Chun Li Zhang;Timothy A. McKinsey;Shurong Chang;Christopher L. Antos

  • Suppression of tumor necrosis factor-induced cell death by inhibitor of apoptosis c-IAP2 is under NF-κB control

    Zhi-Liang Chu;Timothy A. McKinsey;Lily Liu;Jennifer J. Gentry

  • Coupling of a signal response domain in I kappa B alpha to multiple pathways for NF-kappa B activation.

    J. A. Brockman;D. C. Scherer;T. A. Mckinsey;S. M. Hall

  • MEF2: a calcium-dependent regulator of cell division, differentiation and death

    Timothy A McKinsey;Chun Li Zhang;Eric N Olson

  • Histone deacetylases 5 and 9 govern responsiveness of the heart to a subset of stress signals and play redundant roles in heart development

    Shurong Chang;Timothy A. McKinsey;Chun Li Zhang;James A. Richardson

  • Histone Deacetylase 5 Epigenetically Controls Behavioral Adaptations to Chronic Emotional Stimuli

    William Renthal;Ian Maze;Vaishnav Krishnan;Herbert E. Covington

  • Regulation of skeletal myogenesis by association of the MEF2 transcription factor with class II histone deacetylases.

    Jianrong Lu;Timothy A. McKinsey;Chun Li Zhang;Eric N. Olson

  • Protein Kinases C and D Mediate Agonist-Dependent Cardiac Hypertrophy through Nuclear Export of Histone Deacetylase 5

    Rick B. Vega;Brooke C. Harrison;Eric Meadows;Charles R. Roberts

  • Signal-dependent activation of the MEF2 transcription factor by dissociation from histone deacetylases

    Jianrong Lu;Timothy A. McKinsey;Rebekka L. Nicol;Eric N. Olson

  • CaM kinase signaling induces cardiac hypertrophy and activates the MEF2 transcription factor in vivo

    Robert Passier;Hong Zeng;Norbert Frey;Francisco J. Naya

  • Activation of the myocyte enhancer factor-2 transcription factor by calcium/calmodulin-dependent protein kinase-stimulated binding of 14-3-3 to histone deacetylase 5

    Timothy A. McKinsey;Chun Li Zhang;Eric N. Olson

  • Activated glycogen synthase-3β suppresses cardiac hypertrophy in vivo

    Christopher L. Antos;Timothy A. McKinsey;Norbert Frey;William Kutschke

  • Local InsP3-dependent perinuclear Ca2+ signaling in cardiac myocyte excitation-transcription coupling.

    Xu Wu;Tong Zhang;Julie B C Bossuyt;Xiaodong Li

  • MEF2 responds to multiple calcium‐regulated signals in the control of skeletal muscle fiber type

    Hai Wu;Francisco J. Naya;Timothy A. McKinsey;Brian Mercer

  • Control of muscle development by dueling HATs and HDACs.

    Timothy A McKinsey;Chun Li Zhang;Eric N Olson

  • Decoding calcium signals involved in cardiac growth and function

    Norbert Frey;Timothy A. McKinsey;Eric N. Olson

  • Independent Signals Control Expression of the Calcineurin Inhibitory Proteins MCIP1 and MCIP2 in Striated Muscles

    J. Yang;B. Rothermel;R. B. Vega;N. Frey

  • Canonical transient receptor potential channels promote cardiomyocyte hypertrophy through activation of calcineurin signaling

    Erik W. Bush;David B. Hood;Philip J. Papst;Joseph A. Chapo

  • Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo.

    Beverly A Rothermel;Timothy A. McKinsey;Rick B. Vega;Rebekka L. Nicol

Frequent Co-Authors

Eric N. Olson
Eric N. Olson The University of Texas Southwestern Medical Center
Kurt R. Stenmark
Kurt R. Stenmark University of Colorado Anschutz Medical Campus
Michael R. Bristow
Michael R. Bristow University of Colorado Anschutz Medical Campus
Dean W. Ballard
Dean W. Ballard Vanderbilt University
James A. Richardson
James A. Richardson The University of Texas Southwestern Medical Center
Paul P. Tak
Paul P. Tak GlaxoSmithKline (United Kingdom)
Steven R. Houser
Steven R. Houser Temple University
Deepak Srivastava
Deepak Srivastava King's College London
James E. Bradner
James E. Bradner Amgen (United States)
Sheila Collins
Sheila Collins Vanderbilt University Medical Center

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