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Timothy A. McKinsey

Researcher at Anschutz Medical Campus

Publications -  208
Citations -  21571

Timothy A. McKinsey is an academic researcher from Anschutz Medical Campus. The author has contributed to research in topics: Heart failure & Histone deacetylase 5. The author has an hindex of 68, co-authored 179 publications receiving 19784 citations. Previous affiliations of Timothy A. McKinsey include University of Missouri & Vanderbilt University Medical Center.

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

TL;DR: It is suggested that nucleo-cytoplasmic trafficking of HDACs is involved in the control of cellular differentiation, and a mechanism for transcriptional regulation through signal- and differentiation-dependent nuclear export of a chromatin-remodelling enzyme is highlighted.
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Class II Histone Deacetylases Act as Signal-Responsive Repressors of Cardiac Hypertrophy

TL;DR: It is shown that class II HDACs are substrates for a stress-responsive kinase specific for conserved serines that regulate MEF2-HDAC interactions, and act as signal-responsive suppressors of the transcriptional program governing cardiac hypertrophy and heart failure.
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Suppression of tumor necrosis factor-induced cell death by inhibitor of apoptosis c-IAP2 is under NF-κB control

TL;DR: Functional coupling of NF-kappaB and c-IAP2 during the TNF response may provide a signal amplification loop that promotes cell survival rather than death.
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Coupling of a signal response domain in I kappa B alpha to multiple pathways for NF-kappa B activation.

TL;DR: A critical signal response domain in I kappa B alpha is defined that coordinately controls the biologic activities of I k Kappa B alpha and NF-kappa B in response to viral and immune stimuli and is consistent with a causal linkage between the phosphorylation status and proteolytic stability of this cytoplasmic inhibitor.
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MEF2: a calcium-dependent regulator of cell division, differentiation and death

TL;DR: The post-translational mechanisms that confer calcium-sensitivity to MEF2 and its downstream target genes are described, and how this transcription factor can control diverse and mutually exclusive cellular decisions is considered.