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Robert J. Winkfein

Researcher at University of Calgary

Publications -  56
Citations -  3298

Robert J. Winkfein is an academic researcher from University of Calgary. The author has contributed to research in topics: Gene & Complementary DNA. The author has an hindex of 28, co-authored 56 publications receiving 3156 citations.

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A brain-specific activator of cyclin-dependent kinase 5

TL;DR: A full-length complementary DNA clone showed that p25 is a truncated form of a larger protein precursor, p35, which seems to be the predominant form of the protein in crude brain extract, and is the first example of a Cdc2-like kinase with neuronal function.
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Brain proline-directed protein kinase is a neurofilament kinase which displays high sequence homology to p34cdc2.

TL;DR: The results suggest that the brain kinase represents a new category of the cdc2 family, and that some members of thecdc2 kinase family may have major functions unrelated to cell cycle control.
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Molecular identification of the ryanodine receptor pore-forming segment.

TL;DR: It is reported here that single point mutations introduced into this region of the mouse cardiac ryanodine receptor reduce or abolish high affinity [3H]ryanodine binding and single channel analysis revealed that a single substitution of alanine for glycine 4824 within this region reduced the single channel conductance.
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Cardiac ion channel expression and contractile function in mice with deletion of thyroid hormone receptor alpha or beta.

TL;DR: Findings indicate that potassium channel genes that code for K+ channels involved in action potential repolarization, like KV 4.2 and minK, are T3Rα targets and cyclic nucleotide-gated channels, HCN2 and HCN4, are targets of T2Rα, and these transcripts respond markedly to altered T3 signaling concomitant with bradycardia.
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Targeted polyphosphatase expression alters mitochondrial metabolism and inhibits calcium-dependent cell death

TL;DR: Specific reduction of mitochondrial polyP, by polyphosphatase expression, significantly modulates mitochondrial bioenergetics, as indicated by the reduction of inner membrane potential and increased NADH levels.