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K. Ulrich Bayer

Researcher at Anschutz Medical Campus

Publications -  73
Citations -  9939

K. Ulrich Bayer is an academic researcher from Anschutz Medical Campus. The author has contributed to research in topics: Ca2+/calmodulin-dependent protein kinase & Long-term potentiation. The author has an hindex of 33, co-authored 65 publications receiving 8780 citations. Previous affiliations of K. Ulrich Bayer include Stanford University & University of Colorado Hospital.

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Journal ArticleDOI

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
Journal ArticleDOI

Interaction with the NMDA receptor locks CaMKII in an active conformation

K. Ulrich Bayer, +7 more
- 14 Jun 2001 - 
TL;DR: It is shown that regulated CaMKII interaction with two sites on the NMDA receptor subunit NR2B provides a mechanism for the glutamate-induced translocation of the kinase to the synapse in hippocampal neurons.
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CaMKII regulation in information processing and storage

Steven J. Coultrap, +1 more
- 01 Oct 2012 - 
TL;DR: Emerging evidence supports a direct role in information processing, while storage of synaptic information may instead be mediated by regulated interaction of CaMKII with the NMDA receptor (NMDAR) complex.
Journal ArticleDOI

Transition from reversible to persistent binding of CaMKII to postsynaptic sites and NR2B.

K. Ulrich Bayer, +5 more
- 25 Jan 2006 - 
TL;DR: It is shown that CaMKII reversibly translocates to synaptic sites in response to brief stimuli, but its resident time at the synapse increases after longer stimulation, which reflects temporal patterns of synaptic stimulation and supports an initial reversible and Ca2+/CaM-dependent binding at the substrate-binding site.
Journal ArticleDOI

Dual Mechanism of a Natural CaMKII Inhibitor

Rebekah S. Vest, +4 more
- 01 Dec 2007 - 
TL;DR: The inhibitory mechanism of CaM-KIIN is revealed and a powerful new tool for dissecting CaMKII function is established, as CN21 (derived from CaKIN amino acids 43-63) showed full specificity and potency of CaMK II inhibition.