Larry E. Wagner
University of Rochester
49 Papers
201 Citations
Larry E. Wagner is an academic researcher from University of Rochester. The author has contributed to research in topics: Chemistry & Inositol trisphosphate receptor. The author has an hindex of 26, co-authored 45 publications. Previous affiliations of Larry E. Wagner include University of Rochester Medical Center & University of Washington.
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Papers
Phosphorylation of type-1 inositol 1,4,5-trisphosphate receptors by cyclic nucleotide-dependent protein kinases: a mutational analysis of the functionally important sites in the S2+ and S2- splice variants.
TL;DR: It is demonstrated that Ser-1755 is the functionally important residue for phosphoregulation by PKA and PKG in the neuronal variant of the InsP3R-1 and defines the molecular sites phosphorylated in the major variants expressed in neuronal and peripheral tissues.
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Regulation of single inositol 1,4,5‐trisphosphate receptor channel activity by protein kinase A phosphorylation
TL;DR: Biophysical analysis indicated that channel activity can be described by three states: an open state, a long lived closed state which manifests itself as long interburst intervals, and a short‐lived closed state, and the predominant effect of InsP3R‐1 phosphorylation is to increase the likelihood of extended bursting activity and thus markedly augment Ca2+ release.
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Differential regulation of the InsP3 receptor type‐1 and ‐2 single channel properties by InsP3, Ca2+ and ATP
Larry E. Wagner,David I. Yule +1 more
TL;DR: The differing modes of regulation of InsP3R‐1 and InsP4,5‐trisphosphate receptors probably markedly influence the characteristics of intracellular Ca2+ signals observed in cells in which these isoforms are expressed.
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Store-operated Ca2+ entry regulates Ca2+-activated chloride channels and eccrine sweat gland function
Axel R. Concepcion,Martin Vaeth,Larry E. Wagner,Miriam Eckstein,Lee Hecht,Jun Yang,David Crottès,Maximilian Seidl,Hyosup P. Shin,Carl Weidinger,Scott J. Cameron,Stuart E. Turvey,Thomas B. Issekutz,Isabelle Meyts,Rodrigo S. Lacruz,Mario Ćuk,David I. Yule,Stefan Feske +17 more
TL;DR: It is shown that CRAC channel-deficient patients and mice with ectodermal tissue-specific deletion of Orai1 or Stim1 and Stim2 or Stim2 (Stim1/2K14Cre) and human sweat gland cells lacking ORAI1 or STIM1 failed to sweat despite normal sweat gland development.
The volume-regulated anion channel LRRC8C suppresses T cell function by regulating cyclic dinucleotide transport and STING–p53 signaling
Axel R. Concepcion,Larry E. Wagner,Jing He Zhu,Anthony Tao,Jun Yang,Alireza Khodadadi-Jamayran,Yin Hu Wang,Menghan Liu,Rebecca Rose,Drew R. Jones,William A. Coetzee,David I. Yule,Stefan Feske +12 more
TL;DR: In this paper , the authors identify LRRC8C as a critical component of the volume-regulated anion channel (VRAC) in T cells, where its deletion abolishes VRAC currents and RVD.
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