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N. Scott Blair
Researcher at Cincinnati Children's Hospital Medical Center
Publications - 5
Citations - 2408
N. Scott Blair is an academic researcher from Cincinnati Children's Hospital Medical Center. The author has contributed to research in topics: Calcineurin & Endoplasmic reticulum. The author has an hindex of 5, co-authored 5 publications receiving 2268 citations. Previous affiliations of N. Scott Blair include Boston Children's Hospital.
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Journal ArticleDOI
Loss of cyclophilin D reveals a critical role for mitochondrial permeability transition in cell death
Christopher P. Baines,Robert A. Kaiser,Nicole H. Purcell,N. Scott Blair,Hanna Osinska,Michael Hambleton,Eric W. Brunskill,M. Richard Sayen,Roberta A. Gottlieb,Gerald W. Dorn,Jeffrey Robbins,Jeffery D. Molkentin +11 more
TL;DR: Cyclophilin D and the mitochondrial permeability transition are required for mediating Ca2+- and oxidative damage-induced cell death, but not Bcl-2 family member-regulated death.
Journal ArticleDOI
A thrombospondin-dependent pathway for a protective ER stress response
Jeffrey M. Lynch,Marjorie Maillet,Davy Vanhoutte,Aryn Schloemer,Michelle A. Sargent,Michelle A. Sargent,N. Scott Blair,Kaari A. Lynch,Tetsuya Okada,Bruce J. Aronow,Hanna Osinska,Ron Prywes,John N. Lorenz,Kazutoshi Mori,Jack Lawler,Jeffrey Robbins,Jeffery D. Molkentin,Jeffery D. Molkentin +17 more
TL;DR: Thrombospondin can function inside the cell during disease remodeling to augment ER function and protect through a mechanism involving regulation of Atf6α.
Journal ArticleDOI
Plasma membrane Ca2+-ATPase isoform 4 antagonizes cardiac hypertrophy in association with calcineurin inhibition in rodents
Xu Wu,Baojun Chang,N. Scott Blair,Michelle A. Sargent,Allen J. York,Jeffrey Robbins,Gary E. Shull,Jeffery D. Molkentin +7 more
TL;DR: Pmca4b likely reduces the local Ca2+ signals involved in reactive cardiomyocyte hypertrophy via calcineurin regulation, suggesting its potential role in controlling Ca2-dependent signaling effectors such as calcineURin.
Journal ArticleDOI
Dissection of Thrombospondin-4 Domains Involved in Intracellular Adaptive Endoplasmic Reticulum Stress-Responsive Signaling.
Matthew J. Brody,Tobias G. Schips,Davy Vanhoutte,Onur Kanisicak,Jason Karch,Jason Karch,Bryan D. Maliken,N. Scott Blair,Michelle A. Sargent,Michelle A. Sargent,Vikram Prasad,Jeffery D. Molkentin,Jeffery D. Molkentin +12 more
TL;DR: The domains of Thbs4 that mediate interactions with ER proteins, such as BiP and Atf6α, and the domains mediating activation of the ER stress response are dissected, identifying the critical intracellular functional domains of thrombospondin-4, which was formerly thought to have only extracellular functions.
antagonizes cardiac hypertrophy in association with calcineurin inhibition in rodents
Xu Wu,Baojun Chang,N. Scott Blair,Michelle A. Sargent,Allen J. York,Jeffrey Robbins,Gary E. Shull,Jeffery D. Molkentin +7 more
TL;DR: In this article, the authors generated cardiac-specific inducible PMCA4b transgenic mice that displayed normal global Ca2+ transient and cellular contraction levels and reduced cardiac hypertrophy following transverse aortic constriction (TAC) or phenylephrine/Ang II infusion, but showed no reduction in exercise-induced hyper-trophy.