C
Chelsea U Kidwell
Researcher at University of Utah
Publications - 3
Citations - 20
Chelsea U Kidwell is an academic researcher from University of Utah. The author has contributed to research in topics: Peroxin & Mitochondrion. The author has an hindex of 2, co-authored 3 publications receiving 4 citations.
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Journal ArticleDOI
The biochemical basis of mitochondrial dysfunction in Zellweger Spectrum Disorder.
Esther Nuebel,Esther Nuebel,Esther Nuebel,Jeffrey T. Morgan,Jeffrey T. Morgan,Sarah Fogarty,Sarah Fogarty,Jacob M. Winter,Sandra Lettlova,Jordan A. Berg,Yu-Chan Chen,Chelsea U Kidwell,J. Alan Maschek,Katie J. Clowers,Catherine Argyriou,Lingxiao Chen,Ilka Wittig,James E. Cox,Minna Roh-Johnson,Nancy Braverman,Nancy Braverman,Joshua L. Bonkowsky,Steven P. Gygi,Jared Rutter,Jared Rutter +24 more
TL;DR: In this article, the authors investigated the fate of peroxisomal mRNAs and proteins in Zellweger spectrum disorder (ZSD) model systems and found that peroxins were still expressed and a subset of them accumulated on the mitochondrial membrane, which resulted in gross mitochondrial abnormalities and impaired mitochondrial metabolic function.
Posted ContentDOI
Msp1/ATAD1 restores mitochondrial function in Zellweger Spectrum Disease
Esther Nuebel,Jeffrey T. Morgan,Sarah Fogarty,Jacob M. Winter,Sandra Lettlova,Jordan A. Berg,Yu-Chan Chen,Chelsea U Kidwell,J. Alan Maschek,Katie J. Clowers,Catherine Argyriou,Lingxiao Chen,Ilka Wittig,James E. Cox,Minna Roh-Johnson,Nancy Braverman,Steven J. Steinberg,Steven P. Gygi,Jared Rutter +18 more
TL;DR: It is found that loss of peroxisomal import has no effect on peroxin mRNA expression or translational efficiency, and mitochondrial function is rescued in fibroblasts derived from human patients with ZSD by overexpressing ATAD1, an AAA-ATPase that functions in mitochondrial quality control.
Posted ContentDOI
Laterally transferred macrophage mitochondria acts as a signaling source promoting cancer cell proliferation
Chelsea U Kidwell,Joseph R. Casalini,Soorya Pradeep,Sandra D. Scherer,Daniel Greiner,Jarrod S. Johnson,Gregory S. Olson,Jared Rutter,Jared Rutter,Alana L. Welm,Thomas A. Zangle,Thomas A. Zangle,Minna Roh-Johnson,Minna Roh-Johnson +13 more
TL;DR: In this paper, the authors showed that transferred macrophage mitochondria accumulate reactive oxygen species which activate ERK signaling, indicating that transferred mitochondria act as a signaling source that promotes cancer cell proliferation.