Morris F. White
Boston Children's Hospital
344 Papers
5K Citations
Morris F. White is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Insulin receptor & Insulin receptor substrate. The author has an hindex of 117, co-authored 336 publications. Previous affiliations of Morris F. White include University of Vermont & Wayne State University.
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Papers
Insulin receptor substrate 1 (IRS-1) plays a unique role in normal epidermal physiology.
Marianna Sadagurski,Sharon Nofech-Mozes,Galina Weingarten,Morris F. White,Takashi Kadowaki,Efrat Wertheimer +5 more
TL;DR: It is shown for the first time that IRS‐1 but not IRS‐2 has an effect on skin formation and development, being one of the main activators of the differentiation process in skin keratinocytes.
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Ablation of insulin receptor substrates 1 and 2 suppresses Kras-driven lung tumorigenesis
He Xu,Min-Sik Lee,Min-Sik Lee,Pei-Yun Tsai,Pei-Yun Tsai,Ashley Adler,Natasha L. Curry,Saketh Challa,Elizaveta Freinkman,Daniel S. Hitchcock,Kyle D. Copps,Kyle D. Copps,Morris F. White,Morris F. White,Roderick T. Bronson,Michael Marcotrigiano,Yaotang Wu,Clary B. Clish,Nada Y. Kalaany +18 more
TL;DR: Genetic evidence is provided that lung-specific dual ablation of insulin receptor substrates 1/2 (Irs1/Irs2), which mediate insulin and IGF1 signaling, strongly suppresses tumor initiation and dramatically extends the survival of a mouse model of lung cancer with Kras activation and p53 loss.
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Plasma insulin levels predict the development of atherosclerosis when IRS2 deficiency is combined with severe hypercholesterolemia in apolipoprotein E-null mice.
Herminia González-Navarro,Marian Vila-Caballer,María Francisca Pastor,Ángela Vinué,Morris F. White,Deborah J. Burks,Vicente Andrés +6 more
TL;DR: The results suggest that hyperinsulinemia as a result of Irs2 genetic ablation contributes to increased atherosclerosis when combined with severe hypercholesterolemia in the absence of hyperglycaemia, implicating IRS2 as an important modulator of murine hypercholesterololemia-dependent Atherosclerosis.
Phosphatidylcholine transfer protein interacts with thioesterase superfamily member 2 to attenuate insulin signaling.
Baran A. Ersoy,Akansha Tarun,Katharine E. D’Aquino,Nancy J. Hancer,Chinweike Ukomadu,Morris F. White,Thomas Michel,Brendan D. Manning,David E. Cohen +8 more
TL;DR: The authors propose that PC-TP links the changes in membrane composition that occur after feeding or fasting to modulation of the activity of the insulin signaling pathway, and reveal a phospholipid-dependent mechanism that suppresses insulin signaling downstream of its receptor.
Attenuation of accumulation of neointimal lipid by pioglitazone in mice genetically deficient in insulin receptor substrate-2 and apolipoprotein E.
Maria H. Clough,David J. Schneider,Burton E. Sobel,Morris F. White,Morris F. White,Marilyn P. Wadsworth,Douglas J. Taatjes +6 more
TL;DR: Genetically induced intensification of insulin resistance increases atheroma formation and attenuation of insulin resistant mice by treatment with pioglitazone decreases accumulation of lipid in the neointima.