Benjamin A. Clarke
National Institutes of Health
4 Papers
Benjamin A. Clarke is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Sphingolipid & Gene silencing. The author has an hindex of 4, co-authored 4 publications.
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Papers
De Novo Sphingolipid Biosynthesis Is Required for Adipocyte Survival and Metabolic Homeostasis.
Aikaterini Alexaki,Benjamin A. Clarke,Oksana Gavrilova,Yinyan Ma,Hongling Zhu,Xinran Ma,Lingyan Xu,Galina Tuymetova,Bridget C. Larman,Maria L. Allende,Teresa M. Dunn,Richard L. Proia +11 more
TL;DR: It is shown that reduced de novo sphingolipid biosynthesis within adipocytes is associated with adipocyte death, adipose tissue remodeling, and metabolic dysfunction.
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IGF2BP1 overexpression causes fetal-like hemoglobin expression patterns in cultured human adult erythroblasts
Jaira F. de Vasconcellos,Laxminath Tumburu,Colleen Byrnes,Y. Terry Lee,Pauline C. Xu,May Li,Antoinette Rabel,Benjamin A. Clarke,Nicholas R. Guydosh,Richard L. Proia,Jeffery L. Miller +10 more
TL;DR: A focused investigation of a let-7 target named “insulin-like growth-factor 2 mRNA-binding protein 1” (IGF2BP1), for its potential role in reactivating HbF in adult cells, suggests a mechanism for chronoregulation of fetal and adult hemoglobin expression in humans.
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Sphingosine-1-phosphate Phosphatase 2 Regulates Pancreatic Islet β-Cell Endoplasmic Reticulum Stress and Proliferation *
Yoshimitsu Taguchi,Maria L. Allende,Hiroki Mizukami,Emily K. Cook,Oksana Gavrilova,Galina Tuymetova,Benjamin A. Clarke,Weiping Chen,Ana Olivera,Richard L. Proia +9 more
TL;DR: The results show that Sgpp2 deletion causes β-cell endoplasmic reticulum stress, which is a known cause of β- cell dysfunction, and reveal a juncture in the sphingolipid recycling pathway that could impact the development of diabetes.
The Ormdl genes regulate the sphingolipid synthesis pathway to ensure proper myelination and neurologic function in mice.
Benjamin A. Clarke,Saurav Majumder,Hongling Zhu,Y. Terry Lee,Mari Kono,Cuiling Li,Caroline Khanna,Hailey Blain,Ronit Schwartz,Vienna L Huso,Colleen Byrnes,Galina Tuymetova,Teresa M. Dunn,Maria L. Allende,Richard L. Proia +14 more
TL;DR: The data indicate that the Ormdls function to restrain sphingolipid metabolism in order to limit levels of dangerous metabolic intermediates that can interfere with essential physiological processes such as myelination.