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Nitai C. Hait

Researcher at Roswell Park Cancer Institute

Publications -  56
Citations -  7086

Nitai C. Hait is an academic researcher from Roswell Park Cancer Institute. The author has contributed to research in topics: Sphingosine & Sphingosine-1-phosphate. The author has an hindex of 35, co-authored 50 publications receiving 6337 citations. Previous affiliations of Nitai C. Hait include Virginia Commonwealth University.

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Regulation of Histone Acetylation in the Nucleus by Sphingosine-1-Phosphate

TL;DR: Him Hait et al. (p. 1254) report that S1P can also function by direct binding to the nuclear enzymes, histone deacetylases (HDACs) 1 and 2, which are direct intracellular targets of S 1P and link nuclear S1p to epigenetic regulation of gene expression.
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Sphingosine-1-phosphate is a missing cofactor for the E3 ubiquitin ligase TRAF2

TL;DR: The data show that TRAF2 is a novel intracellular target of S1p, and that S1P is the missing cofactor for TRAF 2 E3 ubiquitin ligase activity, indicating a new paradigm for the regulation of lysine-63-linked polyubiquitination.
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SphK1 and SphK2, Sphingosine Kinase Isoenzymes with Opposing Functions in Sphingolipid Metabolism

TL;DR: The results demonstrate that SphK1 and SphK2 have opposing roles in the regulation of ceramide biosynthesis and suggest that the location of sphingosine 1-phosphate production dictates its functions.
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Sphingosine-1-Phosphate Links Persistent STAT3 Activation, Chronic Intestinal Inflammation, and Development of Colitis-Associated Cancer

TL;DR: The prodrug FTY720 decreased SphK1 and S1PR1 expression and eliminated the NF-κB/IL-6/STAT3 amplification cascade and development of CAC, even in Sphk2(-/-) mice, and may be useful in treating colon cancer in individuals with ulcerative colitis.
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Sphingosine kinases, sphingosine 1-phosphate, apoptosis and diseases.

TL;DR: Since sphingolipid metabolism is often dysregulated in many diseases, targeting SphKs is potentially clinically relevant, and the growing recent literature on the regulation and the roles of SphKS and S1P in apoptosis and diseases is reviewed.