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Tathagat Dutta Ray

Researcher at New York University

Publications -  10
Citations -  3575

Tathagat Dutta Ray is an academic researcher from New York University. The author has contributed to research in topics: Inflammation & Tumor necrosis factor alpha. The author has an hindex of 8, co-authored 10 publications receiving 3044 citations. Previous affiliations of Tathagat Dutta Ray include University of Massachusetts Medical School & Boston University.

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Phosphorylation-Driven Assembly of the RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation

TL;DR: The findings suggest that RIP3 controls programmed necrosis by initiating the pronecrotic kinase cascade, and that this is necessary for the inflammatory response against virus infections.
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Inhibition of miR-33a/b in non-human primates raises plasma HDL and lowers VLDL triglycerides

TL;DR: It is shown in African green monkeys that systemic delivery of an anti-miRNA oligonucleotide that targets both miR-33a and miR/b increased hepatic expression of ABCA1 and induced a sustained increase in plasma HDL levels over 12 weeks, establishing a promising therapeutic strategy to raise plasma HDL and lower VLDL triglyceride levels for the treatment of dyslipidaemias that increase cardiovascular disease risk.
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The neuroimmune guidance cue netrin-1 promotes atherosclerosis by inhibiting the emigration of macrophages from plaques

TL;DR: Netrin-1, a neuroimmune guidance cue, was secreted by macrophages in human and mouse atheroma, where it inactivated the migration of macrophage toward chemokines linked to their egress from plaques, establishing a causative role for negative regulators of leukocyte migration in chronic inflammation.
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Netrin-1 promotes adipose tissue macrophage retention and insulin resistance in obesity

TL;DR: It is shown that the neuroimmune guidance cue netrin-1 is highly expressed in obese but not lean adipose tissue of humans and mice, where it directs the retention of macrophages, and hematopoietic deletion of Ntn1 facilitates adipOSE tissue macrophage emigration, reduces inflammation and improves insulin sensitivity.