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Madhulika Dixit

Researcher at Indian Institute of Technology Madras

Publications -  52
Citations -  1863

Madhulika Dixit is an academic researcher from Indian Institute of Technology Madras. The author has contributed to research in topics: Phosphorylation & Insulin. The author has an hindex of 20, co-authored 49 publications receiving 1562 citations. Previous affiliations of Madhulika Dixit include University of Tennessee Health Science Center & Indian Institutes of Technology.

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Role of PECAM-1 in the shear-stress-induced activation of Akt and the endothelial nitric oxide synthase (eNOS) in endothelial cells

TL;DR: The data indicate that the shear-stress-induced activation of Akt and eNOS in endothelial cells is modulated by the tyrosine phosphorylation of PECAM-1 whereas theShear- stress-induced phosphorylated AMPK is controlled by an alternative signaling pathway.
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Role of Polyphenols and Other Phytochemicals on Molecular Signaling

TL;DR: The active antioxidative, antiproliferative, anti-inflammatory, or antiangiogenesis role of various phytochemicals for prevention of chronic diseases is reviewed.
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Nimbolide upregulates RECK by targeting miR-21 and HIF-1α in cell lines and in a hamster oral carcinogenesis model.

TL;DR: Findings provide compelling evidence that targeting RECK, a keystone protein that regulates mediators of invasion and angiogenesis with phytochemicals such as nimbolide may be a robust therapeutic approach to prevent oral cancer progression.
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Astaxanthin Inhibits JAK/STAT-3 Signaling to Abrogate Cell Proliferation, Invasion and Angiogenesis in a Hamster Model of Oral Cancer

TL;DR: Evidence is provided that dietary astaxanthin prevents the development and progression of HBP carcinomas through the inhibition of JAK-2/STAT-3 signaling and its downstream events and astaxAnthin that functions as a potent inhibitor of tumour development and progress by targeting JAK/STAT signaling may be an ideal candidate for cancer chemoprevention.
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Platelet Sarcoplasmic Endoplasmic Reticulum Ca2+-ATPase and μ-Calpain Activity Are Altered in Type 2 Diabetes Mellitus and Restored by Rosiglitazone

TL;DR: In this article, the authors found enhanced tyrosine nitration and inactivation of SERCA-2 and activation of μ-calpain in platelets from patients with type 2 diabetes mellitus.