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Surendra Kumar Nayak

Researcher at Lovely Professional University

Publications -  49
Citations -  1937

Surendra Kumar Nayak is an academic researcher from Lovely Professional University. The author has contributed to research in topics: Catalysis & Melanopsin. The author has an hindex of 17, co-authored 45 publications receiving 1651 citations. Previous affiliations of Surendra Kumar Nayak include SRI International & Salk Institute for Biological Studies.

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Illumination of the melanopsin signaling pathway.

TL;DR: It is found that expression of melanopsin in Xenopus oocytes results in light-dependent activation of membrane currents through the Gαq/Gα11 G protein pathway, with an action spectrum closely matching that of melanpsin-expressing ipRGCs and of behavioral responses to light in mice lacking rods and cones.
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Circadian clock protein cryptochrome regulates the expression of proinflammatory cytokines.

TL;DR: It is shown that absence of the core clock component protein cryptochrome (CRY) leads to constitutive elevation of proinflammatory cytokines in a cell-autonomous manner, and that CRY1 binds to adenylyl cyclase and limits cAMP production.
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Detecting common mental disorders in primary care in India: a comparison of five screening questionnaires.

TL;DR: There is little difference in the ability of these questionnaires to identify cases accurately, but none showed high PPVs without a considerable compromise on sensitivity, so the choice of an optimum cut-off score that yields the best balance between sensitivity and PPV may need to be tailored to individual settings.
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Evolution of the Human Ion Channel Set

TL;DR: Genome comparisons highlight a number of highly conserved channel families that are likely to have non-redundant functions in metazoans and represent some of the best new opportunities for channel target prospecting.
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Parathyroid Hormone (PTH) and PTH-Related Peptide Domains Contributing to Activation of Different PTH Receptor-Mediated Signaling Pathways

TL;DR: Several PTH and PTHrP peptides evaluated in this study promote different patterns of biased agonist signaling and may serve as useful tools to further elucidate therapeutically relevant PTH1R signaling in osteoblasts.