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Peter M. Vassilev

Researcher at Brigham and Women's Hospital

Publications -  53
Citations -  8557

Peter M. Vassilev is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Extracellular & Receptor. The author has an hindex of 36, co-authored 53 publications receiving 8297 citations. Previous affiliations of Peter M. Vassilev include Harvard University & Beth Israel Deaconess Medical Center.

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Journal ArticleDOI

Polycystins 1 and 2 mediate mechanosensation in the primary cilium of kidney cells

TL;DR: PC1 and PC2 contribute to fluid-flow sensation by the primary cilium in renal epithelium and that they both function in the same mechanotransduction pathway, suggesting loss or dysfunction of PC1 or PC2 may lead to polycystic kidney disease.
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Protofibrillar intermediates of amyloid beta-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons.

TL;DR: The results raise the possibility that the preclinical and early clinical progression of AD is driven in part by the accumulation of specific Aβ assembly intermediates formed during the process of fibrillogenesis, and suggest that PF have inherent biological activity similar to that of mature fibrils.
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Cloning and expression of an inwardly rectifying ATP-regulated potassium channel

TL;DR: A complementary DNA encoding an ATP-regulated potassium channel has been isolated by expression cloning from rat kidney and the presence of an H5 region, which is likely to form the ion conduction pathway, indicates that the protein may share a common origin with voltage-gated potassium channel proteins.
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Molecular Cloning and Characterization of a Channel-like Transporter Mediating Intestinal Calcium Absorption

TL;DR: The properties of a calcium transport protein (CaT1) cloned from rat duodenum using an expression cloning strategy in Xenopus laevis oocytes are reported, which likely plays a key role in the intestinal uptake of calcium.
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Reduced immunostaining for the extracellular Ca2+-sensing receptor in primary and uremic secondary hyperparathyroidism.

TL;DR: There is a variable, but substantial, reduction in the immunoreactivity of the Ca2+o-sensing receptor protein in both parathyroid adenomas and uremic hyperparathyroidism, as assessed by immunohistochemistry, that probably results from reduced expression of the receptor protein and may contribute to the increase in the set-point often observed in these patients.