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Robert A. Sikkink

Researcher at Mayo Clinic

Publications -  18
Citations -  867

Robert A. Sikkink is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Calcineurin & Binding site. The author has an hindex of 13, co-authored 18 publications receiving 833 citations. Previous affiliations of Robert A. Sikkink include University of Texas Southwestern Medical Center & University of Rochester.

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Identification of Gene Mutations in Autosomal Dominant Polycystic Kidney Disease through Targeted Resequencing

TL;DR: A strategy to analyze both the PKD1 and PKD2 genes using next-generation sequencing by pooling long-range PCR amplicons and multiplexing bar-coded libraries is developed and validated and is a model for future genetic characterization of large ADPKD populations.
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Failure of Calcineurin Inhibitors to Prevent Pressure-Overload Left Ventricular Hypertrophy in Rats

TL;DR: In this article, the authors showed that calcineurin inhibitors, cyclosporin A (CsA) and FK 506 (0.3 mg · kg −1 · d −1 ) or even higher doses of CsA (10 and 20 mg· kg − 1 · d−1 ) were sufficient to prevent the development of pressure-overload hypertrophy in the spontaneously hypertensive rat and aortic banding.
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Inhibition of calcineurin phosphatase activity by a calcineurin B homologous protein.

TL;DR: It is reported that calcineurin is also the target of a recently identified Ca2+-binding protein, CHP (forcalcineur in homologous protein), which shares a high degree of homology with the regulatory B subunit of calcinesurin and with calmodulin.
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Neelaredoxin, an Iron-binding Protein from the Syphilis Spirochete, Treponema pallidum, Is a Superoxide Reductase

TL;DR: This finding, the first description of a T. pallidum iron-binding protein, indicates that the syphilis spirochete copes with oxidative stress via a primitive mechanism, which, thus far, has not been described in pathogenic bacteria.
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Mate Pair Sequencing of Whole-Genome-Amplified DNA Following Laser Capture Microdissection of Prostate Cancer

TL;DR: A novel methodology to partner laser capture microdissection (LCM) with sequencing platforms, through a whole-genome amplification (WGA) protocol performed in situ directly on LCM engrafted cells, aiding in the derivation of genomic aberrations that initiate cancer and drive cancer progression is presented.