; Collaborative interactions between Investigators in the Section of Nephrology and the Department of Cellular and Molecular Physiology at Yale have historically provided much of the experimental evidence that underlies our current understanding of normal kidney function at the cellular, tubular and whole organ level. And yet, at a time when the development of increasingly sophisticated cell and molecular biology techniques has afforded scientists the ability to manipulate the genes and proteins that control these physiologic, processes, many of the investigators involved in these studies have not acquired the technical skills necessary to identify the mechanism(s) that underlie the phenotype that they uncover. The mission of the Yale O'Brien Kidney Center Renal Physiology and Phenotyping Core (Core A) is to utilize our unique expertise in the rigorous study and understanding of renal physiology to provide highly specialized phenotypic analysis of rodents at the systemic, whole kidney and/or individual nephron segment levels. By providing expertise and training in techniques such as tubule micropuncture, in vitro and in vivo microperfusion, determination of glomerular filtration rates and renal perfusion, and continuous blood pressure measurements. Core A is designed to allow investigators to accurately define the site, mechanism and impact of genetic and/or pharmacologic manipulations on cellular, organ, and whole animal physiology. To achieve this, the Yale O'Brien Kidney Center Renal Physiology and Phenotyping Core takes advantage of 2 major strengths: 1) the specialized equipment needed to provide phenotyping .services at the systemic, whole kidney, and individual nephron segment levels, and 2) experienced and skilled personnel capable of using that equipment to generate reliable and reproducible data that are required for thorough, accurate phenotypic analysis. During the previous funding period, this Core was heavily utilized by Investigators with 19 distinct services provided to more than 40 Investigators supporting studies in 32 manuscripts.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Center Core Grants (P30)
Project #
5P30DK079310-07
Application #
8734393
Study Section
Special Emphasis Panel (ZDK1-GRB-6)
Project Start
Project End
Budget Start
2014-08-01
Budget End
2015-07-31
Support Year
7
Fiscal Year
2014
Total Cost
$311,415
Indirect Cost
$124,379
Name
Yale University
Department
Type
DUNS #
043207562
City
New Haven
State
CT
Country
United States
Zip Code
06520
Lausecker, Franziska; Tian, Xuefei; Inoue, Kazunori et al. (2018) Vinculin is required to maintain glomerular barrier integrity. Kidney Int 93:643-655
Knauf, Felix; Velazquez, Heino; Pfann, Victoria et al. (2018) Characterization of renal NaCl and oxalate transport in Slc26a6-/- mice. Am J Physiol Renal Physiol :
Silva, Luciane M; Jacobs, Damon T; Allard, Bailey A et al. (2018) Inhibition of Hedgehog signaling suppresses proliferation and microcyst formation of human Autosomal Dominant Polycystic Kidney Disease cells. Sci Rep 8:4985
Daga, Ankana; Majmundar, Amar J; Braun, Daniela A et al. (2018) Whole exome sequencing frequently detects a monogenic cause in early onset nephrolithiasis and nephrocalcinosis. Kidney Int 93:204-213
Mansour, Sherry G; Hall, Isaac E; Reese, Peter P et al. (2018) Reliability of deceased-donor procurement kidney biopsy images uploaded in United Network for Organ Sharing. Clin Transplant 32:e13441
Manfredo Vieira, S; Hiltensperger, M; Kumar, V et al. (2018) Translocation of a gut pathobiont drives autoimmunity in mice and humans. Science 359:1156-1161
Greiling, Teri M; Dehner, Carina; Chen, Xinguo et al. (2018) Commensal orthologs of the human autoantigen Ro60 as triggers of autoimmunity in lupus. Sci Transl Med 10:
Nikonova, Anna S; Deneka, Alexander Y; Kiseleva, Anna A et al. (2018) Ganetespib limits ciliation and cystogenesis in autosomal-dominant polycystic kidney disease (ADPKD). FASEB J 32:2735-2746
van der Ven, Amelie T; Kobbe, Birgit; Kohl, Stefan et al. (2018) A homozygous missense variant in VWA2, encoding an interactor of the Fraser-complex, in a patient with vesicoureteral reflux. PLoS One 13:e0191224
Hao, Shoujin; Hao, Mary; Ferreri, Nicholas R (2018) Renal-Specific Silencing of TNF (Tumor Necrosis Factor) Unmasks Salt-Dependent Increases in Blood Pressure via an NKCC2A (Na+-K+-2Cl- Cotransporter Isoform A)-Dependent Mechanism. Hypertension 71:1117-1125

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