; 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
Greenberg, Jason H; Kakajiwala, Aadil; Parikh, Chirag R et al. (2017) Emerging biomarkers of chronic kidney disease in children. Pediatr Nephrol :
Yanda, Murali K; Liu, Qiangni; Cebotaru, Valeriu et al. (2017) Histone deacetylase 6 inhibition reduces cysts by decreasing cAMP and Ca2+ in knock-out mouse models of polycystic kidney disease. J Biol Chem 292:17897-17908
Vivante, Asaf; Ityel, Hadas; Pode-Shakked, Ben et al. (2017) Exome sequencing in Jewish and Arab patients with rhabdomyolysis reveals single-gene etiology in 43% of cases. Pediatr Nephrol 32:2273-2282
Zhou, Han; Tian, Xuefei; Tufro, Alda et al. (2017) Loss of the podocyte glucocorticoid receptor exacerbates proteinuria after injury. Sci Rep 7:9833
Kolodecik, Thomas R; Reed, Anamika M; Date, Kimie et al. (2017) The serum protein renalase reduces injury in experimental pancreatitis. J Biol Chem 292:21047-21059
CastaƱeda-Bueno, Maria; Arroyo, Juan Pablo; Zhang, Junhui et al. (2017) Phosphorylation by PKC and PKA regulate the kinase activity and downstream signaling of WNK4. Proc Natl Acad Sci U S A 114:E879-E886
Li, Yuwen; Caballero, Daniel; Ponsetto, Julian et al. (2017) Response of Npt2a knockout mice to dietary calcium and phosphorus. PLoS One 12:e0176232
Ochi, Akinobu; Chen, Dong; Schulte, Wibke et al. (2017) MIF-2/D-DT enhances proximal tubular cell regeneration through SLPI- and ATF4-dependent mechanisms. Am J Physiol Renal Physiol 313:F767-F780
Vivante, Asaf; Mann, Nina; Yonath, Hagith et al. (2017) A Dominant Mutation in Nuclear Receptor Interacting Protein 1 Causes Urinary Tract Malformations via Dysregulation of Retinoic Acid Signaling. J Am Soc Nephrol 28:2364-2376
Scholl, Ute I; Abriola, Laura; Zhang, Chengbiao et al. (2017) Macrolides selectively inhibit mutant KCNJ5 potassium channels that cause aldosterone-producing adenoma. J Clin Invest 127:2739-2750

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