The Mutant Mouse Core will centralize effort and provide the expertise necessary to maintain stocks of mice with various mutations generated by gene targeting and/or transgene insertion for use by participating investigators. Investigators requiring mice with specific targeted mutations and/or transgenes will be able to obtain the appropriate genotypes in requisite numbers from the Core. The Core is thus responsible for the routine care of founder and breeding animals, the husbandry required to generate the experimental animals, their weaning, application of ear tags for identification, and obtaining genotypes for the relevant gene(s). The Core is also responsible for supplying suitable controls when they are not readily commercially available. Breeding programs will be carried out in coordination with each investigator to obtain the appropriate number of animals of the required genotypes. We will provide the investigators in the PPG renewal the following gene knockout mice;Angiotensin 1 receptor type l a """"""""floxed"""""""" (ATIa-floxed) -/-, angiotensin II receptor type 2 (AT2) -/Y, endothelial nitric oxide synthase (Nos3 or eNOS) -/-, conditional knockouts of the a epithelial sodium channel (ENaC) in both the cortical collecting duct (CCD) alone and the CCD plus the connecting tubule (CNT), and cardiac myocyte specific knockout of the prostaglandin EP4 receptor (CS-EP4) -/-. We will provide the following transgenic mice: NF-KB/luciferase (NF-KB-LUC) Tg, and chicken ovalbumin specific a and p T-cell receptor (OT II) Tg mice. In addition the Core will provide mice, generated by homologous recombination, which have a gain-of-function in the PENaC gene as a mouse model of Liddle's syndrome. In addition the Core will provide the following strains, directly purchased as needed as experimental animals to PPG investigators;Ragl -/-, p47-/-, NZBWF1/J, and NZW/LacJ.
The Mutant Mouse Core of the PPG, Core C will provide genetically modified mice to support the investigations to be conducted in Projects l-IV, as described in those sections. Providing these core services will allow the investigators to concentrate on their experiments without having to concern themselves with the day-to-day husbandry and genotyping of mice.
|Cerniello, Flavia M; Carretero, Oscar A; Longo Carbajosa, Nadia A et al. (2017) MAS1 Receptor Trafficking Involves ERK1/2 Activation Through a ?-Arrestin2-Dependent Pathway. Hypertension 70:982-989|
|Ren, YiLin; Janic, Branislava; Kutskill, Kristopher et al. (2016) Mechanisms of connecting tubule glomerular feedback enhancement by aldosterone. Am J Physiol Renal Physiol 311:F1182-F1188|
|Ramseyer, Vanesa D; Ortiz, Pablo A; Carretero, Oscar A et al. (2016) Angiotensin II-mediated hypertension impairs nitric oxide-induced NKCC2 inhibition in thick ascending limbs. Am J Physiol Renal Physiol 310:F748-F754|
|Gu, Xiaosong; Xu, Jiang; Zhu, Liping et al. (2016) Prostaglandin E2 Reduces Cardiac Contractility via EP3 Receptor. Circ Heart Fail 9:|
|Kumar, Nitin; Nakagawa, Pablo; Janic, Branislava et al. (2016) The anti-inflammatory peptide Ac-SDKP is released from thymosin-?4 by renal meprin-? and prolyl oligopeptidase. Am J Physiol Renal Physiol 310:F1026-34|
|Zhu, Liping; Yang, Xiao-Ping; Janic, Branislava et al. (2016) Ac-SDKP suppresses TNF-?-induced ICAM-1 expression in endothelial cells via inhibition of I?B kinase and NF-?B activation. Am J Physiol Heart Circ Physiol 310:H1176-83|
|Saez, Fara; Hong, Nancy J; Garvin, Jeffrey L (2016) Luminal flow induces NADPH oxidase 4 translocation to the nuclei of thick ascending limbs. Physiol Rep 4:|
|Cerrato, Bruno D; Carretero, Oscar A; Janic, Brana et al. (2016) Heteromerization Between the Bradykinin B2 Receptor and the Angiotensin-(1-7) Mas Receptor: Functional Consequences. Hypertension 68:1039-48|
|González, Germán E; Rhaleb, N-E; D'Ambrosio, Martin A et al. (2016) Cardiac-deleterious role of galectin-3 in chronic angiotensin II-induced hypertension. Am J Physiol Heart Circ Physiol 311:H1287-H1296|
|Gonzalez-Vicente, Agustin; Saikumar, Jagannath H; Massey, Katherine J et al. (2016) Angiotensin II stimulates superoxide production by nitric oxide synthase in thick ascending limbs. Physiol Rep 4:|
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