scholarly journals Retinal Pigment Epithelium Atrophy 1 (rpea1): A New Mouse Model With Retinal Detachment Caused by a Disruption of Protein Kinase C, θ

2016 ◽  
Vol 57 (3) ◽  
pp. 877
Author(s):  
Xiaojie Ji ◽  
Ye Liu ◽  
Ron Hurd ◽  
Jieping Wang ◽  
Bernie Fitzmaurice ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Retinal Pigment Epithelium ◽  
Protein Kinase ◽  
Retinal Detachment ◽  
Mouse Model ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Kinase C ◽  
Retinal Pigment Epithelium Atrophy

Migration of retinal pigment epithelium cells in vitro is regulated by protein kinase C

1995 ◽  
Vol 60 (6) ◽  
pp. 683-695 ◽  
Author(s):  
Todd L. Murphy ◽  
Taiji Sakamoto ◽  
David R. Hinton ◽  
Christine Spee ◽  
Usha Gundimeda ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Retinal Pigment Epithelium ◽  
Protein Kinase ◽  
Pigment Epithelium ◽  
Retinal Pigment ◽  
Kinase C ◽  
Retinal Pigment Epithelium Cells ◽  
Epithelium Cells

scholarly journals Disruption of adenylyl cyclase type V does not rescue the phenotype of cardiac-specific overexpression of Gαq protein-induced cardiomyopathy

2010 ◽  
Vol 299 (5) ◽  
pp. H1459-H1467 ◽  
Author(s):  
Valeriy Timofeyev ◽  
Cliff A. Porter ◽  
Dipika Tuteja ◽  
Hong Qiu ◽  
Ning Li ◽  
...  
Keyword(s):  
Heart Failure ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Mouse Model ◽  
Transgenic Mice ◽  
Cardiac Function ◽  
Adenylyl Cyclase ◽  
Electrical Remodeling ◽  
Kinase C ◽  
Progressive Heart Failure

Adenylyl cyclase (AC) is the principal effector molecule in the β-adrenergic receptor pathway. ACV and ACVI are the two predominant isoforms in mammalian cardiac myocytes. The disparate roles among AC isoforms in cardiac hypertrophy and progression to heart failure have been under intense investigation. Specifically, the salutary effects resulting from the disruption of ACV have been established in multiple models of cardiomyopathy. It has been proposed that a continual activation of ACV through elevated levels of protein kinase C could play an integral role in mediating a hypertrophic response leading to progressive heart failure. Elevated protein kinase C is a common finding in heart failure and was demonstrated in murine cardiomyopathy from cardiac-specific overexpression of Gαq protein. Here we assessed whether the disruption of ACV expression can improve cardiac function, limit electrophysiological remodeling, or improve survival in the Gαq mouse model of heart failure. We directly tested the effects of gene-targeted disruption of ACV in transgenic mice with cardiac-specific overexpression of Gαq protein using multiple techniques to assess the survival, cardiac function, as well as structural and electrical remodeling. Surprisingly, in contrast to other models of cardiomyopathy, ACV disruption did not improve survival or cardiac function, limit cardiac chamber dilation, halt hypertrophy, or prevent electrical remodeling in Gαq transgenic mice. In conclusion, unlike other established models of cardiomyopathy, disrupting ACV expression in the Gαq mouse model is insufficient to overcome several parallel pathophysiological processes leading to progressive heart failure.

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