scholarly journals Interactions between the Regulatory Subunit of Type I Protein Kinase A and p90 Ribosomal S6 Kinase1 Regulate Cardiomyocyte Apoptosis

2013 ◽  
Vol 85 (2) ◽  
pp. 357-367 ◽  
Author(s):  
Xianlong Gao ◽  
Brian Lin ◽  
Sakthivel Sadayappan ◽  
Tarun B. Patel
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Cardiomyocyte Apoptosis ◽  
Regulatory Subunit ◽  
Type I ◽  
Kinase A

Regulatory subunit type I-? of protein kinase A (PRKAR1A): A tumor-suppressor gene for sporadic thyroid cancer

2002 ◽  
Vol 35 (2) ◽  
pp. 182-192 ◽  
Author(s):  
Fabiano Sandrini ◽  
Ludmila Matyakhina ◽  
Nicholas J. Sarlis ◽  
Lawrence S. Kirschner ◽  
Constantine Farmakidis ◽  
...  
Keyword(s):  
Thyroid Cancer ◽  
Protein Kinase ◽  
Tumor Suppressor ◽  
Protein Kinase A ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Regulatory Subunit ◽  
Type I ◽  
Kinase A

Mutations of the gene encoding the protein kinase A type I-α regulatory subunit in patients with the Carney complex

10.1038/79238 ◽  
2000 ◽  
Vol 26 (1) ◽  
pp. 89-92 ◽  
Author(s):  
Lawrence S. Kirschner ◽  
J. Aidan Carney ◽  
Svetlana D. Pack ◽  
Susan E. Taymans ◽  
Christoforos Giatzakis ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Carney Complex ◽  
Regulatory Subunit ◽  
Type I ◽  
Gene Encoding ◽  
Kinase A

scholarly journals Targeting the Regulatory Subunit R2Alpha of Protein Kinase A in Human Glioblastoma through shRNA-Expressing Lentiviral Vectors

Viruses ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1361
Author(s):  
Maira Zorzan ◽  
Claudia Del Vecchio ◽  
Stefania Vogiatzis ◽  
Elisa Saccon ◽  
Cristina Parolin ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Protein Kinase A ◽  
Lentiviral Vectors ◽  
Brain Parenchyma ◽  
Regulatory Subunit ◽  
Glioblastoma Cells ◽  
Cellular Models ◽  
Therapeutic Setting ◽  
Promising Target ◽  
Kinase A

Glioblastoma is the most malignant and most common form of brain tumor, still today associated with a poor 14-months median survival from diagnosis. Protein kinase A, particularly its regulatory subunit R2Alpha, presents a typical intracellular distribution in glioblastoma cells compared to the healthy brain parenchyma and this peculiarity might be exploited in a therapeutic setting. In the present study, a third-generation lentiviral system for delivery of shRNA targeting the regulatory subunit R2Alpha of protein kinase A was developed. Generated lentiviral vectors are able to induce an efficient and stable downregulation of R2Alpha in different cellular models, including non-stem and stem-like glioblastoma cells. In addition, our data suggest a potential correlation between silencing of the regulatory subunit of protein kinase A and reduced viability of tumor cells, apparently due to a reduction in replication rate. Thus, our findings support the role of protein kinase A as a promising target for novel anti-glioma therapies.

The crystal structure of yeast regulatory subunit reveals key evolutionary insights into Protein Kinase A oligomerization

2021 ◽  
pp. 107732
Author(s):  
Nicolás González Bardeci ◽  
Enzo Tofolón ◽  
Felipe Trajtenberg ◽  
Julio Caramelo ◽  
Nicole Larrieux ◽  
...  
Keyword(s):  
Crystal Structure ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Regulatory Subunit ◽  
Kinase A

scholarly journals The Role of Uncoupling Protein 1 in the Metabolism and Adiposity of RIIβ-Protein Kinase A-Deficient Mice

2004 ◽  
Vol 18 (9) ◽  
pp. 2302-2311 ◽  
Author(s):  
Michael A. Nolan ◽  
Maria A. Sikorski ◽  
G. Stanley McKnight
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Protein Kinase ◽  
Protein Kinase A ◽  
Uncoupling Protein ◽  
Mrna Level ◽  
Regulatory Subunit ◽  
Uncoupling Protein 1 ◽  
Brown Adipose ◽  
Kinase A

Abstract Mice lacking the RIIβ regulatory subunit of protein kinase A exhibit a 50% reduction in white adipose tissue stores compared with wild-type littermates and are resistant to diet-induced obesity. RIIβ−/− mice also have an increase in resting oxygen consumption along with a 4-fold increase in the brown adipose-specific mitochondrial uncoupling protein 1 (UCP1). In this study, we examined the basis for UCP1 induction and tested the hypothesis that the induced levels of UCP1 in RIIβ null mice are essential for the lean phenotype. The induction of UCP1 occurred at the protein but not the mRNA level and correlated with an increase in mitochondria in brown adipose tissue. Mice lacking both RIIβ and UCP1 (RIIβ−/−/Ucp1−/−) were created, and the key parameters of metabolism and body composition were studied. We discovered that RIIβ−/− mice exhibit nocturnal hyperactivity in addition to the increased oxygen consumption at rest. Disruption of UCP1 in RIIβ−/− mice reduced basal oxygen consumption but did not prevent the nocturnal hyperactivity. The double knockout animals also retained the lean phenotype of the RIIβ null mice, demonstrating that induction of UCP1 and increased resting oxygen consumption is not the cause of leanness in the RIIβ mutant mice.

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