PRKAR1AMutations and Protein Kinase A Interactions with Other Signaling Pathways in the Adrenal Cortex | Zendy

Audrey RobinsonWhite | Zendy; Elise Meoli | Zendy; Sotirios Stergiopoulos | Zendy; Anélia Horvath | Zendy; Sosipatros A. Boikos | Zendy; Ioannis Bossis | Zendy; Constantine A. Stratakis | Zendy

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PRKAR1AMutations and Protein Kinase A Interactions with Other Signaling Pathways in the Adrenal Cortex

Author(s) -

Audrey RobinsonWhite,

Elise Meoli,

Sotirios Stergiopoulos,

Anélia Horvath,

Sosipatros A. Boikos,

Ioannis Bossis,

Constantine A. Stratakis

Publication year - 2006

Publication title -

the journal of clinical endocrinology and metabolism

Language(s) - English

Resource type - Journals

eISSN - 1945-7197

pISSN - 0021-972X

DOI - 10.1210/jc.2006-0188

Subject(s) - protein kinase a , carney complex , protein subunit , biology , mapk/erk pathway , protein kinase b , kinase , microbiology and biotechnology , signal transduction , gene , biochemistry

Primary pigmented nodular adrenocortical disease, associated with Carney complex, is caused by mutations in PRKAR1A (mt-PRKAR1A), a gene that codes for the regulatory subunit type 1alpha (RIalpha) of cAMP-dependent protein kinase (PKA). PRKAR1A inactivation is associated with dysregulated PKA activity that is thought to result in tumorigenesis. mt-PRKAR1A-bearing lymphocytes from Carney complex patients exhibit enhanced cell proliferation associated with increased expression of the MAPK ERK1/2 pathway.

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