Human PRKAR1B knockout HeLa cell lysate

Supplementary information

This supplementary information is collated from multiple sources and compiled automatically.

PRKAR1B also known as the regulatory subunit type I beta of protein kinase A (PKA) plays an important role in the regulation of cAMP-dependent PKA activity. This protein has a molecular mass of approximately 44 kDa. It binds to the catalytic subunit of PKA inhibiting its activity until cAMP binds which then triggers a conformational change and release of the active catalytic subunit. PRKAR1B is expressed in various tissues with notable abundance in the brain highlighting its significance in neuronal signaling.

Biological function summary

PRKAR1B functions as part of the PKA holoenzyme complex which includes both regulatory and catalytic subunits. The regulatory subunit PRKAR1B directly controls when and where PKA catalytic activity occurs influencing multiple cellular responses. This protein modulates processes like glycogen lipid and protein metabolism by contributing to the precise regulation of cAMP signaling pathways. Its activity affects a range of fundamental cellular functions indicative of its presence in diverse tissues.

Pathways

PRKAR1B is intricately involved in the cAMP signaling pathway and the MAPK/ERK pathway. The cAMP pathway is important for transferring the signals of many hormones and neurotransmitters where PRKAR1B regulates transient PKA activation. In the MAPK/ERK pathway PRKAR1B indirectly influences cellular growth and differentiation by modulating secondary messengers. Proteins such as the catalytic subunits of PKA and CREB a transcription factor interact with PRKAR1B illustrating its central role in cellular responses to external signals.

PRKAR1B has been associated with neurodegenerative diseases like Alzheimer’s and mood disorders such as major depressive disorder. Altered regulation of the cAMP signaling pathway influenced by PRKAR1B affects neuronal survival and function potentially leading to neurodegeneration. Additionally imbalances in PRKAR1B-mediated pathways can contribute to mood disorders. Proteins such as the catalytic subunits of PKA and BDNF (brain-derived neurotrophic factor) interact with PRKAR1B in these contexts indicating its potential as a therapeutic target.