Dibutyryl-cAMP, sodium salt

Supplementary information

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

PKA alpha and beta catalytic subunits also known as protein kinase A catalytic subunits function as enzymes that transfer phosphate groups from ATP to specific proteins. The common alternate names include cAMP-dependent protein kinase catalytic subunits. Each subunit has a different molecular mass with the alpha subunit weighing approximately 40 kDa. These catalytic subunits are components of the larger protein kinase A (PKA) holoenzyme. They express in various tissues including the brain heart and skeletal muscle. The expression can vary indicating distinct functional roles in different tissue types.

Biological function summary

PKA catalytic subunits play a significant role in regulating various cellular processes. They are a part of the PKA holoenzyme complex that becomes activated by cyclic AMP (cAMP) binding to the regulatory subunits. This activation results in the dissociation of the active catalytic subunits which then phosphorylate various target proteins modulating their activity. PKA catalytic subunits including the beta isoform PRKAR2B and PRKAR1A influence processes like metabolism cell cycle progression and neuronal signaling. The prostaglandin E receptor EP2 also known as PTGER2 interacts with these subunits indicating roles in cellular response to extracellular signals like hormones.

Pathways

PKA catalytic subunits are central components of the cAMP signaling pathway which regulates diverse biological functions. In addition to the cAMP pathway PKA also involves in the MAP kinase pathway which influences cell growth and differentiation. Proteins like CREB (cAMP response element-binding protein) serve as significant targets within these pathways. The activation of these pathways by PKA modulates transcription factors and cellular responses illustrating the integration of PKA into broader signaling networks.

PKA catalytic subunits associate with conditions such as Cushing’s syndrome and cardiac hypertrophy. Genetic mutations affecting PRKAR1A a gene encoding a regulatory subunit of PKA relate directly to Cushing’s syndrome due to altered PKA activity. Another example is cardiac hypertrophy where abnormalities in PKA signaling contribute to disease pathogenesis. Connections with other proteins such as those involved in GPCR signaling demonstrate the diverse impact of PKA on various physiological and pathological processes.