| ID | Sequence | Length | GC content |
|---|---|---|---|
| GGAGCUGUCGCCUAGCCGCUAUCGCAGAGUGGAGCGGGGCUGGGAGCAA… | 4386 nt | 0.3878 | |
| AGAACCAUGGAGUCUGGCAGUACCGCCGCCAGUGAGGAGGCACGCAGCC… | 1218 nt | 0.4589 | |
| GAGCUGUGGUGGGCUCCACCCAGUUCGAGCUUCCCGGCUGCUUUGGUUA… | 4307 nt | 0.3854 | |
| AGAGGCGUCAAGGGAGGCCGGAGGGAGAGUGGGGUGGACAGAGGAGCGG… | 4410 nt | 0.3864 | |
| CGCUCACCCUCCCCCAUUUCCUGAAGGACAACGGCUCUAUUUUACUGGG… | 4221 nt | 0.3798 | |
| GGAGCUGUCGCCUAGCCGCUAUCGCAGAGUGGAGCGGGGCUGGGAGCAA… | 4253 nt | 0.3858 | |
| AGAGGCGUCAAGGGAGGCCGGAGGGAGAGUGGGGUGGACAGAGGAGCGG… | 4277 nt | 0.3844 | |
| AUUGACGUCAGUAGCCGAACGCUGAUUGGCUGCGGCCAGGCCGUUUCCG… | 4356 nt | 0.3893 |
cAMP is a signaling molecule important for a variety of cellular functions. cAMP exerts its effects by activating the cAMP-dependent protein kinase, which transduces the signal through phosphorylation of different target proteins. The inactive kinase holoenzyme is a tetramer composed of two regulatory and two catalytic subunits. cAMP causes the dissociation of the inactive holoenzyme into a dimer of regulatory subunits bound to four cAMP and two free monomeric catalytic subunits. Four different regulatory subunits and three catalytic subunits have been identified in humans. This gene encodes one of the regulatory subunits. This protein was found to be a tissue-specific extinguisher that down-regulates the expression of seven liver genes in hepatoma x fibroblast hybrids. Mutations in this gene cause Carney complex (CNC). This gene can fuse to the RET protooncogene by gene rearrangement and form the thyroid tumor-specific chimeric oncogene known as PTC2. A nonconventional nuclear localization sequence (NLS) has been found for this protein which suggests a role in DNA replication via the protein serving as a nuclear transport protein for the second subunit of the Replication Factor C (RFC40). Several alternatively spliced transcript variants encoding two different isoforms have been observed. [provided by RefSeq, Jan 2013] CIViC Summary for PRKAR1A Gene
A study in humans and mice demonstrated that the PRKAR1A is upregulated in whole blood cells and peripheral blood mononuclear cells of patients who develop heart failure after acute myocardial infarction, and is also upregulated in monocytes/macrophages at day 2 post-infarction in mice [Chen et al. DOI:10.3389/fimmu.2022.878876]. A study in human myocardial samples from explanted hearts demonstrated that the PRKAR1A mRNA expression was significantly upregulated in dilated cardiomyopathy (8.16-fold, p < 0.0002) and ischemic cardiomyopathy (4.33-fold, p < 0.002) compared to a healthy control group [Tatrai et al. DOI:10.1016/J.Forsciint.2011.05.010].