PRKAR2B
cAMP-dependent protein kinase type II-beta regulatory subunit
Also known as: KAP3_HUMAN, PRKAR2
Cross-references: UniProt · Ensembl · Human Protein Atlas · GeneCards · NCBI Gene
Protein identityUniProt · HPA
- UniProt accession
- P31323
- Gene
- PRKAR2B
- Ensembl
- ENSG00000005249
- Chromosome
- 7
- Canonical length
- 418 aa
- Protein class
- Predicted intracellular proteins
- Subcellular location
- Golgi apparatus,Centrosome,Basal body,Cytosol
OverviewNCBI Gene
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. The protein encoded by this gene is one of the regulatory subunits. This subunit can be phosphorylated by the activated catalytic subunit. This subunit has been shown to interact with and suppress the transcriptional activity of the cAMP responsive element binding protein 1 (CREB1) in activated T cells. Knockout studies in mice suggest that this subunit may play an important role in regulating energy balance and adiposity. The studies also suggest that this subunit may mediate the gene induction and cataleptic behavior induced by haloperidol. [provided by RefSeq, Jul 2008]
Canonical amino-acid sequenceUniProt
418 residues, UniProt reviewed canonical sequence.
>P31323|PRKAR2B
1 MSIEIPAGLT ELLQGFTVEV LRHQPADLLE FALQHFTRLQ QENERKGTAR FGHEGRTWGD
61 LGAAAGGGTP SKGVNFAEEP MQSDSEDGEE EEAAPADAGA FNAPVINRFT RRASVCAEAY
121 NPDEEEDDAE SRIIHPKTDD QRNRLQEACK DILLFKNLDP EQMSQVLDAM FEKLVKDGEH
181 VIDQGDDGDN FYVIDRGTFD IYVKCDGVGR CVGNYDNRGS FGELALMYNT PRAATITATS
241 PGALWGLDRV TFRRIIVKNN AKKRKMYESF IESLPFLKSL EFSERLKVVD VIGTKVYNDG
301 EQIIAQGDSA DSFFIVESGE VKITMKRKGK SEVEENGAVE IARCSRGQYF GELALVTNKP
361 RAASAHAIGT VKCLAMDVQA FERLLGPCME IMKRNIATYE EQLVALFGTN MDIVEPTALocalizationUniProt · AlphaFold · HPA
Whether an antibody against PRKAR2B can act on the native protein depends on physical access: surface and secreted proteins are reachable by circulating antibodies, intracellular proteins usually are not.
- Antibody reachability
- Cell surface
- Secreted
- No
- Transmembrane segments
- 0
- Mean surface accessibility (rSASA)
- 0.39
- Highest tissue expression
- 160 nTPM
Expression across tissuesHPA
Tissue
- adipose tissue: 160 nTPM
- breast: 50 nTPM
- adrenal gland: 43 nTPM
- cerebral cortex: 31 nTPM
- basal ganglia: 31 nTPM
- ovary: 25 nTPM
Single-cell type
- platelets: 1,661 nCPM
- megakaryocytes: 1,076 nCPM
- adipocytes: 708 nCPM
- megakaryocyte progenitors: 380 nCPM
- megakaryocyte-erythroid progenitors: 372 nCPM
- granulosa cells: 329 nCPM
Immune cell
- myeloid DC: 0.5 nTPM
- total PBMC: 0.5 nTPM
- intermediate monocyte: 0.3 nTPM
- NK-cell: 0.2 nTPM
- plasmacytoid DC: 0.1 nTPM
- basophil: 0 nTPM
Brain region
- cerebral cortex: 11 nTPM
- basal ganglia: 10 nTPM
- midbrain: 9.9 nTPM
- hippocampal formation: 7.4 nTPM
- white matter: 7.2 nTPM
- pons: 6.6 nTPM
Genetic constraint and essentialitygnomAD · DepMap
Does the body need this protein intact? Low LOEUF or a strong DepMap dependency means loss or blockade of the protein is likely to be felt.
- gnomAD LOEUF (loss-of-function intolerance)
- 0.22
- gnomAD pLI
- 1
- gnomAD missense Z
- 2.47
- DepMap mean gene effect
- 0.07
- DepMap dependency class
- none
Cancer expressionTCGA
Across TCGA tumor cohorts, this protein is over-expressed in roughly 6% of surveyed tumor types (aggregate summary; per-cohort expression, alteration, and survival load in the interactive view).
OntologyGO
Biological processes
- adenylate cyclase-activating G protein-coupled receptor signaling pathway
- cellular response to glucagon stimulus
- chemical synaptic transmission
- fatty acid metabolic process
- intracellular signal transduction
- learning
- modulation of chemical synaptic transmission
- negative regulation of cAMP/PKA signal transduction
- negative regulation of inflammatory response to antigenic stimulus
- renal water homeostasis
- response to antipsychotic drug
- vascular endothelial cell response to laminar fluid shear stress
Molecular functions
- cAMP binding
- cAMP-dependent protein kinase inhibitor activity
- cAMP-dependent protein kinase regulator activity
- protein domain specific binding
- protein kinase A catalytic subunit binding
- ubiquitin protein ligase binding
Cellular components
Protein domainsUniProt · Pfam · InterPro
- Cyclic nucleotide-binding domain
- cAMP-dependent protein kinase regulatory subunit, dimerization-anchoring domain
- cAMP-dependent protein kinase regulatory subunit
- RmlC-like jelly roll fold
- Cyclic nucleotide-binding, conserved site
- Cyclic nucleotide-binding domain superfamily
- cAMP-dependent protein kinase regulatory subunit-like
- Cyclic nucleotide-binding domain
- Regulatory subunit of type II PKA R-subunit
KeywordsUniProt
InteractionsUniProt · HPA
Protein binding partners of PRKAR2B in the human serome: UniProt-annotated complex subunits plus reported interactors. Each links to its own Seroatlas record.
Antibody and autoantibody relevanceSeroatlas analysis
Seroatlas reads PRKAR2B as an antibody target. Whether an autoantibody or antibody against PRKAR2B could matter depends on whether native PRKAR2B is physically reachable, whether the body needs it intact, and whether it acts in a disease-relevant tissue.
PRKAR2B is annotated at the cell surface, where native PRKAR2B is exposed to circulating antibodies and is a prime autoantibody target that could block, deplete, or overstimulate it.
Annotation status
The present source text does not explicitly label PRKAR2B as an autoantigen. Seroatlas presents hypothesis context only and does not manufacture a known-serology claim.
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