HCSGD entry for AKAP12


1. General information

Official gene symbolAKAP12
Entrez ID9590
Gene full nameA kinase (PRKA) anchor protein 12
Other gene symbolsAKAP250 SSeCKS
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0005515Protein bindingIPImolecular_function
GO:0005737CytoplasmIDAcellular_component
GO:0005856CytoskeletonIEAcellular_component
GO:0005886Plasma membraneIDAcellular_component
GO:0005938Cell cortexIEAcellular_component
GO:0006605Protein targetingIEAbiological_process
GO:0007186G-protein coupled receptor signaling pathwayTASbiological_process
GO:0008179Adenylate cyclase bindingIPImolecular_function
GO:0010739Positive regulation of protein kinase A signalingIMPbiological_process
GO:0030819Positive regulation of cAMP biosynthetic processIMPbiological_process
GO:0051018Protein kinase A bindingIEAmolecular_function
GO:0090036Regulation of protein kinase C signalingIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.01481351390.31502556510.30319323481.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.2429585449
GSE13712_SHEARUp0.4876943734
GSE13712_STATICDown-0.1655541131
GSE19018Down-0.3188089954
GSE19899_A1Up0.8792997359
GSE19899_A2Up0.0461373094
PubMed_21979375_A1Up0.0576848741
PubMed_21979375_A2Up0.5096495173
GSE35957Down-0.2171582117
GSE36640Down-1.2927023351
GSE54402Up0.3429489237
GSE9593Down-0.2952624876
GSE43922Up0.6650556530
GSE24585Down-0.4510420406
GSE37065Up0.5306971383
GSE28863_A1Up0.9760278111
GSE28863_A2Up0.4008104155
GSE28863_A3Up0.3794181172
GSE28863_A4Down-0.0357286364
GSE48662Up0.1355999127

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Not regulated by compounds

  • Drugs

Not regulated by drugs

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-183-5pMIMAT0000261MIRT005870Immunohistochemistry//Luciferase reporter assay//Microarray//qRT-PCR//Western blotFunctional MTI20979053
hsa-miR-186-5pMIMAT0000456MIRT005871Immunohistochemistry//Luciferase reporter assay//Microarray//qRT-PCR//Western blotFunctional MTI20979053
hsa-miR-186-5pMIMAT0000456MIRT005871CLASHFunctional MTI (Weak)23622248
hsa-miR-1MIMAT0000416MIRT023602ProteomicsFunctional MTI (Weak)18668040
hsa-miR-877-3pMIMAT0004950MIRT036840CLASHFunctional MTI (Weak)23622248
hsa-miR-181a-5pMIMAT0000256MIRT047327CLASHFunctional MTI (Weak)23622248
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  • mirRecord
No target information from mirRecord

6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 4 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

22811901Pivotal Role of AKAP12 in the Regulation of Cellular Adhesion Dynamics: Control of Cytoskeletal Architecture, Cell Migration, and Mitogenic Signaling
22811901AKAP12/SSeCKS/Gravin (AKAP12) is a scaffold protein for PKA and PKC which controls actin-cytoskeleton reorganization in a spatiotemporal manner
22811901AKAP12 also acts as a tumor suppressor which regulates cell-cycle progression and inhibits Src-mediated oncogenic signaling and cytoskeletal pathways
22811901Downregulation of AKAP12 induces the formation of thickened, longitudinal stress fibers and the proliferation of adhesion complexes
22811901AKAP12-null mouse embryonic fibroblasts exhibit hyperactivation of PKC, premature cellular senescence, and defects in cytokinesis, relating to the loss of PKC scaffolding activity by AKAP12
22811901The paper describes the regulatory and scaffolding functions of AKAP12 and how it regulates cell adhesion, signaling, and oncogenic suppression
22684366Scaffolding proteins such as SSeCKS/Gravin/AKAP12 ("AKAP12") are thought to control oncogenic signaling pathways by regulating key mediators in a spatiotemporal manner
22684366The downregulation of AKAP12 in many human cancers, often associated with promoter hypermethylation, or the loss of its locus at 6q24-25
22684366The forced re-expression of AKAP12 in cancer cell lines suppresses in vitro parameters of oncogenic growth, invasiveness, and cell motility through its ability to scaffold protein kinase C (PKC), F-actin, cyclins, Src, and phosphoinositides, and possibly through additional scaffolding domains for PKA, calmodulin, beta1,4-galactosyltransferase-polypeptide-1, beta2-adrenergic receptors, and cAMP-specific 3',5'-cyclic phosphodiesterase 4D
22684366Moreover, AKAP12 re-expression in tumor models results in metastasis suppression through the inhibition of Src-regulated, VEGF-mediated neovascularization at distal sites
21779438Emerging data suggest that SSeCKS/Gravin/AKAP12 ("AKAP12"), originally identified as an autoantigen in cases of myasthenia gravis, controls multiple biological processes through its ability to scaffold key signaling proteins such as protein kinase (PK) C and A, calmodulin, cyclins, phosphoinositides, "long" beta-1,4 galactosyltransferase (GalTase) isoform, Src, as well as the actin cytoskeleton in a spatiotemporal manner
21779438Specialized functions attributed to AKAP12 include the suppression of cancer malignancy, especially aspects of metastatic progression, regulation of blood-brain and blood-retina barrier formation, and resensitization of beta2-adrenergic pain receptors
21779438Recent data identify a direct role for AKAP12 in cytokinesis completion, further suggesting a function as a negative regulator of cell senescence
21779438The current review will discuss the emerging knowledge base of AKAP12-related biological roles and how the factors that affect AKAP12 expression or that interact with AKAP12 at the protein level control cancer progression and blood-tissue barrier formation
21099353Rb-dependent cellular senescence, multinucleation and susceptibility to oncogenic transformation through PKC scaffolding by SSeCKS/AKAP12
21099353Although p53 and Rb pathways are activated in the absence of Akap12, senescence is dependent on Rb
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