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AKT2 (v-akt murine thymoma viral oncogene homolog 2)

Written2007-07Deborah A. Altomare, Joseph R. Testa
Fox Chase Cancer Center, 333 Cottman Avenue, Philadelphia, PA 19111, USA

(Note : for Links provided by Atlas : click)

Identity

Other namesPKBBETA (PKB beta)
PKBB (protein kinase B, beta)
RAC-PK-Beta (rac protein kinase beta)
HGNC (Hugo) AKT2
LocusID (NCBI) 208
Atlas_Id 517
Location 19q13.2  [Link to chromosome band 19q13]
Location_base_pair Starts at 40736224 and ends at 40791302 bp from pter ( according to hg19-Feb_2009)  [Mapping AKT2.png]
 
Fusion genes
(updated 2016)
AKT2 (19q13.2) / AKT2 (19q13.2)AKT2 (19q13.2) / BLOC1S1 (12q13.2)AKT2 (19q13.2) / DNAJC3 (13q32.1)
AKT2 (19q13.2) / U2AF2 (19q13.42)AKT2 (19q13.2) / UPF1 (19p13.11)BCAM (19q13.32) / AKT2 (19q13.2)
C19orf47 (19q13.2) / AKT2 (19q13.2)CES4A (16q22.1) / AKT2 (19q13.2)RPS8 (1p34.1) / AKT2 (19q13.2)
ZIC1 (3q24) / AKT2 (19q13.2)
Note Details concerning the local order of the human AKT2 locus can be found at ensembl.org. Human AKT2 is found in chromosome 19, position 45,428,706-45,483,107. < or > symbols indicate the orientation of the genes. M3K10 is Mitogen-activated protein kinase kinase kinase 10 gene. CNTD2 is a gene encoding Cyclin N-terminal domain-containing protein.
Location in the mouse: chromosome 7 in band B1

DNA/RNA

 
  Genomic organization of human AKT2. Open boxes indicate untranslated regions and shaded boxes indicate coding regions of the gene. The ATG transcription start site is located in exon 2 and the TGA termination codon is located in exon 14.
Description The entire gene is about 54.4 Kb and contains 14 exons. The open reading frame of the coding region is 1,445 bp.
Transcription Transcript length: 4,623 bp
Pseudogene No human pseudogene known. A mouse Akt2 pseudogene was cloned and mapped to proximal mouse chromosome 11 by fluorescence in situ hybridization.

Protein

 
  AKT proteins contain an amino terminal pleckstrin homology (PH) domain, followed by a short helical region and kinase domain that terminates in a regulatory hydrophobic motif. Activation of AKT kinases is a multi-step process that involves both membrane translocation and phosphorylation. AKT activation occurs by means of stimulation of the growth factor receptor-associated phosphatidylinositol 3-kinase (PI3K). PI3K generates 3'-phosphorylated phosphoinositides, i.e., phosphatidylinositol-3,4,5-trisphosphate (PIP3) and phosphatidylinositol-3,4-bisphosphate (PIP2) at the plasma membrane. Both phospholipids bind with high affinity to the PH domain, mediating membrane translocation of AKT. At the membrane, AKT2 is phosphorylated at two sites, threonine 309 (T309) and serine 474 (S474).
Description AKT2 protein consists of 481 amino acids, with a molecular weight of 55,769 Da.
Expression Found in all human cell types so far analyzed; insulin responsive tissues such as normal brown fat, skeletal muscle and liver exhibit the highest expression levels of AKT2/Akt2.
Localisation Predominantly cytoplasmic; also found at the plasma membrane and in the nucleus following its activation.
Function AKT proteins mediate a variety of cellular functions, ranging from control of cell proliferation and survival to modulation of intermediary metabolism and angiogenesis. Such pleiotropic effects are the consequence of phosphorylation of numerous substrates, some of which are listed below. Most substrates share the consensus sequence for AKT phosphorylation, RXRXXS/T. For example, activated AKT exerts anti-apoptotic activity in part by preventing the release of cytochrome c from mitochondria, and phosphorylating and inactivating the pro-apoptotic factors BAD and pro-caspase-9. AKT also activates IkappaB kinase (IKK), a positive regulator of NF-kappaB, which results in the transcription of anti-apoptotic genes. AKT phosphorylates and inactivates FOXO transcription factors, which mediate the expression of genes critical for apoptosis, such as the Fas ligand gene.
AKT activation mediates cell cycle progression by phosphorylation and inhibition of glycogen synthase kinase 3 beta to inhibit cyclin D1 degradation. AKT phosphorylates the cell cycle inhibitors p21WAF1 and p27Kip1 near the nuclear localization signal to induce cytoplasmic retention of these cell cycle inhibitors. Moreover, phosphorylation of AKT kinases also results in increased translation of cyclin D1, D3 and E transcripts.
AKT activates the downstream mTOR kinase by inhibiting a complex formed by the tumor suppressor proteins TSC1 and TSC2, also known as hamartin and tuberin, respectively. mTOR broadly mediates cell growth and proliferation by regulating ribosomal biogenesis and protein translation and can regulate response to nutrients by restricting cell cycle progression in the presence of suboptimal growth conditions.
AKT signaling also contributes to other cellular processes considered to be cancer hallmarks. AKT promotes the phosphorylation and translocation of Mdm2 into the nucleus, where it downregulates p53 and thereby antagonizes p53-mediated cell cycle checkpoints. AKT signaling is linked to tumor cell migration, and it contributes to tumor invasion and metastasis by promoting the secretion of matrix metalloproteinases. Moreover, vascular endothelial growth factor (VEGF) effects on cell survival have been shown to be mediated by the Flk1/VEGFR2-PI3K-AKT pathway. In other cellular processes, AKT has been shown to phosphorylate human telomerase reverse transcriptase (hTERT), thereby stimulating telomerase activity and replication. Collectively, these findings implicate up-regulation of the AKT pathway in many aspects of tumorigenesis.
Homology All three AKT kinases belong to the more general class of AGC kinases (related to AMP/GMP kinase and protein kinase C). The kinase domain of AKT shares high similarity with other members of the AGC family of kinases such as PKA, PKC, p70 S6K, and p90 RSK. The sequence identities among the three AKTs in the kinase domain exceed 87%. The three AKT kinases are identical in the ATP binding region, except for one residue: Ala 230 of AKT1 is conserved in AKT2 (Ala 232), but switches to Val 228 in AKT3. In addition, each of the three AKT kinases has a carboxy terminal extension of about 40 amino acids.
Human AKT2 is 98.1% similar to M. musculus Akt2; 97.7% similar to the R. norvegicus homolog; 61.3% similar to D. melanogaster protein kinase RAC; 52.4% similar to C. elegans Akt/PKB serine/threonine kinase; 47.7% similar to S. cerevisiae protein kinase (see UniGene Hs.631535)

Mutations

Germinal Insulin resistance and a diabetes mellitus-like syndrome have been described in knockout mice lacking Akt2.
Somatic Individuals carrying a G-to-A transition in the AKT2 gene resulting in an Arg-to-His substitution at codon 274 (R274H) were found to be markedly hyperinsulinemic. However, a large case-control study showed that variation in and around the AKT2 locus is unlikely to contribute significantly to increased risk of type 2 diabetes.
Mutations in AKT2 are uncommon in human tumors. For example, AKT2 mutations have been reported in 1 of 51 gastric carcinomas and 2 of 79 lung carcinomas. The mutations consisted of one missense mutation and 2 splice site mutations in an intron.

Implicated in

Note
Entity Various cancers
Prognosis Frequent activation of AKT has been reported in a broad range of human cancers including various carcinomas, glioblastoma multiforme, and hematological malignancies. In some of these tumor types, AKT activation has been shown to correlate with advanced disease and/or poor prognosis. AKT is a major mediator of survival signals that protect cells from undergoing apoptosis and, thus, is a potentially important therapeutic target. Ovarian cancer cell lines with either constitutive AKT1 activity or AKT2 gene amplification have been shown to be highly resistant to paclitaxel compared to cells with low AKT levels.
 
Hyperactivation of AKT kinases have been reported in a wide assortment of human solid tumors and hematological malignancies. Activation of growth factor receptors either by ligand stimulation or receptor overexpression/mutation is one of the mechanisms leading to the upregulation of AKT signaling. Other mechanisms include activation of oncoproteins and inactivation of tumor suppressors intersecting the AKT signal transduction pathway. AKT is now known to be a central player in a signaling pathway consisting of many components that have been implicated in tumorigenesis, including upstream phosphatidylinositol 3-kinase (PI3K) and PTEN (Phosphatase and Tensin homologue deleted on chromosome Ten). Several proteins, such as AKT, eIF4E, and the subunits of PI3K, can act as oncoproteins when activated or overexpressed. Germline mutations in PTEN, LKB1, TSC2/TSC1, and VHL are linked with different dominantly-inherited cancer syndromes. Each of these tumor suppressors is a negative regulator of the AKT pathway which, when deregulated, results in altered translation of cancer-related mRNAs that regulate cellular processes such as cell cycle progression, growth, cell survival, invasion, and communication with the extracellular environment.
Oncogenesis In 1992, amplification and overexpression of AKT2 was reported in a subset of ovarian carcinomas. AKT2 was shown to be amplified and overexpressed in 2 of 8 ovarian carcinoma cell lines and 2 of 15 primary ovarian tumors. Recently, amplification of AKT2 was found in 18.2% of high-grade ovarian carcinomas.
Amplification and/or overexpression of AKT2 was reported in 10-20% of primary pancreatic carcinomas and pancreatic cancer cell lines. PANC1 and ASPC1 cell lines exhibited 30-fold and 50-fold amplification of AKT2, respectively, and highly elevated levels of AKT2 RNA and protein. As an early indication of the potential importance of molecularly targeting the AKT pathway, AKT2 expression and tumorigenicity of PANC1 cells in nude mice was markedly inhibited by transfection with an antisense AKT2 construct but not with a control AKT2 construct in the sense orientation. Through the use of in vitro kinase assays, activation of the AKT2 kinase has been observed in about 40% of ovarian and pancreatic cancers.
  

Bibliography

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Citation

This paper should be referenced as such :
Altomare, DA ; Testa, JR
AKT2 (v-akt murine thymoma viral oncogene homolog 2)
Atlas Genet Cytogenet Oncol Haematol. 2008;12(1):20-23.
Free journal version : [ pdf ]   [ DOI ]
On line version : http://AtlasGeneticsOncology.org/Genes/AKT2ID517ch19q13.html


Other Solid tumors implicated (Data extracted from papers in the Atlas) [ 2 ]
  Breast: Ductal carcinoma
Ovarian tumours : an overview
Pancreatic tumors: an overview

External links

Nomenclature
HGNC (Hugo)AKT2   392
Cards
AtlasAKT2ID517ch19q13
Entrez_Gene (NCBI)AKT2  208  v-akt murine thymoma viral oncogene homolog 2
AliasesHIHGHH; PKBB; PKBBETA; PRKBB; 
RAC-BETA
GeneCards (Weizmann)AKT2
Ensembl hg19 (Hinxton)ENSG00000105221 [Gene_View]  chr19:40736224-40791302 [Contig_View]  AKT2 [Vega]
Ensembl hg38 (Hinxton)ENSG00000105221 [Gene_View]  chr19:40736224-40791302 [Contig_View]  AKT2 [Vega]
ICGC DataPortalENSG00000105221
TCGA cBioPortalAKT2
AceView (NCBI)AKT2
Genatlas (Paris)AKT2
WikiGenes208
SOURCE (Princeton)AKT2
Genomic and cartography
GoldenPath hg19 (UCSC)AKT2  -     chr19:40736224-40791302 -  19q13.1-q13.2   [Description]    (hg19-Feb_2009)
GoldenPath hg38 (UCSC)AKT2  -     19q13.1-q13.2   [Description]    (hg38-Dec_2013)
EnsemblAKT2 - 19q13.1-q13.2 [CytoView hg19]  AKT2 - 19q13.1-q13.2 [CytoView hg38]
Mapping of homologs : NCBIAKT2 [Mapview hg19]  AKT2 [Mapview hg38]
OMIM125853   164731   240900   
Gene and transcription
Genbank (Entrez)AK054771 AK055779 AK122839 AK294453 AK304209
RefSeq transcript (Entrez)NM_001243027 NM_001243028 NM_001626
RefSeq genomic (Entrez)NC_000019 NC_018930 NG_012038 NT_011109 NW_004929415
Consensus coding sequences : CCDS (NCBI)AKT2
Cluster EST : UnigeneHs.631535 [ NCBI ]
CGAP (NCI)Hs.631535
Alternative Splicing GalleryENSG00000105221
Gene ExpressionAKT2 [ NCBI-GEO ]   AKT2 [ EBI - ARRAY_EXPRESS ]   AKT2 [ SEEK ]   AKT2 [ MEM ]
Gene Expression Viewer (FireBrowse)AKT2 [ Firebrowse - Broad ]
SOURCE (Princeton)Expression in : [Datasets]   [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
GenevisibleExpression in : [tissues]  [cell-lines]  [cancer]  [perturbations]  
BioGPS (Tissue expression)208
GTEX Portal (Tissue expression)AKT2
Protein : pattern, domain, 3D structure
UniProt/SwissProtP31751 (Uniprot)
NextProtP31751  [Sequence]  [Exons]  [Medical]  [Publications]
With graphics : InterProP31751
Splice isoforms : SwissVarP31751 (Swissvar)
Catalytic activity : Enzyme2.7.11.1 [ Enzyme-Expasy ]   2.7.11.12.7.11.1 [ IntEnz-EBI ]   2.7.11.1 [ BRENDA ]   2.7.11.1 [ KEGG ]   
PhosPhoSitePlusP31751
Domaine pattern : Prosite (Expaxy)AGC_KINASE_CTER (PS51285)    PH_DOMAIN (PS50003)    PROTEIN_KINASE_ATP (PS00107)    PROTEIN_KINASE_DOM (PS50011)    PROTEIN_KINASE_ST (PS00108)   
Domains : Interpro (EBI)AGC-kinase_C    Kinase-like_dom    PH_dom-like    PH_domain    Pkinase_C    Prot_kinase_dom    Protein_kinase_ATP_BS    Ser/Thr_dual-sp_kinase    Ser/Thr_kinase_AS   
Domain families : Pfam (Sanger)PH (PF00169)    Pkinase (PF00069)    Pkinase_C (PF00433)   
Domain families : Pfam (NCBI)pfam00169    pfam00069    pfam00433   
Domain families : Smart (EMBL)PH (SM00233)  S_TK_X (SM00133)  S_TKc (SM00220)  
DMDM Disease mutations208
Blocks (Seattle)AKT2
PDB (SRS)1GZK    1GZN    1GZO    1MRV    1MRY    1O6K    1O6L    1P6S    2JDO    2JDR    2UW9    2X39    2XH5    3D0E    3E87    3E88    3E8D   
PDB (PDBSum)1GZK    1GZN    1GZO    1MRV    1MRY    1O6K    1O6L    1P6S    2JDO    2JDR    2UW9    2X39    2XH5    3D0E    3E87    3E88    3E8D   
PDB (IMB)1GZK    1GZN    1GZO    1MRV    1MRY    1O6K    1O6L    1P6S    2JDO    2JDR    2UW9    2X39    2XH5    3D0E    3E87    3E88    3E8D   
PDB (RSDB)1GZK    1GZN    1GZO    1MRV    1MRY    1O6K    1O6L    1P6S    2JDO    2JDR    2UW9    2X39    2XH5    3D0E    3E87    3E88    3E8D   
Structural Biology KnowledgeBase1GZK    1GZN    1GZO    1MRV    1MRY    1O6K    1O6L    1P6S    2JDO    2JDR    2UW9    2X39    2XH5    3D0E    3E87    3E88    3E8D   
SCOP (Structural Classification of Proteins)1GZK    1GZN    1GZO    1MRV    1MRY    1O6K    1O6L    1P6S    2JDO    2JDR    2UW9    2X39    2XH5    3D0E    3E87    3E88    3E8D   
CATH (Classification of proteins structures)1GZK    1GZN    1GZO    1MRV    1MRY    1O6K    1O6L    1P6S    2JDO    2JDR    2UW9    2X39    2XH5    3D0E    3E87    3E88    3E8D   
SuperfamilyP31751
Human Protein AtlasENSG00000105221
Peptide AtlasP31751
HPRD01262
IPIIPI00012870   IPI01011038   IPI01010542   IPI00784816   IPI00440705   IPI00816059   IPI00977463   IPI00790293   IPI00798192   IPI00788928   IPI00797131   IPI00797722   IPI00795867   IPI00794313   
Protein Interaction databases
DIP (DOE-UCLA)P31751
IntAct (EBI)P31751
FunCoupENSG00000105221
BioGRIDAKT2
STRING (EMBL)AKT2
ZODIACAKT2
Ontologies - Pathways
QuickGOP31751
Ontology : AmiGOpositive regulation of protein phosphorylation  protein serine/threonine kinase activity  protein serine/threonine kinase activity  protein kinase C binding  protein binding  ATP binding  nucleus  nucleus  nucleoplasm  early endosome  cytosol  plasma membrane  plasma membrane  cell cortex  glycogen biosynthetic process  glucose metabolic process  regulation of translation  cellular protein modification process  response to osmotic stress  signal transduction  insulin receptor signaling pathway  insulin receptor signaling pathway  carbohydrate transport  positive regulation of signal transduction  negative regulation of plasma membrane long-chain fatty acid transport  positive regulation of glucose metabolic process  response to muscle activity  peptidyl-serine phosphorylation  regulation of cell migration  positive regulation of cell migration  positive regulation of vesicle fusion  response to nutrient levels  positive regulation of fatty acid beta-oxidation  peripheral nervous system myelin maintenance  ruffle membrane  insulin-responsive compartment  cellular response to insulin stimulus  negative regulation of RNA splicing  positive regulation of peptidyl-serine phosphorylation  intracellular signal transduction  negative regulation of cysteine-type endopeptidase activity involved in apoptotic process  protein kinase B signaling  positive regulation of nitric oxide biosynthetic process  fat cell differentiation  positive regulation of glycogen biosynthetic process  positive regulation of transcription from RNA polymerase II promoter  positive regulation of glucose import  positive regulation of positive chemotaxis  mammary gland epithelial cell differentiation  intracellular protein transmembrane transport  regulation of cell cycle arrest  cellular response to organic cyclic compound  protein localization to plasma membrane  positive regulation of protein targeting to membrane  activation of GTPase activity  positive regulation of cell motility  positive regulation of glucose import in response to insulin stimulus  
Ontology : EGO-EBIpositive regulation of protein phosphorylation  protein serine/threonine kinase activity  protein serine/threonine kinase activity  protein kinase C binding  protein binding  ATP binding  nucleus  nucleus  nucleoplasm  early endosome  cytosol  plasma membrane  plasma membrane  cell cortex  glycogen biosynthetic process  glucose metabolic process  regulation of translation  cellular protein modification process  response to osmotic stress  signal transduction  insulin receptor signaling pathway  insulin receptor signaling pathway  carbohydrate transport  positive regulation of signal transduction  negative regulation of plasma membrane long-chain fatty acid transport  positive regulation of glucose metabolic process  response to muscle activity  peptidyl-serine phosphorylation  regulation of cell migration  positive regulation of cell migration  positive regulation of vesicle fusion  response to nutrient levels  positive regulation of fatty acid beta-oxidation  peripheral nervous system myelin maintenance  ruffle membrane  insulin-responsive compartment  cellular response to insulin stimulus  negative regulation of RNA splicing  positive regulation of peptidyl-serine phosphorylation  intracellular signal transduction  negative regulation of cysteine-type endopeptidase activity involved in apoptotic process  protein kinase B signaling  positive regulation of nitric oxide biosynthetic process  fat cell differentiation  positive regulation of glycogen biosynthetic process  positive regulation of transcription from RNA polymerase II promoter  positive regulation of glucose import  positive regulation of positive chemotaxis  mammary gland epithelial cell differentiation  intracellular protein transmembrane transport  regulation of cell cycle arrest  cellular response to organic cyclic compound  protein localization to plasma membrane  positive regulation of protein targeting to membrane  activation of GTPase activity  positive regulation of cell motility  positive regulation of glucose import in response to insulin stimulus  
Pathways : KEGGMAPK signaling pathway    ErbB signaling pathway    Ras signaling pathway    Rap1 signaling pathway    Chemokine signaling pathway    HIF-1 signaling pathway    FoxO signaling pathway    mTOR signaling pathway    PI3K-Akt signaling pathway    Apoptosis    Adrenergic signaling in cardiomyocytes    VEGF signaling pathway    Osteoclast differentiation    Focal adhesion    Tight junction    Toll-like receptor signaling pathway    Jak-STAT signaling pathway    T cell receptor signaling pathway    B cell receptor signaling pathway    Fc epsilon RI signaling pathway    Fc gamma R-mediated phagocytosis    TNF signaling pathway    Neurotrophin signaling pathway    Cholinergic synapse    Dopaminergic synapse    Insulin signaling pathway    Progesterone-mediated oocyte maturation    Estrogen signaling pathway    Prolactin signaling pathway    Thyroid hormone signaling pathway    Adipocytokine signaling pathway    Non-alcoholic fatty liver disease (NAFLD)    Carbohydrate digestion and absorption    Chagas disease (American trypanosomiasis)    Toxoplasmosis    Tuberculosis    Hepatitis C    Hepatitis B    Measles    Influenza A    HTLV-I infection    Epstein-Barr virus infection    Pathways in cancer    Proteoglycans in cancer    Colorectal cancer    Renal cell carcinoma    Pancreatic cancer    Endometrial cancer    Glioma    Prostate cancer    Melanoma    Chronic myeloid leukemia    Acute myeloid leukemia    Small cell lung cancer    Non-small cell lung cancer   
REACTOMEP31751 [protein]
REACTOME PathwaysR-HSA-5628897 TP53 Regulates Metabolic Genes [pathway]
REACTOME PathwaysR-HSA-1358803 Downregulation of ERBB2:ERBB3 signaling [pathway]
REACTOME PathwaysR-HSA-165158 Activation of AKT2 [pathway]
REACTOME PathwaysR-HSA-165181 Inhibition of TSC complex formation by PKB [pathway]
REACTOME PathwaysR-HSA-1257604 PIP3 activates AKT signaling [pathway]
REACTOME PathwaysR-HSA-5674400 Constitutive Signaling by AKT1 E17K in Cancer [pathway]
REACTOME PathwaysR-HSA-389513 CTLA4 inhibitory signaling [pathway]
REACTOME PathwaysR-HSA-389357 CD28 dependent PI3K/Akt signaling [pathway]
REACTOME PathwaysR-HSA-211163 AKT-mediated inactivation of FOXO1A [pathway]
REACTOME PathwaysR-HSA-1445148 Translocation of GLUT4 to the plasma membrane [pathway]
REACTOME PathwaysR-HSA-165160 PDE3B signalling [pathway]
REACTOME PathwaysR-HSA-165158 Activation of AKT2 [pathway]
REACTOME PathwaysR-HSA-198323 AKT phosphorylates targets in the cytosol [pathway]
REACTOME PathwaysR-HSA-199418 Negative regulation of the PI3K/AKT network [pathway]
REACTOME PathwaysR-HSA-3769402 deactivation of the beta-catenin transactivating complex [pathway]
REACTOME PathwaysR-HSA-111447 Activation of BAD and translocation to mitochondria [pathway]
REACTOME PathwaysR-HSA-392451 G beta:gamma signalling through PI3Kgamma [pathway]
REACTOME PathwaysR-HSA-198693 AKT phosphorylates targets in the nucleus [pathway]
REACTOME PathwaysR-HSA-5218920 VEGFR2 mediated vascular permeability [pathway]
REACTOME PathwaysR-HSA-114604 GPVI-mediated activation cascade [pathway]
REACTOME PathwaysR-HSA-165160 PDE3B signalling [pathway]
NDEx Network
Atlas of Cancer Signalling NetworkAKT2
Wikipedia pathwaysAKT2
Orthology - Evolution
OrthoDB208
GeneTree (enSembl)ENSG00000105221
Phylogenetic Trees/Animal Genes : TreeFamAKT2
Homologs : HomoloGeneAKT2
Homology/Alignments : Family Browser (UCSC)AKT2
Gene fusions - Rearrangements
Fusion : MitelmanAKT2/UPF1 [19q13.2/19p13.11]  
Fusion: TCGAAKT2 19q13.2 UPF1 19p13.11 LGG
Polymorphisms : SNP, variants
NCBI Variation ViewerAKT2 [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)AKT2
dbVarAKT2
ClinVarAKT2
1000_GenomesAKT2 
Exome Variant ServerAKT2
ExAC (Exome Aggregation Consortium)AKT2 (select the gene name)
Genetic variants : HAPMAP208
Genomic Variants (DGV)AKT2 [DGVbeta]
Mutations
ICGC Data PortalAKT2 
TCGA Data PortalAKT2 
Broad Tumor PortalAKT2
OASIS PortalAKT2 [ Somatic mutations - Copy number]
Cancer Gene: CensusAKT2 
Somatic Mutations in Cancer : COSMICAKT2 
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD - Leiden Open Variation Database
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
LOVD (Leiden Open Variation Database)MSeqDR-LSDB Mitochondrial Disease Locus Specific Database
BioMutasearch AKT2
DgiDB (Drug Gene Interaction Database)AKT2
DoCM (Curated mutations)AKT2 (select the gene name)
CIViC (Clinical Interpretations of Variants in Cancer)AKT2 (select a term)
intoGenAKT2
Impact of mutations[PolyPhen2] [SIFT Human Coding SNP] [Buck Institute : MutDB] [Mutation Assessor] 
Diseases
DECIPHER (Syndromes)19:40736224-40791302  ENSG00000105221
CONAN: Copy Number AnalysisAKT2 
Mutations and Diseases : HGMDAKT2
OMIM125853    164731    240900   
MedgenAKT2
Genetic Testing Registry AKT2
NextProtP31751 [Medical]
TSGene208
GENETestsAKT2
Huge Navigator AKT2 [HugePedia]
snp3D : Map Gene to Disease208
BioCentury BCIQAKT2
ClinGenAKT2 (curated)
Clinical trials, drugs, therapy
Chemical/Protein Interactions : CTD208
Chemical/Pharm GKB GenePA24685
Drug Sensitivity AKT2
Clinical trialAKT2
Miscellaneous
canSAR (ICR)AKT2 (select the gene name)
Other database326445
Other databaseID ENSG00000105221
Probes
Litterature
PubMed269 Pubmed reference(s) in Entrez
GeneRIFsGene References Into Functions (Entrez)
CoreMineAKT2
EVEXAKT2
GoPubMedAKT2
iHOPAKT2
REVIEW articlesautomatic search in PubMed
Last year publicationsautomatic search in PubMed

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indexed on : Sat Jun 11 12:56:26 CEST 2016

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