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V-akt murine thymoma viral oncogene homolog 2

Akt2, Akt3, PKBbeta
This gene is a putative oncogene encoding a protein belonging to a subfamily of serine/threonine kinases containing SH2-like (Src homology 2-like) domains. The gene was shown to be amplified and overexpressed in 2 of 8 ovarian carcinoma cell lines and 2 of 15 primary ovarian tumors. Overexpression contributes to the malignant phenotype of a subset of human ductal pancreatic cancers. The encoded protein is a general protein kinase capable of phophorylating several known proteins. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: Akt, PI3K, Insulin, HAD, CAN
Papers using Akt2 antibodies
PHI-base update: additions to the pathogen host interaction database
Zhou Yan et al., In BMC Genomics, 2007
... AKT1, which encodes a series of carboxyl-activating enzymes, and AKT2 are involved in the biosynthesis of the AK-toxin ...
mTORC2 Protein-mediated Protein Kinase B (Akt) Serine 473 Phosphorylation Is Not Required for Akt1 Activity in Human Platelets*
Hers Ingeborg et al., In The Journal of Biological Chemistry, 2006
... p38, and Akt2 (L79BZ) antibodies were from Cell Signaling Technologies (New England Biolabs, ...
Inositol 1,4,5-trisphosphate [correction of tris-phosphate] activation of inositol trisphosphate [correction of tris-phosphate] receptor Ca2+ channel by ligand tuning of Ca2+ inhibition
Stöckli Jacqueline et al., In The Journal of Biological Chemistry, 1997
... The Akt1-specific and Akt2-specific inhibitors were previously described (20) and were obtained from Merck.
Akt2 phosphorylates Synip to regulate docking and fusion of GLUT4-containing vesicles
Mori Masatomo et al., In The Journal of Cell Biology, 1997
... purchased from Cell Signaling Technology, and Akt1- and Akt2-specific antibodies and siRNA for Akt1 and Akt2 were obtained from Upstate Cell Signaling Solutions ...
Papers on Akt2
Diverse involvement of isoforms and gene aberrations of Akt in human lung carcinomas.
Ooi et al., Saitama, Japan. In Cancer Sci, 09 May 2015
Immunohistochemical staining for 108 cases revealed overexpression of total-Akt, Akt1, Akt2 and Akt3 in 61.1%, 47.2%, 40.7%, 23.1%, respectively and phosphorylated-Akt in 42.6%.
Activation of TGF-β-induced non-Smad signaling pathways during Th17 differentiation.
Kleiter et al., Regensburg, Germany. In Immunol Cell Biol, 01 May 2015
Using protein antibody arrays we found an increase of expression and phosphorylation of the following Smad-independent signaling molecules in Th17-polarized wild-type T cells: AKT1(Tyr474), AKT2 (Ser474), ERK1-p44/42 MAPK(Tyr204), mTOR(Thr2446), p38 MAPK(Thr180), Rac1/cdc42(Ser71), SAPK/JNK(Tyr185) and SP1(Thr739).
Rapid depot-specific activation of adipocyte precursor cells at the onset of obesity.
Rodeheffer et al., New Haven, United States. In Nat Cell Biol, 30 Apr 2015
Furthermore, we find that in multiple models of obesity, the activation of APs is dependent on the phosphoinositide 3-kinase (PI3K)-AKT2 pathway; however, the development of WAT does not require AKT2.
AKT phosphorylates H3-threonine 45 to facilitate termination of gene transcription in response to DNA damage.
Youn et al., Seoul, South Korea. In Nucleic Acids Res, 26 Apr 2015
AKT1 was more effective than AKT2 in phosphorylating H3-T45.
All akt isoforms (akt1, akt2, akt3) are involved in normal hearing, but only akt2 and akt3 are involved in auditory hair cell survival in the Mammalian inner ear.
Bodmer et al., Basel, Switzerland. In Plos One, Dec 2014
Our results further indicate that Akt2 and Akt3 enhance hair cell resistance to ototoxicity, while Akt1 does not.
mTOR Signaling in Epilepsy: Insights from Malformations of Cortical Development.
Crino, Philadelphia, United States. In Cold Spring Harb Perspect Med, Dec 2014
Mutations in mTOR regulatory genes (e.g., TSC1, TSC2, AKT3, DEPDC5) have been associated with several focal MCD highly associated with epilepsy such as tuberous sclerosis complex (TSC), hemimegalencephaly (HME; brain malformation associated with dramatic enlargement of one brain hemisphere), and cortical dysplasia.
MiRNA-615-5p Functions as a Tumor Suppressor in Pancreatic Ductal Adenocarcinoma by Targeting AKT2.
Chen et al., Beijing, China. In Plos One, Dec 2014
Effects of miR-615-5p on AKT2 were examined by dual-luciferase reporter assay.
De novo CCND2 mutations leading to stabilization of cyclin D2 cause megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome.
Sheridan et al., Seattle, United States. In Nat Genet, May 2014
The PI3K-AKT pathway modulates GSK-3β activity, and cells from individuals with PIK3CA, PIK3R2 or AKT3 mutations showed similar CCND2 accumulation.
Role of Akt in human malignant glioma: from oncogenesis to tumor aggressiveness.
Verrelle et al., Clermont-Ferrand, France. In J Neurooncol, Apr 2014
More recently, the actions of the two other isoforms, Akt2 and Akt3 have emerged in glioma.
Comparative genomic hybridisation array and DNA sequencing to direct treatment of metastatic breast cancer: a multicentre, prospective trial (SAFIR01/UNICANCER).
Bonnefoi et al., Villejuif, France. In Lancet Oncol, Mar 2014
117 (39%) of 297 patients with genomic tests available presented with rare genomic alterations (defined as occurring in less than 5% of the general population), including AKT1 mutations, and EGFR, MDM2, FGFR2, AKT2, IGF1R, and MET high-level amplifications.
Advances in small bowel neuroendocrine neoplasia.
Beutler et al., Rochester, United States. In Curr Opin Gastroenterol, Mar 2014
Candidate therapeutically relevant alterations were found to affect SRC, SMAD genes, aurora kinase A, epidermal growth factor receptor, heat shock protein 90, and platelet-derived growth factor receptor as well as mutually exclusive amplification of RAC-alpha serine/threonine-protein kinase (AKT1) or AKT2 and other alterations of PI3K/Akt/mTOR signaling genes.
The AKT genes and their roles in various disorders.
Cohen, Halifax, Canada. In Am J Med Genet A, 2013
Both AKT2 and AKT3, although important, have more limited distributions.
AKT2 is essential to maintain podocyte viability and function during chronic kidney disease.
Terzi et al., Paris, France. In Nat Med, 2013
Here we show that Akt2 activation has an essential role in podocyte protection after nephron reduction.
The role of the dysfunctional akt-related pathway in cancer: establishment and maintenance of a malignant cell phenotype, resistance to therapy, and future strategies for drug development.
Romano, Philadelphia, United States. In Scientifica (cairo), 2012
Akt is present in three isoforms: Akt1, Akt2, and Akt3, which may be alternatively named PKB α , PKB β , and PKB γ , respectively.
Single-neuron sequencing analysis of L1 retrotransposition and somatic mutation in the human brain.
Walsh et al., Boston, United States. In Cell, 2012
We then genotyped single cortical cells to characterize the mosaicism of a somatic AKT3 mutation identified in a child with hemimegalencephaly.
ADP-stimulated activation of Akt during integrin outside-in signaling promotes platelet spreading by inhibiting glycogen synthase kinase-3β.
Du et al., Chicago, United States. In Arterioscler Thromb Vasc Biol, 2012
Results demonstrate that integrin outside-in signaling and platelet spreading requires Src family kinase-dependent and ADP receptor-amplified activation of the PI3K-Akt-GSK-3beta pathway.
De novo somatic mutations in components of the PI3K-AKT3-mTOR pathway cause hemimegalencephaly.
Gleeson et al., San Diego, United States. In Nat Genet, 2012
Exome sequencing and mass spectrometry analysis in paired brain-blood samples from individuals with hemimegalencephaly (20 cases) identified de novo somatic mutations in 30% of affected individuals in the PIK3CA, AKT3 and MTOR genes.
De novo germline and postzygotic mutations in AKT3, PIK3R2 and PIK3CA cause a spectrum of related megalencephaly syndromes.
Dobyns et al., Seattle, United States. In Nat Genet, 2012
identified mutations in AKT3, PIK3R2 and PIK3CA in 11 unrelated families with megalencephaly-capillary malformation and megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndromes
Akt1 and Akt2 protein kinases differentially contribute to macrophage polarization.
Tsatsanis et al., Irákleion, Greece. In Proc Natl Acad Sci U S A, 2012
Akt kinases differentially contribute to macrophage polarization, with Akt1 ablation giving rise to an M1 and Akt2 ablation resulting in an M2 phenotype
Akt3 deficiency in macrophages promotes foam cell formation and atherosclerosis in mice.
Podrez et al., Cleveland, United States. In Cell Metab, 2012
nonredundant atheroprotective role for Akt3 exerted via the previously unknown link between the Akt signaling pathway and cholesterol metabolism.
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