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anti-Mouse (Murine) AKT Antibodies:
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Human Polyclonal AKT Primary Antibody for IHC, WB - ABIN361978
Kim, Lee, Kim, Bahk: A Proteomic approach for protein-profiling the oncogenic ras induced transformation (H-, K-, and N-Ras) in NIH/3T3 mouse embryonic fibroblasts. in Proteomics 2008
Show all 21 Pubmed References
Human Polyclonal AKT Primary Antibody for IHC, WB - ABIN362584
Bahk, Cho, Kim: A cross-talk between oncogenic Ras and tumor suppressor PTEN through FAK Tyr861 phosphorylation in NIH/3T3 mouse embryonic fibroblasts. in Biochemical and biophysical research communications 2008
Show all 15 Pubmed References
Human Polyclonal AKT Primary Antibody for CyTOF, FACS - ABIN4900619
Wang, Yue, Kim, Fu, Khuri, Sun: Enhancing mammalian target of rapamycin (mTOR)-targeted cancer therapy by preventing mTOR/raptor inhibition-initiated, mTOR/rictor-independent Akt activation. in Cancer research 2008
Show all 12 Pubmed References
Human Monoclonal AKT Primary Antibody for IHC, IHC (p) - ABIN252685
Luty, Rodeberg, Parness, Vyas: Antiparallel segregation of notch components in the immunological synapse directs reciprocal signaling in allogeneic Th:DC conjugates. in Journal of immunology (Baltimore, Md. : 1950) 2007
Show all 8 Pubmed References
Human Monoclonal AKT Primary Antibody for ICS - ABIN1177030
Prinz, Mendler, Masouris, Durner, Oberneder, Noessner: High DGK-α and disabled MAPK pathways cause dysfunction of human tumor-infiltrating CD8+ T cells that is reversible by pharmacologic intervention. in Journal of immunology (Baltimore, Md. : 1950) 2012
Show all 7 Pubmed References
Human Polyclonal AKT Primary Antibody for IP, WB - ABIN223018
Artwohl, Muth, Kosulin, de Martin, Hölzenbein, Rainer, Freudenthaler, Huttary, Schmetterer, Waldhäusl, Baumgartner-Parzer: R-(+)-alpha-lipoic acid inhibits endothelial cell apoptosis and proliferation: involvement of Akt and retinoblastoma protein/E2F-1. in American journal of physiology. Endocrinology and metabolism 2007
Show all 6 Pubmed References
Human Monoclonal AKT Primary Antibody for WB - ABIN4279016
Nair, Shishodia, Ahn, Kunnumakkara, Sethi, Aggarwal: Deguelin, an Akt inhibitor, suppresses IkappaBalpha kinase activation leading to suppression of NF-kappaB-regulated gene expression, potentiation of apoptosis, and inhibition of cellular invasion. in Journal of immunology (Baltimore, Md. : 1950) 2006
Show all 6 Pubmed References
Human Polyclonal AKT Primary Antibody for IF, IHC - ABIN361980
Tremblay, Krebs, Dombrowski, Brehm, Bernroider, Roth, Nowotny, Waldhäusl, Marette, Roden: Overactivation of S6 kinase 1 as a cause of human insulin resistance during increased amino acid availability. in Diabetes 2005
Show all 10 Pubmed References
Human Polyclonal AKT Primary Antibody for ELISA, FACS - ABIN4278995
Sagatys, Garrett, Boulware, Kelley, Malafa, Cheng, Sebti, Coppola: Activation of the serine/threonine protein kinase Akt during the progression of Barrett neoplasia. in Human pathology 2007
Show all 5 Pubmed References
Human Monoclonal AKT Primary Antibody for ICS - ABIN1177029
Alessi, Andjelkovic, Caudwell, Cron, Morrice, Cohen, Hemmings: Mechanism of activation of protein kinase B by insulin and IGF-1. in The EMBO journal 1997
Show all 5 Pubmed References
The metabolic defects of cycG (show CCNG1 Antibodies) mutant animals are abrogated by a concomitant loss of Wdb, CycG (show CCNG1 Antibodies) presumably influences Akt1 activity at the PP2A (show PPP2R2B Antibodies) nexus; Well rounded (Wrd), another B' subunit of PP2A (show PPP2R2B Antibodies) in Drosophila, binds CycG (show CCNG1 Antibodies) similar to Wdb, and that its loss ameliorates some, but not all, of the metabolic defects of cycG (show CCNG1 Antibodies) mutants.
Our findings demonstrated that lovastatin restored LRRK2 (show LRRK2 Antibodies)-G2019S neurite degeneration by augmenting Akt/NRF2 (show NFE2L2 Antibodies) pathway and inhibiting downstream GSK3b (show GSK3b Antibodies) activity, which decreased phospho-tau levels. We suggested that lovastatin is a potential disease-modifying agent for LRRK2 (show LRRK2 Antibodies)-G2019S parkinsonism.
subtle manipulation of foxo (show FOXO Antibodies) through Akt1 can enhance survival during adverse nutrient conditions in Drosophila.
The developmental delay of these novel Akt1 hypomorphs results in a latent phenotype uncovered by generation of somatic clones
these data show that Drosophila Trbl has a conserved role to bind Akt and block Akt-mediated insulin signaling, and implicate Trib proteins as novel sites of signaling pathway integration that link nutrient availability with cell growth and proliferation
AKT1 and caspase-dependent regulation of Acn stability adjusts basal autophagy levels.
Akt1 governs two critical elements of synapse development, neurotransmitter receptor (show GRIN1 Antibodies) localization, and postsynaptic membrane elaboration
Tsc2 (show TSC2 Antibodies) mutants showed a dramatic decrease in the levels of phosphorylated Akt, and interestingly, Akt mutants phenocopied Tsc2 (show TSC2 Antibodies) mutants, leading to the hypothesis that Tsc2 (show TSC2 Antibodies) and Akt might work via the same genetic pathway to regulate synapse growth.
Hippo signaling not only blocks cell division and promotes apoptosis, but also regulates cellular growth by inhibiting the Akt pathway activity.
Regeneration of Drosophila sensory neuron axons and dendrites is regulated by the Akt pathway involving Pten (show PTEN Antibodies) and microRNA bantam.
CIPK23 and AtKC1 exhibit distinct effects; however, they act synergistically and balance K(+) uptake/leakage to modulate AKT1-mediated low potassium responses in Arabidopsis.
results suggest that NO decreases K(+) absorption by promoting the synthesis of vitamin B6 PLP (show FNTA Antibodies), which further represses the activity of K(+) channel (show KCNC4 Antibodies) AKT1 in Arabidopsis.
Examination of the athak5 atakt1 double mutant, revealing novel aspects of an uptake system as yet unidentified by genetic means.
AKT1 is regulated by CIPK23 in guard cells and is involved in water stress responses.
These findings provide further insights into the signaling network consisting of CBL (show CBL Antibodies)-CIPK-PP2C interactions in the activation of the AKT1 channel.
Electrophysiological results showed that AtKC1 inhibited the AKT1-mediated inward K(+) currents and negatively shifted the voltage dependence of AKT1 channels.
AtHAK5 and AKT1 are vital for plant growth and development at low K+ concentrations.
In the range between 0.01 and 0.05 mM K+ AtHAK5 and AtAKT1 are the only contributors to K+ acquisition. At higher K+ concentrations, unknown systems come into operation and participate together with AtAKT1 in low-affinity K+ uptake.
CIPK23 directly phosphorylates the K+ transporter AKT1
Data show that interacting calcium sensors (CBL1 and CBL9) together with CIPK23, but not either alone, activated the AKT1 channel in a Ca(2 (show CA2 Antibodies)+)-dependent manner, connecting the Ca(2 (show CA2 Antibodies)+) signal to K(+) uptake through activation of a K(+) channel (show KCNC4 Antibodies).
Besides, both in vivo and in votro studies suggested that K145 stimulated insulin (show INS Antibodies) dependent Akt phosphorylation and subsequently activates FoxO1 (show FOXO1 Antibodies) phosphorylation therefore inhibited gluconeogenetic genes expression including PEPCK (show PEPCK Antibodies) and G6pase (show G6PC Antibodies). Our study figures out a potential extent increase the value of developing K145 as therapeutic candidate for diabetes.
C5a in vitro caused activation (phosphorylation) of MAPKs and Akt in cardiomyocytes, which required availability of both C5a receptors. These data suggest that polymicrobial sepsis causes cardiac dysfunction that appears to be linked to activation of MAPKs and Akt in heart.
High Akt1 expression is associated with hepatocarcinogenesis.
Findings indicate that the energy-sensing LKB1 (show STK11 Antibodies)-AMPK (show PRKAA1 Antibodies) pathway regulates IGF1 (show IGF1 Antibodies) secretion in mouse primary hepatocytes, which in turn regulates activation of the IGF1R (show IGF1R Antibodies)-PKB (show AKT2 Antibodies) pathway.
data suggested that PPARbeta (show PPARD Antibodies)-regulated PDK1 (show PDPK1 Antibodies)/Akt and E2f (show E2F1 Antibodies) signaling that controls metabolism and proliferation is involved in the normal progression of liver regeneration
This work suggests that a switch in substrate specificity coupled to the phosphorylation status of Akt may lead to alternative cell fates and demonstrates that proteins involved with alternative splicing are important factors in T cell fate decisions.
Suppression of Akt1-beta-catenin (show CTNNB1 Antibodies) pathway in advanced prostate cancer promotes TGFbeta1 (show TGFB1 Antibodies)-mediated epithelial to mesenchymal transition and metastasis.
TSC1 (show TSC1 Antibodies)/TSC2 (show TSC2 Antibodies) complex upregulation of OPN (show SPP1 Antibodies) expression is mediated by transcription factor SOX9 (show SOX9 Antibodies) in an mTOR (show FRAP1 Antibodies)-independent manner. Moreover, ablation of OPN (show SPP1 Antibodies) by deficient TSC1 (show TSC1 Antibodies)/TSC2 (show TSC2 Antibodies) complex contributed to inactivation of AKT in TSC (show SLC12A3 Antibodies) cells
Our results suggest that increasing Akt/ NF-kappaB (show NFKB1 Antibodies) is a crucial mediator of skin aging, which can increase the susceptibility of cell transformation.
findings highlight a pivotal link between an epigenetic regulator, WHSC1, and key intracellular signaling molecules, AKT, RICTOR, and Rac1, to drive prostate cancer metastasis.
elevated Th17 cells secrete IL-17A (show IL17A Antibodies) by which promotes the proliferation and resistance to daunorubicin in B-cell acute lymphoblastic leukemia cells through activation of Akt signaling.
We hypothesize that sporadic meningothelial and transitional subtype meningiomas are a forme fruste or microform of Proteus syndrome, and activation of the AKT/PI3K (show PIK3CA Antibodies) pathway drives hyperostosis in both non-syndromic, and Proteus-related meningiomas.
Transforming growth factor-beta1 upregulation triggers pulmonary artery smooth muscle cell proliferation and apoptosis imbalance in rats with hypoxic pulmonary hypertension via the PTEN (show PTEN Antibodies)/AKT pathways
High AKT1 expression is associated with lung cancer.
High AKT1 expression is associated with gastric cancer.
High AKT1 expression is associated with ovarian cancer.
AKT/GSK-3beta (show GSK3b Antibodies)-mediated stabilization of SP1 (show PSG1 Antibodies) is required for TGF-beta (show TGFB1 Antibodies) induced up-regulation of NKG2DLs.
RanBP9 (show RANBP9 Antibodies)/TSSC3 (show PHLDA2 Antibodies) complex cooperatively suppress metastasis via downregulation of Src (show SRC Antibodies)-dependent Akt pathway to expedite mitochondrial-associated anoikis.
miR (show MLXIP Antibodies)-137 suppresses the phosphorylation of AKT.
High AKT1 expression is associated with gallbladder cancer.
These results indicate glycine enhances muscle protein mass under an inflammatory condition. The beneficial roles of glycine on the muscle are closely associated with maintaining Akt-mTOR (show FRAP1 Antibodies)-FOXO1 (show FOXO1 Antibodies) signaling and suppressing the activation of TLR4 (show TLR4 Antibodies) and/or NOD2 (show NOD2 Antibodies) signaling pathways.
Data show that homocysteine (Hcy) can ameliorate the endothelium-independent hypoxic coronary vasoconstriction, in which the inhibition of PI3K/Akt signaling pathway may be involved.
In pigs, lactose synthesis was significantly elevated with the increase of milk production and AKT1 could positively regulate lactose synthesis.
In conclusion, our observations reveal that PRRSV triggers the activation of FAK-PI3K-AKT-Rac1 signaling pathway to facilitate its entry into cells.
Host PI3K and Akt1 play a role in viral gene expression, leading to an increase in porcine reproductive and respiratory syndrome virus replication.
Activity of AKT is not essential for induction of germinal vesicle breakdown in porcine oocytes but plays a substantial role during progression of meiosis to MI/MII-stage.
IL-4 induced activation of Akt/SREBP-1/lipid biosynthesis in EC, resulting in protection against membrane attack complex and melittin, in association with mitochondrial protection.
findings show that megalin (show LRP2 Antibodies) is the sensor that determines whether cells will be protected or injured by albumin (show ALB Antibodies); it binds protein kinase B (PKB) in a D-3-phosphorylated phospholipid-insensitive manner, anchoring PKB in the luminal plasma membrane [
protein kinase B (PKB/Akt)was localized in the granulosa cells of primordial follicles and in the basal layers of the granulosa cells of preantral and antral follicles, but were not localized in atretic follicles and corpora lutea
Akt signaling in porcine patellofemoral joint cartilage is dependent upon frequency of loading, cartilage zone, and the time interval between loading and cartilage harvest.
the measurement of levels of PI3K-Akt pathway components in FCs from ovarian follicles carrying oocytes with distinct developmental competences is a useful tool to identify putative molecular pathways involved in the acquisition of oocyte competence.
These results demonstrate that activation of AKT is required for gonadotropin regulation of CTNNB1 (show CTNNB1 Antibodies) accumulation and subsequent ovarian E2 production.
Caveolin-1 (show CAV1 Antibodies) scaffolding domain residue phenylalanine 92 modulates Akt signaling
TG2 (show TGM2 Antibodies) contributes to 5-hydroxytryptamine-induced distal pulmonary artery smooth muscle cell proliferation via promotion of AKT signaling, likely via its serotonylation.
results suggest that PI3K-Akt activity is important for the internalization of S. aureus and phosphorylation of GSK-3alpha, GSK-3beta (show GSK3b Antibodies), and NF-kappaB (show NFKB1 Antibodies).
The current study was designed to determine mechanisms underlying 20-hydroxyeicosatetraenoic acid -stimulated nitric oxide (NO) release, and particularly the role of NADPH oxidase (show NOX1 Antibodies), reactive oxygen species, and PI3-kinase (show PIK3CA Antibodies) in stimulated NO release.
PI3K/Akt and p53 (show TP53 Antibodies) are redox-regulated in bovine aortic endothelial cells exposed to hydrogen peroxide
Thus our data demonstrate that hypoxia-induced adventitial fibroblast proliferation requires activation and interaction of PI3K, Akt, mTOR (show FRAP1 Antibodies), p70S6K (show RPS6KB1 Antibodies), and ERK1/2 (show MAPK1/3 Antibodies).
Gab1 (show GAB1 Antibodies) tyrosine phosphorylation is stimulated by flow shear stress to mediate protein kinase B and endothelial nitric-oxide synthase (show NOS3 Antibodies) activation in endothelial cells
Losartan metabolite stimulates eNOS (show NOS3 Antibodies) phosphorylation and suppresses tumor necrosis factor alpha (show TNF Antibodies)-induced endothelial cell apoptosis by activating AKT1.
The serine-threonine protein kinase encoded by the AKT1 gene is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Mutations in this gene have been associated with the Proteus syndrome. Multiple alternatively spliced transcript variants have been found for this gene.
RAC-alpha serine/threonine-protein kinase
, protein kinase B
, v-akt murine thymoma viral oncogene homolog 1
, Akt kinase
, dAkt kinase
, related to PKA to PKC protein kinases
, related to the A and C kinases
, AKT1 kinase
, PKB alpha
, protein kinase B alpha
, protein kinase B-alpha
, proto-oncogene c-AKT
, related to A and C kinases
, proto-oncogene c-Akt
, rac protein kinase alpha
, RAC protein kinase alpha RAC-PK alpha
, murine thymoma viral (v-akt) oncogene homolog 1
, thymoma viral proto-oncogene 1
, protein kinase Akt-1
, protein kinase B, alpha
, serine/threonine protein kinase
, v-akt murine thymoma viral oncogene-like 1
, v-akt murine thymoma viral oncogene-like protein 1