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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
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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
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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
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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
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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
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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
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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
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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
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Dog (Canine) Monoclonal AKT Primary Antibody for ICS - ABIN1176874
Alessi, Andjelkovic, Caudwell, Cron, Morrice, Cohen, Hemmings: Mechanism of activation of protein kinase B by insulin and IGF-1. in The EMBO journal 1997
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Human Monoclonal AKT Primary Antibody for ICS - ABIN1177027
Cantley, Neel: New insights into tumor suppression: PTEN suppresses tumor formation by restraining the phosphoinositide 3-kinase/AKT pathway. in Proceedings of the National Academy of Sciences of the United States of America 1999
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High AKT1 expression is associated with hypercholesterolemia.
Authors show here that cyclin F (显示 CCNF 抗体), a substrate receptor F-box protein (显示 FBXW10 抗体) for the SCF (显示 KITLG 抗体) (Skp1 (显示 SKP1 抗体)/Cul1 (显示 CUL1 抗体)/F-box) family of E3 ubiquitin ligases, is a bona fide AKT substrate.
Data suggest that PLSCR1 (显示 PLSCR1 抗体) is involved in viral entry; here, herpes simplex viruses activate PLSCR1 (显示 PLSCR1 抗体) and up-regulate flipping of phosphatidylserines and AKT to outside of plasma membrane shortly following HSV-1 or HSV-2 exposure. (PLSCR1 (显示 PLSCR1 抗体) = phospholipid scramblase 1 (显示 PLSCR1 抗体); AKT = proto-oncogene c-Akt)
that AKT and mTOR proteins are involved in oral squamous cell carcinoma biology and that GSK3beta itself may drive cervical lymph node metastatic spread of oral squamous cell carcinoma cells
enigma (显示 PDLIM1 抗体) siRNA-transfected cells, cell viability, and the protein levels of AKT and survivin (显示 BIRC5 抗体) decreased.
Data indicate connector enhancer of kinase suppressor of Ras 1 (显示 CNKSR1 抗体) protein (CNK1 (显示 CNKSR1 抗体)) as a molecular platform that controls c-raf (显示 RAF1 抗体) protein (RAF (显示 RAF1 抗体)) and c-akt protein (AKT) signalling and determines cell fate decisions in a cell type- and cell stage-dependent manner.
ITGA6 (显示 ITGA6 抗体) might be involved in a mechanism that underlies radiation resistance and that ITGA6 (显示 ITGA6 抗体) could be a potential target for therapies aimed at overcoming radiation resistance in breast cancer.
High Expressions of AKT1 is associated with metastasis of esophageal squamous cell carcinoma.
mutp53 augments insulin (显示 INS 抗体)-induced AKT1 activation by binding and inhibiting the tumor suppressor DAB2IP (DAB2-interacting protein (显示 DAB2IP 抗体)) in the cytoplasm
High AKT1 expression is associated with oncogenicity and chemoresistance in hepatocellular carcinoma.
The authors find in Mus (显示 TRPV6 抗体) musculus, each AKT isoform has a unique expression pattern in the hippocampus. AKT1, but not AKT2 (显示 AKT2 抗体) or AKT3 (显示 AKT3 抗体), is required for late long term potetiation (LTD) through regulating activity-induced protein synthesis. Interestingly, AKT activity inhibits mGluR (显示 GRM8 抗体)-LTD, with overlapping functions for AKT1 and AKT3 (显示 AKT3 抗体).
At 3days after the first tamoxifen injection, Akt1(-/-)/iAkt2 KO hearts showed decreased expression of connexin43 (Cx43 (显示 GJA1 抗体)) and connexin-interacting protein zonula occludens-1 (ZO-1 (显示 TJP1 抗体)). Furthermore, Akt1/2 silencing significantly decreased both Cx43 (显示 GJA1 抗体) and ZO-1 (显示 TJP1 抗体) expression
AKT1 plays an important role in the underlying pathomechanism.
Findings suggest that Akt1 deficiency modulates GABAergic interneurons and GABA A receptor expression, contributing to hippocampus-dependent cognitive functional impairment.
Saliva (显示 RAG1AP1 抗体)-induced enhancement of Akt pathway activation was observed in tick-borne encephalitis virus-infected dendritic cells.
FSTL1 (显示 FSTL1 抗体) may exert its actions through the modulation of Akt signaling.
Building upon previous work suggesting that FAK (显示 PTK2 抗体)-Akt1 binding is mediated by the FAK (显示 PTK2 抗体) F1 lobe, we demonstrated that independently expressing the F1 domain in human Caco-2 or murine CT-26 (显示 DDX53 抗体) colon cancer cells by transient or stable inducible plasmid expression respectively prevents the stimulation of cancer cell adhesion by increased extracellular pressure.
Findings suggest an important role for effector-like memory CD8 (显示 CD8A 抗体)(+) T cells in tumor immune surveillance and indicate proto-oncogene (显示 RAB1A 抗体) proteins c-akt (Akt) as a key signaling node in the development of protective memory CD8 (显示 CD8A 抗体)(+) T-cell responses.
data showed that Klotho (显示 KL 抗体) protects Tac (显示 IL2RA 抗体)-induced oxidative stress by negatively regulating the PI3K/AKT pathway and subsequently enhancing FoxO3a (显示 FOXO3 抗体)-mediated MnSOD (显示 SOD2 抗体) expression.
findings indicate that simvastatin exerts a protective effect against ionizing radiation-induced damage in the mouse thymus, which may be partially attributed to the activation of the AKT/sirtuin 1 (显示 SIRT1 抗体) pathway.
The metabolic defects of cycG (显示 CCNG1 抗体) mutant animals are abrogated by a concomitant loss of Wdb, CycG (显示 CCNG1 抗体) presumably influences Akt1 activity at the PP2A (显示 PPP2R2B 抗体) nexus; Well rounded (Wrd), another B' subunit of PP2A (显示 PPP2R2B 抗体) in Drosophila, binds CycG (显示 CCNG1 抗体) similar to Wdb, and that its loss ameliorates some, but not all, of the metabolic defects of cycG (显示 CCNG1 抗体) mutants.
Our findings demonstrated that lovastatin restored LRRK2-G2019S neurite degeneration by augmenting Akt/NRF2 pathway and inhibiting downstream GSK3b activity, which decreased phospho-tau levels. We suggested that lovastatin is a potential disease-modifying agent for LRRK2-G2019S parkinsonism.
subtle manipulation of foxo (显示 FOXO 抗体) 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 (显示 GRIN1 抗体) localization, and postsynaptic membrane elaboration
Tsc2 (显示 TSC2 抗体) mutants showed a dramatic decrease in the levels of phosphorylated Akt, and interestingly, Akt mutants phenocopied Tsc2 (显示 TSC2 抗体) mutants, leading to the hypothesis that Tsc2 (显示 TSC2 抗体) 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 and microRNA bantam.
Thus, activation of STAT3 (显示 STAT3 抗体) and inactivation of AKT signaling are involved in structural regression of the corpus luteum.
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 (显示 CTNNB1 抗体) accumulation and subsequent ovarian E2 production.
Caveolin-1 (显示 CAV1 抗体) scaffolding domain residue phenylalanine 92 modulates Akt signaling
TG2 (显示 TGM2 抗体) 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, and NF-kappaB (显示 NFKB1 抗体).
The current study was designed to determine mechanisms underlying 20-hydroxyeicosatetraenoic acid -stimulated nitric oxide (NO) release, and particularly the role of NADPH oxidase (显示 NOX1 抗体), reactive oxygen species, and PI3-kinase (显示 PIK3CA 抗体) in stimulated NO release.
PI3K/Akt and p53 (显示 TP53 抗体) 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, p70S6K, and ERK1/2.
Gab1 tyrosine phosphorylation is stimulated by flow shear stress to mediate protein kinase B and endothelial nitric-oxide synthase (显示 NOS3 抗体) activation in endothelial cells
These findings highlight novel and essential roles of PFKFB4 (显示 PFKFB4 抗体) activity in later stages of neural crest (NC) development that are wired into the NC gene regulatory network.
SCF (显示 KITLG 抗体) is a critical regulatory factor for conceptus development and implantation during pregnancy in pigs.
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 (显示 FRAP1 抗体)-FOXO1 (显示 FOXO1 抗体) signaling and suppressing the activation of TLR4 (显示 TLR4 抗体) and/or NOD2 (显示 NOD2 抗体) 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 (显示 LRP2 抗体) is the sensor that determines whether cells will be protected or injured by albumin (显示 ALB 抗体); 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
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 (显示 FNTA 抗体), which further represses the activity of K(+) channel (显示 KCNC4 抗体) 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 (显示 CBL 抗体)-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 (显示 CA2 抗体)+)-dependent manner, connecting the Ca(2 (显示 CA2 抗体)+) signal to K(+) uptake through activation of a K(+) channel (显示 KCNC4 抗体).
the LIN-28/let-7/AKT/DAF-16 axis is a program that plays an important role in balancing reproduction and somatic maintenance.
this study shows that akt-1 and akt-2 negatively regulate DNA-damage-induced apoptosis in the C. elegans germline and the antiapoptotic activity of akt-1 is independent of its target gene daf-16 but dependent on cep-1/p53 (显示 TP53 抗体).
Modulation of pptr-1 affects insulin (显示 INS 抗体)/IGF-1 (显示 IGF1 抗体) signaling pathway-associated phenotypes including life span, dauer, stress resistance, and fat storage; study shows that PPTR-1 functions by regulating worm AKT-1 phosphorylation at Thr (显示 TRH 抗体) 350.
Exogenous AKT was transcribed, and AKT was overexpressed, inducing the phosphorylation of p70S6K (显示 RPS6KB1 抗体) (Thr389) and 4E-BP1 (显示 EIF4EBP1 抗体) (Thr37/46) in goat fetal fibroblasts.
findings suggested that the expressions of the cardiac CACNA1C (显示 CACNA1C 抗体) were under the CLOCK-BMAL1 (显示 ARNTL 抗体) regulation, probably through the PI3K-Akt signal pathway
This study has identified Akt as a novel intracellular pathway required for neural crest differentiation.
Overexpression of human Akt1 enhances adipogenesis and leads to lipoma formation in zebrafish.
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 alpha
, proto-oncogene c-Akt
, rac protein kinase alpha
, AKT1 kinase
, protein kinase B-alpha
, proto-oncogene c-AKT
, related to A and C kinases
, Akt kinase
, dAkt kinase
, protein kinase B
, related to PKA to PKC protein kinases
, related to the A and C kinases
, actin, cytoplasmic 1
, gamma non-muscle actin
, RAC protein kinase alpha RAC-PK alpha
, murine thymoma viral (v-akt) oncogene homolog 1
, thymoma viral proto-oncogene 1
, v-akt murine thymoma viral oncogene-like protein 1
, serine/threonine protein kinase
, protein kinase Akt-1
, protein kinase B, alpha
, v-akt murine thymoma viral oncogene homolog 1
, v-akt murine thymoma viral oncogene-like 1