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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 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 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 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 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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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 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
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Human Polyclonal AKT Primary Antibody for IHC, WB - ABIN362586
Xu, Stippec, Lazrak, Huang, Cobb: WNK1 activates SGK1 by a phosphatidylinositol 3-kinase-dependent and non-catalytic mechanism. in The Journal of biological chemistry 2005
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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 (显示 LRRK2 抗体)-G2019S neurite degeneration by augmenting Akt/NRF2 (显示 NFE2L2 抗体) pathway and inhibiting downstream GSK3b (显示 GSK3b 抗体) activity, which decreased phospho-tau levels. We suggested that lovastatin is a potential disease-modifying agent for LRRK2 (显示 LRRK2 抗体)-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 (显示 PTEN 抗体) 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 (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).
Tideglusib significantly reduced cerebral infarct volume at both 24h and 7days after HI injury. Tideglusib also increased phosphorylated GSK-3beta (显示 GSK3b 抗体)(Ser9) and Akt(Ser473)
Therefore our study identifies a compartmentalized PtdIns(3,4,5)P3/AKT/GSK3beta (显示 GSK3b 抗体) signaling axis at cilia in SHH (显示 SHH 抗体)-dependent medulloblastoma that is regulated by INPP5E (显示 INPP5E 抗体) to maintain tumor cell cilia, promote SHH (显示 SHH 抗体) signaling and thereby medulloblastoma progression.
mTORC2 (显示 CRTC2 抗体) complex is responsible for phosphorylating Akt at S(473).
FHL2 (显示 FHL2 抗体) facilitates ovarian granulosa cell tumor progression via controlling AKT1 transcription.
Omentin (显示 ITLN1 抗体) protects against lipopysaccharides-induced acute respiratory distress syndrome through suppressing pulmonary inflammation and promoti (显示 NOS3 抗体)ng endothelial barrier via an Akt/NOS3-dependent mechanism.
AIM2 (显示 AIM2 抗体) contributes to the maintenance of intestinal integrity via Akt and protects against Salmonella mucosal infection.
Following transepithelial migration, neutrophils adhesion to ICAM-1 (显示 ICAM1 抗体) resulted in activation of Akt and beta-catenin (显示 CTNNB1 抗体) signaling, increased epithelial-cell proliferation, and wound healing.
Besides, both in vivo and in votro studies suggested that K145 stimulated insulin (显示 INS 抗体) dependent Akt phosphorylation and subsequently activates FoxO1 (显示 FOXO1 抗体) phosphorylation therefore inhibited gluconeogenetic genes expression including PEPCK (显示 PEPCK 抗体) and G6pase (显示 G6PC 抗体). 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.
ILT3 (显示 LILRB4 抗体) may functionally contribute to a regulatory network controlling tumor progression by suppressing the Akt pathway.
Extracellular polyamines induced proliferation and cancer cell migration by inducing ODC (显示 ODC1 抗体) and SSAT (显示 SAT1 抗体) expression, and the Akt1-mediated pathway.
The impact of AKT1 on glucocorticoid receptor (GR (显示 NR3C1 抗体))-induced transcriptional activity in cooperation with phospho-serine/threonine-binding protein 14-3-3 (显示 YWHAQ 抗体), was examined.
These findings identify phospho-AKT in the primary tumor and miR (显示 MLXIP 抗体)-200c later during tumor progression as prognostic molecules.
This study showed that the induction level of IL-32 (显示 IL32 抗体) was increased in chronic rhinosinusitis with nasal polyps compared to normal nasal mucosa and that LPS (显示 IRF6 抗体)-induced IL-32 (显示 IL32 抗体) expression in nasal polyp-derived fibroblasts was regulated via the TLR4 (显示 TLR4 抗体)/JNK (显示 MAPK8 抗体)/AKT/CREB (显示 CREB1 抗体) signaling pathway.
Phosphorylation of MITF (显示 MITF 抗体) by AKT affects its downstream targets and causes TP53 (显示 TP53 抗体)-dependent cell senescence
IL-1beta (显示 IL1B 抗体) induced apoptosis and the expression of catabolic mediators by inducing autophagy, and the autophagy in part was mediated through the activation of AKT/mTOR (显示 FRAP1 抗体)/P70S6K (显示 RPS6KB1 抗体) signaling pathway in human osteoarthritis chondrocytes.
KRAS mutations and AKT activation are present in Wilms tumors (WT) and may represent novel therapeutic targets for this tumor.
High AKT1 expression is associated with Lung 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 (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
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 (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 (显示 GSK3b 抗体), 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 (显示 FRAP1 抗体), p70S6K (显示 RPS6KB1 抗体), and ERK1/2 (显示 MAPK1/3 抗体).
Gab1 (显示 GAB1 抗体) 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
Losartan metabolite stimulates eNOS (显示 NOS3 抗体) phosphorylation and suppresses tumor necrosis factor alpha (显示 TNF 抗体)-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 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
, actin, cytoplasmic 1
, Akt kinase
, dAkt kinase
, protein kinase B
, related to PKA to PKC protein kinases
, related to the A and C kinases
, 5C actin
, actin 5 C
, actin 5C
, actin 5c
, actin A1
, cellular cytoskeletal beta-actin
, gamma non-muscle actin
, beta 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