Use your antibodies-online credentials, if available.
Il n’y a pas de produits dans votre liste de comparaison.
Votre panier est vide.
Afficher toutes les espèces
Afficher tous les synonymes
Sélectionnez vos espèces et l'application
anti-Human AKT Anticorps:
anti-Mouse (Murine) AKT Anticorps:
anti-Rat (Rattus) AKT Anticorps:
Vous arrivez à notre recherche pré-filtrée.
Human Polyclonal AKT Primary Antibody pour 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. dans Proteomics 2008
Show all 21 Pubmed References
Human Polyclonal AKT Primary Antibody pour 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. dans Cancer research 2008
Show all 16 Pubmed References
Human Polyclonal AKT Primary Antibody pour 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. dans Biochemical and biophysical research communications 2008
Show all 15 Pubmed References
Human Monoclonal AKT Primary Antibody pour 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. dans Journal of immunology (Baltimore, Md. : 1950) 2007
Show all 8 Pubmed References
Human Monoclonal AKT Primary Antibody pour 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. dans Journal of immunology (Baltimore, Md. : 1950) 2012
Show all 7 Pubmed References
Human Polyclonal AKT Primary Antibody pour 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. dans American journal of physiology. Endocrinology and metabolism 2007
Show all 6 Pubmed References
Human Monoclonal AKT Primary Antibody pour 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. dans Journal of immunology (Baltimore, Md. : 1950) 2006
Show all 6 Pubmed References
Human Polyclonal AKT Primary Antibody pour 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. dans Diabetes 2005
Show all 10 Pubmed References
Human Polyclonal AKT Primary Antibody pour IHC, WB - ABIN362586
Xu, Stippec, Lazrak, Huang, Cobb: WNK1 activates SGK1 by a phosphatidylinositol 3-kinase-dependent and non-catalytic mechanism. dans The Journal of biological chemistry 2005
Show all 9 Pubmed References
Human Polyclonal AKT Primary Antibody pour 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. dans Human pathology 2007
Show all 5 Pubmed References
TMCO1 (Montrer TMCO1 Anticorps) recruited the PH domain and leucine-rich repeat protein phosphatase 2 (PHLPP2 (Montrer PHLPP2 Anticorps)) to dephosphorylate pAKT1(serine 473) (S473). Mutagenesis at S60 of the TMCO1 (Montrer TMCO1 Anticorps) protein released TMCO1 (Montrer TMCO1 Anticorps)-induced cell-cycle arrest and restored the AKT pathway in BFTC905 cells. Stable TMCO1 (Montrer TMCO1 Anticorps) (wild-type) overexpression suppressed, whereas T33A and S60A mutants recovered, tumor size in xenograft mice.
AKT inhibition led to decreased FMRP (Montrer FMR1 Anticorps) levels, as expected due to the known FMR1/FMRP (Montrer FMR1 Anticorps) negative feedback loop. But rFSH and the mTOR (Montrer FRAP1 Anticorps) inhibition increased them, indicating a decoupling of this FMR1/FMRP (Montrer FMR1 Anticorps) negative feedback loop in our model system
Combined targeting of AKT and SRC (Montrer SRC Anticorps) resulted in a synergistic efficacy against human pancreatic cancer growth and metastasis
IGF-1R (Montrer IGF1R Anticorps) and AKT inhibitors further increased apoptosis by Nutlin-3a in parental MHM cells and the cisplatin-resistant clones, confirming IGF-1R (Montrer IGF1R Anticorps)/AKT signaling promotes apoptosis resistance.
The results of the present study revealed a correlation between BAFF (Montrer TNFSF13B Anticorps) and the PI3K (Montrer PIK3CA Anticorps)/Akt/mTOR (Montrer FRAP1 Anticorps) signaling pathway, and it is hypothesized that they are involved in the pathogenesis of lupus nephritis
results reveal how alterations in FBXO31 (Montrer FBXO5 Anticorps) phosphorylation, mediated by AKT and ATM (Montrer ATM Anticorps), underlie physiological regulation of FBXO31 (Montrer FBXO5 Anticorps) levels in unstressed and genotoxically stressed cells
By monitoring single-cell dynamics in each of these contexts, the authors identified PI3K (Montrer PIK3CA Anticorps)/Akt regulation of glycolysis as a multifaceted modulator of single-cell metabolic dynamics that is required to maintain metabolic stability in proliferating cells.
Mycobacterial trehalose 6,6'-dimycolate modulates transendothelial migration of neutrophils upon mycobacterial infection through prolonged AKT phosphorylation.
High AKT1 expression is associated with non-small cell lung cancer metastasis.
Knockdown of MTDH (Montrer MTDH Anticorps) expression also upregulated PTEN and suppressed pAKT protein expression in Caki2 cells. In conclusion, the present study is the first, to the best of our knowledge, to provide evidence suggesting that miRNA30a5p suppresses tumor human renal cancer cell proliferation via the MTDH (Montrer MTDH Anticorps)/PTEN/AKT pathway
CYP2E1 (Montrer CYP2E1 Anticorps)-induced oxidative stress may be responsible for ethanol-induced suppression of Akt phosphorylation and pharmacological modulation of Akt in liver may be an effective strategy for the treatment of ethanol-induced fatty liver.
The authors find in Mus (Montrer TRPV6 Anticorps) musculus, each AKT isoform has a unique expression pattern in the hippocampus. AKT1, but not AKT2 (Montrer AKT2 Anticorps) or AKT3 (Montrer AKT3 Anticorps), is required for late long term potetiation (LTD) through regulating activity-induced protein synthesis. Interestingly, AKT activity inhibits mGluR (Montrer GRM8 Anticorps)-LTD, with overlapping functions for AKT1 and AKT3 (Montrer AKT3 Anticorps).
At 3days after the first tamoxifen injection, Akt1(-/-)/iAkt2 KO hearts showed decreased expression of connexin43 (Cx43 (Montrer GJA1 Anticorps)) and connexin-interacting protein zonula occludens-1 (ZO-1 (Montrer TJP1 Anticorps)). Furthermore, Akt1/2 silencing significantly decreased both Cx43 (Montrer GJA1 Anticorps) and ZO-1 (Montrer TJP1 Anticorps) 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 (Montrer RAG1AP1 Anticorps)-induced enhancement of Akt pathway activation was observed in tick-borne encephalitis virus-infected dendritic cells.
FSTL1 (Montrer FSTL1 Anticorps) may exert its actions through the modulation of Akt signaling.
Building upon previous work suggesting that FAK (Montrer PTK2 Anticorps)-Akt1 binding is mediated by the FAK (Montrer PTK2 Anticorps) F1 lobe, we demonstrated that independently expressing the F1 domain in human Caco-2 or murine CT-26 (Montrer DDX53 Anticorps) 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 (Montrer CD8A Anticorps)(+) T cells in tumor immune surveillance and indicate proto-oncogene (Montrer RAB1A Anticorps) proteins c-akt (Akt) as a key signaling node in the development of protective memory CD8 (Montrer CD8A Anticorps)(+) T-cell responses.
data showed that Klotho (Montrer KL Anticorps) protects Tac (Montrer IL2RA Anticorps)-induced oxidative stress by negatively regulating the PI3K/AKT pathway and subsequently enhancing FoxO3a (Montrer FOXO3 Anticorps)-mediated MnSOD (Montrer SOD2 Anticorps) expression.
The metabolic defects of cycG (Montrer CCNG1 Anticorps) mutant animals are abrogated by a concomitant loss of Wdb, CycG (Montrer CCNG1 Anticorps) presumably influences Akt1 activity at the PP2A (Montrer PPP2R2B Anticorps) nexus; Well rounded (Wrd), another B' subunit of PP2A (Montrer PPP2R2B Anticorps) in Drosophila, binds CycG (Montrer CCNG1 Anticorps) similar to Wdb, and that its loss ameliorates some, but not all, of the metabolic defects of cycG (Montrer CCNG1 Anticorps) 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 (Montrer FOXO Anticorps) 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 (Montrer GRIN1 Anticorps) localization, and postsynaptic membrane elaboration
Tsc2 (Montrer TSC2 Anticorps) mutants showed a dramatic decrease in the levels of phosphorylated Akt, and interestingly, Akt mutants phenocopied Tsc2 (Montrer TSC2 Anticorps) mutants, leading to the hypothesis that Tsc2 (Montrer TSC2 Anticorps) 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 (Montrer STAT3 Anticorps) 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 (Montrer CTNNB1 Anticorps) accumulation and subsequent ovarian E2 production.
Caveolin-1 (Montrer CAV1 Anticorps) scaffolding domain residue phenylalanine 92 modulates Akt signaling
TG2 (Montrer TGM2 Anticorps) 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 (Montrer NFKB1 Anticorps).
The current study was designed to determine mechanisms underlying 20-hydroxyeicosatetraenoic acid -stimulated nitric oxide (NO) release, and particularly the role of NADPH oxidase (Montrer NOX1 Anticorps), reactive oxygen species, and PI3-kinase (Montrer PIK3CA Anticorps) in stimulated NO release.
PI3K/Akt and p53 (Montrer TP53 Anticorps) 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 (Montrer NOS3 Anticorps) activation in endothelial cells
These findings highlight novel and essential roles of PFKFB4 (Montrer PFKFB4 Anticorps) activity in later stages of neural crest (NC) development that are wired into the NC gene regulatory network.
SCF (Montrer KITLG Anticorps) 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 (Montrer FRAP1 Anticorps)-FOXO1 (Montrer FOXO1 Anticorps) signaling and suppressing the activation of TLR4 (Montrer TLR4 Anticorps) and/or NOD2 (Montrer NOD2 Anticorps) 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 (Montrer LRP2 Anticorps) is the sensor that determines whether cells will be protected or injured by albumin (Montrer ALB Anticorps); 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 (Montrer FNTA Anticorps), which further represses the activity of K(+) channel (Montrer KCNC4 Anticorps) 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 (Montrer CBL Anticorps)-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 (Montrer CA2 Anticorps)+)-dependent manner, connecting the Ca(2 (Montrer CA2 Anticorps)+) signal to K(+) uptake through activation of a K(+) channel (Montrer KCNC4 Anticorps).
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 (Montrer TP53 Anticorps).
Modulation of pptr-1 affects insulin (Montrer INS Anticorps)/IGF-1 (Montrer IGF1 Anticorps) 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 (Montrer TRH Anticorps) 350.
Exogenous AKT was transcribed, and AKT was overexpressed, inducing the phosphorylation of p70S6K (Montrer RPS6KB1 Anticorps) (Thr389) and 4E-BP1 (Montrer EIF4EBP1 Anticorps) (Thr37/46) in goat fetal fibroblasts.
findings suggested that the expressions of the cardiac CACNA1C (Montrer CACNA1C Anticorps) were under the CLOCK-BMAL1 (Montrer ARNTL Anticorps) 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