产品: 总AKT1/2/3 抗体
货号: AF6261
描述: Rabbit polyclonal antibody to pan-AKT1/2/3
应用: WB IHC IF/ICC IP
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat, Monkey
预测: Pig, Horse, Dog, Chicken, Xenopus
蛋白号: P31749 | P31751 | Q9Y243
RRID: AB_2835121

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   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

货期: 当天发货

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500, IP 1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat, Monkey
克隆:
Polyclonal
特异性:
pan-AKT1/2/3 Antibody detects endogenous levels of total pan-AKT1/2/3.
RRID:
AB_2835121
引用格式: Affinity Biosciences Cat# AF6261, RRID:AB_2835121.
偶联:
Unconjugated. 130
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
别名:

展开/折叠

AKT 1; AKT; AKT1; AKT1_HUMAN; MGC99656; PKB; PKB-ALPHA; PRKBA; Protein Kinase B Alpha; Protein kinase B; Proto-oncogene c-Akt; RAC Alpha; RAC; RAC-alpha serine/threonine-protein kinase; RAC-PK-alpha; Akt2; AKT2_HUMAN; HIHGHH; murine thymoma viral (v-akt) homolog-2; PKB; PKB beta; PKBB; PKBBETA; PRKBB; Protein kinase Akt 2; Protein kinase Akt-2; Protein kinase B beta; rac protein kinase beta; RAC-BETA; RAC-beta serine/threonine-protein kinase; RAC-PK-beta; v akt murine thymoma viral oncogene homolog 2; Akt3; AKT3 kinase; AKT3_HUMAN; DKFZp434N0250; MPPH; PKB gamma; PKBG; PRKBG; Protein kinase Akt-3; Protein Kinase AKT3; Protein kinase B gamma; RAC gamma; RAC gamma serine/threonine protein kinase; RAC-gamma serine/threonine-protein kinase; RAC-PK-gamma; RACPK Gamma; Serine threonine protein kinase Akt 3; Serine threonine protein kinase Akt3; STK 2; STK-2; STK2; V akt murine thymoma viral oncogene homolog 3 (protein kinase B, gamma); V akt murine thymoma viral oncogene homolog 3; V akt murine thymoma viral oncogene homolog 3 protein kinase B gamma;

抗原和靶标

免疫原:

A synthesized peptide derived from human Akt, corresponding to a region within the internal amino acids.

基因/基因ID:
描述:
an AGC kinase that plays a critical role in controlling the balance between survival and AP0ptosis. Phosphorylated and activated by PDK1 in the PI3 kinase pathway.

文献引用

1). Antibacterial and Angiogenic (2A) Bio-Heterojunctions Facilitate Infectious Ischemic Wound Regeneration via an Endogenous-Exogenous Bistimulatory Strategy. Advanced materials (Deerfield Beach, Fla.), 2024 (PubMed: 37848208) [IF=27.4]

2). Thread-structural microneedles loaded with engineered exosomes for annulus fibrosus repair by regulating mitophagy recovery and extracellular matrix homeostasis. Bioactive materials, 2024 (PubMed: 38515611) [IF=18.9]

3). MTH1 protects platelet mitochondria from oxidative damage and regulates platelet function and thrombosis. Nature Communications, 2023 (PubMed: 37563135) [IF=16.6]

Application: WB    Species: Mouse    Sample:

Fig. 4 Dysregulated protein phosphorylation in MTH1-deficient platelets after thrombin stimulation. a MTH1fl/fl or MTH1−/− platelets were treated with thrombin (1 U/ml) for 3 min followed by quantitative phosphoproteomics assay. b Differentially expressed phosphopeptides between two groups were presented as volcano map. X-axis shows the fold change (logarithmic conversion based on 2) and Y-axis shows the P-value (logarithmic conversion based on 10). Red dots represented the differentially upregulated phosphopeptides with significance and Blue dots showed the differentially downregulated phosphopeptides with significance. KEGG pathway analysis between control and MTH1-deficient platelets under the condition of resting (MA/NA) (c) or stimulation (MB/NB) (d). e MTH1fl/fl or MTH1−/− platelets were stimulated with thrombin (1 U/ml) followed by measuring the phosphorylation level of p38 MAPK, AKT, PLCβ3 and RhoA. The data were quantified based on three independent experiments (mean ± SD, n = 3 independent isolated platelets, two-way ANOVA with Sidak multiple comparisons test). f The number of differentially expressed phosphopeptides among the four groups. g Details of the 2 differentially expressed phosphopeptides localized in the mitochondria with significance identified from the comparison of control and MTH1-deficient platelets after thrombin stimulation (n = 3 independent experiments, two-tailed unpaired Student’s t test).

4). Aberrant translation regulated by METTL1/WDR4‐mediated tRNA N7‐methylguanosine modification drives head and neck squamous cell carcinoma progression. Cancer Communications, 2022 (PubMed: 35179319) [IF=16.2]

Application: WB    Species: Human    Sample: METTL1‐KO cells

FIGURE 4 METTL1‐mediated m7G tRNA modification regulates the activity of the PI3K/AKT/mTOR signaling pathway. (A) Scatterplot of the TRs in METTL1‐WT and METTL1‐KO SCC15 cells. TRs were calculated by dividing the ribosome‐binding transcript signals by input RNA‐seq signals. (B) KEGG pathway analysis of the genes with decreased TRs upon METTL1 knockout. (C) The PI3K/AKT/mTOR signaling pathway was enriched in RNC‐seq datasets by GSEA (NES = 1.64, FDR = 0.165, P < 0.001). (D) Western blotting of PI3K/AKT/mTOR signaling pathway proteins and downstream proteins using the indicated antibodies. (E) qRT‐PCR analysis of PIK3CA with RNC and input samples in SCC9 and SCC15 cells. (F) The protein levels of PI3K, AKT, and p‐AKT in METTL1‐WT, METTL1‐KO, PI3K‐transfected METTL1‐KO cells (KO + PIK3CA) and 5 μg/mL SC79‐treated METTL1‐KO cells cultured with (KO + SC79). (G‐I) The proliferation (G), migration (H) and invasion abilities (I) were partially restored after transfecting METTL1‐KO cells with the PI3K plasmid or activating AKT. Data are presented as the mean ± SD and analyzed by Student's t‐test. *, P < 0.05, **, P < 0.01, ***, P < 0.001. Abbreviations: PI3K/AKT/mTOR: phosphatidylinositol‐3‐kinase/protein kinase B/mammalian target of rapamycin; METTL1: Methyltransferase‐like 1; WT: wild‐type; KO: knockout; TRs: translation ratios; KEGG: Koto Encyclopedia of Genes and Genomes; GSEA: gene set enrichment analysis; NES: normalized enrichment score; FDR: false discovery rate; qRT‐PCR: quantitative real‐time PCR; RNC: Ribosome nascent‐chain complex‐bound; MMP9: matrix metalloprotein 9; Bcl‐2: B‐cell lymphoma‐2; P‐S6K: phosphorylation of S6 kinase; BAX: Bcl‐2‐associated X protein; PIK3CA: phosphatidylinositol‐4,5‐bisphosphate 3‐kinase, catalytic subunit alpha; SD: standard deviation

5). Glucagon Enhances Chemotherapy Efficacy By Inhibition of Tumor Vessels in Colorectal Cancer. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024 (PubMed: 38072640) [IF=15.1]

6). A rationally designed CD19 monoclonal antibody-triptolide conjugate for the treatment of systemic lupus erythematosus. Acta pharmaceutica Sinica. B, 2024 (PubMed: 39525579) [IF=14.7]

7). Polydatin accelerates osteoporotic bone repair by inducing the osteogenesis-angiogenesis coupling of bone marrow mesenchymal stem cells via the PI3K/AKT/GSK-3β/β-catenin pathway. International journal of surgery (London, England), 2024 (PubMed: 39248296) [IF=12.5]

Application: WB    Species: Rat    Sample:

Figure 3. The effect of POL action was via the PI3K/AKT/GSK3-β/β-catenin pathway. (A-B) The protein expression levels of total PI3K, p-PI3K, total AKT, pAKT, total GSK3β, p-GSK3β, total β-catenin, and p-β-catenin were evaluated by western blot (n = 3); (C) Images of immunofluorescence staining for β-catenin (scale bar = 100 μm); (D-E) Quantification of immunofluorescence staining for β-catenin (n = 5). Data were presented as mean ± SEM. Compared with control group: * P < 0.05, **P < 0.01, ***P < 0.001. Compared with POL group: ##P < 0.01, ### P < 0.001.

8). Polydatin accelerates osteoporotic bone repair by inducing the osteogenesis-angiogenesis coupling of bone marrow mesenchymal stem cells via the PI3K/AKT/GSK-3β/β-catenin pathway. International journal of surgery (London, England), 2025 (PubMed: 39248296) [IF=12.5]

9). iNOS contributes to heart failure with preserved ejection fraction through mitochondrial dysfunction and Akt S-nitrosylation. Journal of Advanced Research, 2023 (PubMed: 36585107) [IF=11.4]

Application: WB    Species: Rat    Sample: heart tissue

Fig. 2. iNOS inhibition reduced nitrative stress and Akt S-nitrosylation in HFpEF heart. (A-B) The interactions of iNOS with other proteins were identified using the STRING database. iNOS (Nos2) directly interacted with Akt (A). The confidence score of the interaction of iNOS and other proteins is shown in B. (C) Urinary nitrite/nitrate concentration in mice from different experimental groups. n = 4 per group. (D-E) Representative immunostaining and semi-quantification of S-nitrosylated Akt (SNO-Akt) levels in heart tissue samples. n = 6 per group. (F-H) Representative immunostaining and semi-quantification of S-nitrosylated Akt and iNOS expression levels in neonatal rat cardiomyocytes transfected with plasmids. n = 6 per group for the detection of S-nitrosylated Akt. n = 3 per group for the detection of iNOS expression. (I-J) Representative immunostaining and semi-quantification of S-nitrosylated Akt in AC16 human cardiomyocyte cells transfected with mutated Akt plasmids. The data are shown as mean ± SEM and were analyzed using one-way ANOVA followed by Tukey’s post hoc test (C-E), or Student’s t-tests (F-H) ,or two-way ANOVA with Bonferroni post hoc test (I-J). *, P < 0.05. **, P < 0.01. ***, P < 0.0005. ****, P < 0.0001. ns, no significant.

10). LncRNA AK023391 promotes tumorigenesis and invasion of gastric cancer through activation of the PI3K/Akt signaling pathway. Journal of Experimental & Clinical Cancer Research, 2017 (PubMed: 29282102) [IF=11.3]

Application: WB    Species: human    Sample: Gastric cancer cells

Fig. 8 | LncRNA AK023391 was involved in the regulation of the PI3K/Akt signaling pathway.e-f Western blotting validation of the effects of AK023391 knockdown on the expression of PI3K/Akt, NF-κB, p53, and FOXO3a pathways, and their downstream transcription factors c-myb, cyclinB1/G2, and BCL-6 in HGC 27, AGS, and SGC-7901 cells

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