pan-AKT1/2/3 Antibody - #AF6259

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产品: 总AKT1/2/3 抗体
货号: AF6259
描述: Rabbit polyclonal antibody to pan-AKT1/2/3
应用: WB IHC IF/ICC
文献验证: WB, IHC
反应: Human, Mouse, Rat, Monkey
预测: Pig, Bovine, Horse, Dog, Chicken, Xenopus
蛋白号: P31749 | P31751 | Q9Y243
RRID: AB_2835120

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 200ul RMB¥ 3000 现货

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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
*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_2835120
引用格式: Affinity Biosciences Cat# AF6259, RRID:AB_2835120.
偶联:
Unconjugated.
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 C-terminal amino acids.

基因/基因ID:
AKT1(207) | AKT2(208) | AKT3(10000)
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.

研究领域

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

· Cellular Processes > Cell growth and death > Apoptosis.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Signaling pathways regulating pluripotency of stem cells.   (View pathway)

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > ErbB signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Ras signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Rap1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cGMP-PKG signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > cAMP signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > HIF-1 signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > FoxO signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Sphingolipid signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Phospholipase D signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > mTOR signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > AMPK signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Apelin signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > Jak-STAT signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > TNF signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > EGFR tyrosine kinase inhibitor resistance.

· Human Diseases > Drug resistance: Antineoplastic > Endocrine resistance.

· Human Diseases > Drug resistance: Antineoplastic > Platinum drug resistance.

· Human Diseases > Endocrine and metabolic diseases > Insulin resistance.

· Human Diseases > Endocrine and metabolic diseases > Non-alcoholic fatty liver disease (NAFLD).

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Measles.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > HTLV-I infection.

· Human Diseases > Infectious diseases: Viral > Epstein-Barr virus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Proteoglycans in cancer.

· Human Diseases > Cancers: Specific types > Colorectal cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Renal cell carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Pancreatic cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Endometrial cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Glioma.   (View pathway)

· Human Diseases > Cancers: Specific types > Prostate cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Melanoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Chronic myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Acute myeloid leukemia.   (View pathway)

· Human Diseases > Cancers: Specific types > Small cell lung cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Non-small cell lung cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Breast cancer.   (View pathway)

· Human Diseases > Cancers: Specific types > Hepatocellular carcinoma.   (View pathway)

· Human Diseases > Cancers: Specific types > Gastric cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Central carbon metabolism in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > Choline metabolism in cancer.   (View pathway)

· Organismal Systems > Immune system > Chemokine signaling pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway.   (View pathway)

· Organismal Systems > Aging > Longevity regulating pathway - multiple species.   (View pathway)

· Organismal Systems > Circulatory system > Adrenergic signaling in cardiomyocytes.   (View pathway)

· Organismal Systems > Development > Osteoclast differentiation.   (View pathway)

· Organismal Systems > Immune system > Platelet activation.   (View pathway)

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > T cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > B cell receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Fc epsilon RI signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Fc gamma R-mediated phagocytosis.   (View pathway)

· Organismal Systems > Nervous system > Neurotrophin signaling pathway.   (View pathway)

· Organismal Systems > Nervous system > Cholinergic synapse.

· Organismal Systems > Nervous system > Dopaminergic synapse.

· Organismal Systems > Endocrine system > Insulin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Progesterone-mediated oocyte maturation.

· Organismal Systems > Endocrine system > Estrogen signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Prolactin signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Thyroid hormone signaling pathway.   (View pathway)

· Organismal Systems > Endocrine system > Adipocytokine signaling pathway.

· Organismal Systems > Endocrine system > Glucagon signaling pathway.

· Organismal Systems > Endocrine system > Regulation of lipolysis in adipocytes.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

· Organismal Systems > Digestive system > Carbohydrate digestion and absorption.

文献引用

1). RIPK1-dependent necroptosis promotes vasculogenic mimicry formation via eIF4E in triple-negative breast cancer. Cell Death & Disease, 2023 [IF=8.1]

Application: WB    Species: human    Sample: MDA-MB-231and MCF-7cells

Fig. 2: RIPK1-dependent necroptosis in triple-negative breast cancer regulates eIF4E expression via p-AKT. A–D Necroptosis and RIPK1 expression promote the expression of p-AKT and eIF4E in MDA-MB-231 (A, B) and MCF-7 (C, D) cells, as shown by Western blotting and quantitative analysis. SH-RIPK1 and control MDA-MB-231 cells were treated with TZA or N + TZA. EX-RIPK1 control MCF-7 cells were treated with the same method. E The p-AKT inhibitor MK-2206 inhibited eIF4E expression in MDA-MB-231 cells, as shown by Western blotting and quantitative analysis. MDA-MB-231 cells were treated with MK-2206 at the indicated concentrations (0μM, 2μM, 4μM and 8μM). F MK-2206 (8 μM) blocked the expression of eIF4E in necroptosis, as shown by Western blotting and quantitative analysis. G, H Immunofluorescence staining results showed the effect of necroptosis and RIPK1 expression levels on the expression and localization of eIF4E in MDA-MB-231 (G) and MCF-7 (H) cells. Data are representative of three independent experiments (*P 
2). Djulis Hull Improves Insulin Resistance and Modulates the Gut Microbiota in High-Fat Diet (HFD)-Induced Hyperglycaemia. Antioxidants, 2021 (PubMed: 35052549) [IF=7.0]

Application: WB    Species: Mice    Sample: epididymal white adipose tissue

Figure 5 Effect of djulis hull crude extract on the expression of proteins involved in glucose transportation in (A) epididymal white adipose tissue (eWAT) and (B) the liver of high-fat diet-induced hyperglycaemia. ND: normal diet; HFD: high-fat diet; HCE: high dosage of crude extract. Values represent the mean ± SEM (n = 6). The statistical methods used one-way ANOVA, and the values with different letters are significantly different at p < 0.05.
3). NLRP3 inflammasome blocked the glycolytic pathway via targeting to PKLR in arsenic-induced hepatic insulin resistance. Ecotoxicology and environmental safety, 2021 (PubMed: 34364127) [IF=6.2]

Application: WB    Species: Rat    Sample: livers

Fig. 6. Glycolysis was modulated by NLRP3 inflammasome via interaction with PKLR. L-02 cells were transfected with plasmid encoding PKLR for 12 h. The cells were pretreated with 200 ng/ml LPS for 2 h, and then treated with 4 μM NaAsO2 for 48 h. (A) The expression of NLRP3 inflammasome-associated proteins in L-02 cells was analyzed by Western blot. (B–E) The relative expression of PKLR, NLRP3, caspase-1 and IL-1β was shown as the percentage of β-actin. (F) L-02 cells were stimulated with 100 nM insulin for 10 min at the end of treatment. The expression of p-AKT and p-GSK3β was analyzed by Western blot. (G) The relative expression of p-AKT (Ser 473) was shown as the percentage of AKT. (H) The relative expression of p-GSK3β (Ser 9) was shown as the percentage of GSK3β. Results were means ± SEM, and n = 3. *P 
4). Baicalin Attenuates Panton-Valentine Leukocidin (PVL)-Induced Cytoskeleton Rearrangement via Regulating the RhoA/ROCK/LIMK and PI3K/AKT/GSK-3β Pathways in Bovine Mammary Epithelial Cells. International journal of molecular sciences, 2023 (PubMed: 37833969) [IF=5.6]

Application: WB    Species: bovine    Sample: BMECs

Figure 3. Effects of rPVL on the regulation of RhoA/ROCK/LIMK/Cofilin and PI3K/AKT/GSK-3β signaling pathways and phosphorylation of cofilin and tau hyperphosphorylation in the rPVL-treated BMECs. Representative immunoblot bands for RhoA, p-ROCK2(Tyr722), ROCK2, p-LIMK1/2(Thr508/Thr505), p-cofilin (Ser3), and cofilin (A); p-PI3K (Tyr458/Tyr199), PI3K, p-AKT(Ser473), AKT, GSK-3β(Ser9), GSK-3β, p-tau (Ser396), and tau (B); GAPDH was used as a control. rPVL was used at a 100 ng/mL concentration. Data are expressed as mean ± standard deviation of three independent experiments. * 0.01 < p < 0.05, ** p < 0.01 (one-way ANOVA with Dunnett’s multiple comparison tests), ns: not significant.
5). Rictor regulates the vasculogenic mimicry of melanoma via the AKT-MMP-2/9 pathway. Journal of Cellular and Molecular Medicine, 2017 (PubMed: 28699701) [IF=5.3]

Application: IHC    Species: human    Sample:

Fig. 1 Rictor is overexpressed in invasive melanoma and correlated with VM. (A), IHC staining of (a) Rictor, (c) AKT, (e) MMP-2 expression. b, d, f were negative controls without primary antibodies for Rictor, AKT, MMP-2, respectively.
6). Effect of EphA2 knockdown on melanoma metastasis depends on intrinsic ephrinA1 level. Cellular Oncology, 2020 (PubMed: 32291572) [IF=4.9]

Application: WB    Species: Human    Sample: MUM-2B and A375 cells

Fig. 5 Colony formation via ligand-independent EphA2 signaling is Akt dependent. (a) Effect of EphA2 downregulation on the phosphorylation of EphA2, Akt and ERK. (b) Changes in EphA2 phosphorylation after pretreatment of cells with the Akt signaling inhibitor MK-2206 or the RSK inhibitor BI-D1870. (c) Cells were stimulated with ephrinA1-Fc or Fc, after which lysates were blotted for phosphorylation of EphA2 and Akt. (d) Colony formation of MUM-2B and A375 cells after treatment with ephrinA1-Fc for 15 min. (e) MUM-2B and A375 cells pretreated with ephrinA1-Fc or Fc for 15 min were stained with pS897- EphA2 or pTyr588-EphA2 (red) and DAPI (blue) for confocal microscopy analysis. Scale bars, 50 µm and 10 µm
7). Prediction of the mechanisms of Xiaoai Jiedu Recipe in the treatment of breast cancer: A comprehensive approach study with experimental validation. JOURNAL OF ETHNOPHARMACOLOGY, 2020 (PubMed: 31981747) [IF=4.8]

Application: WB    Species: Human    Sample: breast cancer cells

Fig. 8. Western blotting analysis showed the activation of PI3K- Akt signal pathway was suppressed after alone or in combined administration of quercetin and ursolic acid at the concentration of 40 μM for 24 h. β- actin was used as a loading control. The bands were quantified by densitometry scanning by using Image J. *p < 0.05 vs control.
8). Inhibition of B7-H4 promotes hepatocellular carcinoma cell apoptosis and autophagy through the PI3K signaling pathway. International Immunopharmacology, 2020 (PubMed: 32805693) [IF=4.8]

Application: WB    Species: Human    Sample: Huh7 and Hep3B cells

Fig. 4. Expression change of PI3K/AKT/mTOR signaling pathway in Huh7 and Hep3B cells after B7-H4 siRNA treatment. ** siRNA vs NC, P < 0.05.
9). An Injectable Sustained Release Hydrogel of Hyaluronic Acid Loaded with β-Ecdysterone Ameliorates Cartilage Damage in Osteoarthritis via Activating Autophagy. Advanced Therapeutics, 2023 [IF=4.6]
10). PTGER3 knockdown inhibits the vulnerability of triple-negative breast cancer to ferroptosis. Cancer science, 2024 (PubMed: 38566528) [IF=4.5]

Application: WB    Species: Human    Sample:

FIGURE 5 Activation of the PI3K‐AKT pathway in prostaglandin E receptor 3 (PTGER3)‐downregulated triple‐negative breast cancer (TNBC) cells. (A) KEGG pathway enrichment of PTGER3‐related genes identified the PI3K‐AKT pathway as the top‐ranked pathway. (B) GSEA analysis showed that low PTGER3 expression was closely associated with the PI3K‐AKT pathway. (C) Western blotting showed that PTGER3 knockdown promoted AKT phosphorylation in MDA‐MB‐231 cells, whereas PTGER3 overexpression inhibited AKT phosphorylation. (D) Following the addition of MK‐2206 to MDA‐MB‐231 cells with altered PTGER3 expression, the expression of p‐AKT decreased, but GPX4 expression did not change significantly. (E, F) Evaluation of GSH content in cells after different treatments. (G, H) Quantitative analysis using the DHE probe to determine reactive oxygen species (ROS) levels in cells after different treatments (erastin: 2 μM; MK‐2206: 5 μM; Fer‐1: 5 μM) Scale bars: 100 μm. Data are presented as the mean ± SD. One‐way ANOVA.
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