产品: 磷酸化 总AKT1/2/3 (Thr308) 抗体
货号: AF3262
描述: Rabbit polyclonal antibody to Phospho-pan-AKT1/2/3 (Thr308)
应用: WB IHC IF/ICC
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat
预测: Pig, Zebrafish, Bovine, Horse, Dog, Chicken, Xenopus
蛋白号: P31749 | P31751 | Q9Y243
RRID: AB_2834688

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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
克隆:
Polyclonal
特异性:
Phospho-pan-AKT1/2/3 (Thr308) Antibody detects endogenous levels of pan-AKT1/2/3 only when phosphorylated at Threonine 308.
RRID:
AB_2834688
引用格式: Affinity Biosciences Cat# AF3262, RRID:AB_2834688.
偶联:
Unconjugated.
纯化:
The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.
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 around the phosphorylation site of Thr308.

基因/基因ID:
描述:
Akt2 an AGC kinase. Plays critical roles in glucose metabolism and the development or maintenance of proper adipose tissue and islet mass for which other Akt/PKB isoforms are unable to fully compensate. Amplified and overexpressed in human ovarian carcinoma cell lines and amplified in some primary ovarian and pancreatic tumors. Antisense blocks invasiveness in xenografts.

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). Sulindac (K-80003) with nab-paclitaxel and gemcitabine overcomes drug-resistant pancreatic cancer. Molecular cancer, 2024 (PubMed: 39350121) [IF=37.3]

Application: WB    Species: Mouse    Sample: PDAC cells

Fig. 6. cFAM124A activates PI3K/Akt pathway through tRXRα to cause GEM resistance in PDAC, and K-80003 can reverse this effect. A, Western blot analysis of Akt, p-Akt (Ser473), p-Akt (Thr308), and cleaved caspase 3/8 expression after 6 h of treatment with different inhibitors and GEM treatment. B, IC50 values for GEM in PDAC cells overexpressing cFAM124A and control cells after 6 h of treatment with different inhibitors and GEM treatment. C, Necrosis in 3D tumor microspheres based on PI staining (red) and after 6 h of treatment with different inhibitors and GEM treatment. Scale bar, 100 μm. D, Colony formation by cells overexpressing cFAM124A after 6 h of treatment with different inhibitors and GEM treatment in 6-well dishes (800 cells/well) for 2 weeks. Each inhibitor, copanlisib (2 nM, pan-PI3K inhibitor) or K-80003 (5 nM, tRXRα-dependent Akt activation inhibitor). Quantitative data are shown on the right. E, Subcutaneous xenograft model of mice in the different groups treated with GEM (40 mg/kg i.p. 2×/week for 4 weeks), copanlisib (1 mg/kg, iv. 2×/week for 4 weeks), or K-80003 (20 mg/ kg i.p. 2×/week for 4 weeks) at 2 weeks after subcutaneous injection of 5 × 106 cells overexpressing cFAM124A and control cells. Representative images of tumors are shown (n = 5). F, Body weights of subcutaneous tumor-bearing mice in the indicated groups (n = 5). G, Volcano plot showing upregulated and downregulated protein between EV-PATU8988T and cFAM124A-PATU8988T cells. H, Western blot analysis of RXRα, Akt, p-Akt (Ser473), and p-Akt (Thr308) expression in PDAC cells overexpressing cFAM124A or with cFAM124A knockout and control cells. I, cFAM124A increased RXRα protein degradation: Indicated PDAC cell lines were incubated with CHX for indicated time periods before western blot analysis of RXRα and GAPDH expression. Representative images are shown (left). J, Indicated PDAC cell lines were incubated with MG132 and then with CHX for indicated time periods before western blot analysis of RXRα and GAPDH expression. Representative images are shown (left)

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

3). Butylparaben induced zebrafish (Danio rerio) kidney injury by down-regulating the PI3K-AKT pathway. Journal of hazardous materials, 2024 (PubMed: 38565019) [IF=12.2]

4). Inhibition of Bcl-2 Synergistically Enhances the Antileukemic Activity of Midostaurin and Gilteritinib in Preclinical Models of FLT3-mutated Acute Myeloid Leukemia. CLINICAL CANCER RESEARCH, 2019 (PubMed: 31320594) [IF=10.0]

Application: WB    Species: mouse    Sample: AML cell

Figure 2. |Combination of midostaurin and venetoclax mitigates venetoclax-induced upregulation of p-ERK and prevents rebound of p-ERK during midostaurin treatment. (A558 C) FLT3-ITD AML cell lines MOLM-13, MV4-11, and primary patient sample AML#171 were treated with midostaurin alone or in combination with venetoclax for up to 24 hours. Representative Western blots generated using whole cell lysates are shown. Densitometry measurements, shown below the corresponding blot, were normalized to β-actin and expressed as fold change compared to vehicle control.

5). Antileukemic activity and mechanism of action of the novel PI3K and histone deacetylase dual inhibitor CUDC-907 in acute myeloid leukemia. HAEMATOLOGICA, 2019 (PubMed: 30819918) [IF=8.2]

Application: WB    Species: human    Sample: MOLM-13 cells

Figure S1. | CUDC-907 treatment inhibits PI3K/Akt and HDACs in AML cell lines. (A) The structure of CUDC-907. (B&C) U937 (panel B) and MOLM-13 (panel C) cells were treated with variable concentrations of CUDC-907 for 3 hours. Whole cell lysates were subjected to Western blotting.

6). Paeonol ameliorates hyperlipidemia and autophagy in mice by regulating Nrf2 and AMPK/mTOR pathways. Phytomedicine : international journal of phytotherapy and phytopharmacology (PubMed: 38943694) [IF=7.9]

7). Melatonin improves synapse development by PI3K/Akt signaling in a mouse model of autism spectrum disorder. Neural regeneration research, 2024 (PubMed: 38051907) [IF=5.9]

Application: WB    Species: Mouse    Sample:

Figure 4 The effects of MT on the expression of GAD67, synaptic-associated proteins, and the PI3K/Akt signaling pathway in Ctnnd2 KO mice. (A) Representative western blot showing the expression levels of GAD67, ELKS, p-Syn, and Syn in the indicated groups. (B–D) Relative protein expression normalized to total protein or β-actin: GAD67 (B), ELKS (C), p-Syn (D). (E) Representative western blot showing the expression levels of p-PI3K, PI3K, p-Akt (Ser473), p-Akt (Thr308), and Akt in the indicated groups. (F–H) Relative protein expression normalized to total protein: p-PI3K (F), p-Akt (Ser473) (G), and p-Akt (Thr308) (H). Data are presented as the mean ± SEM (all groups: n = 3, performed in triplicate). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 (one-way analysis of variance followed by Tukey's multiple comparison tests). Akt: Protein kinase B; Ctnnd2: delta catenin 2; GAD67: glutamate decarboxylase 67; KO: knock out; MT: melatonin; p-Akt: phospho-Akt; PI3K: phosphatidylinositol-3 kinase; p-PI3K: phospho-PI3K; p-Syn: phospho-Syn; Syn: Synapsin I; WT: wild-type.

8). Magnolol Alleviates Inflammatory Responses and Lipid Accumulation by AMP-Activated Protein Kinase-Dependent Peroxisome Proliferator-Activated Receptor α Activation. Frontiers in Immunology, 2018 (PubMed: 29467759) [IF=5.7]

Application: WB    Species: mouse    Sample: Liver

FigUre 9 | Effect of magnolol (MG) treatment on AMPK, peroxisome proliferator-activated receptor α (PPARα), AKT, and sterol regulatory element-binding protein1c (SREBP-1c) in tyloxapol (Ty)-induced hyperlipidemia mice. Mice were administered MG (10 and 20 mg/kg) for 1 h. Afterward, the mice were injected with Ty(500 mg/kg) for 12 h. Liver tissues were gathered and analyzed by western blot. (a) Effects of MG on P-acetyl-CoA carboxylase (ACC), ACC, P-AMPKα, AMPKα,P-AKT, AKT, PPARα, SREBP-1c, P-P65, P65, and TLR4 were measured by western blot analysis.

Application: IF/ICC    Species: mouse    Sample: HepG2 cells

FigUre 5 | Effect of magnolol (MG) on the expression of proteins related to hepatic steatosis in HepG2 cells. Cells were exposed to MG (4 µg/mL) with or without oleic acid (OA) (120 µM) for up to 24 h. Afterward, immunofluorescence for peroxisome proliferator-activated receptor α (PPARα), SREBP-1c, P-AKT, and P-AMPKα(red) and the nuclear dye DAPI (blue), and scale bars represent 100 µm. All data are expressed as the mean ± SD of three independent experiments.

9). Targeting PI3K, mTOR, ERK, and Bcl-2 signaling network shows superior antileukemic activity against AML ex vivo. BIOCHEMICAL PHARMACOLOGY, 2018 (PubMed: 29208365) [IF=5.3]

10). Geniposide alleviates non-alcohol fatty liver disease via regulating Nrf2/AMPK/mTOR signalling pathways. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, 2020 (PubMed: 32293113) [IF=5.3]

Application: WB    Species: Human    Sample: HepG2 cells

Figure 2 Effect of GEN on the expression of Nrf2‐related signalling proteins in OA (660 μmol/L) and PA (330 μmol/L)‐induced HepG2 cells. GEN was added into HepG2 cells prior 1 h to stimulation of OA and PA for 18 h. A‐C, Protein expression of Nrf2, PPARα, PPARγ in nucleus and HO‐1 in cytoplasm was detected by Western blot. (D and E) Protein expression of P‐ACC, ACC, P‐AKT, AKT, P‐AMPKα, AMPKα, P‐AMPKβ and AMPKβ was detected by Western blot. F‐H, Protein expression of PI3K, P‐mTORC, mTORC, P‐S6K, S6K, P‐S6, S6, SREBP‐1c and HMGB1 was detected by Western blot. The similar results were collected from three dependent experiments. All data were expressed by mean ± SEM (n = 5 in each group). ## P < .01 vs Control Group; *P < .05 and **P < .01 vs OA and PA Group

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