製品: Phospho-AKT1 (Ser473) Antibody
カタログ: AF8355
タンパク質の説明: Rabbit polyclonal antibody to Phospho-AKT1 (Ser473)
アプリケーション: WB IF/ICC
Cited expt.: WB
反応性: Human, Mouse, Rat, Monkey
予測: Pig, Zebrafish, Bovine, Horse, Dog, Chicken, Xenopus
分子量: 60kDa; 56kD(Calculated).
ユニプロット: P31749
RRID: AB_2840417

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製品説明

ソース:
Rabbit
アプリケーション:
WB 1:1000-3000, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

反応性:
Human,Mouse,Rat,Monkey
予測:
Pig(100%), Zebrafish(100%), Bovine(92%), Horse(100%), Dog(100%), Chicken(100%), Xenopus(100%)
クローナリティ:
Polyclonal
特異性:
Phospho-AKT1 (Ser473) Antibody detects endogenous levels of AKT1 only when phosphorylated at Ser473.
RRID:
AB_2840417
引用形式: Affinity Biosciences Cat# AF8355, RRID:AB_2840417.
コンジュゲート:
Unconjugated.
精製:
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.
別名:

折りたたみ/展開

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;

免疫原

免疫原:

A synthesized peptide derived from human AKT1 around the phosphorylation site of Ser473.

Uniprot:
遺伝子(ID):
発現特異性:
P31749 AKT1_HUMAN:

Expressed in prostate cancer and levels increase from the normal to the malignant state (at protein level). Expressed in all human cell types so far analyzed. The Tyr-176 phosphorylated form shows a significant increase in expression in breast cancers during the progressive stages i.e. normal to hyperplasia (ADH), ductal carcinoma in situ (DCIS), invasive ductal carcinoma (IDC) and lymph node metastatic (LNMM) stages.

タンパク質配列:
MSDVAIVKEGWLHKRGEYIKTWRPRYFLLKNDGTFIGYKERPQDVDQREAPLNNFSVAQCQLMKTERPRPNTFIIRCLQWTTVIERTFHVETPEEREEWTTAIQTVADGLKKQEEEEMDFRSGSPSDNSGAEEMEVSLAKPKHRVTMNEFEYLKLLGKGTFGKVILVKEKATGRYYAMKILKKEVIVAKDEVAHTLTENRVLQNSRHPFLTALKYSFQTHDRLCFVMEYANGGELFFHLSRERVFSEDRARFYGAEIVSALDYLHSEKNVVYRDLKLENLMLDKDGHIKITDFGLCKEGIKDGATMKTFCGTPEYLAPEVLEDNDYGRAVDWWGLGVVMYEMMCGRLPFYNQDHEKLFELILMEEIRFPRTLGPEAKSLLSGLLKKDPKQRLGGGSEDAKEIMQHRFFAGIVWQHVYEKKLSPPFKPQVTSETDTRYFDEEFTAQMITITPPDQDDSMECVDSERRPHFPQFSYSASGTA

種類予測

種類予測:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Dog
100
Xenopus
100
Zebrafish
100
Chicken
100
Bovine
92
Sheep
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

研究背景

機能:

AKT1 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface (By similarity). Phosphorylation of PTPN1 at 'Ser-50' negatively modulates its phosphatase activity preventing dephosphorylation of the insulin receptor and the attenuation of insulin signaling (By similarity). Phosphorylation of TBC1D4 triggers the binding of this effector to inhibitory 14-3-3 proteins, which is required for insulin-stimulated glucose transport. AKT regulates also the storage of glucose in the form of glycogen by phosphorylating GSK3A at 'Ser-21' and GSK3B at 'Ser-9', resulting in inhibition of its kinase activity (By similarity). Phosphorylation of GSK3 isoforms by AKT is also thought to be one mechanism by which cell proliferation is driven (By similarity). AKT regulates also cell survival via the phosphorylation of MAP3K5 (apoptosis signal-related kinase). Phosphorylation of 'Ser-83' decreases MAP3K5 kinase activity stimulated by oxidative stress and thereby prevents apoptosis. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1. AKT is involved in the phosphorylation of members of the FOXO factors (Forkhead family of transcription factors), leading to binding of 14-3-3 proteins and cytoplasmic localization. In particular, FOXO1 is phosphorylated at 'Thr-24', 'Ser-256' and 'Ser-319'. FOXO3 and FOXO4 are phosphorylated on equivalent sites. AKT has an important role in the regulation of NF-kappa-B-dependent gene transcription and positively regulates the activity of CREB1 (cyclic AMP (cAMP)-response element binding protein). The phosphorylation of CREB1 induces the binding of accessory proteins that are necessary for the transcription of pro-survival genes such as BCL2 and MCL1. AKT phosphorylates 'Ser-454' on ATP citrate lyase (ACLY), thereby potentially regulating ACLY activity and fatty acid synthesis (By similarity). Activates the 3B isoform of cyclic nucleotide phosphodiesterase (PDE3B) via phosphorylation of 'Ser-273', resulting in reduced cyclic AMP levels and inhibition of lipolysis (By similarity). Phosphorylates PIKFYVE on 'Ser-318', which results in increased PI(3)P-5 activity (By similarity). The Rho GTPase-activating protein DLC1 is another substrate and its phosphorylation is implicated in the regulation cell proliferation and cell growth. AKT plays a role as key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation (By similarity). Signals downstream of phosphatidylinositol 3-kinase (PI(3)K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). AKT mediates the antiapoptotic effects of IGF-I (By similarity). Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly. May be involved in the regulation of the placental development (By similarity). Phosphorylates STK4/MST1 at 'Thr-120' and 'Thr-387' leading to inhibition of its: kinase activity, nuclear translocation, autophosphorylation and ability to phosphorylate FOXO3. Phosphorylates STK3/MST2 at 'Thr-117' and 'Thr-384' leading to inhibition of its: cleavage, kinase activity, autophosphorylation at Thr-180, binding to RASSF1 and nuclear translocation. Phosphorylates SRPK2 and enhances its kinase activity towards SRSF2 and ACIN1 and promotes its nuclear translocation. Phosphorylates RAF1 at 'Ser-259' and negatively regulates its activity. Phosphorylation of BAD stimulates its pro-apoptotic activity. Phosphorylates KAT6A at 'Thr-369' and this phosphorylation inhibits the interaction of KAT6A with PML and negatively regulates its acetylation activity towards p53/TP53. Phosphorylates palladin (PALLD), modulating cytoskeletal organization and cell motility. Phosphorylates prohibitin (PHB), playing an important role in cell metabolism and proliferation. Phosphorylates CDKN1A, for which phosphorylation at 'Thr-145' induces its release from CDK2 and cytoplasmic relocalization. These recent findings indicate that the AKT1 isoform has a more specific role in cell motility and proliferation. Phosphorylates CLK2 thereby controlling cell survival to ionizing radiation.

PTMs:

O-GlcNAcylation at Thr-305 and Thr-312 inhibits activating phosphorylation at Thr-308 via disrupting the interaction between AKT1 and PDPK1. O-GlcNAcylation at Ser-473 also probably interferes with phosphorylation at this site.

Phosphorylation on Thr-308, Ser-473 and Tyr-474 is required for full activity. Activated TNK2 phosphorylates it on Tyr-176 resulting in its binding to the anionic plasma membrane phospholipid PA. This phosphorylated form localizes to the cell membrane, where it is targeted by PDPK1 and PDPK2 for further phosphorylations on Thr-308 and Ser-473 leading to its activation. Ser-473 phosphorylation by mTORC2 favors Thr-308 phosphorylation by PDPK1. Phosphorylated at Thr-308 and Ser-473 by IKBKE and TBK1. Ser-473 phosphorylation is enhanced by interaction with AGAP2 isoform 2 (PIKE-A). Ser-473 phosphorylation is enhanced in focal cortical dysplasias with Taylor-type balloon cells. Ser-473 phosphorylation is enhanced by signaling through activated FLT3 (By similarity). Ser-473 is dephosphorylated by PHLPP. Dephosphorylated at Thr-308 and Ser-473 by PP2A phosphatase. The phosphorylated form of PPP2R5B is required for bridging AKT1 with PP2A phosphatase. Ser-473 is dephosphorylated by CPPED1, leading to termination of signaling.

Ubiquitinated via 'Lys-48'-linked polyubiquitination by ZNRF1, leading to its degradation by the proteasome (By similarity). Ubiquitinated; undergoes both 'Lys-48'- and 'Lys-63'-linked polyubiquitination. TRAF6-induced 'Lys-63'-linked AKT1 ubiquitination is critical for phosphorylation and activation. When ubiquitinated, it translocates to the plasma membrane, where it becomes phosphorylated. When fully phosphorylated and translocated into the nucleus, undergoes 'Lys-48'-polyubiquitination catalyzed by TTC3, leading to its degradation by the proteasome. Also ubiquitinated by TRIM13 leading to its proteasomal degradation. Phosphorylated, undergoes 'Lys-48'-linked polyubiquitination preferentially at Lys-284 catalyzed by MUL1, leading to its proteasomal degradation.

Acetylated on Lys-14 and Lys-20 by the histone acetyltransferases EP300 and KAT2B. Acetylation results in reduced phosphorylation and inhibition of activity. Deacetylated at Lys-14 and Lys-20 by SIRT1. SIRT1-mediated deacetylation relieves the inhibition.

細胞の位置付け:

Cytoplasm. Nucleus. Cell membrane.
Note: Nucleus after activation by integrin-linked protein kinase 1 (ILK1). Nuclear translocation is enhanced by interaction with TCL1A. Phosphorylation on Tyr-176 by TNK2 results in its localization to the cell membrane where it is targeted for further phosphorylations on Thr-308 and Ser-473 leading to its activation and the activated form translocates to the nucleus. Colocalizes with WDFY2 in intracellular vesicles (PubMed:16792529).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
組織特異性:

Expressed in prostate cancer and levels increase from the normal to the malignant state (at protein level). Expressed in all human cell types so far analyzed. The Tyr-176 phosphorylated form shows a significant increase in expression in breast cancers during the progressive stages i.e. normal to hyperplasia (ADH), ductal carcinoma in situ (DCIS), invasive ductal carcinoma (IDC) and lymph node metastatic (LNMM) stages.

タンパク質ファミリー:

Binding of the PH domain to phosphatidylinositol 3,4,5-trisphosphate (PI(3,4,5)P3) following phosphatidylinositol 3-kinase alpha (PIK3CA) activity results in its targeting to the plasma membrane. The PH domain mediates interaction with TNK2 and Tyr-176 is also essential for this interaction.

The AGC-kinase C-terminal mediates interaction with THEM4.

Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. RAC subfamily.

研究領域

· 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.

参考文献

1). Oxyberberine, an absorbed metabolite of berberine, possess superior hypoglycemic effect via regulating the PI3K/Akt and Nrf2 signaling pathways. BIOMEDICINE & PHARMACOTHERAPY, 2021 (PubMed: 33524788) [IF=6.9]

2). p75NTR-/- mice exhibit an alveolar bone loss phenotype and inhibited PI3K/Akt/β-catenin pathway. CELL PROLIFERATION, 2020 (PubMed: 32215984) [IF=5.9]

Application: WB    Species: Mice    Sample: mandibular RNA and protein

FIGURE 3 PI3K/Akt pathway is downregulated in p75NTR−/− EMSCs. (A) Cluster analysis showed the differentially expressed genes between WT and p75NTR−/− EMSCs after cultured in osteogenic induction medium for 7 d. (B) Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analysis of RNA-seq data. The top ten enriched pathways are shown. (C) The expression levels of PI3K, p-PI3K, Akt, p-Akt and β-catenin were detected by Western blot analysis during osteogenic induction. Grayscale analysis was performed, and (D) the levels of β-catenin proteins were expressed relative to the levels of GAPDH, (E) phosphorylation of PI3K and Akt were analysed, and the results were represented as fraction of the control. (F) The expression levels of PI3K, Akt and β-catenin were detected by real-time PCR normalized to GAPDH. All experiments were repeated at least three times. adjusted P-value (Padj) < .05, *P < .05, ***P < .001, ns = no significant difference

3). Hu’po Anshen Decoction Accelerated Fracture-Healing in a Rat Model of Traumatic Brain Injury Through Activation of PI3K/AKT Pathway. Frontiers in Pharmacology, 2022 [IF=5.6]

Application: WB    Species: Rat    Sample:

FIGURE 9. HPASD promoted the expressions of osteogenic factors in the rat model of traumatic brain injury by activating PI3K/AKT pathway. (A) The mRNA expression levels of osteogenic factors, COL1A1, RUNX2, BMP2, Aggrecan, and inflammation-related factor, MMP13 were evaluated by real-time PCR (B) Representative western blots and quantitative analysis of the VEGFA, COL1A1, RUNX2, BMP2, Aggrecan, MMP13, PI3K p85, p-AKT (Thr308), p-AKT (Ser473), and AKT in the callus tissues of TBI rats in each group. *p < 0.05, **p < 0.01 vs. Fracture-only group; ▲p < 0.05, ▲▲p < 0.01 vs. Fracture + TBI group [unpaired Student’s t-test].

4). Buxuhuayu Decoction Accelerates Angiogenesis by Activating the PI3K-Akt-eNOS Signalling Pathway in a Streptozotocin-Induced Diabetic Ulcer Rat Model. JOURNAL OF ETHNOPHARMACOLOGY, 2021 (PubMed: 33581257) [IF=4.8]

Application: WB    Species: Rat    Sample:

Fig. 13. The protein expressions of p-PI3K, p-AKT1, and p-eNOS by Western blot at 7 days after administration. n = 3 for each group. Quantifications of the bands (b–d) (mean±SEM). Compared with CG, *P < 0.05 and **P < 0.01; Compared with MG, #P < 0.05, ##P < 0.01, &P < 0.05 and &&P < 0.01.

5). LAIR-1 overexpression inhibits osteosarcoma epithelial-mesenchymal transition via GLUT1-related energy metabolism. World Journal of Surgical Oncology, 2020 (PubMed: 32563267) [IF=3.2]

Application: WB    Species: Human    Sample: OS cells

Fig. 3 LAIR-1 overexpression in HOS cells inhibits the expression of EMT-associated transcription factors by decreasing p-Foxo1 expression. a Expression of Twist1 in untreated HOS cells (Blank) and corresponding LV-NC- and LV-LAIR-1-overexpressing transfectants was analyzed by qPCR. b Twist1, N-cadherin, p-Foxo1, total Foxo1, p-Akt, and total Akt expression were analyzed by western blotting in blank, LV-NC-overexpressing, and LV-LAIR-1-overexpressing OS cells. c Twist1, p-Foxo1, and total Foxo1 expression were analyzed by western blotting in blank, negative control (NC) siRNA, and Foxo1 siRNA (siFoxo1)-transfected OS cells. Representative immunofluorescence staining for Twist1 (d) and Foxo1 (e) in HOS cells (left). Cell nuclei were stained with DAPI (blue). Scale bar = 20 μm. The statistical data for the images are shown in histograms (right). *P < 0.05, **P < 0.01. Results represent at least three independent experiments.

6). LAIR-1 overexpression inhibits epithelial–mesenchymal transition in osteosarcoma via GLUT1-related energy metabolism. World Journal of Surgical Oncology, 2020 [IF=3.2]

Application: WB    Species: Human    Sample: OS cells

Fig. 3 LAIR-1 overexpression in HOS cells inhibits the expression of EMT-associated transcription factors by decreasing p-Foxo1 expression. a Expression of Twist1 in untreated HOS cells (Blank) and corresponding LV-NC- and LV-LAIR-1-overexpressing transfectants was analyzed by qPCR. b Twist1, N-cadherin, p-Foxo1, total Foxo1, p-Akt, and total Akt expression were analyzed by western blotting in blank, LV-NC-overexpressing, and LV-LAIR-1-overexpressing OS cells. c Twist1, p-Foxo1, and total Foxo1 expression were analyzed by western blotting in blank, negative control (NC) siRNA, and Foxo1 siRNA (siFoxo1)-transfected OS cells. Representative immunofluorescence staining for Twist1 (d) and Foxo1 (e) in HOS cells (left). Cell nuclei were stained with DAPI (blue). Scale bar = 20 μm. The statistical data for the images are shown in histograms (right). *P < 0.05, **P < 0.01. Results represent at least three independent experiments.

7). The role of RRS1 in breast cancer cells metastasis and AEG-1/AKT/c-Myc signaling pathway. Neoplasma, 2024 (PubMed: 39267538) [IF=2.0]

8). Bellidifolin from Gentianella acuta (Michx.) Hulten protects H9c2 cells from hydrogen peroxide-induced injury via the PI3K-Akt signal pathway. Toxicology Reports, 2022 (PubMed: 36518482)

Application: WB    Species: Rat    Sample: H9c2 cells

Fig. 10 Expression of GSK-3β and Akt. (A), (B): Validation of RNA-seq data by qRT-PCR. (C), (D), (E): Validation of protein expression by western blot. (means ± SD, n = 3). ***P 

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