Phospho-AKT1/2/3 (Ser473) Antibody - #AF0016

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产品: 磷酸化 AKT1/2/3 (Ser473) 抗体
货号: AF0016
描述: Rabbit polyclonal antibody to Phospho-AKT1/2/3 (Ser473)
应用: WB IHC IF/ICC
文献验证: WB, IHC, IF/ICC
反应: Human, Mouse, Rat, Monkey
预测: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken
蛋白号: P31749 | P31751 | Q9Y243
RRID: AB_2810275

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IF/ICC Protocol

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:
Phospho-pan-AKT1/2/3 (Ser473) Antibody detects endogenous levels of pan-AKT1/2/3 only when phosphorylated at Sersine 473.
RRID:
AB_2810275
引用格式: Affinity Biosciences Cat# AF0016, RRID:AB_2810275.
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 Ser473.

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. Mediates survival signals downstream of PI3 kinase and several growth factor receptors by phosphorylating AP0pototic proteins. First found in a mouse transforming retrovirus. Tumorigenic in a mouse lymphoma model and activated (by phospho-Akt staining) and/or overexpressed in a number of cancers including breast, prostate, lung, pancreatic, liver, ovarian and colorectal. Inhibitor: RX-0201. Substrates include tuberin, Bad, Forkhead transcription factors, caspase-9, and glycogen synthase kinase-3.

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). CircVAPA promotes small cell lung cancer progression by modulating the miR-377-3p and miR-494-3p/IGF1R/AKT axis. Molecular Cancer, 2022 (PubMed: 35668527) [IF=37.3]

Application: WB    Species: Human    Sample: SCLC cells

Fig. 6 circVAPA promotes the progression of SCLC through the miR-377-3p and miR-494-3p/IGF1R/AKT axis. a and b Western blot analysis of the effects of circVAPA or miR-377-3p/miR-494-3p on IGF1R, AKT, and its downstream protein expression in SCLC cells. 377 inhi, miR-377 inhibitor, 494 inhi, miR-494 inhibitor; 377 mimic, miR-377 mimic; 494 mimic, miR-494 mimic. c Western blot analysis of the effect of overexpressing circVAPA or silencing IGF1R on AKT and its downstream protein expression in SCLC cells. d Western blot analysis of the effect of overexpressing circVAPA or IGF1R inhibitor (drug BMS-536924) on AKT and its downstream protein expression in SCLC cells. e The relative luciferase activities were detected in 293T cells after co-transfection with Lu-IGF1R-WT and mimic-NC or the circVAPA overexpression plasmid or miR-377-3p/miR-494-3p mimics, respectively. The firefly luciferase activities were measured and normalized to renilla luciferase activities (F/R). f-g Representative images of immunohistochemistry analysis of IGF1R (f) and p-AKT (g) in three independent SCLC cases. Scale bar, 50 μm. SCR, siRNA with scrambled sequences; si-circVAPA, the co-transfection of two independent siRNAs target circVAPA; EV, the empty vector; circVAPA, the circVAPA overexpression plasmid; miR-377 mimic/miR-494 mimic, transiently overexpressing miR-377-3p/miR-494-3p, respectively; miR-377 inhibitor/miR-494 inhibitor, transiently suppressing miR-377-3p/miR-494-3p, respectively; si-IGF1R, an independent siRNA targeting IGF1R; IGF1Ri, the addition of IGF1R inhibitor (drug BMS-536924). (All data are presented as the mean ± SD; ns, no significance; *P < 0.05; **P < 0.01; ***P < 0.001 by two-tailed Student’s t-test). Three independent assays were performed in the above assays. *** miR-377/miR-494 in this article represents miR-377-3p/miR-494-3p, respectively

Application: IHC    Species: Human    Sample: SCLC cells

Fig. 6 circVAPA promotes the progression of SCLC through the miR-377-3p and miR-494-3p/IGF1R/AKT axis. a and b Western blot analysis of the effects of circVAPA or miR-377-3p/miR-494-3p on IGF1R, AKT, and its downstream protein expression in SCLC cells. 377 inhi, miR-377 inhibitor, 494 inhi, miR-494 inhibitor; 377 mimic, miR-377 mimic; 494 mimic, miR-494 mimic. c Western blot analysis of the effect of overexpressing circVAPA or silencing IGF1R on AKT and its downstream protein expression in SCLC cells. d Western blot analysis of the effect of overexpressing circVAPA or IGF1R inhibitor (drug BMS-536924) on AKT and its downstream protein expression in SCLC cells. e The relative luciferase activities were detected in 293T cells after co-transfection with Lu-IGF1R-WT and mimic-NC or the circVAPA overexpression plasmid or miR-377-3p/miR-494-3p mimics, respectively. The firefly luciferase activities were measured and normalized to renilla luciferase activities (F/R). f-g Representative images of immunohistochemistry analysis of IGF1R (f) and p-AKT (g) in three independent SCLC cases. Scale bar, 50 μm. SCR, siRNA with scrambled sequences; si-circVAPA, the co-transfection of two independent siRNAs target circVAPA; EV, the empty vector; circVAPA, the circVAPA overexpression plasmid; miR-377 mimic/miR-494 mimic, transiently overexpressing miR-377-3p/miR-494-3p, respectively; miR-377 inhibitor/miR-494 inhibitor, transiently suppressing miR-377-3p/miR-494-3p, respectively; si-IGF1R, an independent siRNA targeting IGF1R; IGF1Ri, the addition of IGF1R inhibitor (drug BMS-536924). (All data are presented as the mean ± SD; ns, no significance; *P < 0.05; **P < 0.01; ***P < 0.001 by two-tailed Student’s t-test). Three independent assays were performed in the above assays. *** miR-377/miR-494 in this article represents miR-377-3p/miR-494-3p, respectively
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). 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
4). Sleep Deprivation Triggers the Excessive Activation of Ovarian Primordial Follicles via β2 Adrenergic Receptor Signaling. Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024 (PubMed: 39229959) [IF=15.1]
5). Gut Metabolite Indole-3-Propionic Acid Regulates Macrophage Autophagy Through PPT1 Inhibiting Aging-Related Myocardial Fibrosis. Advanced Science, 2025 [IF=14.1]

Application: WB    Species: Mouse    Sample:

Figure 9 IPA regulates macrophage autophagy via PI3K-AKT-mTOR pathway. A) Heat map of differentially expressed genes. B) Venn diagram of differentially expressed genes. C) KEGG pathway enrichment bubble diagram of differentially expressed genes. D) mCherry-GFP-LC3B immunofluorescence staining representative images. Magnification: 200×, scale bar = 20 µm. E) Representative images immunofluorescence staining of LC3B. Magnification: 200×, scale bar = 20 µm. F,G) Representative images and statistical analysis of mTOR, p-mTOR, PI3K, p-PI3K, AKT, p-AKT, P62, Beclin1 and LC3B at protein level. (n =4–6, data are expressed as mean ± SEM, **p < 0.01 vs the Young group; ##p < 0.01 vs the Aged group).
6). Targeting TM4SF1 promotes tumor senescence enhancing CD8+ T cell cytotoxic function in hepatocellular carcinoma. Clinical and molecular hepatology, 2024 (PubMed: 39736265) [IF=14.0]
7). The combination of CUDC-907 and gilteritinib shows promising in vitro and in vivo antileukemic activity against FLT3-ITD AML. Blood Cancer Journal, 2021 (PubMed: 34099621) [IF=12.9]

Application: WB    Species: Human    Sample: MV4-11 cells

Fig. 5 CUDC-907 and gilteritinib induce complimentary and cooperatively altered activity within the MAPK/ERK and JAK2/STAT5 pathways. A MV4-11 cells were treated with gilteritinib, CUDC-907, both, or neither for 4, 8, 12, or 24 h. Western blots were generated utilizing whole-cell lysates, with representative blots shown, and densitometry displayed below each blot. Densitometry was assessed via comparison to vehicle control and normalized to β-actin. B A primary FLT3-ITD positive AML patient sample was treated with gilteritinib and/or CUDC-907 for 24 h. Densitometry was assessed via comparison to vehicle control and normalized to β-actin. C, D MOLM-13 and MV4-11 cells were treated using CUDC- 907 either with or without AZD1480, a selective JAK2 inhibitor, for 24 h. Flow cytometry analysis of annexin V/PI stained cells is shown in the upper panels and western blot analyses of phosphorylated STAT5 are shown in the lower panels. ***p < 0.001 compared to single-drug treatments. E MOLM-13, MV4-11, and primary patient sample AML#213 were treated with gilteritinib, CUDC-907, both, or vehicle control for 24 h. Western blotting was performed to analyze expression of members of the Bcl-2 family. Densitometry was measured via comparison to vehicle control and normalized to β-actin. F Mcl-1 overexpression and red fluorescent protein (RFP) control MV4-11 cells were generated using lentivirus particles as described in the “Methods” section. Whole-cell lysates were subjected to western blotting to confirm overexpression (upper panel). The cells were then treated with vehicle control, gilteritinib, CUDC-907, or in combination for 24 h, and then annexin V/PI staining and flow cytometry analysis were performed (lower panel). ***p < 0.001 compared to RFP under the same drug treatment. G, H shRNA knockdown of Bim, Bak, and Bax, or nontemplate control (NTC) was performed in MV4-11 cells. Whole-cell lysates were subjected to western blotting (upper panels). Cells were treated with vehicle control, gilteritinib, CUDC-907, or in combination for 24 h. Annexin V/PI staining and flow cytometry analysis results are shown (lower panels). ***p < 0.001 compared to NTC for the same drug treatment.
8). Arsenic induces hepatic insulin resistance via mtROS-NLRP3 inflammasome pathway. JOURNAL OF HAZARDOUS MATERIALS, 2020 (PubMed: 32544768) [IF=12.2]

Application: WB    Species: rat    Sample: liver

Fig.2 The effect of NaAsO2 on mitophagy, ox-mtDNA and NLRP3 inflammation in rats liver. Male SD rats were treated with 2.5, 5 mg/kg of NaAsO2 for 3 months. Liver coefficient (A). The level of serum ALT and AST were determined by commercial reagent kits (B-C). H&E staining of liver sections after NaAsO2 administration (D). scale bar = 500 μm. NAS in rat liver (E). Cytosolic fractions were analyzed by Western blot analysis. GAPDH was used as an internal control. The relative expression of MPO was shown as the percentage of GAPDH (F-G). The level of ox￾mtDNA was measured with an ELISA kit (H). Mitochondria fractions were analyzed by Western blot analysis. VDAC1, mitochondria marker protein, was used as an Journal Pre-proof internal control. The protein level and densitometric analyses of PINK1, Parkin, LC3B in rats liver tissues (I-L). The protein level and densitometric analyses of NLRP3, IL-1β, IL-18 expressed in rat liver tissues (M-T). Results are mean ± SEM of 5 rats. *P < 0.05 compare with the control group.
9). 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: IHC    Species: human    Sample: xenograft tumor

Fig. 9 | Knockdown of AK023391 inhibited tumor growth in vivo. d IHC analysis of the expression levels of Ki-67, p-FOXO3a, p-PI3K, p-Akt, and p-NF-κB in xenograft tumor tissues treated with si-AK023391 and in the NC group (original magnification, ×200).

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
10). High yield engineered nanovesicles from ADSC with enriched miR-21-5p promote angiogenesis in adipose tissue regeneration. Biomaterials Research, 2022 (PubMed: 36528594) [IF=11.3]

Application: WB    Species: Human    Sample: HUVECs

Fig. 6 miR-21-5p abundant in ADSC-NVs inhibits PTEN and activates PI3K/AKT signaling in HUVECs. First, HUVECs were transfected with miR-21-5p mimic or inhibitor. qRT-PCR assay was then conducted to determine the relative expression level of miR-21-5p (A) and PTEN (B) in the mimic, mimic negative control (mimic NC), inhibitor, and inhibitor negative control (inhibitor NC) groups (n = 3 per group). qRT-PCR assay of the relative expression level of angiogenetic VEGF and Ang-1 mRNA (C), and apoptosis associated mRNA expression of Bax and Bcl-2 (D) in the mimic, mimic NC, inhibitor, and inhibitor NC groups (n = 3 per group). E Western blot assay for protein level of PTEN. F-G Western blot assay for protein level of VEGF, Ang-1, Bax, and Bcl-2. H Western blot assay of PI3K, Akt, and p-Akt protein level. Next, HUVECs were treated with/without ADSC-NVs for 24 h and collected for analysis. I qRT-PCR analysis of the relative expression level of miR-21-5p (n = 3 per group). J qRT-PCR analysis of relative expression level of PTEN and PI3K (n = 3 per group). K Western blot assay for protein levels of PTEN and PI3K. L Western blot assay for protein levels of Akt and p-Akt. ns, no significant difference, *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001
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