产品: Phospho-PI3K p85 alpha (Tyr607) 抗体
货号: AF3241
来源: Rabbit
应用: WB, IHC, IF/ICC, ELISA(peptide)
反应: Human, Mouse, Rat, Pig
预测: Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
分子量: 80kD; 84kD(Calculated).
蛋白号: P27986
RRID: AB_2834667

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

货期: 当天发货

产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-500, ELISA(peptide) 1:20000-1:40000
*The optimal dilutions should be determined by the end user.
反应:
Human,Mouse,Rat,Pig
预测:
Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(86%), Xenopus(86%)
克隆:
Polyclonal
特异性:
Phospho-PI3K p85 alpha (Tyr607) Antibody detects endogenous levels of PI3K p85 alpha only when phosphorylated at Tyrosine 607.
RRID:
AB_2834667
引用格式: Affinity Biosciences Cat# AF3241, RRID:AB_2834667.
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

GRB 1; GRB1; p85 alpha; p85; P85A_HUMAN; Phosphatidylinositol 3 kinase associated p 85 alpha; Phosphatidylinositol 3 kinase regulatory 1; Phosphatidylinositol 3 kinase regulatory subunit alpha; Phosphatidylinositol 3 kinase regulatory subunit polypeptide 1 (p85 alpha); Phosphatidylinositol 3-kinase 85 kDa regulatory subunit alpha; Phosphatidylinositol 3-kinase regulatory subunit alpha; Phosphoinositide 3 kinase regulatory subunit 1 (alpha); Phosphoinositide 3 kinase regulatory subunit 1 (p85 alpha); Phosphoinositide 3 kinase regulatory subunit 1; Phosphoinositide 3 kinase regulatory subunit polypeptide 1 (p85 alpha); PI3 kinase p85 subunit alpha; PI3-kinase regulatory subunit alpha; PI3-kinase subunit p85-alpha; PI3K; PI3K regulatory subunit alpha; Pik3r1; PtdIns 3 kinase p85 alpha; PtdIns-3-kinase regulatory subunit alpha; PtdIns-3-kinase regulatory subunit p85-alpha;

抗原和靶标

免疫原:
Uniprot:
基因/基因ID:
表达特异性:
P27986 P85A_HUMAN:

Isoform 2 is expressed in skeletal muscle and brain, and at lower levels in kidney and cardiac muscle. Isoform 2 and isoform 4 are present in skeletal muscle (at protein level).

蛋白描述:
PIK3R1 is a regulatory subunit of phosphoinositide-3-kinase. Mediates binding to a subset of tyrosine-phosphorylated proteins through its SH2 domain. Acts as an adapter, mediating the association of the p110 catalytic unit of the alpha, beta and delta enzymes to the plasma membrane, where p110 phosphorylates inositol lipids. May play an additional role in the regulation of the actin cytoskeleton. Necessary for the insulin-stimulated increase in glucose uptake and glycogen synthesis in insulin-sensitive tissues. Its SH2 domains interacts with the YTHM motif of phosphorylated INSR in vitro. Defects in PIK3R1 are a cause of severe insulin resistance. Four alternatively spliced isoforms have been described.
蛋白序列:
MSAEGYQYRALYDYKKEREEDIDLHLGDILTVNKGSLVALGFSDGQEARPEEIGWLNGYNETTGERGDFPGTYVEYIGRKKISPPTPKPRPPRPLPVAPGSSKTEADVEQQALTLPDLAEQFAPPDIAPPLLIKLVEAIEKKGLECSTLYRTQSSSNLAELRQLLDCDTPSVDLEMIDVHVLADAFKRYLLDLPNPVIPAAVYSEMISLAPEVQSSEEYIQLLKKLIRSPSIPHQYWLTLQYLLKHFFKLSQTSSKNLLNARVLSEIFSPMLFRFSAASSDNTENLIKVIEILISTEWNERQPAPALPPKPPKPTTVANNGMNNNMSLQDAEWYWGDISREEVNEKLRDTADGTFLVRDASTKMHGDYTLTLRKGGNNKLIKIFHRDGKYGFSDPLTFSSVVELINHYRNESLAQYNPKLDVKLLYPVSKYQQDQVVKEDNIEAVGKKLHEYNTQFQEKSREYDRLYEEYTRTSQEIQMKRTAIEAFNETIKIFEEQCQTQERYSKEYIEKFKREGNEKEIQRIMHNYDKLKSRISEIIDSRRRLEEDLKKQAAEYREIDKRMNSIKPDLIQLRKTRDQYLMWLTQKGVRQKKLNEWLGNENTEDQYSLVEDDEDLPHHDEKTWNVGSSNRNKAENLLRGKRDGTFLVRESSKQGCYACSVVVDGEVKHCVINKTATGYGFAEPYNLYSSLKELVLHYQHTSLVQHNDSLNVTLAYPVYAQQRR

种属预测

种属预测:

score>80的预测可信度较高,可尝试用于WB检测。*预测模型主要基于免疫原序列比对,结果仅作参考,不作为质保凭据。

Species
Results
Score
Horse
100
Bovine
100
Sheep
100
Dog
100
Rabbit
100
Xenopus
86
Chicken
86
Zebrafish
67
Pig
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

翻译修饰 - P27986 作为底物

Site PTM Type Enzyme
Ubiquitination
S2 Acetylation
Y12 Phosphorylation
S43 Phosphorylation
Y59 Phosphorylation
Y73 Phosphorylation
Y76 Phosphorylation
S83 Phosphorylation P17612 (PRKACA)
T86 Phosphorylation
S147 Phosphorylation
T148 Phosphorylation
T152 Phosphorylation
S154 Phosphorylation
Y203 Phosphorylation P07949 (RET)
S208 Phosphorylation
S265 Phosphorylation
S269 Phosphorylation
S279 Phosphorylation
K346 Ubiquitination
Y368 Phosphorylation P06213 (INSR)
T369 Phosphorylation
K379 Ubiquitination
K419 Ubiquitination
Y426 Phosphorylation
K438 Ubiquitination
K448 Ubiquitination
Y452 Phosphorylation
T454 Phosphorylation
K459 Sumoylation
K459 Ubiquitination
Y463 Phosphorylation
Y467 Phosphorylation
Y470 Phosphorylation
T471 Phosphorylation
T490 Phosphorylation
Y504 Phosphorylation
K506 Ubiquitination
Y508 Phosphorylation P09619 (PDGFRB)
K513 Ubiquitination
R514 Methylation
K519 Ubiquitination
R523 Methylation
Y528 Phosphorylation
K530 Acetylation
S541 Phosphorylation
Y556 Phosphorylation
K567 Ubiquitination
T576 Phosphorylation
Y580 Phosphorylation P06213 (INSR)
T603 Phosphorylation
Y607 Phosphorylation P06213 (INSR) , P12931 (SRC)
S608 Phosphorylation P42336 (PIK3CA) , P68400 (CSNK2A1)
T623 Phosphorylation
S628 Phosphorylation
S629 Phosphorylation
K633 Ubiquitination
S652 Phosphorylation Q15139 (PRKD1)
Y657 Phosphorylation
K674 Ubiquitination
Y679 Phosphorylation
Y688 Phosphorylation
S690 Phosphorylation

研究背景

功能:

Binds to activated (phosphorylated) protein-Tyr kinases, through its SH2 domain, and acts as an adapter, mediating the association of the p110 catalytic unit to the plasma membrane. Necessary for the insulin-stimulated increase in glucose uptake and glycogen synthesis in insulin-sensitive tissues. Plays an important role in signaling in response to FGFR1, FGFR2, FGFR3, FGFR4, KITLG/SCF, KIT, PDGFRA and PDGFRB. Likewise, plays a role in ITGB2 signaling. Modulates the cellular response to ER stress by promoting nuclear translocation of XBP1 isoform 2 in a ER stress- and/or insulin-dependent manner during metabolic overloading in the liver and hence plays a role in glucose tolerance improvement.

翻译修饰:

Polyubiquitinated in T-cells by CBLB; which does not promote proteasomal degradation but impairs association with CD28 and CD3Z upon T-cell activation.

Phosphorylated. Tyrosine phosphorylated in response to signaling by FGFR1, FGFR2, FGFR3 and FGFR4. Phosphorylated by CSF1R. Phosphorylated by ERBB4. Phosphorylated on tyrosine residues by TEK/TIE2. Dephosphorylated by PTPRJ. Phosphorylated by PIK3CA at Ser-608; phosphorylation is stimulated by insulin and PDGF. The relevance of phosphorylation by PIK3CA is however unclear (By similarity). Phosphorylated in response to KIT and KITLG/SCF. Phosphorylated by FGR.

组织特异性:

Isoform 2 is expressed in skeletal muscle and brain, and at lower levels in kidney and cardiac muscle. Isoform 2 and isoform 4 are present in skeletal muscle (at protein level).

亚基结构:

Heterodimer of a regulatory subunit PIK3R1 and a p110 catalytic subunit (PIK3CA, PIK3CB or PIK3CD). Interacts (via SH2 domains) with CCDC88A/GIV (tyrosine-phosphorylated form); the interaction enables recruitment of PIK3R1 to the EGFR receptor, enhancing PI3K activity and cell migration. Interacts (via SH2 domain) with CSF1R (tyrosine phosphorylated). Interacts with PIK3R2; the interaction is dissociated in an insulin-dependent manner (By similarity). Interacts with XBP1 isoform 2; the interaction is direct and induces translocation of XBP1 isoform 2 into the nucleus in a ER stress- and/or insulin-dependent but PI3K-independent manner. Interacts with FER. Interacts (via SH2 domain) with TEK/TIE2 (tyrosine phosphorylated). Interacts with PTK2/FAK1 (By similarity). Interacts with phosphorylated TOM1L1. Interacts with phosphorylated LIME1 upon TCR and/or BCR activation. Interacts with SOCS7. Interacts with RUFY3. Interacts (via SH2 domain) with CSF1R (tyrosine phosphorylated). Interacts with LYN (via SH3 domain); this enhances enzyme activity (By similarity). Interacts with phosphorylated LAT, LAX1 and TRAT1 upon TCR activation. Interacts with CBLB. The SH2 domains interact with the YTHM motif of phosphorylated INSR in vitro. Also interacts with tyrosine-phosphorylated IGF1R in vitro. Interacts with CD28 and CD3Z upon T-cell activation. Interacts with IRS1 and phosphorylated IRS4, as well as with NISCH and HCST. Interacts with FASLG, KIT and BCR. Interacts with AXL, FGFR1, FGFR2, FGFR3 and FGFR4 (phosphorylated). Interacts with FGR and HCK. Interacts with PDGFRA (tyrosine phosphorylated) and PDGFRB (tyrosine phosphorylated). Interacts with ERBB4 (phosphorylated). Interacts with NTRK1 (phosphorylated upon ligand-binding). Interacts with FAM83B; activates the PI3K/AKT signaling cascade. Interacts with APPL1 and APPL2 (By similarity). Interacts with SRC.

(Microbial infection) Interacts with HIV-1 Nef to activate the Nef associated p21-activated kinase (PAK). This interaction depends on the C-terminus of both proteins and leads to increased production of HIV.

(Microbial infection) Interacts with HCV NS5A.

(Microbial infection) Interacts with herpes simplex virus 1 UL46; this interaction activates the PI3K/AKT pathway.

(Microbial infection) Interacts with herpes simplex virus 1 UL46 and varicella virus ORF12; this interaction activates the PI3K/AKT pathway.

蛋白家族:

The SH3 domain mediates the binding to CBLB, and to HIV-1 Nef.

Belongs to the PI3K p85 subunit family.

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)

· Cellular Processes > Cell motility > Regulation of actin cytoskeleton.   (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 > 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 > Phosphatidylinositol signaling system.

· 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 > 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 > Type II diabetes mellitus.

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

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

· Human Diseases > Infectious diseases: Bacterial > Bacterial invasion of epithelial cells.

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

· Human Diseases > Infectious diseases: Parasitic > Amoebiasis.

· 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 > Viral carcinogenesis.

· 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 > Development > Axon guidance.   (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 > Natural killer cell mediated cytotoxicity.   (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 > Immune system > Leukocyte transendothelial migration.   (View pathway)

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

· Organismal Systems > Nervous system > Cholinergic synapse.

· Organismal Systems > Sensory system > Inflammatory mediator regulation of TRP channels.   (View pathway)

· 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 > Regulation of lipolysis in adipocytes.

· Organismal Systems > Endocrine system > Relaxin signaling pathway.

· Organismal Systems > Excretory system > Aldosterone-regulated sodium reabsorption.

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

文献引用

1). Li W et al. Circular RNA TGFBR2 acts as a ceRNA to suppress nasopharyngeal carcinoma progression by sponging miR-107. Cancer Lett 2020 Nov 4;S0304-3835(20)30586-3. (PubMed: 33160003) [IF=9.756]

Application: WB    Species: human    Sample: NPC cells

Fig.3 m TGFBR2 and PI3K/Akt pathway protein levels after miR-107 overexpression and inhibition in NPC cells.

Application: WB    Species: human    Sample: NPC cells

Fig. 4. TGFBR2 mediates the effects of miR-107 on the proliferation and migration of nasopharyngeal carcinoma (NPC) cells. HNE1 cells overexpressing miR-107 were transfected with TGFBR2-expressing plasmids, and 5–8F cells with miR-107 knockdown were transfected with TGFBR2 siRNA. a–b Expression of TGFBR2 mRNA in qRT-PCR. c–d Expression of TGFBR2 and PI3K/Akt pathway proteins. e–f CCK-8 assays were performed to detect cell viability. g–h The potential of cells to replicate and self-renew was reflected by colony-forming capacity. i–j Rate of wound healing represented the migratory potential of cells. k–l Transwell assays showed the invasive potential of cells. m–n Cell apoptotic ability was evaluated using an apoptosis assay. o–p Protein markers of epithelial-mesenchymal transition (EMT; E-cadherin, N-cadherin, and vimentin) were detected by Western blot analysis. The values are expressed as the mean ± SD from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.

Application: WB    Species: human    Sample: NPC cells

Fig. 4. TGFBR2 mediates the effects of miR-107 on the proliferation and migration of nasopharyngeal carcinoma (NPC) cells. HNE1 cells overexpressing miR-107 were transfected with TGFBR2-expressing plasmids, and 5–8F cells with miR-107 knockdown were transfected with TGFBR2 siRNA. a–b Expression of TGFBR2 mRNA in qRT-PCR. c–d Expression of TGFBR2 and PI3K/Akt pathway proteins. e–f CCK-8 assays were performed to detect cell viability. g–h The potential of cells to replicate and self-renew was reflected by colony-forming capacity. i–j Rate of wound healing represented the migratory potential of cells. k–l Transwell assays showed the invasive potential of cells. m–n Cell apoptotic ability was evaluated using an apoptosis assay. o–p Protein markers of epithelial-mesenchymal transition (EMT; E-cadherin, N-cadherin, and vimentin) were detected by Western blot analysis. The values are expressed as the mean ± SD from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.

Application: WB    Species: human    Sample: NPC cells

Fig. 7. circTGFBR2 promotes nasopharyngeal carcinoma (NPC) progression by the sponging activity of miR-107 and upregulation of TGFBR2. HNE1 cells were cotransfected with circTGFBR2 and miR-107 or NC; 5–8F cells were co-transfected with si-circTGFBR2 plus miR-107 inhibitor or si-NC. a–b CCK-8 assays were performed to detect cell viability. c–d The potential of cells to replicate and self-renew was reflected by colony-forming capacity. e–f Migratory potential of cells was examined in cells by wound healing assay. g–h Invasive potential of cells was assessed by Transwell assays. i–j Apoptotic ability of cells was evaluated by an apoptosis assay. k–l Protein markers of EMT (E-cadherin, N-cadherin, and vimentin) were detected by Western blot analysis. m–n TGFBR2 and PI3K/Akt pathway protein levels were detected. o–p TGFBR2 levels were detected by immunofluorescence assay. q Positive correlation between TGFBR2 and miR-107 expression in NPC tissues. The values are expressed as the mean ± SD from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.

Application: WB    Species: human    Sample: NPC cells

Fig. 7. circTGFBR2 promotes nasopharyngeal carcinoma (NPC) progression by the sponging activity of miR-107 and upregulation of TGFBR2. HNE1 cells were cotransfected with circTGFBR2 and miR-107 or NC; 5–8F cells were co-transfected with si-circTGFBR2 plus miR-107 inhibitor or si-NC. a–b CCK-8 assays were performed to detect cell viability. c–d The potential of cells to replicate and self-renew was reflected by colony-forming capacity. e–f Migratory potential of cells was examined in cells by wound healing assay. g–h Invasive potential of cells was assessed by Transwell assays. i–j Apoptotic ability of cells was evaluated by an apoptosis assay. k–l Protein markers of EMT (E-cadherin, N-cadherin, and vimentin) were detected by Western blot analysis. m–n TGFBR2 and PI3K/Akt pathway protein levels were detected. o–p TGFBR2 levels were detected by immunofluorescence assay. q Positive correlation between TGFBR2 and miR-107 expression in NPC tissues. The values are expressed as the mean ± SD from three independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001.

2). Xi X et al. ACT001, a novel PAI-1 inhibitor, exerts synergistic effects in combination with cisplatin by inhibiting PI3K/AKT pathway in glioma. Cell Death Dis 2019 Oct 7;10(10):757 (PubMed: 31591377) [IF=9.685]

3). Dou R et al. Suppression of steroid 5α-reductase type I promotes cellular apoptosis and autophagy via PI3K/Akt/mTOR pathway in multiple myeloma. Cell Death Dis 2021 Feb 24;12(2):206. (PubMed: 33627630) [IF=9.685]

Application: WB    Species: human    Sample: ARP1 and H929 cells

Fig. 5 |SRD5A1 knockdown induces autophagy via PI3K/Akt/mTOR pathway. Expression of a marker protein in PI3K/Akt/mTOR signaling was detected by western blotting in ARP1 and H929 cells.

4). Wang Y et al. p75NTR-/- mice exhibit an alveolar bone loss phenotype and inhibited PI3K/Akt/β-catenin pathway. Cell Prolif 2020 Mar 25:e12800 (PubMed: 32215984) [IF=8.755]

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

5). Shang L et al. Prolyl hydroxylases positively regulated LPS-induced inflammation in human gingival fibroblasts via TLR4/MyD88-mediated AKT/NF-κB and MAPK pathways. Cell Prolif 2018 Aug 9:e12516 (PubMed: 30091492) [IF=8.755]

6). Li Y et al. LncRNA NORAD Mediates the Proliferation and Apoptosis of Diffuse Large-B-Cell Lymphoma via Regulation of miR-345-3p/TRAF6 Axis. Arch Med Res 2022 Apr;53(3):271-279. (PubMed: 35164979) [IF=8.323]

7). Zhu J et al. Liubao brick tea activates the PI3K-Akt signaling pathway to lower blood glucose, metabolic disorders and insulin resistance via altering the intestinal flora. Food Res Int 2021 Oct;148:110594. (PubMed: 34507739) [IF=7.425]

8). Lu Y et al. Protective effects of Danzhi jiangtang capsule on vascular endothelial damages induced by high-fat diet and palmitic acid. Biomed Pharmacother 2018 Nov;107:1631-1640 (PubMed: 30257381) [IF=7.419]

9). Shen F et al. CEMIP promotes ovarian cancer development and progression via the PI3K/AKT signaling pathway. Biomed Pharmacother 2019 Mar 26;114:108787 (PubMed: 30925458) [IF=7.419]

10). Liao L et al. Leonurine Ameliorates Oxidative Stress and Insufficient Angiogenesis by Regulating the PI3K/Akt-eNOS Signaling Pathway in H2O2-Induced HUVECs. Oxid Med Cell Longev 2021 Aug 3;2021:9919466. (PubMed: 34394836) [IF=7.310]

Application: WB    Species: Human    Sample: HUVECs

Figure 8 Effect of LEO on protein expression of PI3K, p-PI3K, Akt, p-Akt, eNOS, and p-eNOS in HUVEC. Values are presented as means ± S.D. (n = 3). #P < 0.05, ##P < 0.01, and ###P < 0.001 vs. control group; ∗P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001 vs. H2O2 group.

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