PI3 kinase P110 alpha Antibody - #AF5112

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Product: PI3 kinase P110 alpha Antibody
Catalog: AF5112
Description: Rabbit polyclonal antibody to PI3 kinase P110 alpha
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Sheep, Rabbit, Dog, Chicken
Mol.Wt.: 110 kDa; 124kD(Calculated).
Uniprot: P42336
RRID: AB_2837598

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
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: 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.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(92%)
Clonality:
Polyclonal
Specificity:
PI3 kinase P110 alpha Antibody detects endogenous levels of total PI3 kinase P110 alpha.
RRID:
AB_2837598
Cite Format: Affinity Biosciences Cat# AF5112, RRID:AB_2837598.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
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.
Alias:

Fold/Unfold

5-bisphosphate 3-kinase 110 kDa catalytic subunit alpha; 5-bisphosphate 3-kinase catalytic subunit alpha isoform; caPI3K; CLOVE; CWS5; MCAP; MCM; MCMTC; MGC142161; MGC142163; p110 alpha; p110alpha; Phosphatidylinositol 3 kinase catalytic alpha polypeptide; Phosphatidylinositol 3 kinase catalytic 110 KD alpha; Phosphatidylinositol 4 5 bisphosphate 3 kinase catalytic subunit alpha; Phosphatidylinositol 4 5 bisphosphate 3 kinase catalytic subunit alpha isoform; Phosphatidylinositol 4,5 bisphosphate 3 kinase 110 kDa catalytic subunit alpha; Phosphatidylinositol-4; Phosphoinositide 3 kinase catalytic alpha polypeptide; PI3 kinase p110 subunit alpha; PI3-kinase subunit alpha; PI3K; PI3K-alpha; PI3KC A; PIK3C A; Pik3ca; PK3CA; PK3CA_HUMAN; PtdIns 3 kinase p110; PtdIns-3-kinase subunit alpha; PtdIns-3-kinase subunit p110-alpha; Serine/threonine protein kinase PIK3CA;

Immunogens

Immunogen:
Uniprot:

P42336(PK3CA_HUMAN) >>Visit HPA database.

Gene(ID):
PIK3CA(5290)
Description:
Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns (Phosphatidylinositol), PtdIns4P (Phosphatidylinositol 4-phosphate) and PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Participates in cellular signaling in response to various growth factors.
Sequence:
MPPRPSSGELWGIHLMPPRILVECLLPNGMIVTLECLREATLITIKHELFKEARKYPLHQLLQDESSYIFVSVTQEAEREEFFDETRRLCDLRLFQPFLKVIEPVGNREEKILNREIGFAIGMPVCEFDMVKDPEVQDFRRNILNVCKEAVDLRDLNSPHSRAMYVYPPNVESSPELPKHIYNKLDKGQIIVVIWVIVSPNNDKQKYTLKINHDCVPEQVIAEAIRKKTRSMLLSSEQLKLCVLEYQGKYILKVCGCDEYFLEKYPLSQYKYIRSCIMLGRMPNLMLMAKESLYSQLPMDCFTMPSYSRRISTATPYMNGETSTKSLWVINSALRIKILCATYVNVNIRDIDKIYVRTGIYHGGEPLCDNVNTQRVPCSNPRWNEWLNYDIYIPDLPRAARLCLSICSVKGRKGAKEEHCPLAWGNINLFDYTDTLVSGKMALNLWPVPHGLEDLLNPIGVTGSNPNKETPCLELEFDWFSSVVKFPDMSVIEEHANWSVSREAGFSYSHAGLSNRLARDNELRENDKEQLKAISTRDPLSEITEQEKDFLWSHRHYCVTIPEILPKLLLSVKWNSRDEVAQMYCLVKDWPPIKPEQAMELLDCNYPDPMVRGFAVRCLEKYLTDDKLSQYLIQLVQVLKYEQYLDNLLVRFLLKKALTNQRIGHFFFWHLKSEMHNKTVSQRFGLLLESYCRACGMYLKHLNRQVEAMEKLINLTDILKQEKKDETQKVQMKFLVEQMRRPDFMDALQGFLSPLNPAHQLGNLRLEECRIMSSAKRPLWLNWENPDIMSELLFQNNEIIFKNGDDLRQDMLTLQIIRIMENIWQNQGLDLRMLPYGCLSIGDCVGLIEVVRNSHTIMQIQCKGGLKGALQFNSHTLHQWLKDKNKGEIYDAAIDLFTRSCAGYCVATFILGIGDRHNSNIMVKDDGQLFHIDFGHFLDHKKKKFGYKRERVPFVLTQDFLIVISKGAQECTKTREFERFQEMCYKAYLAIRQHANLFINLFSMMLGSGMPELQSFDDIAYIRKTLALDKTEQEALEYFMKQMNDAHHGGWTTKMDWIFHTIKQHALN

Predictions

Predictions:

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

PTMs - P42336 As Substrate

Site PTM Type Enzyme
S6 Phosphorylation
K100 Ubiquitination
K148 Ubiquitination
K184 Ubiquitination
Y246 Phosphorylation
Y294 Phosphorylation
S306 Phosphorylation
S312 Phosphorylation
T313 Phosphorylation
T315 Phosphorylation
Y317 Phosphorylation
S332 Phosphorylation
Y355 Phosphorylation
Y361 Phosphorylation
S507 Phosphorylation
Y508 Phosphorylation
S509 Phosphorylation
K532 Ubiquitination
Y584 Phosphorylation
Y698 Phosphorylation
K863 Ubiquitination
S874 Phosphorylation
T876 Phosphorylation
T957 Phosphorylation
K973 Ubiquitination
K1030 Ubiquitination
Y1038 Phosphorylation

PTMs - P42336 As Enzyme

Substrate Site Source
P09493 (TPM1) S61 Uniprot
P23443 (RPS6KB1) T252 Uniprot
P23443-1 (RPS6KB1) T390 Uniprot
P23443 (RPS6KB1) T412 Uniprot
P27986 (PIK3R1) S608 Uniprot
P32927 (CSF2RB) S585 Uniprot

Research Backgrounds

Function:

Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns (Phosphatidylinositol), PtdIns4P (Phosphatidylinositol 4-phosphate) and PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Participates in cellular signaling in response to various growth factors. Involved in the activation of AKT1 upon stimulation by receptor tyrosine kinases ligands such as EGF, insulin, IGF1, VEGFA and PDGF. Involved in signaling via insulin-receptor substrate (IRS) proteins. Essential in endothelial cell migration during vascular development through VEGFA signaling, possibly by regulating RhoA activity. Required for lymphatic vasculature development, possibly by binding to RAS and by activation by EGF and FGF2, but not by PDGF. Regulates invadopodia formation through the PDPK1-AKT1 pathway. Participates in cardiomyogenesis in embryonic stem cells through a AKT1 pathway. Participates in vasculogenesis in embryonic stem cells through PDK1 and protein kinase C pathway. Also has serine-protein kinase activity: phosphorylates PIK3R1 (p85alpha regulatory subunit), EIF4EBP1 and HRAS. Plays a role in the positive regulation of phagocytosis and pinocytosis (By similarity).

Subunit Structure:

Heterodimer of a catalytic subunit PIK3CA and a p85 regulatory subunit (PIK3R1, PIK3R2 or PIK3R3). Interacts with IRS1 in nuclear extracts (By similarity). Interacts with RUFY3 (By similarity). Interacts with RASD2 (By similarity). Interacts with APPL1. Interacts with HRAS and KRAS (By similarity). Interaction with HRAS/KRAS is required for PI3K pathway signaling and cell proliferation stimulated by EGF and FGF2 (By similarity). Interacts with FAM83B; activates the PI3K/AKT signaling cascade.

Family&Domains:

The PI3K-ABD domain and the PI3K-RBD domain interact with the PI3K/PI4K kinase domain. The C2 PI3K-type domain may facilitate the recruitment to the plasma membrane. The inhibitory interactions with PIK3R1 are mediated by the PI3K-ABD domain and the C2 PI3K-type domain with the iSH2 (inter-SH2) region of PIK3R1, and the C2 PI3K-type domain, the PI3K helical domain, and the PI3K/PI4K kinase domain with the nSH2 (N-terminal SH2) region of PIK3R1.

Belongs to the PI3/PI4-kinase family.

Research Fields

· 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: Overview > MicroRNAs 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)

· Metabolism > Carbohydrate metabolism > Inositol phosphate metabolism.

· 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.

References

1). Aberrant translation regulated by METTL1/WDR4‐mediated tRNA N7‐methylguanosine modification drives head and neck squamous cell carcinoma progression. Cancer Communications (PubMed: 35179319) [IF=16.2]

Application: WB    Species: Mice    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
2). Epimedin C Alleviates Glucocorticoid-Induced Suppression of Osteogenic Differentiation by Modulating PI3K/AKT/RUNX2 Signaling Pathway. Frontiers in Pharmacology (PubMed: 35860032) [IF=5.6]
3). Niaoduqing alleviates podocyte injury in high glucose model via regulating multiple targets and AGE/RAGE pathway: Network pharmacology and experimental validation. Frontiers in Pharmacology (PubMed: 36923354) [IF=5.6]

Application: WB    Species: Mouse    Sample: MPC5 cells

FIGURE 9 Three major ingredients of Niaoduqing (Que + Lut + Kae) participated in the regulation of AGE/RAGE signaling pathway in diabetic complications (hsa04933). (A) The protein expression and phosphorylation levels of PI3K, AKT and NF-κB in MPC5 cells were detected by Western blot. (B) The mRNA expression levels of Rage, Tnf-α, Il-6, Tgf-β1 and Col1a1 in MPC5 cells were determined by RT-qPCR. (C) The detail of AGE/RAGE signaling pathway in diabetic complications (hsa04933). Boxes represented the detected sites. Red boxes indicated the positive results, while green boxes indicated the inconclusive results. Data represented the mean ± SD of triplicate independent experiments; *p < 0.05, **p < 0.01, ***p < 0.001, NS, non-statistically significant.
4). Axl deficiency promotes the neuroinvasion of Japanese encephalitis virus by enhancing IL-1α production from pyroptotic macrophages. Journal of Virology (PubMed: 32611752) [IF=5.4]

Application: IF/ICC    Species: mouse    Sample: peritoneal macrophages

Fig. 13. | Effects of Axl on the expression of cell death regulatory proteins in the in situ peritoneal macrophages. (D-E) IF staining of PI3K-p110(D) and phosphorylated Akt (pAkt,E) of the in situ peritoneal macrophages. Scale bar=20 μm
5). NPR3, transcriptionally regulated by POU2F1, inhibits osteosarcoma cell growth through blocking the PI3K/AKT pathway. CELLULAR SIGNALLING (PubMed: 34229087) [IF=4.8]

Application: WB    Species: Human    Sample: OS cell

Fig. 3. NPR3 inhibits the PI3K/AKT pathway in OS cell lines. U2OS cells were transfected with NPR3 overexpression vector or empty vector. HOS cells were transfected with NPR3 shRNAs or NC shRNA. After 48 h transfection, the protein expression levels of PI3K, p-AKT, and AKT were detected by western blot (a and b). After HOS cells were transfected with sh-NPR3 or sh-NC, OS cells were treated with or without PI3K inhibitor LY294002 (25 μ M). The viability of HOS cells was assessed by CCK-8 assay (c); Cell cycle distribution was measured by flow cytometry (d). *P < 0.05, **P < 0.01, and ***P < 0.001 vs parental/sh-NC + vehicle group; % P < 0.05, %% P < 0.01, and %%% P < 0.001 vs sh-NPR3 + vehicle group. n = 3.
6). DHW-221, a Dual PI3K/mTOR Inhibitor, Overcomes Multidrug Resistance by Targeting P-Glycoprotein (P-gp/ABCB1) and Akt-Mediated FOXO3a Nuclear Translocation in Non-small Cell Lung Cancer. Frontiers in Oncology (PubMed: 35646704) [IF=4.7]

Application: WB    Species: Human    Sample: A549 cells

Figure 5 DHW-221-triggered mitochondrial apoptosis is linked to Akt-mediated FOXO3a nuclear translocation in A549/Taxol cells. (A, B) Comparison and the expression levels of PI3K/Akt/FOXO3a signaling pathway related proteins in A549 and A549/Taxol cells were determined by Western blot, in the presence and absence of DHW-221 and GDC-0980. Statistical comparisons were performed with unpaired Student’s t-test (n = 3) in Panel (A). *p < 0.05, **p < 0.01 versus A549. Statistical comparisons were performed with one-way ANOVA followed by Dunnett’s post-hoc test for multiple comparisons in Panel (B) (n = 3). *p < 0.05, **p < 0.01, ***p < 0.001 versus control. (C, E) The FOXO3a and p-FOXO3a expressions in the nuclear and cytoplasmic fractions of A549/Taxol cells were detected by Western blot. Proliferating cell nuclear antigen (PCNA) was selected as nucleoprotein internal control. The quantitative results were shown in Panel (E). (D) Immunofluorescence staining of FOXO3a in A549/Taxol cells was carried out to evaluate the effect of DHW-221 on FOXO3a nuclear translocation. Scale bar = 20 µm. The histograms indicated the percentage of the cells in each condition exhibiting FOXO3a nuclear mean fluorescence intensity (positive cells, green fluorescence) by ImageJ. (F) FOXO3a degradation in A549/Taxol cells with or without DHW-221 co-treatment in different time spot when protein biosynthesis was blocked with 20 µM cycloheximide (CHX). FOXO3a stability was analyzed relative to control by ImageJ software. (G) FOXO3a proteins levels in the presence of MG132 (0.20 μM) or 2.40 μM DHW-221-treated A549/Taxol cells at 24 h. Statistical comparisons were performed with one-way ANOVA followed by Dunnett’s post-hoc test for multiple comparisons (n = 3). Data were presented as mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001 versus control.
7). Gualou-Xiebai-Banxia decoction protects against type II diabetes with acute myocardial ischemia by attenuating oxidative stress and apoptosis via PI3K/Akt/eNOS signaling. Chinese Journal of Natural Medicines (PubMed: 33781449) [IF=4.6]

Application: WB    Species: rat    Sample: circulation Endothelial progenitor cells (CEPCs)

Fig. 7 GXB activated the PI3K/Akt/eNOS signaling in CEPCs of T2DM-AMI rats. (A) Western-blot analysis of total and phosphorylated PI3K, Akt, and eNOS in CEPCs from each group; GAPDH was used as an internal reference protein. (B) Ratio of phosphorylated/total PI3K, Akt, and eNOS in EPCs from the indicated groups. (C) The relative expression of Pi3k, Akt and eNos mRNA changes in CEPCs from the different groups. Data were shown as mean ± SD (n = 8). ΔP < 0.05, ΔΔP < 0.01 vs control; *P < 0.05, **P < 0.01 vs model
8). The anti-migration and anti-invasion effects of Bruceine D in human triple-negative breast cancer MDA-MB-231 cells. Experimental and Therapeutic Medicine (PubMed: 31853299) [IF=2.7]

Application: WB    Species: human    Sample: MDA-MB-231 cells

Figure 4.| BD inhibits the activation of the PI3K/AKT pathway in MDA-MB-231 cells. (A) The protein levels of PI3K, AKT and p-AKT were evaluated using western blotting.

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