Phospho-PI3K p85 alpha (Tyr607) Antibody

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

FIGURE 3 PI3K/Akt pathway is downregulated in p75NTR−/− EMSCs.

Fig.

Figure 4.

Figure 4:| Efect of LQZS on phosphorylation levels of EGFR, PI3K, and AKT in lung tissues of rats with AECOPD.

Fig.

Figure 6 FGFRL1 regulates ENO1 expression and the PI3K/Akt pathway.

Figure 4.

Fig.

Figure 6 Effects of Huangqin decoction (HQD) on colonic expression levels of Ras-phosphoinositide-3-kinase (PI3K)-Akt-hypoxia inducible factor 1 alpha (HIF-1α) pathway proteins assessed by Western blot in dextran sulfate sodium (DSS)-induced colitis mice (A).

Fig.

Figure 4.

Figure 5 circKIF4A promotes bladder cancer progression via the circKIF4A-miR-375/1231-NOTCH2 axis.

Figure 5.

Figure 5 Effects of miR-654-3p upregulation on cisplatin-induced apoptosis and migration of OVC cells.

FIGURE 6 miR‐145 and SOX9 exerted their impacts through PI3K/AKT signaling pathway.

FIGURE 4 MEG3 regulates the PTEN/PI3K/AKT signalling in primary SCs.

Fig.

FIGURE 5 FMN inhibits myostatin‐mediated dephosphorylation on the PI3K/Akt/FoxO3a signalling pathway in the muscle of CKD rats and C2C12 myotubes.

Fig.

Figure 3 Activation of PI3K/AKT signaling in the femoral vein tissue of mice with DVT.

Fig.

Figure 7 QLD inhibits MMP-9 and affects the PI3K/AKT pathway.

FIGURE 5 Inhibition of PI3K/Akt/mTOR signaling pathway of NSCLC cells by SIRT6 overexpression and radiation therapy.

Figure 7 Overexpression of FABP4 suppresses the phosphorylation of PI3K and AKT.

Figure 3 ZJJ activated the hippocampal insulin signaling pathway in diabetic rats.

Figure 4 ZJJ activated the neuronal insulin signaling pathway in diabetic rats.

Figure 8 Effect of LEO on protein expression of PI3K, p-PI3K, Akt, p-Akt, eNOS, and p-eNOS in HUVEC.

Figure 4 Wogonin inhibits PI3K/Akt/ NF-κB Signaling pathway in diabetic mice.

Figure 4 Notoginsenoside R1 inhibits the KRAS/PI3K/Akt pathway via YBX3.

Figure 6 Effect of BG on PI3K/Akt signaling with respect to restoring the blood-spinal cord barrier and to anti-apoptosis in SH-SY5Y cells.

FIGURE 4 | ASIV attenuated ferroptosis-related indicators in the ADR-reduced renal damage.

Fig.

Figure 11 Effect of YQ on insulin secretion-related proteins in pancreas islet.

Fig.

Figure 7 FA inhibited the TGF-β1-induced activation of NOX4/ROS and PI3K/Akt pathway.

FIGURE 6 | RB ameliorated insulin resistance by upregulating the PI3K/AKT/TXNIP cascade signaling pathway in vitro.

Fig.

FIGURE 5 Protein levels of PI3K, AKT, Bcl‐2, Bax, and cleaved‐Caspase 3 were detected by Western blotting.

Figure 5 MiR-216b modulates PC EMT through the PI3K/AKT pathway.

Fig.

FIGURE 4 Signaling pathways involved in A1/A2 astrocyte activation were regulated by PBM.

Fig.

Figure 6 Effect of BG on PI3K/Akt signaling with respect to restoring the blood-spinal cord barrier and to anti-apoptosis in SH-SY5Y cells.

Figure 6 Periplocymarin (PPM) modulates gene expression involved in PI3K/AKT signaling pathway.

Figure 7 The effect of periplocymarin (PPM) on colorectal cancer cells in nude mice.

FIGURE 4 Effects of surfactin on key protein in insulin signaling pathway in IR‐HepG2 cells.

Fig.

Figure 8 RAC prevented the activation of the PI3K/AKT/mTOR and MAPK pathway.

Figure 4 CD147 upregulates HIF-1α expression through the activated PI3K/AKT/mTOR signaling pathway.

Figure 8 Effect of LBAG on the expression of autophagy and PI3K/AKT pathway-related proteins in H9c2 cells with H/R injury.

Figure 5 Expression levels of PI3K/Akt/GSK-3β pathway-related proteins in intestinal tissue of NEC mice.

Figure 2 IHC of GPNMB, EGFR, p-PI3K, and Ki-67 in ESCC.

Figure 5.

Figure 10 APL extract upregulated PI3K/Akt signaling of Iso-induced mice.

FIGURE 9 (A) Distribution of p-PI3K, p-IKK, p-NF-κB, and p-AKT positive cells in the synovial tissue of the ankle joint in each group (immunohistochemical method, ×100).

Fig.

Figure 7 Western blot analysis of the proteins.

Figure 3.

Figure 6 High-dose VC inhibited the PI3K/AKT/mTOR signaling pathway in CLP-Induced sepsis rats.

FIGURE 10 Metformin reduced the activation of NF-κB and inhibited the PI3K/AKT/mTOR/HIF-1α signaling pathway in the gastric tissues of Atp4a−/− mice.

FIGURE 6 Effects of Ginsenoside Rb1 and Ginsenoside CK on Apoptosis-related Pathways Proteins in HGC-27 (A) Apoptosis-related pathways PI3K, p-PI3K, AKT, p-AKT bands.

Fig.

FIGURE 6.

Product:	Phospho-PI3K p85 alpha (Tyr607) Antibody
Catalog:	AF3241
Description:	Rabbit polyclonal antibody to Phospho-PI3K p85 alpha (Tyr607)
Application:	WB IHC IF/ICC
Reactivity:	Human, Mouse, Rat, Pig
Prediction:	Bovine, Horse, Sheep, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.:	80kDa; 84kD(Calculated).
Uniprot:	P27986
RRID:	AB_2834667

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Blocking peptides are peptides that bind specifically to the target antibody and block antibody binding. These peptide usually contains the epitope recognized by the antibody. Antibodies bound to the blocking peptide no longer bind to the epitope on the target protein. By comparing the staining from the blocked antibody versus the antibody alone, one can see which staining is specific.

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MSDS

Data Sheet

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Product Info

Source:

Rabbit

Application:

WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-500
*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,Pig

Prediction:

Bovine(100%), Horse(100%), Sheep(100%), Rabbit(100%), Dog(100%), Chicken(86%), Xenopus(86%)

Clonality:

Polyclonal

Specificity:

Phospho-PI3K p85 alpha (Tyr607) Antibody detects endogenous levels of PI3K p85 alpha only when phosphorylated at Tyrosine 607.

RRID:

AB_2834667
Cite Format: Affinity Biosciences Cat# AF3241, RRID:AB_2834667.

Conjugate:

Unconjugated.

Purification:

The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho-peptide and non-phospho-peptide affinity columns.

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

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;

Immunogens

Immunogen:

Uniprot:

P27986(P85A_HUMAN) >>Visit HPA database.

Gene(ID):

PIK3R1(5295)

Expression:

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).

Description:

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.

Sequence:

P27986 P85A_HUMAN:
Protein BLAST With
NCBI/
ExPASy/
Uniprot

MSAEGYQYRALYDYKKEREEDIDLHLGDILTVNKGSLVALGFSDGQEARPEEIGWLNGYNETTGERGDFPGTYVEYIGRKKISPPTPKPRPPRPLPVAPGSSKTEADVEQQALTLPDLAEQFAPPDIAPPLLIKLVEAIEKKGLECSTLYRTQSSSNLAELRQLLDCDTPSVDLEMIDVHVLADAFKRYLLDLPNPVIPAAVYSEMISLAPEVQSSEEYIQLLKKLIRSPSIPHQYWLTLQYLLKHFFKLSQTSSKNLLNARVLSEIFSPMLFRFSAASSDNTENLIKVIEILISTEWNERQPAPALPPKPPKPTTVANNGMNNNMSLQDAEWYWGDISREEVNEKLRDTADGTFLVRDASTKMHGDYTLTLRKGGNNKLIKIFHRDGKYGFSDPLTFSSVVELINHYRNESLAQYNPKLDVKLLYPVSKYQQDQVVKEDNIEAVGKKLHEYNTQFQEKSREYDRLYEEYTRTSQEIQMKRTAIEAFNETIKIFEEQCQTQERYSKEYIEKFKREGNEKEIQRIMHNYDKLKSRISEIIDSRRRLEEDLKKQAAEYREIDKRMNSIKPDLIQLRKTRDQYLMWLTQKGVRQKKLNEWLGNENTEDQYSLVEDDEDLPHHDEKTWNVGSSNRNKAENLLRGKRDGTFLVRESSKQGCYACSVVVDGEVKHCVINKTATGYGFAEPYNLYSSLKELVLHYQHTSLVQHNDSLNVTLAYPVYAQQRR

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

Horse

100

Bovine

100

Sheep

100

Dog

100

Rabbit

100

Xenopus

Chicken

Zebrafish

Pig

Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - P27986 As Substrate

P27986

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

Research Backgrounds

P27986_P85A_HUMAN

Function:

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.

PTMs:

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.

Tissue Specificity:

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).

Subunit Structure:

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.

Family&Domains:

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

Belongs to the PI3K p85 subunit 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: 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.

References

1). ITGB6 modulates resistance to anti-CD276 therapy in head and neck cancer by promoting PF4+ macrophage infiltration. Nature communications, 2024 (PubMed: 39152118) [IF=16.6]

2). Simvastatin-enhanced bioinspired exosome mimetics regulate osteogenesis and angiogenesis for the treatment of glucocorticoid-induced osteonecrosis of the femoral head. Chemical Engineering Journal, 2023 [IF=15.1]

3). Circular RNA TGFBR2 acts as a ceRNA to suppress nasopharyngeal carcinoma progression by sponging miR-107. CANCER LETTERS, 2021 (PubMed: 33160003) [IF=9.7]

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.

4). Chemotactic recruitment of genetically engineered cell membrane-camouflaged metal-organic framework nanoparticles for ischemic osteonecrosis treatment. Acta biomaterialia, 2024 (PubMed: 39029641) [IF=9.7]

5). TREM-1 governs NLRP3 inflammasome activation of macrophages by firing up glycolysis in acute lung injury. International Journal of Biological Sciences, 2023 (PubMed: 36594089) [IF=9.2]

6). ACT001, a novel PAI-1 inhibitor, exerts synergistic effects in combination with cisplatin by inhibiting PI3K/AKT pathway in glioma. Cell Death & Disease, 2019 (PubMed: 31591377) [IF=9.0]

7). Blockade of FGF2/FGFR2 partially overcomes bone marrow mesenchymal stromal cells mediated progression of T-cell acute lymphoblastic leukaemia. Cell Death & Disease, 2022 (PubMed: 36333298) [IF=9.0]

8). Suppression of steroid 5α-reductase type I promotes cellular apoptosis and autophagy via PI3K/Akt/mTOR pathway in multiple myeloma. Cell Death & Disease, 2021 (PubMed: 33627630) [IF=9.0]

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.

9). Eosinophil peroxidase promotes bronchial epithelial cells to secrete asthma-related factors and induces the early stage of airway remodeling. Clinical immunology (Orlando, Fla.), 2024 (PubMed: 38663494) [IF=8.6]

10). Prolyl hydroxylases positively regulated LPS-induced inflammation in human gingival fibroblasts via TLR4/MyD88-mediated AKT/NF-κB and MAPK pathways. CELL PROLIFERATION, 2018 (PubMed: 30091492) [IF=8.5]

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Affinity Biosciences tests all products strictly. Citations are provided as a resource for additional applications that have not been validated by Affinity Biosciences. Please choose the appropriate format for each application and consult Materials and Methods sections for additional details about the use of any product in these publications.

For Research Use Only.
Not for use in diagnostic or therapeutic procedures. Not for resale. Not for distribution without written consent. Affinity Biosciences will not be held responsible for patent infringement or other violations that may occur with the use of our products. Affinity Biosciences, Affinity Biosciences Logo and all other trademarks are the property of Affinity Biosciences LTD.

Phospho-PI3K p85 alpha (Tyr607) Antibody - #AF3241

Related products

Related Downloads

MSDS

Data Sheet

COA

Protocols

WB Handbook

IHC Protocol

IF/ICC Protocol

Product Info

Immunogens

Predictions

PTMs - P27986 As Substrate

Research Backgrounds

Research Fields

References

Restrictive clause