Product: Phospho-PTEN (Ser370) Antibody
Catalog: AF3351
Description: Rabbit polyclonal antibody to Phospho-PTEN (Ser370)
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Bovine, Horse, Rabbit, Dog, Chicken, Xenopus
Mol.Wt.: 54kDa; 47kD(Calculated).
Uniprot: P60484
RRID: AB_2834766

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 100ul $280 In stock
 200ul $350 In stock

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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%), Rabbit(100%), Dog(100%), Chicken(100%), Xenopus(100%)
Clonality:
Polyclonal
Specificity:
Phospho-PTEN (Ser370) Antibody detects endogenous levels of PTEN only when phosphorylated at Serine 370.
RRID:
AB_2834766
Cite Format: Affinity Biosciences Cat# AF3351, RRID:AB_2834766.
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

10q23del; BZS; DEC; GLM2; MGC11227; MHAM; MMAC1; MMAC1 phosphatase and tensin homolog deleted on chromosome 10; Mutated in multiple advanced cancers 1; Phosphatase and tensin homolog; Phosphatase and tensin like protein; Phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN; Pten; PTEN_HUMAN; PTEN1; TEP1;

Immunogens

Immunogen:
Uniprot:
Gene(ID):
Expression:
P60484 PTEN_HUMAN:

Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.

Description:
PTEN a phosphoinositide 3-phosphatase (PIP3) and a tumor suppressor implicated in a wide variety of human cancers. Dephosphorylates inositol phospholipids generated by the activation of the phosphoinositide 3 kinase (PI3K).
Sequence:
MTAIIKEIVSRNKRRYQEDGFDLDLTYIYPNIIAMGFPAERLEGVYRNNIDDVVRFLDSKHKNHYKIYNLCAERHYDTAKFNCRVAQYPFEDHNPPQLELIKPFCEDLDQWLSEDDNHVAAIHCKAGKGRTGVMICAYLLHRGKFLKAQEALDFYGEVRTRDKKGVTIPSQRRYVYYYSYLLKNHLDYRPVALLFHKMMFETIPMFSGGTCNPQFVVCQLKVKIYSSNSGPTRREDKFMYFEFPQPLPVCGDIKVEFFHKQNKMLKKDKMFHFWVNTFFIPGPEETSEKVENGSLCDQEIDSICSIERADNDKEYLVLTLTKNDLDKANKDKANRYFSPNFKVKLYFTKTVEEPSNPEASSSTSVTPDVSDNEPDHYRYSDTTDSDPENEPFDEDQHTQITKV

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

PTMs - P60484 As Substrate

Site PTM Type Enzyme
Ubiquitination
T2 Acetylation
K6 Acetylation
K6 Ubiquitination
K13 Ubiquitination
Y27 Phosphorylation P06213 (INSR)
Y46 Phosphorylation P12931 (SRC)
K66 Ubiquitination
Y68 Phosphorylation P12931 (SRC)
K80 Ubiquitination
S113 Phosphorylation Q13315 (ATM)
K125 Acetylation
K128 Acetylation
Y138 Phosphorylation
Y155 Phosphorylation P12931 (SRC)
K163 Acetylation
K164 Acetylation
Y174 Phosphorylation P12931 (SRC) , P06213 (INSR)
Y176 Phosphorylation
Y177 Phosphorylation
Y178 Phosphorylation
S179 Phosphorylation
Y180 Phosphorylation
K223 Ubiquitination
S227 Phosphorylation
S229 Phosphorylation Q13464 (ROCK1)
T232 Phosphorylation Q13464 (ROCK1)
Y240 Phosphorylation P12931 (SRC) , P21802 (FGFR2) , P07948 (LYN) , P22607 (FGFR3) , P06239 (LCK)
K254 Sumoylation
K266 Sumoylation
K289 Sumoylation
K289 Ubiquitination
S294 Phosphorylation
S302 Phosphorylation
Y315 Phosphorylation P12931 (SRC) , P06239 (LCK)
T319 Phosphorylation
T321 Phosphorylation
K332 Acetylation
Y336 Phosphorylation P42685 (FRK)
S362 Phosphorylation P49841 (GSK3B)
T366 Phosphorylation P49841 (GSK3B) , Q9H4B4 (PLK3)
S370 Phosphorylation P68400 (CSNK2A1) , Q9H4B4 (PLK3)
Y377 Phosphorylation P12931 (SRC)
S380 Phosphorylation Q15831 (STK11) , Q05513 (PRKCZ) , P68400 (CSNK2A1) , P53350 (PLK1)
T382 Phosphorylation Q15831 (STK11) , P68400 (CSNK2A1) , Q05513 (PRKCZ) , P53350 (PLK1)
T383 Phosphorylation P53350 (PLK1) , P68400 (CSNK2A1) , Q05513 (PRKCZ) , Q15831 (STK11)
S385 Phosphorylation Q15831 (STK11) , P68400 (CSNK2A1)
T398 Phosphorylation Q13315 (ATM)
T401 Phosphorylation
K402 Acetylation

Research Backgrounds

Function:

Tumor suppressor. Acts as a dual-specificity protein phosphatase, dephosphorylating tyrosine-, serine- and threonine-phosphorylated proteins. Also acts as a lipid phosphatase, removing the phosphate in the D3 position of the inositol ring from phosphatidylinositol 3,4,5-trisphosphate, phosphatidylinositol 3,4-diphosphate, phosphatidylinositol 3-phosphate and inositol 1,3,4,5-tetrakisphosphate with order of substrate preference in vitro PtdIns(3,4,5)P3 > PtdIns(3,4)P2 > PtdIns3P > Ins(1,3,4,5)P4. The lipid phosphatase activity is critical for its tumor suppressor function. Antagonizes the PI3K-AKT/PKB signaling pathway by dephosphorylating phosphoinositides and thereby modulating cell cycle progression and cell survival. The unphosphorylated form cooperates with AIP1 to suppress AKT1 activation. Dephosphorylates tyrosine-phosphorylated focal adhesion kinase and inhibits cell migration and integrin-mediated cell spreading and focal adhesion formation. Plays a role as a key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation. May be a negative regulator of insulin signaling and glucose metabolism in adipose tissue. The nuclear monoubiquitinated form possesses greater apoptotic potential, whereas the cytoplasmic nonubiquitinated form induces less tumor suppressive ability. In motile cells, suppresses the formation of lateral pseudopods and thereby promotes cell polarization and directed movement.

Functional kinase, like isoform 1 it antagonizes the PI3K-AKT/PKB signaling pathway. Plays a role in mitochondrial energetic metabolism by promoting COX activity and ATP production, via collaboration with isoform 1 in increasing protein levels of PINK1.

PTMs:

Constitutively phosphorylated by CK2 under normal conditions. Phosphorylated in vitro by MAST1, MAST2, MAST3 and STK11. Phosphorylation results in an inhibited activity towards PIP3. Phosphorylation can both inhibit or promote PDZ-binding. Phosphorylation at Tyr-336 by FRK/PTK5 protects this protein from ubiquitin-mediated degradation probably by inhibiting its binding to NEDD4. Phosphorylation by ROCK1 is essential for its stability and activity. Phosphorylation by PLK3 promotes its stability and prevents its degradation by the proteasome.

Monoubiquitinated; monoubiquitination is increased in presence of retinoic acid. Deubiquitinated by USP7; leading to its nuclear exclusion. Monoubiquitination of one of either Lys-13 and Lys-289 amino acid is sufficient to modulate PTEN compartmentalization. Ubiquitinated by XIAP/BIRC4.

Subcellular Location:

Cytoplasm. Nucleus. Nucleus>PML body.
Note: Monoubiquitinated form is nuclear. Nonubiquitinated form is cytoplasmic. Colocalized with PML and USP7 in PML nuclear bodies (PubMed:18716620). XIAP/BIRC4 promotes its nuclear localization (PubMed:19473982).

Secreted.
Note: May be secreted via a classical signal peptide and reenter into cells with the help of a poly-Arg motif.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.

Subunit Structure:

Monomer. The unphosphorylated form interacts with the second PDZ domain of AIP1 and with DLG1 and MAST2 in vitro. Interacts with MAGI2, MAGI3, MAST1 and MAST3, but neither with MAST4 nor with DLG5; interaction with MAGI2 increases protein stability. Interacts with NEDD4. Interacts with NDFIP1 and NDFIP2; in the presence of NEDD4 or ITCH, this interaction promotes PTEN ubiquitination. Interacts (via C2 domain) with FRK. Interacts with USP7; the interaction is direct. Interacts with ROCK1 (By similarity). Interacts with XIAP/BIRC4. Interacts with STK11; the interaction phosphorylates PTEN. Interacts with PPP1R16B. Interacts with NOP53; regulates PTEN phosphorylation and increases its stability.

Family&Domains:

The C2 domain binds phospholipid membranes in vitro in a Ca(2+)-independent manner; this binding is important for its tumor suppressor function.

Belongs to the PTEN phosphatase protein family.

Research Fields

· Cellular Processes > Cell growth and death > p53 signaling pathway.   (View pathway)

· Cellular Processes > Transport and catabolism > Autophagy - animal.   (View pathway)

· Cellular Processes > Cell growth and death > Cellular senescence.   (View pathway)

· Cellular Processes > Cellular community - eukaryotes > Focal adhesion.   (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 > mTOR signaling pathway.   (View pathway)

· Environmental Information Processing > Signal transduction > PI3K-Akt signaling pathway.   (View pathway)

· Human Diseases > Drug resistance: Antineoplastic > EGFR tyrosine kinase inhibitor resistance.

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

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Cancers: Overview > Pathways in cancer.   (View pathway)

· Human Diseases > Cancers: Overview > MicroRNAs in cancer.

· 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 > 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: Overview > Central carbon metabolism in cancer.   (View pathway)

· Metabolism > Carbohydrate metabolism > Inositol phosphate metabolism.

References

1). Melatonin prevents cyclophosphamide-induced primordial follicle loss by inhibiting ovarian granulosa cell apoptosis and maintaining AMH expression. Frontiers in Endocrinology, 2022 (PubMed: 35992124) [IF=5.2]

Application: WB    Species: Mice    Sample:

Figure 3 Effect of Mel on expression of AMH and oxidative stress in ovaries of six-week-old female mice 14 days after Cyc chemotherapy (Day 18). (A) AMH was expressed in granulosa cells of secondary and early antral follicles in Sal, Cyc, Mel, and Mel + Cyc groups (n = 6). Bar = 200 μm. (B) Cyc combined with Mel therapy prevented the decrease of serum AMH and LH levels but there was no significant change in serum FSH levels (n = 6). (C) Biochemical analysis of the ovarian CAT, SOD activities, and MDA levels (n = 6). (D) Phosphorylation levels of PTEN and FOXO3a did not change significantly after treatment with Cyc and Mel (n = 6). a,b Values with different letters are significantly different from each other.

2). β-elemene alleviates esophageal fibrosis after endoscopic submucosal dissection via the FAP-mediated PTEN-PI3K/AKT signaling pathway. Heliyon, 2024 (PubMed: 38807882) [IF=4.0]

Application: WB    Species: Human    Sample: PHEGFs

Fig. 3 β-elemene suppressed the proliferation and promoted the apoptosis of PHEGFs. (A) Endoscopic view after ESD and PHEGFs culture at different stages. (B) The primary cells were identified as fibroblasts by immunocytochemistry. (C) Flow cytometry detection of PHEGFs apoptosis rate after β-elemene intervention (n = 3). (D) CCK-8 to assess the proliferation of PHEGFs after β-elemene intervention (n = 3). (E) Flod change of FAP, p-PTEN, p-PI3K, and p-AKT (n = 3).*P < 0.05 versus the control group.

3). MicroRNA‑21‑5p acts via the PTEN/Akt/FOXO3a signaling pathway to prevent cardiomyocyte injury caused by high glucose/high fat conditions. Experimental and Therapeutic Medicine, 2022 (PubMed: 35222707) [IF=2.7]

Application: WB    Species: Rat    Sample: H9c2 cells

Figure 2 Effects of high levels of glucose and fat on expression of apoptosis-related and PTEN/Akt/FOXO3a proteins in H9c2 cells. **P<0.01 compared with the control group (n=6 in each group). HG-HF, high glucose-high fat; p-, phosphorylated.

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