Anti-PTEN (phospho T366 + S370) antibody [EP229] (ab109454)
- Product nameAnti-PTEN (phospho T366 + S370) antibody [EP229]See all PTEN primary antibodies ...
- DescriptionRabbit monoclonal [EP229] to PTEN (phospho T366 + S370)
- Specificityab109454 only detects PTEN phosphorylated on T366 or S370.
- Tested applicationsWB, IP, IHC-P, ICC more details
- Species reactivityReacts with: Human
Does not react withMouse, Rat
A phospho-specific peptide corresponding to residues surrounding Threonine 366 and Serine 370 of Human PTEN.
- Positive controlHeLa cell lysates, treated with Calyculin A; Human breast ductal carcinoma tissue.
- General notesProduced under U.S. Patent No. 5,675,063.
- Storage instructionsStore at -20°C. Stable for 12 months at -20°C
- Storage bufferPBS 49%,Sodium azide 0.01%,Glycerol 50%,BSA 0.05%
- PurityTissue culture supernatant
- Clonality Monoclonal
- Clone numberEP229
Our Abpromise guarantee covers the use of ab109454 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||WB: 1/1000 - 1/10000. Detects a band of approximately 54 kDa (predicted molecular weight: 47 kDa).|
|IHC-P||IHC-P: 1/100 - 1/250. Perform heat mediated antigen retrieval before commencing with IHC staining protocol.|
|ICC||ICC: 1/100 - 1/250.|
- FunctionTumor 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.
- Tissue specificityExpressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.
- Involvement in diseaseDefects in PTEN are a cause of Cowden disease (CD) [MIM:158350]; also known as Cowden syndrome (CS). CD is an autosomal dominant cancer predisposition syndrome associated with elevated risk for tumors of the breast, thyroid and skin. The predominant phenotype for CD is multiple hamartoma syndrome, in many organ systems including the breast (70% of CD patients), thyroid (40-60%), skin, CNS (40%), gastrointestinal tract. Affected individuals are at an increased risk of both breast and thyroid cancers. Trichilemmomas (benign tumors of the hair follicle infundibulum), and mucocutaneous papillomatosis (99%) are hallmarks of CD.
Defects in PTEN are the cause of Lhermitte-Duclos disease (LDD) [MIM:158350]; also known as cerebelloparenchymal disorder VI. LDD is characterized by dysplastic gangliocytoma of the cerebellum which often results in cerebellar signs and seizures. LDD and CD seem to be the same entity, and are considered as hamartoma-neoplasia syndromes.
Defects in PTEN are a cause of Bannayan-Zonana syndrome (BZS) [MIM:153480]; also known as Ruvalcaba-Myhre-Smith syndrome (RMSS) or Bannayan-Riley-Ruvalcaba syndrome (BRRS). In BZS there seems not to be an increased risk of malignancy. It has a partial clinical overlap with CD. BZS is characterized by the classic triad of macrocephaly, lipomatosis and pigmented macules of the gland penis.
Defects in PTEN are a cause of head and neck squamous cell carcinomas (HNSCC) [MIM:275355]; also known as squamous cell carcinoma of the head and neck.
Defects in PTEN are a cause of susceptibility to endometrial cancer [MIM:608089].
Note=PTEN mutations are found in a subset of patients with Proteus syndrome, a genetically heterogeneous condition. The molecular diagnosis of PTEN mutation positive cases classifies Proteus syndrome patients as part of the PTEN hamartoma syndrome spectrum. As such, patients surviving the early years of Proteus syndrome are likely at a greater risk of developing malignancies.
Defects in PTEN are a cause of susceptibility to glioma type 2 (GLM2) [MIM:613028]. Gliomas are central nervous system neoplasms derived from glial cells and comprise astrocytomas, glioblastoma multiforme, oligodendrogliomas, and ependymomas.
Defects in PTEN are a cause of VACTERL association with hydrocephalus (VACTERL-H) [MIM:276950]. VACTERL is an acronym for vertebral anomalies, anal atresia, congenital cardiac disease, tracheoesophageal fistula, renal anomalies, radial dysplasia, and other limb defects.
Defects in PTEN may be a cause of susceptibility to prostate cancer (PC) [MIM:176807]. It is a malignancy originating in tissues of the prostate. Most prostate cancers are adenocarcinomas that develop in the acini of the prostatic ducts. Other rare histopathologic types of prostate cancer that occur in approximately 5% of patients include small cell carcinoma, mucinous carcinoma, prostatic ductal carcinoma, transitional cell carcinoma, squamous cell carcinoma, basal cell carcinoma, adenoid cystic carcinoma (basaloid), signet-ring cell carcinoma and neuroendocrine carcinoma.
Defects in PTEN are a cause of macrocephaly/autism syndrome (MCEPHAS) [MIM:605309]. Patients have autism spectrum disorders and macrocephaly, with head circumferences ranging from +2.5 to +8 SD for age and sex (average head circumference +4.0 SD).
Note=A microdeletion of chromosome 10q23 involving BMPR1A and PTEN is a cause of chromosome 10q23 deletion syndrome, which shows overlapping features of the following three disorders: Bannayan-Zonana syndrome, Cowden disease and juvenile polyposis syndrome.
- Sequence similaritiesContains 1 C2 tensin-type domain.
Contains 1 phosphatase tensin-type domain.
- DomainThe C2 domain binds phospholipid membranes in vitro in a Ca(2+)-independent manner; this binding is important for its tumor suppressor function.
modificationsPhosphorylated in vitro by MAST1, MAST2 and MAST3. 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.
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 comportmentalization.
- Cellular localizationCytoplasm. Nucleus. Nucleus > PML body. Monoubiquitinated form is nuclear. Nonubiquitinated form is cytoplasmic. Colocalized with PML and USP7 in PML nuclear bodies.
- 10q23del antibody5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN antibodyBZS antibody
- DEC antibodyGLM2 antibodyMGC11227 antibodyMHAM antibodyMMAC1 antibodyMMAC1 phosphatase and tensin homolog deleted on chromosome 10 antibodyMutated in multiple advanced cancers 1 antibodyPhosphatase and tensin homolog antibodyPhosphatase and tensin like protein antibodyPhosphatidylinositol-3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN antibodyPten antibodyPTEN_HUMAN antibodyPTEN1 antibodyTEP1 antibody
Anti-PTEN (phospho T366 + S370) antibody [EP229] images
All lanes : Anti-PTEN (phospho T366 + S370) antibody [EP229] (ab109454) at 1/1000 dilution
Lane 1 : HeLa cell lysates, untreated
Lane 2 : HeLa cell lysates, treated with Calyculin A
Lysates/proteins at 10 µg per lane.
Predicted band size : 47 kDa
Observed band size : 54 kDa (why is the actual band size different from the predicted?)
ab109454 at 1/100 dilution staining PTEN in Human breast ductal carcinoma by Immunohistochemistry, Paraffin-embedded tissue.