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Key Documents

SAB4300044

Sigma-Aldrich

Anti-phospho-PTEN (pSer380/pThr382/pThr383) antibody produced in rabbit

affinity isolated antibody

Synonyme(s) :

Anti-10q23del antibody produced in rabbit, Anti-BZS antibody produced in rabbit, Anti-MGC11227 antibody produced in rabbit, Anti-MHAM antibody produced in rabbit, Anti-phosphatase and tensin homolog antibody produced in rabbit

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About This Item

Numéro MDL:
Code UNSPSC :
12352203
Nomenclature NACRES :
NA.41

Source biologique

rabbit

Niveau de qualité

Conjugué

unconjugated

Forme d'anticorps

affinity isolated antibody

Type de produit anticorps

primary antibodies

Clone

polyclonal

Forme

buffered aqueous solution

Poids mol.

~54 kDa

Espèces réactives

human, rat, mouse

Concentration

1 mg/mL

Technique(s)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): 1:50-1:100
indirect immunofluorescence: 1:100-1:200
western blot: 1:500-1:1000

Isotype

IgG

Séquence immunogène

(R-Y-SP-D-TP-TP-D-S)

Numéro d'accès NCBI

Numéro d'accès UniProt

Conditions d'expédition

wet ice

Température de stockage

−20°C

Modification post-traductionnelle de la cible

phosphorylation (pSer380/pThr382/pThr383)

Informations sur le gène

human ... PTEN(5728)

Immunogène

Peptide sequence around phosphorylation site of threonine 380/382/383 (R-Y-S(p)-D-T(p)-T(p)-D-S), according to the protein PTEN.

Caractéristiques et avantages

Evaluate our antibodies with complete peace of mind. If the antibody does not perform in your application, we will issue a full credit or replacement antibody. Learn more.

Description de la cible

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. May be a negative regulator of insulin signaling and glucose metabolism in adipose tissue.

Forme physique

Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol

Clause de non-responsabilité

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.

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Code de la classe de stockage

10 - Combustible liquids

Classe de danger pour l'eau (WGK)

WGK 1

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


Certificats d'analyse (COA)

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Consulter la Bibliothèque de documents

Prerna Malaney et al.
Cell cycle (Georgetown, Tex.), 17(8), 947-962 (2017-11-08)
PTEN phosphorylation at its C-terminal (C-tail) serine/threonine cluster negatively regulates its tumor suppressor function. However, the consequence of such inhibition and its downstream effects in driving lung cancer remain unexplored. Herein, we ascertain the molecular mechanisms by which phosphorylation compromises
Kasra Khalaj et al.
American journal of respiratory and critical care medicine, 206(4), 476-487 (2022-06-08)
Rationale: Pulmonary hypoplasia secondary to congenital diaphragmatic hernia is characterized by reduced branching morphogenesis, which is responsible for poor clinical outcomes. Administration of amniotic fluid stem cell extracellular vesicles (AFSC-EVs) rescues branching morphogenesis in rodent fetal models of pulmonary hypoplasia.
Lili Liu et al.
Bioscience reports, 40(5) (2020-05-19)
The present study aims to reveal the molecular mechanism of peroxisome proliferator-activated receptor γ (PPARγ) on sepsis-induced acute lung injury (ALI). To do that, the rat injury model was established using cecal ligation and perforation (CLP) method, followed by different

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