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Key Documents

SAB4300044

Sigma-Aldrich

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

affinity isolated antibody

Synonym(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

MDL number:
MFCD02097285
UNSPSC Code:
12352203
NACRES:
NA.41

biological source

rabbit

Quality Level

100

conjugate

unconjugated

antibody form

affinity isolated antibody

antibody product type

primary antibodies

clone

polyclonal

form

buffered aqueous solution

mol wt

~54 kDa

species reactivity

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

immunogen sequence

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

NCBI accession no.

NP_000305.3

UniProt accession no.

P60484

shipped in

wet ice

storage temp.

−20°C

target post-translational modification

phosphorylation (pSer380/pThr382/pThr383)

Gene Information

human ... PTEN(5728)

Immunogen

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.

Features and Benefits

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.

Target description

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.

Physical form

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

Disclaimer

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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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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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