phosphatase and tensin homolog (mutated in multiple advanced cancers 1).
phosphatase and tensin homolog
Mutated in multiple advanced cancers 1
MMAC1 phosphatase and tensin homolog deleted on chromosome 10
Background Information
PTEN acts as a dual-specificity protein phosphatase, dephosphorylating tyrosine-, serine- and threonine- phosphorylated proteins. It 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. PTEN 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. It dephosphorylates tyrosine-phosphorylated focal adhesion kinase and inhibits cell migration and integrin-mediated cell spreading and focal adhesion formation. PTEN may be a negative regulator of insulin signaling and glucose metabolism in adipose tissue. Recent research shows a role for PTEN in addiction.
Product Information
Format
Purified
Control
MCF7 cells
Presentation
Rabbit monoclonal IgG in buffer containing 60% storage buffer (50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 0.01% sodium azide and 0.05% BSA) and 40% glycerol.
Applications
Application
Please note that this product will not be available for sale after March 15, 2015. Please select one of the other antibodies against this target. Anti-PTEN Rabbit Antibody detects level of PTEN & has been published & validated for use in FC, IF, IH, IH(P), IP & WB.
Key Applications
Western Blotting
Flow Cytometry
Immunofluorescence
Immunohistochemistry
Immunohistochemistry (Paraffin)
Immunoprecipitation
Application Notes
Immunoprecipitation:
A 1:50 dilution of a previous lot of this antibody immunoprecipitated PTEN from MCF-7 cell lysate using protein G:agarose beads.
Flow Cytometry:
A 1:20 dilution of a previous lot of this antibody stained cells for intracellular staining for flow cytometry analysis.
Immunohistochemistry:
A 1:50 dilution of a previous lot of this antibody was used for detection of PTEN in immunohistochemical analysis of paraffin-embedded human thyroid gland carcinoma.
Immunfluorescence Staining:
1:50 dilution of a previous lot of this antibody was used for Immunfluorescence staining of paraformaldehyde fixed cells.
Biological Information
Immunogen
KLH-conjugated synthetic peptide corresponding to the C-terminal region of human PTEN.
Epitope
C-terminus
Host
Rabbit
Specificity
This antibody recognizes the C-terminal domain of PTEN.
This gene was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency. The protein encoded this gene is a phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase. It contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, this protein preferentially dephosphorylates phosphoinositide substrates. It negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells and functions as a tumor suppressor by negatively regulating AKT/PKB signaling pathway.
FUNCTION: SwissProt: P60484 # 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.
COFACTOR: Magnesium.
SIZE: 403 amino acids; 47166 Da
SUBUNIT: Monomer. The unphosphorylated form interacts with the second PDZ domain of AIP1 and with DLG1 and MAST2 in vitro.
SUBCELLULAR LOCATION: Cytoplasm.
TISSUE SPECIFICITY: Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.
DOMAIN: SwissProt: P60484 The C2 domain binds phospholipid membranes in vitro in a Ca(2+)-independent manner; this binding is important for its tumor suppressor function.
PTM: Phosphorylation results in an inhibited activity towards PIP3. Phosphorylation can both inhibit and promote PDZ-binding.
DISEASE: SwissProt: P60484 # Mutations of PTEN are found in a large number of cancers. & Defects 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-Riley-Smith 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 squamous cell carcinoma of the head and neck (HNSCC) [MIM:275355]. & Defects in PTEN are a cause of susceptibility to endometrial cancer [MIM:608089]. & Defects in PTEN are a cause of Proteus syndrome [MIM:176920]. Proteus syndrome is a hamartomatous disorder characterized by overgrowth of multiple tissues, connective tissue and epidermal naevi, and vascular malformations. These presentations are usually apparent at birth or soon after and continue to develop as the patient ages. It is named after the Greek god Proteus who, legend has it, could change his shape at will to avoid capture. Tumors, mostly benign but some malignant, have also been reported in Proteus syndrome, generally presenting by the age of 20 years and including papillary adenocarcinoma of the testis, meningioma, and cystadenoma of the ovaries. & Defects in PTEN are a cause of oligodendroglioma [MIM:137800]; also called oligodendroblastoma or familial glioma of brain. Oligodendroglioma is a usually benign neoplasm derived from and composed of oligodendrogliocytes in varying stages of differentiation. The majority are seen in adults in the white matter of the brain. & Defects in PTEN are a cause of VACTERL association with hydrocephalus [MIM:276950]; which includes also VATER association with hydrocephalus. 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 are involved in prostate cancer [MIM:176807]. & Defects in PTEN are a cause of macrocephaly/autism syndrome [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).
Western Blot Analysis:
A 1:500 dilution of the lot detected endogenous PTEN in lysates from MCF7 cells.
Usage Statement
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.
Storage and Shipping Information
Storage Conditions
Stable for 1 year at -20ºC from date of receipt.
Handling Recommendations:
Upon first thaw, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerol-containing solutions to become frozen during storage.
Packaging Information
Material Size
100 µL
原厂资料：
Key Spec Table
Species Reactivity
Key Applications
Host
Format
Antibody Type
R, H, M
WB, FC, IF, IHC, IH(P), IP
Rb
Purified
Monoclonal Antibody
Description
Catalogue Number
04-409
Brand Family
Upstate
Trade Name
Upstate
Description
Anti-PTEN rabbit monoclonal Antibody
Alternate Names
phosphatase and tensin homolog (mutated in multiple advanced cancers 1).
phosphatase and tensin homolog
Mutated in multiple advanced cancers 1
MMAC1 phosphatase and tensin homolog deleted on chromosome 10
Background Information
PTEN acts as a dual-specificity protein phosphatase, dephosphorylating tyrosine-, serine- and threonine- phosphorylated proteins. It 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. PTEN 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. It dephosphorylates tyrosine-phosphorylated focal adhesion kinase and inhibits cell migration and integrin-mediated cell spreading and focal adhesion formation. PTEN may be a negative regulator of insulin signaling and glucose metabolism in adipose tissue. Recent research shows a role for PTEN in addiction.
Product Information
Format
Purified
Control
MCF7 cells
Presentation
Rabbit monoclonal IgG in buffer containing 60% storage buffer (50 mM Tris-Glycine (pH 7.4), 0.15 M NaCl, 0.01% sodium azide and 0.05% BSA) and 40% glycerol.
Applications
Application
Please note that this product will not be available for sale after March 15, 2015. Please select one of the other antibodies against this target. Anti-PTEN Rabbit Antibody detects level of PTEN & has been published & validated for use in FC, IF, IH, IH(P), IP & WB.
Key Applications
Western Blotting
Flow Cytometry
Immunofluorescence
Immunohistochemistry
Immunohistochemistry (Paraffin)
Immunoprecipitation
Application Notes
Immunoprecipitation:
A 1:50 dilution of a previous lot of this antibody immunoprecipitated PTEN from MCF-7 cell lysate using protein G:agarose beads.
Flow Cytometry:
A 1:20 dilution of a previous lot of this antibody stained cells for intracellular staining for flow cytometry analysis.
Immunohistochemistry:
A 1:50 dilution of a previous lot of this antibody was used for detection of PTEN in immunohistochemical analysis of paraffin-embedded human thyroid gland carcinoma.
Immunfluorescence Staining:
1:50 dilution of a previous lot of this antibody was used for Immunfluorescence staining of paraformaldehyde fixed cells.
Biological Information
Immunogen
KLH-conjugated synthetic peptide corresponding to the C-terminal region of human PTEN.
Epitope
C-terminus
Host
Rabbit
Specificity
This antibody recognizes the C-terminal domain of PTEN.
This gene was identified as a tumor suppressor that is mutated in a large number of cancers at high frequency. The protein encoded this gene is a phosphatidylinositol-3,4,5-trisphosphate 3-phosphatase. It contains a tensin like domain as well as a catalytic domain similar to that of the dual specificity protein tyrosine phosphatases. Unlike most of the protein tyrosine phosphatases, this protein preferentially dephosphorylates phosphoinositide substrates. It negatively regulates intracellular levels of phosphatidylinositol-3,4,5-trisphosphate in cells and functions as a tumor suppressor by negatively regulating AKT/PKB signaling pathway.
FUNCTION: SwissProt: P60484 # 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.
COFACTOR: Magnesium.
SIZE: 403 amino acids; 47166 Da
SUBUNIT: Monomer. The unphosphorylated form interacts with the second PDZ domain of AIP1 and with DLG1 and MAST2 in vitro.
SUBCELLULAR LOCATION: Cytoplasm.
TISSUE SPECIFICITY: Expressed at a relatively high level in all adult tissues, including heart, brain, placenta, lung, liver, muscle, kidney and pancreas.
DOMAIN: SwissProt: P60484 The C2 domain binds phospholipid membranes in vitro in a Ca(2+)-independent manner; this binding is important for its tumor suppressor function.
PTM: Phosphorylation results in an inhibited activity towards PIP3. Phosphorylation can both inhibit and promote PDZ-binding.
DISEASE: SwissProt: P60484 # Mutations of PTEN are found in a large number of cancers. & Defects 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-Riley-Smith 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 squamous cell carcinoma of the head and neck (HNSCC) [MIM:275355]. & Defects in PTEN are a cause of susceptibility to endometrial cancer [MIM:608089]. & Defects in PTEN are a cause of Proteus syndrome [MIM:176920]. Proteus syndrome is a hamartomatous disorder characterized by overgrowth of multiple tissues, connective tissue and epidermal naevi, and vascular malformations. These presentations are usually apparent at birth or soon after and continue to develop as the patient ages. It is named after the Greek god Proteus who, legend has it, could change his shape at will to avoid capture. Tumors, mostly benign but some malignant, have also been reported in Proteus syndrome, generally presenting by the age of 20 years and including papillary adenocarcinoma of the testis, meningioma, and cystadenoma of the ovaries. & Defects in PTEN are a cause of oligodendroglioma [MIM:137800]; also called oligodendroblastoma or familial glioma of brain. Oligodendroglioma is a usually benign neoplasm derived from and composed of oligodendrogliocytes in varying stages of differentiation. The majority are seen in adults in the white matter of the brain. & Defects in PTEN are a cause of VACTERL association with hydrocephalus [MIM:276950]; which includes also VATER association with hydrocephalus. 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 are involved in prostate cancer [MIM:176807]. & Defects in PTEN are a cause of macrocephaly/autism syndrome [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).
Western Blot Analysis:
A 1:500 dilution of the lot detected endogenous PTEN in lysates from MCF7 cells.
Usage Statement
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.
Storage and Shipping Information
Storage Conditions
Stable for 1 year at -20ºC from date of receipt.
Handling Recommendations:
Upon first thaw, and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance. Note: Variability in freezer temperatures below -20°C may cause glycerol-containing solutions to become frozen during storage.
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