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P6244

Sigma-Aldrich

Protein Tyrosine Phosphatase 1B human

recombinant, expressed in E. coli

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Synonym(s):
PTP-1B
MDL number:

recombinant

expressed in E. coli

Quality Level

form

solution

specific activity

≥20 units/mg protein

mol wt

37.4 kDa

concentration

≥0.5 mg/mL

UniProt accession no.

relevant disease(s)

diabetes; obesity; cancer

shipped in

dry ice

storage temp.

−70°C

Gene Information

human ... PTPN1(5770)

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This Item
SRP0212SRP0216SRP5074
Sigma-Aldrich

Sigma-Aldrich

SRP0216

SHP-1 Active human

form

solution

form

aqueous solution

form

aqueous solution

form

buffered aqueous glycerol solution

specific activity

≥20 units/mg protein

specific activity

-

specific activity

-

specific activity

2040-2760 nmol/min·mg

mol wt

37.4 kDa

mol wt

63.3 kDa

mol wt

95 kDa

mol wt

~61 kDa

concentration

≥0.5 mg/mL

concentration

0.84 mg/mL

concentration

1 mg/mL

concentration

-

UniProt accession no.

P18031

UniProt accession no.

P18031

UniProt accession no.

P29350

UniProt accession no.

-

General description

Protein tyrosine phosphatase 1B human (PTP1B) is encoded by the gene PTPN1. In human chromosome, the gene PTPN1 is localized on 20q13.13. The protein has 37 kDa catalytic domain and the C-terminal hydrophobic residues targets the protein to the cytoplasmic side of the endoplasmic reticulum membrane.

Application

Protein Tyrosine Phosphatase 1B (PTP1B) human has been used in treating cell lysate prior to immunoprecipitation and protein pull-down studies. It has also been used in PTP1B activity assay and also for the evaluation of inhibitors like betulinic acid (BA) and sodium orthovanadate (Na3VO4), and 6-chloro-3-formyl-7-methylchromone (CFM) on PTP1B.
Protein tyrosine phosphatase 1B (PTP1B) is a pharmaceutical target used to study the treatment of various diseases such as obesity, cancer and type II diabetes mellitus.
The inhibitory effect of 8-(4-chlorophenylthio)-cAMP and 8-(4-chlorophenylthio)-cGMP on protein tyrosine phosphatase-1B has been assayed.

Biochem/physiol Actions

PTP-1B is a recombinant, non-transmembrane protein expressed in E. coli containing amino acid residues 1-322 of human PTP-1B. It has a molecular mass of 37.4 kDa. It is an abundant intracellular enzyme that is thought to act as a negative regulator of certain signaling pathways. It dephosphorylates tyrosine-phosphorylated proteins and peptides, and is usually localized in the cytostolic domain of the ER.
PTP1B dephosphorylates c-Src in several human breast cancer cell lines has a regulatory role for PTP1B in the control of c-Src kinase activity. PTP1B is regulates the cardiovascular effects of leptin. PTP1B controls the JAK/STAT signaling pathway by dephosphorylation of JAK2.
Polymorphism in the gene PTPN1 is associated with type 2 diabetes and obesity.

Unit Definition

One unit will hydrolyze 1.0 μmole of a phosphopeptide, EGFR fragment 988-998, per minute at pH 7.2 at 30 °C

Physical form

Supplied as a solution in 50 mM HEPES (pH 7.2), 1 mM EDTA, 5 mM DTT, and 0.05% NP-40

Storage Class Code

12 - Non Combustible Liquids

WGK

WGK 1

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


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p66Shc couples mechanical signals to RhoA through FAK-dependent recruitment of p115-RhoGEF and GEF-H1
Wu RF, et al.
Molecular and Cellular Biology, MCB-00194 (2016)
A colorimetric biosensor based on guanidinium recognition for the assay of protein tyrosine phosphatase 1B and its inhibitors
Lv J, et al.
New. J. Chem., 41(23), 14414-14419 (2017)
Analysis of common PTPN1 gene variants in type 2 diabetes, obesity and associated phenotypes in the French population
Cheyssac C, et al.
BMC Medical Genetics, 7(1), 44-44 (2006)
Shaowei Wang et al.
Frontiers in microbiology, 12, 715773-715773 (2021-08-03)
Human PTEN, a dual-phosphatase tumor suppressor, is frequently dysregulated by alternative splicing. Fungi harbor PTEN homologs, but alternative splicing of fungal PTENs has not been reported as far as we know. Here, we described an alternative splicing case in the
PTP1B: from the sidelines to the front lines!
Tonks NK
Febs Letters, 546(1), 140-148 (2003)

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