PTPN1 Knockout BEAS-2B Cell Line

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PTPN1 Knockout BEAS-2B Cell Line
Cat.No.:

EDC90245

Species:

Human

Cell Name:

BEAS-2B

Gene:

PTPN1

Gene ID:

5770

Size:

1×10⁶cells

PTPN1 Knockout BEAS-2B Cell Line is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performotion Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDC90245
Product Name PTPN1 Knockout BEAS-2B Cell Line
Species Human
Cell Line BEAS-2B
Gene ID
Gene PTPN1
Summary
The protein encoded by this gene is the founding member of the protein tyrosine phosphatase (PTP) family, which was isolated and identified based on its enzymatic activity and amino acid sequence. PTPs catalyze the hydrolysis of the phosphate monoesters specifically on tyrosine residues. Members of the PTP family share a highly conserved catalytic motif, which is essential for the catalytic activity. PTPs are known to be signaling molecules that regulate a variety of cellular processes including cell growth, differentiation, mitotic cycle, and oncogenic transformation. This PTP has been shown to act as a negative regulator of insulin signaling by dephosphorylating the phosphotryosine residues of insulin receptor kinase. This PTP was also reported to dephosphorylate epidermal growth factor receptor kinase, as well as JAK2 and TYK2 kinases, which implicated the role of this PTP in cell growth control, and cell response to interferon stimulation. Two transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Jul 2013]
Digestion Time 2 min
Morphology Adherent
Passage Ratio 1:3-1:2，3-5 days
Complete Culture Medium BEGM kit (Lonza/Clonetics，CC-3170)
Freezing Medium 92.5% Complete medium + 7.5% DMSO
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
LociSTR Info (Sample Cell)
Sample Cell Line: BEAS-2B		STR Info (Cell bank)
Cell Line: BEAS-2B
Allele1Allele2Allele1Allele2
Amelogenin X Y X Y
D5S818 12 13 12 13
D13S317 13 13
D7S820 10 13 10 13
D16S539 12 12
vWA 17 18 17 18
TH01 7 9.3 7 9.3
TPOX 6 11 6 11
CSF1PO 9 12 9 12
D19S433 13.2 15.2 13.2 15.2
D21S11 28 30 28 30
D18S51 18 19 18 19
D6S1043 12 18
D3S1358 15 17 15 17
Penta D 2.2 13 2.2 13
D2S441 11 11.3 11 11.3
D8S1179 13 15 13 15
Penta E 5 8 5 8
D12S391 17 18 17 18
D2S1338 22 23 22 23
FGA 20 24 20 24
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.

FAQ

The choice depends on whether you are studying PTPN1 (PTP1B)'s role as the principal negative regulator of insulin and leptin receptor signaling or its emerging functions in cancer biology and airway epithelial signaling. The Knockout line is the standard tool for asking whether PTP1B is required for dephosphorylating IR, IRS-1/2, JAK2, and other RTK substrates — PTP1B is a major therapeutic target for type 2 diabetes and obesity. Overexpression is useful for studying PTP1B's reported tumor-promoting effects in some cancer contexts. For airway epithelial signaling research, the EDITGENE PTP1B Knockout in BEAS-2B is highly relevant — BEAS-2B is a non-tumorigenic human bronchial epithelial cell line, and PTP1B regulates EGFR and other respiratory epithelial RTK signaling. Rescue with wild-type or catalytically-dead (C215S) PTP1B is the standard specificity control. The knockout serves as a critical specificity tool for PTP1B inhibitors (trodusquemine/MSI-1436, JTT-551) in metabolic disease therapeutic development.
Primary applications: • Insulin signaling: phospho-IR, phospho-IRS-1, and phospho-AKT analysis to assess PTP1B's negative regulation of insulin signaling in bronchial epithelial context. • Leptin signaling: phospho-STAT3 analysis given PTP1B's role in dephosphorylating JAK2. • Airway EGFR signaling: phospho-EGFR analysis given PTP1B's role in RTK regulation in respiratory epithelium. • PTP1B inhibitor specificity: critical genetic control for trodusquemine, JTT-551, and other PTP1B-targeting compounds in metabolic disease research. EDITGENE recommends this model for researchers investigating insulin/leptin signaling, airway epithelial biology, and PTP1B-targeted metabolic disease pharmacology.
Yes. PTP1B rescue experiments are well-established for tyrosine phosphatase research: • Construct design: use a codon-modified PTPN1 sequence with a small C-terminal tag (FLAG, HA). PTP1B has N-terminal catalytic phosphatase domain and C-terminal ER-anchoring tail — preserve both elements. • Catalytically-dead rescue: the C215S mutation in the active site cysteine abolishes phosphatase activity and is the standard specificity control. • Substrate-trap rescue: D181A (substrate-trap mutant) generates a catalytically inactive form that retains substrate binding — invaluable for identifying PTP1B substrates by mass spectrometry. • Functional readout: rescue should restore IR, IRS-1, EGFR, and STAT3 dephosphorylation patterns. BEAS-2B is a non-tumorigenic bronchial epithelial cell line — transduction with lentivirus is supported and standard rescue protocols apply.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

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