In Stock Cell Lines
Homo sapiens (Human)
Breast (mammary gland)
Adherent
The PTPN11 Knockout T-47D Cell Line is a CRISPR/Cas9-edited human knockout cell line that eliminates SHP2 tyrosine phosphatase function in ER-positive T-47D breast cancer cells. SHP2 transduces signals from receptors such as EGFR and HER2 through GRB2/SOS to activate RAS-MAPK and PI3K-AKT cascades, driving proliferation via ERK, AKT, and downstream effectors like cyclin D1. This model enables dissection of hormone receptor?Cgrowth factor crosstalk, pathway interrogation, and drug resistance studies in breast cancer. It is ideal for assays including Western blotting, proliferation measurements, and phospho-protein analysis, supporting research into SHP2-dependent oncogenic signaling.
ARSF Knockout HAP1 Polyclonal Cells
Cat. No. ARG21910
LYN Knockout HT29 Polyclonal Cells
Cat. No. ARG13843
FIBP Knockout A549 Polyclonal Cells
Cat. No. ARG10159
DNAJC1 Knockout HAP1 Polyclonal Cells
Cat. No. ARG39165
MCOLN1 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7251
DGCR2 Knockout 786-O Polyclonal Cells
Cat. No. ARG5681
The PTPN11 Knockout T-47D Cell Line is a human knockout cell line generated by CRISPR/Cas9-mediated disruption of the PTPN11 gene in T-47D epithelial cells. This loss-of-function model enables the study of SHP2 phosphatase in a hormone-responsive breast cancer context. The product is supplied as a live cell stock for expansion and experimental use.
T-47D is a hypotetraploid human breast ductal carcinoma cell line derived from a pleural effusion metastasis. It expresses estrogen receptor (ER), progesterone receptor (PR), and androgen receptor (AR), making it a widely used model for ER-positive breast cancer. These cells retain signaling dependencies on hormone receptors and growth factor pathways, which are coordinated in part by SHP2.
PTPN11 encodes SHP2, a non-receptor tyrosine phosphatase that acts as a crucial positive signal transducer downstream of receptor tyrosine kinases (RTKs) and cytokine receptors. Following activation by upstream regulators such as EGFR, HER2, PDGFR, FGFR, cytokines, and integrins, SHP2 associates with scaffold proteins GAB1, GAB2, and IRS-1, recruits GRB2, and activates SOS1-mediated RAS signaling. This triggers the RAF-MEK-ERK cascade and concurrently engages PI3K-AKT signaling via the p85 subunit. SHP2 also interfaces with JAK-STAT pathways, promoting transcription of cyclin D1 and c-FOS through ERK and STAT3. Thus, SHP2 amplifies proliferative and survival signals from diverse extracellular inputs.
Within T-47D cells, SHP2 integrates signals from hormone receptors and RTKs to drive ER-positive breast cancer growth. PTPN11 knockout disrupts RAS-MAPK and PI3K-AKT activation, reducing downstream phosphorylation of ERK and AKT, diminishing cyclin D1 expression, and impairing hormone-driven proliferation. Consequently, this knockout line serves as a precise tool to dissect SHP2-dependent mechanisms in hormone receptor signaling crosstalk and to evaluate its role in oncogenic transformation and drug resistance.
This cell line is suitable for investigating breast cancer signal transduction, SHP2 functional dynamics, and therapeutic resistance. Representative applications include Western blotting for phospho-ERK and phospho-AKT, cell proliferation and colony formation assays, migration assays, immunofluorescence, RT-qPCR for target gene expression, and drug sensitivity profiling against endocrine agents or kinase inhibitors. It also provides a cellular framework for studying SHP2-related pathologies such as Noonan syndrome and juvenile myelomonocytic leukemia within solid tumor biology. For additional information, please contact Ascent Research.
