In Stock Cell Lines
Homo sapiens (Human)
Breast (mammary gland)
Adherent
The PTPN11 Knockout BT-549 Cell Line is a CRISPR/Cas9-edited human knockout model in which the PTPN11 gene encoding the SHP-2 phosphatase has been disrupted. Derived from a triple-negative breast cancer (TNBC) epithelial line with mesenchymal features, this tool enables loss-of-function studies of SHP-2 in an aggressive carcinoma context. SHP-2 positively regulates RAS-MAPK, JAK-STAT, and PI3K-AKT pathways downstream of RTKs, and interacts with adaptors such as GAB1 and kinases like ERK. This knockout line supports drug target validation for SHP-2 inhibitors, signaling mechanism dissection, and functional genomics screens. Key assays include western blot for phospho-ERK and migration/invasion tests.
CYBB Knockout 769-P Polyclonal Cells
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MTFR1 Knockout jurkat Polyclonal Cells
Cat. No. ARG13744
CDKN1B Knockout CAL27 Polyclonal Cells
Cat. No. ARG11608
Osr2 Knockout CAL27 Polyclonal Cells
Cat. No. ARG11524
LDHAL6B Knockout Hela Polyclonal Cells
Cat. No. ARG7884
MCCC2 Knockout MES-OV Polyclonal Cells
Cat. No. ARG6398
The PTPN11 Knockout BT-549 Cell Line is a CRISPR/Cas9-edited human knockout cell line that disrupts the PTPN11 gene, encoding the SHP-2 non-receptor tyrosine phosphatase. This loss-of-function model provides a powerful tool for studying SHP-2-dependent signaling in an epithelial carcinoma context. The gene disruption is achieved through targeted CRISPR/Cas9-mediated editing, resulting in loss of functional SHP-2 protein.
The parental BT-549 line originates from a mammary ductal carcinoma of a 72-year-old female and is characterized by a triple-negative phenotype??lacking estrogen receptor, progesterone receptor, and HER2 amplification. These cells exhibit a mesenchymal morphology and invasive properties, making them a representative model for aggressive triple-negative breast cancer (TNBC). They grow as an adherent monolayer and are widely employed to investigate mechanisms of metastasis and therapeutic resistance.
SHP-2 is a ubiquitously expressed protein tyrosine phosphatase that positively regulates RAS-MAPK signaling downstream of RTKs such as EGFR and PDGFR. It is recruited to phosphotyrosine-containing adaptors like GAB1 and GAB2, where it dephosphorylates inhibitory tyrosine residues on SPRED, sustaining ERK activation. SHP-2 also interfaces with JAK-STAT and PI3K-AKT pathways through interactions with JAK2, STAT3, and focal adhesion components paxillin and FAK. Key pathway components include EGFR, GAB1, SHP-2, GRB2, SOS, RAS, RAF, MEK, ERK, and transcription factors ELK-1 and c-Fos.
In BT-549 TNBC cells, SHP-2 activity drives proliferation and migration via sustained ERK and AKT signaling. Disruption of PTPN11 is expected to attenuate these oncogenic processes, impairing tumor cell invasiveness and anchorage-independent growth. Given their mesenchymal characteristics, BT-549 cells rely on integrin-mediated adhesion dynamics, and SHP-2 loss may further compromise this by altering paxillin/FAK signaling. Thus, this knockout line enables targeted investigation of SHP-2 contributions to TNBC aggressiveness.
The PTPN11 Knockout BT-549 Cell Line is ideal for functional analysis of SHP-2 in breast cancer, validation of inhibitors like SHP099, and CRISPR-based screens. Representative assays include western blot for SHP-2 and phospho-ERK, MTS proliferation, transwell migration/invasion, immunofluorescence for paxillin, and RT-qPCR for DUSP6 and ETV5. This model also supports in vivo xenograft studies of tumor growth. For inquiries, contact Ascent Research.
