In Stock Cell Lines
The SETD2 Knockout MeT-5A Cell Line is a CRISPR/Cas9-edited knockout cell line derived from human pleural mesothelial MeT-5A cells, providing a loss-of-function model for SETD2, the histone methyltransferase that catalyzes H3K36me3. Disruption of SETD2 impairs transcriptional elongation, DNA mismatch repair, and alternative splicing, contributing to genomic instability. SETD2 functions in complexes with RNA Polymerase II, MSH2/MSH6, and hnRNP L, and is regulated by p53. This knockout line is highly relevant for mesothelioma research, DNA damage repair studies, and epigenetic regulation, with applications including Western blotting for H3K36me3, immunofluorescence for ??H2AX foci, and RNA-seq for splicing analysis. For additional information, please contact Ascent Research.
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The SETD2 Knockout MeT-5A Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the MeT-5A human pleural mesothelial cell line, with targeted disruption of the SETD2 gene. This loss-of-function model eliminates SETD2 protein expression, enabling reproducible analysis without transient silencing artifacts. The knockout was generated via CRISPR/Cas9-mediated gene disruption, ensuring specific ablation of SETD2 function within the native host cell background. This product is suitable for applications in cancer biology, epigenetics, and DNA repair research.
The parental MeT-5A line originates from human pleural mesothelial cells immortalized with SV40 large T-antigen. These non-tumorigenic cells retain key mesothelial characteristics: forming protective monolayers, secreting glycosaminoglycans and surfactant, and mediating inflammatory and fibrotic responses. SV40 immortalization permits continuous culture without full transformation, making MeT-5A an ideal model for early events in mesothelial biology and malignant conversion. This background is particularly relevant for mesothelioma research, as pleural mesothelial cells are targets of asbestos-induced carcinogenesis.
SETD2 encodes a histone methyltransferase that trimethylates H3K36, a mark coordinating transcriptional elongation, DNA mismatch repair, and alternative splicing. H3K36me3 facilitates RNA Polymerase II elongation via SUPT6H and IWS1, recruits the mismatch repair complex MSH2/MSH6, and influences splicing through hnRNP L and the FACT complex. SETD2 is regulated by p53 and DNA damage kinases ATM/ATR, and promotes expression of p53 targets like p21 and BAX. Loss of SETD2 impairs these processes, leading to increased mutation rates, aberrant splicing, and genomic instability.
In pleural mesothelial cells, SETD2 knockout is significant for dissecting asbestos-induced carcinogenesis. MeT-5A cells provide a non-malignant platform to study how SETD2 deficiency promotes transformation. Loss of H3K36me3 compromises DNA repair, allowing mutation accumulation upon genotoxic exposure. This model recapitulates genetic alterations seen in mesothelioma and enables investigation of interactions with p53 signaling and epithelial-mesenchymal transition pathways relevant to tumor progression.
This knockout cell line supports diverse experiments: Western blotting for global H3K36me3, RT-qPCR for p53 targets, and RNA-seq for splicing analysis. Immunofluorescence for ??H2AX foci visualizes DNA breaks; cell viability and flow cytometry assays probe stress responses and apoptosis. ChIP-qPCR maps H3K36me3 enrichment, and comet assay quantifies DNA damage. Applications include mesothelioma research, epigenetics, and drug sensitivity studies. For further details, contact Ascent Research.
