In Stock Cell Lines
Homo sapiens (Human)
Bone (bone marrow)
Suspension
The BTG2 Knockout TMD8 Cell Line is a CRISPR/Cas9-edited human B lymphocyte cell line with targeted disruption of the BTG2 tumor suppressor gene. Derived from an activated B-cell-like diffuse large B-cell lymphoma (DLBCL) background, this model enables loss-of-function studies of a key p53-regulated antiproliferative factor. BTG2 is transcriptionally induced by TP53 and interacts with CNOT7/CNOT8 and PRMT1 to mediate cell cycle arrest and apoptosis. Applications include studying BTG2-dependent signaling in lymphomagenesis, screening for synthetic lethal interactions, and evaluating compounds that restore p53 function. The model is compatible with proliferation, apoptosis, and omics-based assays for mechanistic and translational research.
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The BTG2 Knockout TMD8 Cell Line is a CRISPR/Cas9-mediated gene disruption model that stably ablates BTG2 expression in the TMD8 human B lymphocyte cell line. This product, provided as a live, ready-to-use knockout cell line, ensures consistent target gene inactivation across passages, avoiding the pitfalls of transient transfection or RNA interference. The constitutive loss-of-function system is ideal for long-term studies of tumor suppression, cell cycle regulation, and apoptosis in hematological malignancies.
The TMD8 host cell line derives from a patient with activated B-cell-like diffuse large B-cell lymphoma (DLBCL), a highly aggressive non-Hodgkin lymphoma subtype. This ABC-DLBCL line recapitulates key pathogenic features, including chronic active B-cell receptor signaling, constitutive NF-??B activation, and dependence on downstream survival pathways. TMD8 cells are widely used in preclinical research to model lymphomagenesis, drug response, and resistance mechanisms, providing a clinically relevant context for BTG2 functional studies.
BTG2 is a well-established tumor suppressor that enforces G1/S cell cycle arrest and promotes apoptosis primarily through the p53 signaling pathway. In response to genotoxic stress, TP53 directly transactivates BTG2, whereas oncogenic signals like NF-??B and miR-21 transcriptionally repress it. Once expressed, BTG2 physically interacts with the CNOT7/CNOT8 deadenylase complex to modulate mRNA turnover and with PRMT1 to facilitate protein arginine methylation, altering the activity of key growth regulators. Consequently, BTG2 downregulates the cell cycle driver CCND1 and upregulates the CDK inhibitor CDKN1A (p21). In B-cell malignancies, BTG2 also antagonizes the transcriptional repressor BCL6, a master oncogene in DLBCL, reinforcing its tumor-suppressive function within the DNA damage response and apoptotic signaling networks.
In the TMD8 ABC-DLBCL model, BTG2 inactivation mirrors the frequent disruption of p53-mediated growth control observed in lymphoma patients. This knockout cell line enables rigorous investigation of how BTG2 loss cooperates with aberrant NF-??B and BCR signaling to drive uncontrolled proliferation and apoptotic resistance. It offers a powerful system for studying synthetic lethal interactions that arise specifically in BTG2-null lymphoma cells and for screening chemical libraries to identify agents that compensate for BTG2 deficiency or reactivate downstream p53 effectors.
Researchers can employ this BTG2 knockout line in apoptosis assays (annexin V), cell cycle analysis (flow cytometry), and proliferation measurements (MTS/MTT). RNA-seq defines BTG2-dependent transcriptomes, while co-immunoprecipitation reveals interactions with CNOT7/CNOT8 or PRMT1. Drug sensitivity screening identifies vulnerabilities specific to BTG2-deficient lymphoma cells. For further assistance, please contact Ascent Research.
