The BAD Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human osteosarcoma cell line 143B. This product provides a heterogeneous pool of cells with targeted disruption of the BAD gene, enabling loss-of-function studies in a bone cancer background.
The 143B cell line is a widely used human osteosarcoma model established from a bone tumor. These adherent cells exhibit a transformed phenotype and retain key features of osteosarcoma, making them suitable for cancer biology research, particularly in studying bone malignancy, tumor progression, and therapeutic responses.
BAD encodes a BH3-only protein that functions as a critical activator of the intrinsic apoptosis pathway. Under apoptotic stimuli, dephosphorylated BAD interacts with and inhibits anti-apoptotic Bcl-2 family members such as Bcl-2 and Bcl-xL, relieving their suppression of the pro-apoptotic effectors Bax and Bak. This leads to mitochondrial outer membrane permeabilization, cytochrome c release, and subsequent caspase cascade activation. In survival signaling, kinases including AKT, PKA, and RSK phosphorylate BAD, promoting its association with 14-3-3 scaffold proteins and cytoplasmic sequestration, thereby preventing its pro-apoptotic functions. Thus, BAD serves as a key node integrating growth factor and stress signals to control cell fate.
In the 143B osteosarcoma background, disruption of BAD provides a powerful tool to dissect apoptotic signaling and survival mechanisms relevant to bone cancer. Osteosarcoma cells often exhibit dysregulated PI3K/AKT signaling that promotes cell survival partly through BAD phosphorylation. Loss of BAD in this context allows investigation of intrinsic and acquired resistance to apoptosis, a hallmark of cancer. This polyclonal knockout model enables researchers to study how the absence of BAD influences cellular responses to chemotherapeutic agents, targeted therapies, and microenvironmental stress signals.
Researchers can employ this BAD knockout model for a variety of advanced applications, including dissecting BAD-dependent and -independent apoptotic pathways, evaluating chemosensitivity and BH3 mimetic responses, and analyzing protein?Cprotein interactions within the Bcl-2 family network. Common experimental readouts include western blotting for total and phosphorylated BAD, Annexin V flow cytometry to quantify apoptosis, cytochrome c release assays to assess mitochondrial outer membrane permeabilization, co-immunoprecipitation to probe binding partners, and caspase activity or cell viability measurements. This product is an essential resource for apoptosis and cancer biology investigations. For additional information, please contact Ascent Research.
