The AIFM2 Knockout T-47D Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast ductal carcinoma line. This product comprises a heterogeneous pool of gene-disrupted cells, offering a loss-of-function model for investigating the cellular roles of apoptosis-inducing factor mitochondrion-associated 2 (AIFM2). Unlike monoclonal cell lines, the polyclonal format provides a broader representation of knockout effects, minimizing clonal artifacts and enabling robust analysis in a physiologically relevant cellular background.
The T-47D host cell line is a well-characterized model of hormone-responsive breast cancer, originally isolated from a metastatic pleural effusion. These cells express estrogen and progesterone receptors and are extensively employed in studies of endocrine signaling, hormone-dependent proliferation, and mechanisms of endocrine therapy resistance. The T-47D background provides a context for examining AIFM2 function in relation to estrogen receptor-driven pathways and apoptotic signaling in breast cancer.
AIFM2 functions as a p53-inducible mitochondrial flavoprotein oxidoreductase that, upon apoptotic stimulation, translocates to the nucleus and mediates caspase-independent chromatin condensation and DNA fragmentation. Its activity is regulated by upstream factors including TP53, oxidative stress signals, and NF-??B. AIFM2 interacts with Bcl-2 family proteins, mitochondrial flavoproteins, and HADHA, and acts within a network involving BAX and cytochrome c, ultimately executing cell death through non-caspase-dependent mechanisms. In addition to its pro-apoptotic role, AIFM2 contributes to mitochondrial redox homeostasis and participates in the cellular response to oxidative damage.
This AIFM2 knockout model in T-47D cells is particularly valuable for dissecting the interplay between mitochondrial apoptosis and hormone-driven survival pathways in breast cancer. The loss of AIFM2 function may shed light on p53-regulated cell death mechanisms and their modulation in the context of estrogen receptor signaling. Furthermore, this system enables investigation of AIFM2??s contribution to chemosensitivity, as its deletion may alter cellular responses to agents such as tamoxifen and doxorubicin. By utilizing a polyclonal knockout population, researchers can capture the phenotypic variability inherent in a heterogeneous tumor cell environment, providing insights into adaptive resistance mechanisms.
This cell product is ideally suited for a range of experimental applications, including mechanistic studies of caspase-independent cell death, p53 signaling, and mitochondrial dysfunction in breast cancer. Researchers can employ these polyclonal knockout cells in apoptosis assays using Annexin V and TUNEL staining, monitor AIFM2 localization via immunofluorescence, and quantify gene expression through Western blotting and RT-qPCR. Drug sensitivity assays, such as dose-response studies with tamoxifen or doxorubicin, coupled with flow cytometry-based cell death analysis, will help define the role of AIFM2 in therapeutic resistance. For further information or to place an order, please contact Ascent Research.
