BTN1A1 Knockout T-47D Polyclonal Cells are a population of CRISPR/Cas9-edited human breast ductal carcinoma cells featuring targeted disruption of the BTN1A1 gene. This polyclonal knockout product offers a genetically diverse pool of loss-of-function variants, suitable for studying the multifaceted functions of BTN1A1 in mammary epithelial biology and breast cancer pathogenesis. By leveraging CRISPR/Cas9-mediated gene disruption, researchers can interrogate BTN1A1-dependent processes without clonal isolation, preserving biological heterogeneity.
T-47D is a human breast ductal carcinoma cell line derived from a pleural effusion of a ductal carcinoma, representing a widely used estrogen receptor-positive (ER+), progesterone receptor-positive (PR+), and HER2-low breast cancer model. These epithelial cells retain hormone responsiveness and are commonly employed to study luminal A/basal-like breast cancer subtypes, hormone-dependent proliferation, and endocrine therapy resistance. Their well-documented growth requirements and signaling characteristics make them an ideal chassis for functional genomics studies using CRISPR/Cas9-edited knockouts.
BTN1A1 encodes a transmembrane immunoglobulin-like protein predominantly expressed in mammary epithelial cells. It functions as a key regulator of milk fat globule secretion by anchoring lipid droplets to the apical plasma membrane through its interaction with xanthine oxidoreductase (XOR) and the lipid droplet coat protein perilipin-2 (ADPH). BTN1A1 signaling is influenced by prolactin via the JAK2/STAT5 pathway and glucocorticoid receptor activity. Downstream, BTN1A1 modulates T cell activation and immune checkpoint regulation, partly through interactions with the butyrophilin family members BTN2A1 and BTN3A1, and influences XOR-mediated redox signaling. While its role in lactation is well established, emerging evidence suggests that BTN1A1 may act as a tumor suppressor in breast cancer, possibly by maintaining epithelial integrity and immune surveillance.
In the T-47D background, knockout of BTN1A1 provides a powerful model for dissecting the intersection of lipid metabolism, immune modulation, and breast cancer progression. Disruption of BTN1A1 in ER+ breast cancer cells is expected to impair lipid secretion pathways and may enhance tumor cell immunogenicity by altering the expression of immunoregulatory molecules. This polyclonal knockout population is particularly valuable for studying the tumor-suppressive functions of BTN1A1, as loss in a hormone-sensitive carcinoma context can reveal its potential role in limiting cell proliferation, migration, and immune evasion. The model also enables exploration of crosstalk between prolactin/JAK2/STAT5 signaling and BTN1A1-dependent immune checkpoint regulation.
Researchers can employ BTN1A1 Knockout T-47D Polyclonal Cells in a diverse array of experimental workflows. Typical applications include western blotting and RT-qPCR to confirm target ablation, immunofluorescence to assess lipid droplet dynamics, MTT assays to measure proliferation changes, Boyden chamber migration assays to investigate invasive potential, and T cell co-culture activation assays to evaluate immune modulatory effects. This knockout model also supports studies of lactation biology, breast cancer tumor suppressor mechanisms, and the development of immune checkpoint-targeted therapies. For further technical information or to place an order, please contact Ascent Research.
