The BTN1A1 Knockout PaTu 8988t Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed for targeted gene disruption of BTN1A1. This product provides a loss-of-function model derived from the PaTu 8988t host cell line, enabling researchers to interrogate the specific contributions of BTN1A1 in cellular processes. By introducing Cas9-mediated DNA cleavage, the BTN1A1 gene is disrupted without claiming a specific editing pattern, ensuring a relevant experimental tool for functional genomics.
The parental PaTu 8988t cell line originates from a liver metastasis of pancreatic ductal adenocarcinoma (PDAC), establishing it as a well-characterized model of metastatic pancreatic cancer. These epithelial cells retain key features of aggressive PDAC, including invasive potential and characteristic signaling pathway alterations. Consequently, this host background is particularly suited for studying molecular mechanisms underlying pancreatic cancer progression and metastasis, providing a physiologically pertinent context for investigating tumor biology.
BTN1A1 encodes butyrophilin subfamily 1 member A1, a protein originally characterized as mediating milk fat globule secretion in mammary epithelia. Mechanistically, BTN1A1 interacts with xanthine oxidoreductase (XDH) and perilipin-2 (PLIN2) at the endoplasmic reticulum membrane, facilitating the formation and secretion of lipid droplets. This process is regulated upstream by prolactin receptor signaling and the transcription factor STAT5. Additionally, BTN1A1 is implicated in immune regulation, potentially acting as an immune checkpoint modulator, and interacts with the related butyrophilin BTN2A2. In pancreatic cancer cells, BTN1A1 may influence lipid metabolism and immune evasion, although its exact roles remain to be fully elucidated.
Knocking out BTN1A1 in the PaTu 8988t metastatic PDAC model enables dissection of its functions in a cancer-relevant system. Given the metabolic reprogramming and immune escape mechanisms inherent to pancreatic tumors, disrupting BTN1A1 may impair lipid droplet secretion and alter immune cell interactions, potentially affecting tumor growth and metastatic capacity. This polyclonal knockout population allows researchers to assess how loss of BTN1A1 modulates lipid homeostasis, influences immune checkpoint molecule interactions, and impacts the aggressive phenotype of PDAC cells.
This BTN1A1 knockout polyclonal cell product is amenable to a range of experimental approaches. Researchers can assess lipid droplet dynamics using BODIPY staining, perform co-immunoprecipitation to study interactions with XDH or PLIN2, and quantify transcript and protein expression via RT-qPCR and western blotting. Functional readouts may include transwell invasion assays to evaluate metastatic potential and immune cell co-culture experiments to probe immune modulation. Phospho-signaling analyses can further elucidate altered pathways downstream of BTN1A1 loss. For further technical details or ordering information, please contact Ascent Research.
