The KAT7 Knockout T-47D Polyclonal Cells are a pool of CRISPR/Cas9-edited cells targeting the KAT7 gene in the human T-47D breast ductal carcinoma line. This polyclonal knockout population is generated by CRISPR/Cas9-mediated gene disruption, providing a heterogeneous loss-of-function model that avoids clonal selection artifacts and retains the inherent genetic diversity of the parental cell line. It serves as a robust tool for dissecting KAT7’s roles in chromatin modification, transcriptional regulation, and cell cycle progression.
The T-47D host cell line was derived from the pleural effusion of a 54-year-old female with metastatic ductal breast carcinoma. It is an ER??-positive, progesterone receptor-positive luminal A breast cancer model that requires estrogen for growth. T-47D cells faithfully mimic hormone-responsive breast cancer, making them a widely used system for studying estrogen signaling, endocrine therapy resistance, and the molecular basis of luminal subtype proliferation.
KAT7 (MYST2/HBO1) is a histone acetyltransferase that acetylates histone H4 at lysines 5, 8, and 12, facilitating chromatin relaxation. It coactivates ER?? to drive expression of target genes like TFF1. Upstream, KAT7 is regulated by CDKs and ATR/ATM; downstream, it licenses DNA replication origins by promoting MCM2-7 helicase loading. KAT7 operates in complexes with JADE, BRPF, and ING4/ING5 proteins, linking mitogenic signaling to transcriptional and replicative processes.
In T-47D cells, KAT7 is essential for estrogen-dependent proliferation. By acetylating histone H4, it permits ER?? recruitment to chromatin, leading to activation of cell cycle regulators such as Cyclin D1. Disruption of KAT7 impairs ER??-mediated transcription and blocks cell cycle progression, while also potentially causing replication stress due to defective origin licensing. This knockout model thus enables dissection of the epigenetic circuitry sustaining luminal A breast cancer growth and provides a platform for assessing KAT7 as a drug target.
This product supports a broad range of assays: Western blotting for H4K5ac/H4K8ac/H4K12ac; RT-qPCR for TFF1; proliferation (MTS/MTT) and colony formation assays; cell cycle analysis by flow cytometry; ChIP-qPCR for histone acetylation at ER binding sites or replication origins; and DNA fiber assays for replication fork dynamics. Key applications include estrogen receptor signaling studies, histone acetylation research, DNA replication regulation, and epigenetic drug validation. For additional information, please contact Ascent Research.
