The KLF6 Knockout HEK293T Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human KLF6 gene in HEK293T cells. This heterogeneous pool arises from CRISPR/Cas9-mediated disruption of the endogenous KLF6 locus, providing a loss-of-function model to study KLF6 deficiency without clonal selection artifacts.
HEK293T cells are a derivative of the HEK293 human embryonic kidney line that constitutively expresses the SV40 large T-antigen, enabling episomal replication of SV40 origin-containing plasmids and high-level transient protein expression and viral production. These cells are highly amenable to transfection and widely employed for protein expression, lentiviral packaging, and signaling studies, making them a versatile platform for generating and analyzing knockout models.
KLF6 is a zinc-finger transcription factor and tumor suppressor that integrates signals from TGF-??1, p53, EGF, HGF, and cytokines. It interacts with co-regulators including SP1, Smad3, HDAC1, and c-Jun to exert transcriptional control. KLF6 directly activates the CDK inhibitor p21/CDKN1A and the adhesion protein E-cadherin, leading to cell cycle arrest and enhanced cell?Ccell adhesion, and represses pro-proliferative and pro-invasive genes such as cyclin D1, c-Myc, and MMPs. In the canonical TGF-?? pathway, KLF6 operates downstream of TGFBR1/2?CSMAD2/3?CSMAD4 to mediate growth-inhibitory and apoptotic signals; its disruption uncouples TGF-?? stimulation from these tumor-suppressive outcomes.
Using HEK293T cells, which retain many native signaling pathways despite being transformed, the KLF6 knockout polyclonal population permits analysis of altered cell cycle regulation, apoptotic sensitivity, and response to chemotherapeutics or targeted agents. This model also supports transient and stable transfection for rescue or overexpression experiments, facilitating the dissection of KLF6-dependent transcriptional networks. Because HEK293T cells are a staple in signal transduction research, this knockout tool integrates seamlessly into existing assay workflows for studying growth factor signaling and tumor suppressor biology.
This product is applicable to a variety of experimental contexts, including mechanistic studies of prostate, liver, and colorectal cancer, drug sensitivity and resistance screening, and fibrosis research. Key assays include RT-qPCR and Western blotting for target validation, proliferation (MTT, BrdU) and apoptosis (Annexin V) measurements, migration/invasion testing, and genome-wide approaches such as RNA-seq and ChIP-qPCR. Researchers can employ this model to explore KLF6??s role in tumor suppression and response to therapy. For further information, please contact Ascent Research.
