The C6orf120 Knockout HAP1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the C6orf120 gene in the HAP1 cell line. This polyclonal format delivers a heterogeneous population of gene-edited cells, enabling loss-of-function studies without clonal selection artifacts. The knockout model facilitates investigation of C6orf120??s biological role in signaling networks and disease contexts, particularly in apoptosis and cell proliferation regulation.
HAP1 is a human near-haploid chronic myeloid leukemia (CML) cell line derived from the KBM-7 line. Its male origin and stable haploid karyotype make it exceptionally suited for CRISPR-based gene editing, as disruption of a single allele eliminates gene function without requiring biallelic targeting. The near-haploid genome simplifies interpretation of knockout phenotypes, establishing HAP1 as a workhorse for genetic perturbation studies in cancer and signal transduction research.
The C6orf120 gene encodes a poorly characterized protein that is transcriptionally regulated by TGF-beta signaling. Upon TGF-beta receptor activation, phosphorylated SMAD2 and SMAD3 complex with SMAD4 and translocate to the nucleus, where they modulate C6orf120 expression. C6orf120 functions downstream of TGF-beta and may act as a pro-apoptotic factor, promoting the expression of BCL2 family members BAX and BIM, which are key initiators of mitochondrial outer membrane permeabilization. This cascade leads to caspase-3 activation and execution of apoptosis. While direct interacting factors remain unknown, C6orf120 integrates into the TGF-beta/apoptosis axis and potentially influences cell fate decisions.
In the HAP1 background, knockout of C6orf120 creates a clean loss-of-function model to dissect its contribution to TGF-beta-mediated cell death. The haploid state ensures that the CRISPR-mediated gene disruption yields a complete loss of protein function, eliminating confounding effects from a second allele. The polyclonal nature of the population preserves cellular heterogeneity, allowing observation of phenotypic variability and reducing the risk of clonal bias. This setup is valuable for correlating genotype with apoptotic response and for mapping genetic interactions in a near-isogenic context.
This knockout cell population is suitable for a range of research applications, including mechanistic studies of TGF-beta-induced apoptosis, cancer cell biology, and genetic interaction screening in haploid cells. Representative assays include western blotting for BAX, BIM, and cleaved caspase-3; RT-qPCR for TGF-beta target genes; flow cytometry for cell cycle and apoptosis (Annexin V/PI staining); cell viability assays (MTT/Resazurin); and phospho-SMAD analysis. By providing a defined genetic perturbation, these cells support pathway dissection, drug response profiling, and functional genomics studies. For further information or technical support, please contact Ascent Research.
