The KLF13 Knockout HAP1 Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population of the human HAP1 cell line, designed to disrupt the KLF13 gene. This loss-of-function model enables systematic investigation of KLF13-dependent transcriptional control, proliferation, and apoptosis without the need for clonal isolation. The polyclonal nature captures editing heterogeneity, offering a robust tool for functional genomics and pathway dissection in cancer biology, erythropoiesis, and immune regulation contexts.
HAP1 is a near-haploid cell line derived from the KBM-7 chronic myeloid leukemia (CML) background, widely adopted for genetic screens due to its haploidy. This feature facilitates CRISPR/Cas9-mediated gene disruption and simplifies genotype?Cphenotype correlations, as most genes exist in a single copy. The stable epithelial morphology and compatibility with high-throughput assays make HAP1 an ideal host for knockout generation, ensuring that KLF13 loss yields a complete functional readout in a clean genetic setting.
KLF13 encodes a Kr??ppel-like factor transcription factor that binds GC-rich promoters and acts as a context-dependent activator or repressor. It is regulated by GATA1, TGF-??, and ERK signaling, and interacts with cofactors mSin3A, HDAC1, and SP1. Direct transcriptional targets include BCL2L11 (Bim), gamma-globin, and CDKN1A (p21), thereby linking KLF13 to apoptosis, erythroid differentiation, and cell cycle arrest. Its activity interfaces with the TGF-?? pathway through SMAD2/3 and with the MAPK/ERK cascade via ERK1/2, integrating extracellular signals with growth and survival decisions.
Leveraging the CML-derived HAP1 background, this KLF13 knockout model is particularly relevant for studying hematological malignancies and solid tumors where KLF13 is dysregulated. The polyclonal population mirrors clonal heterogeneity observed in cancer, while the haploid genome ensures penetrant phenotypic readouts. In this system, apoptosis assessments via BCL2L11 and proliferation assays through CDKN1A or cell cycle analysis become highly interpretable, enabling precise dissection of KLF13??s role in oncogenic processes and therapeutic responses.
Representative applications include transcriptome analysis by RNA-seq, protein-level knockout validation by Western blotting, and functional assays such as Annexin V?Cbased apoptosis detection, MTT proliferation tests, and flow cytometry for cell cycle profiling. Reporter gene assays and drug sensitivity screens facilitate investigation of TGF-?? and MAPK pathway interventions. These polyclonal cells support functional genomics, drug target validation, and erythropoiesis research. For additional product details and technical support, please contact Ascent Research.
