The JMY Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to eliminate JMY (Junction Mediating and Regulatory Protein) expression in the HAP1 human near-haploid cell line. This genetically disrupted pool provides a loss-of-function model for investigating JMY-dependent cellular processes without the confounding effects of wild-type protein. Through targeted gene disruption using CRISPR/Cas9 technology, these cells enable robust interrogation of JMY??s dual role as a transcriptional co-activator for p53 and an actin nucleation factor.
HAP1 is a near-haploid cell line derived from the KBM-7 chronic myeloid leukemia (CML) line, retaining a haploid karyotype for most chromosomes except a portion of chromosome 8. As a hematopoietic progenitor model, HAP1 cells are widely utilized for functional genomics and cancer biology studies due to their stable haploid state, which simplifies gene editing and eliminates allelic variation. The CML origin provides a relevant context for examining tumor suppressor pathways and DNA damage responses in a leukemia background.
JMY is a multifunctional protein that acts as a p53 cofactor, enhancing p53-dependent transcription of pro-apoptotic genes such as BAX and PUMA, and independently promotes actin polymerization by activating the Arp2/3 complex. DNA damage triggers JMY phosphorylation via ATM/ATR kinases, while Rho GTPases regulate its actin nucleator activity. In the nucleus, JMY interacts with p53 and p300/CBP to drive cell cycle arrest and apoptosis. In the cytoplasm, it cooperates with the WAVE complex and Arp2/3 to control cell migration. JMY also associates with STRAP, linking TGF-?? and DNA damage responses.
In the haploid HAP1 background, JMY disruption ensures a complete loss-of-function phenotype, enabling unambiguous study of JMY??s roles in p53-mediated cell fate and actin dynamics. This model is particularly powerful for dissecting DNA damage-induced apoptosis and migration pathways in leukemia cells, providing a clean system for mechanistic studies without allelic interference.
These polyclonal knockout cells are suitable for western blotting, RT-qPCR, immunofluorescence, apoptosis and migration/invasion assays, co-immunoprecipitation, reporter gene assays, and flow cytometry. Applications include functional genomics, p53 signaling, DNA damage response, cancer cell motility, and neurodevelopmental disorder research. For further information, please contact Ascent Research.
