The DNAJA1 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the near-haploid HAP1 human cell line. This product provides targeted disruption of the DNAJA1 gene, eliminating functional DNAJA1 protein. The polyclonal nature offers a heterogeneous allele pool suitable for robust loss-of-function experiments without clonal selection.
HAP1 is a male, BCR-ABL positive chronic myeloid leukemia cell line with a near-haploid karyotype. Originating from a CML patient, its hemizygous genome facilitates unambiguous genotype-phenotype correlations, making it ideal for knockout studies. The cells retain key oncogenic signaling, including BCR-ABL, and are widely used in gene function research.
DNAJA1 encodes an Hsp40 co-chaperone that stimulates Hsp70 ATPase activity, critical for protein folding, trafficking, and degradation. It is regulated by heat shock factor 1 (HSF1), ER stress sensors IRE1/PERK, and TNF-??. DNAJA1 interacts with Hsp70, Hsp90, p53, Bcl-2, and Apaf-1, and modulates downstream targets such as Akt1, JNK, and the androgen receptor. Thus, DNAJA1 integrates chaperone function with apoptosis, stress responses, and survival signaling.
In HAP1 cells, DNAJA1 knockout disrupts proteostasis, impairing Hsp70-mediated protein quality control and potentially activating the unfolded protein response. Given its role in p53 and JNK pathways, the knockout is expected to alter apoptotic sensitivity and proliferation. The haploid background enhances phenotypic penetrance, providing a clear model to dissect DNAJA1??s contributions to oncogenic and stress signaling networks.
Applications include protein quality control studies, stress response dissection, and co-chaperone function in cancer research. These cells are suitable for functional genomics screens, drug target validation, and signaling pathway analysis using assays such as Western blotting, co-immunoprecipitation, apoptosis assays, and proteasome activity measurements. They support investigation of DNAJA1 in leukemia and other malignancies. For additional information, please contact Ascent Research.
