DTD1 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated in the K-562 leukemia cell line. This product consists of a pooled population of cells carrying targeted disruption of the DTD1 gene via CRISPR/Cas9-mediated genome editing. The polyclonal format provides a broad representation of editing outcomes, enabling researchers to study loss-of-function effects without bias from clonal selection. These cells serve as a versatile model for investigating DTD1-dependent processes in a hematopoietic cancer background.
The K-562 cell line is a widely used model derived from a female patient with chronic myelogenous leukemia (CML) in blast crisis. These cells carry the Philadelphia chromosome, resulting in a BCR-ABL1 fusion oncogene that drives aberrant tyrosine kinase signaling. K-562 cells are undifferentiated, multipotent progenitors that can be induced to differentiate along erythroid, monocytic, and megakaryocytic lineages, making them a robust platform for studying hematopoietic differentiation, oncogene addiction, and cancer biology.
DTD1 encodes a D-aminoacyl-tRNA deacylase that hydrolytically removes D-amino acids from mischarged tRNAs, such as D-Tyr-tRNA(Tyr), to prevent their incorporation into nascent polypeptides. This enzyme operates as a homodimer and interacts directly with D-aminoacylated tRNA substrates. DTD1 expression is putatively regulated by the MYC and mTORC1 signaling pathways, linking its function to cellular growth and metabolic cues. By maintaining the stereochemical purity of the proteome, DTD1 safeguards ribosomal elongation fidelity and supports proteostasis, with downstream effects on stress responses and cell survival.
In the K-562 leukemia background, loss of DTD1 is expected to cause accumulation of D-aminoacylated tRNAs, leading to aberrant protein synthesis and proteotoxic stress. Given the dependency of CML cells on robust proteostatic mechanisms to manage the oncogenic stress imposed by BCR-ABL1, DTD1 knockout may sensitize these cells to proteasome inhibitors or other modulators of protein quality control. This model thus provides a means to explore the intersection of translational fidelity and leukemia cell biology, and to investigate potential synthetic lethal relationships.
These DTD1 Knockout K-562 Polyclonal Cells are suitable for a variety of research applications, including mechanistic studies of translational fidelity and D-amino acid metabolism in cancer, elucidation of DTD1’s role in proteotoxic stress responses, and functional modeling of DTD1-deficiency-related neurodevelopmental disorders. The population can be employed in assays such as Western blotting and RT-qPCR for knockout confirmation, aminoacylation assays to monitor D-aminoacyl-tRNA accumulation, proteomics to detect D-amino acid incorporation, cell viability and apoptosis assays, drug sensitivity testing with proteasome inhibitors, and transcriptomic profiling via RNA-seq. For additional product information and technical support, please contact Ascent Research.
