The DTWD1 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human K-562 cell line. This product offers a heterogeneous loss-of-function model for studying DTWD1, a putative tRNA-modifying enzyme. The polyclonal pool contains cells with various CRISPR-induced disruptions, enabling robust functional assays without clonal artifacts.
K-562 is a female-derived chronic myelogenous leukemia (CML) cell line isolated during blast crisis. These suspension lymphoblasts harbor the Philadelphia chromosome, resulting in BCR-ABL1 fusion, and serve as a classical in vitro model for CML pathogenesis and therapeutic research. The line??s well-documented molecular landscape facilitates detailed studies of gene function in a leukemic context.
The DTWD1 gene encodes a predicted tRNA-modifying enzyme involved in wobble uridine modification, a process that enhances translational efficiency and fidelity. While its direct interactors and regulators remain poorly characterized, DTWD1 likely acts within a network of tRNA modification enzymes, including methyltransferases and uridine modification complexes. Its activity is hypothesized to modulate the translation of codon-biased mRNAs, such as those encoding cell cycle regulators or stress-responsive proteins. Disruption of DTWD1 may therefore alter the proteomic landscape of cells, particularly under conditions requiring rapid protein synthesis.
In the K-562 leukemia background, loss of DTWD1 function could compromise the efficient translation of proteins essential for proliferation and survival. This polyclonal knockout model captures a spectrum of editing outcomes, allowing researchers to explore how varying degrees of DTWD1 disruption affect leukemic traits. By impairing tRNA modification, DTWD1 knockout may sensitize cells to metabolic stress or chemotherapeutic agents, providing a platform to study translational control in hematologic malignancies. The lack of established disease associations highlights the value of this tool for uncovering novel roles of tRNA modifications in cancer.
These cells support diverse experimental workflows, including proliferation assays, drug sensitivity screens, and translation efficiency measurements using ribosome profiling or polysome fractionation. Western blotting, RT-qPCR, and flow cytometry can confirm knockout and assess downstream phenotypic changes. RNA-seq may reveal transcriptome-wide shifts in codon usage or stress responses. Metabolic assays provide insights into altered energetic demands. Researchers investigating tRNA biology, leukemia signaling, or translational regulation will find this model indispensable. For additional information, contact Ascent Research.
