The ELAVL2 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the ELAVL2 gene in the K-562 human chronic myelogenous leukemia cell line. This genetically heterogeneous pool carries diverse indels within ELAVL2, providing a loss-of-function model for studying ELAVL2’s role in a robust, disease-relevant setting. The live cells are delivered ready for expansion and immediate experimental use.
K-562 is a suspension cell line derived from a CML patient in blast crisis, characterized by the Philadelphia chromosome and BCR-ABL1 fusion oncogene. It serves as a classic model for CML and hematopoietic differentiation, capable of undergoing erythroid, granulocytic, or monocytic maturation upon stimulation. This background allows the exploration of post-transcriptional regulation in leukemia and hematopoietic processes.
ELAVL2 encodes an RNA-binding protein that recognizes AU-rich elements (AREs) in 3?? UTRs, stabilizing target mRNAs and enhancing their translation. In neuronal systems, ELAVL2 is regulated by NeuroD1, REST, and BDNF, and modulates expression of targets such as FOS, CDKN1A, GAP43, and NEFL. It interacts with ELAVL1, ELAVL3, ELAVL4, and RNA polymerase II, and is functionally linked to the RNA exosome and translation initiation complexes, constituting a key node in post-transcriptional control.
In the K-562 leukemia context, ELAVL2 knockout may alter the stability of ARE-containing transcripts involved in proliferation and differentiation, potentially impacting the leukemic phenotype. This model allows the dissection of ELAVL2’s non-neuronal functions, including its influence on hematopoietic differentiation and leukemia cell maintenance. It offers a system to identify ELAVL2-dependent mRNA regulatory networks in cancer cells.
Applications include RIP-seq to map ELAVL2?CRNA interactions, RNA-seq for transcriptome-wide analysis, and RT-qPCR/western blotting for validation of specific targets. Flow cytometry enables assessment of differentiation markers or cell cycle effects. The polyclonal format serves as a suitable CRISPR control and provides a platform for investigating post-transcriptional gene regulation in leukemia. For technical inquiries, please contact Ascent Research.
