The HDHD2 Knockout Jurkat Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal knockout cell population targeting the HDHD2 gene in the Jurkat host background. This gene disruption model is generated without clonal isolation, yielding a mixed population of knockout cells suitable for pooled functional studies of pseudouridine metabolism in a T-cell leukemia context.
The Jurkat cell line is an immortalized human T lymphoblastoid line derived from an acute T cell leukemia patient. Jurkat cells serve as a widely adopted model for T-cell receptor signaling, activation responses, and T-cell acute lymphoblastic leukemia (T-ALL) pathology, recapitulating key features of malignant T-cell growth.
HDHD2 encodes pseudouridine monophosphatase, which catalyzes the dephosphorylation of pseudouridine 5??-phosphate to pseudouridine, a central step in the pyrimidine salvage pathway and RNA modification turnover. Transcription factors such as MYC and E2F1, known regulators of nucleotide metabolism, may modulate HDHD2 expression. Downstream, pseudouridine is further processed by uridine phosphorylase to uracil and ribose-1-phosphate, linking pseudouridine recycling to nucleotide pool homeostasis. Through its enzymatic function, HDHD2 impacts the balance of modified nucleosides and the dynamics of RNA pseudouridylation in Jurkat T-ALL cells.
In the Jurkat T-ALL model, HDHD2 disruption permits exploration of how pseudouridine metabolism influences malignant T-cell proliferation, survival, and signaling. Given that nucleotide imbalances and altered RNA modifications are characteristic of many cancers, this polyclonal knockout line offers a physiologically relevant platform to dissect metabolic vulnerabilities driven by oncogenic transcriptional programs.
This product is well-suited for a range of research applications, including Western blotting for HDHD2 expression, LC-MS-based nucleotide metabolite analysis, RNA pseudouridine profiling, and proliferation or apoptosis assays to assess cellular fitness. Metabolic flux analyses can elucidate compensatory pyrimidine salvage pathways. For additional information or assistance with experimental design, please contact Ascent Research.
