HMMR Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in which the HMMR gene has been disrupted. This polyclonal format provides a heterogeneous mixture of Jurkat cells carrying diverse loss-of-function edits, enabling robust assessment of HMMR-dependent phenotypes without clonal selection bias. The knockout model is suitable for dissecting HMMR-mediated processes in a human T-lymphocyte context.
The Jurkat cell line is an immortalized human T-lymphocyte line originally derived from the peripheral blood of a 14-year-old male patient with acute T-cell leukemia. Jurkat cells are widely used as a model system for studying T-cell receptor signaling, activation, and apoptosis. Their leukemic origin and T-cell characteristics make them particularly relevant for investigating pathways that control lymphocyte proliferation, migration, and survival.
HMMR encodes a hyaluronan receptor that promotes cell motility, proliferation, and mitotic spindle integrity. Stimuli such as TGF-??, EGF, and hyaluronan upregulate HMMR via AP-1 and NF-??B transcription factors. Downstream, HMMR activates ERK1/2 and AKT, promoting FAK phosphorylation and Cyclin D1 expression, and regulates Rho GTPases and MMPs. At the spindle, HMMR interacts with TPX2 and SRC, ensuring chromosome segregation, and cooperates with CD44 in hyaluronan signaling.
In Jurkat T lymphocytes, HMMR contributes to processes essential for leukemic cell behavior, including migratory capacity, proliferative signaling, and cell cycle progression. Disruption of HMMR in this polyclonal knockout allows researchers to interrogate hyaluronan-mediated signaling in T-cell leukemia. The loss of HMMR can reveal alterations in ERK and AKT pathway activity, impacting targets such as Cyclin D1 and MMPs, and may impair mitotic spindle assembly via disrupted HMMR?CTPX2 interactions, providing insights into chromosome instability.
This polyclonal knockout population supports diverse functional assays including Transwell migration, wound healing, proliferation, flow cytometric hyaluronan binding and cell cycle analysis, Western blotting for phospho-ERK/AKT, apoptosis assays, and drug sensitivity dose-response curves. Applications encompass T-cell migration, hyaluronan signaling, cell cycle regulation, and drug screening, advancing cancer biology and immunotherapy research. For further details, please contact Ascent Research.
