ANKRD26 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat human T lymphocyte line. This pool of cells contains targeted disruption of the ANKRD26 gene, providing a loss-of-function model without clonal selection. The polyclonal nature preserves a diverse genetic background while abolishing ANKRD26 expression, suitable for studying ANKRD26-dependent processes in a T-cell context.
The Jurkat host cell line is an immortalized T lymphocyte derived from T-cell leukemia, widely used in immunology and oncology research. These cells model adaptive immune functions, including cytokine production and cell-mediated immunity, and offer a well-characterized signaling framework for analyzing pathways relevant to hematopoietic malignancies.
ANKRD26 acts as a negative regulator of thrombopoietin (TPO) signaling by interacting with the MPL receptor and adaptors GRB2 and SHC1 to modulate downstream cascades. TPO binding to MPL triggers JAK2-mediated STAT5 phosphorylation and activates the MAPK/ERK pathway via RAF1-MAP2K1-MAPK1/3 (ERK1/2), along with PI3K-AKT signaling. ANKRD26 is transcriptionally controlled by RUNX1, GATA1, and FLI1. Its loss leads to hyperactivation of MAPK1/3 and upregulation of targets such as MYC, CCND1, and BCL2 family members, resulting in dysregulated proliferation and survival.
In Jurkat cells, ANKRD26 knockout reveals crosstalk between thrombopoietin pathways and T-lymphocyte signaling. Although ANKRD26 is primarily linked to megakaryopoiesis and platelet production, Jurkat cells express components of the MPL?CJAK2?CSTAT5 axis, making this model valuable for examining how ANKRD26 loss affects MAPK/ERK and AKT-driven proliferation and apoptosis in a leukemia-relevant background. This polyclonal population enables dissection of ANKRD26??s tumor-suppressive or oncogenic potential and serves as a platform for studying inherited bone marrow failure syndromes.
This knockout product supports a range of applications, including mechanistic signaling studies, disease modeling of ANKRD26-related thrombocytopenia and acute myeloid leukemia, drug screening, and functional genomics. Compatible assays include Western blotting for phospho-ERK, RT-qPCR for megakaryocytic transcripts, flow cytometry for platelet glycoproteins, luciferase reporter assays, and proliferation measurements. For additional information, please contact Ascent Research.
