The ALDH1A2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with targeted disruption of the ALDH1A2 gene. This polyclonal format provides a heterogeneous pool of edited cells, avoiding clonal biases and enabling robust loss-of-function studies. The knockout is achieved through CRISPR/Cas9-mediated gene disruption, offering a versatile model to dissect retinoic acid signaling in a T cell background.
The Jurkat cell line, derived from the peripheral blood of a patient with acute T cell leukemia, is a classic model for T cell receptor signaling, activation, apoptosis, and T-ALL pathogenesis. Jurkat cells produce IL-2 upon stimulation, exhibit early T cell differentiation markers, and are widely used in immunological and cancer research. Their genetic tractability makes them ideal for gene editing to study T cell biology and leukemogenesis.
ALDH1A2 encodes retinaldehyde dehydrogenase 2 (RALDH2), which catalyzes the NAD+-dependent oxidation of retinaldehyde to retinoic acid, a key morphogen. Retinoic acid binds CRABPs and activates nuclear receptors RAR??/RXR??, regulating transcription of target genes such as HOX, CDKN1A (p21), CYP26A1, and Bcl-2 family members. ALDH1A2 is regulated by FOXC1, PBX1, FGF, and Wnt signaling, and participates in retinoic acid auto-regulation. Its disruption impairs retinoic acid biosynthesis, affecting differentiation, immune function, and developmental signaling.
In Jurkat T cells, ALDH1A2 knockout provides a model to investigate the role of intrinsic retinoic acid synthesis in T cell biology and leukemia. Retinoic acid signaling influences T cell differentiation, apoptosis, and chemosensitivity, with altered pathways implicated in T-ALL. Ablating RALDH2 activity allows dissection of autocrine/paracrine retinoid effects and gene regulatory networks. This model is valuable for exploring retinoic acid-based differentiation therapy and resistance mechanisms in T-ALL.
Applications include functional analysis of retinoic acid signaling in T cells, drug screening for pathway modulators, and transcriptomic profiling. Knockout validation by western blot and RT-qPCR of target genes (e.g., CYP26A1, HOXA1), flow cytometry for differentiation markers, retinoic acid reporter assays, and RNA-seq are typical. Enzymatic conversion assays directly measure activity. For further details, contact Ascent Research.
