The ALDH7A1 Knockout Jurkat Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T-cell leukemia line, providing targeted disruption of the ALDH7A1 gene. This loss-of-function model enables study of aldehyde dehydrogenase 7A1 activity in a lymphocytic background, supporting research into lysine catabolism, aldehyde detoxification, and related neurological disorders. The polyclonal pool minimizes clonal artifacts, allowing robust functional analyses across heterogeneous knockout populations.
Jurkat cells are an immortalized human T lymphocyte line widely used to model T-cell receptor (TCR) signaling, immune activation, and cytokine production. These suspension cells proliferate rapidly and maintain key signaling pathways governing apoptosis, NF-??B activation, and interleukin expression. Their genetic tractability and well-characterized oxidative stress response make them suitable for dissecting the metabolic and signaling consequences of ALDH7A1 ablation, especially given the link between aldehyde metabolism and immune function.
ALDH7A1 encodes an NAD+-dependent aldehyde dehydrogenase that oxidizes ??-aminoadipic semialdehyde to ??-aminoadipate in the lysine degradation pathway, utilizing NAD+ and forming a homotetramer. It acts downstream of AASS and upstream of DHTKD1, OGDHL, DLST, and DLD, linking lysine catabolism to the TCA cycle. Transcription is regulated by NFE2L2 and PPARGC1A and modulated by glucocorticoids. Impaired function causes accumulation of piperideine-6-carboxylate (P6C), which sequesters pyridoxal phosphate (PLP) and disrupts neurotransmitter metabolism, modeling pyridoxine-dependent epilepsy and hyperpipecolatemia. ALDH7A1 knockout also perturbs NADH production and aldehyde detoxification, with potential effects on oxidative stress responses.
In Jurkat T cells, ALDH7A1 disruption illuminates the intersection of metabolic reprogramming and immune signaling. T lymphocytes require redox balance and metabolic flux for activation; aldehyde accumulation may exacerbate oxidative stress, alter NF-??B-mediated transcription, and impair cytokine secretion. PLP sequestration by P6C can indirectly influence T-cell differentiation and function. Thus, this model tests whether lysine degradation intermediates modulate TCR signaling or apoptosis sensitivity, broadening ALDH7A1 relevance beyond neurology.
Applications include lysine flux analysis via LC-MS metabolite profiling, P6C and ??-aminoadipate quantification, and PLP measurement. Cells are suitable for ALDH7A1 enzyme activity assays, immunoblotting, and RT-qPCR of pathway components. Under oxidative challenge, apoptosis assays explore aldehyde toxicity, and electrophysiological methods may probe excitotoxicity in differentiated or fused systems. For details, contact Ascent Research.
