The KIAA1191 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the KIAA1191 gene in the human Jurkat T lymphoblast cell line. This gene disruption model creates a heterogeneous loss-of-function population, enabling robust investigation of KIAA1191-dependent mTORC1 signaling while avoiding the selection biases of clonal lines.
Jurkat cells are an immortalized T lymphocyte line derived from human acute T-cell leukemia, widely employed as a model for T-cell signaling and leukemia biology. They offer a physiologically relevant context for studying TCR-mediated pathways, metabolic regulation, and oncogenic signaling, with genetic tractability suited for CRISPR-based knockout experiments.
KIAA1191 functions as a positive regulator of mTORC1 at the lysosomal surface, where it interacts with Rag GTPases (RagA, RagC) and the Ragulator complex (LAMTOR1-5) to promote mTOR binding to RPTOR. Upstream signals such as growth factors (insulin), amino acids (leucine, arginine), and cytokines (IL-2) activate this machinery. Active mTORC1 phosphorylates downstream targets RPS6KB1 (S6K) and EIF4EBP1 (4E-BP1) to drive protein synthesis, while inhibiting ULK1 and TFEB to suppress autophagy and lysosomal biogenesis. KIAA1191 knockout disrupts amino acid-dependent mTORC1 activation, providing a defined tool to dissect these signaling events.
In Jurkat cells, KIAA1191-mediated mTORC1 activation integrates nutrient and growth factor cues essential for T-cell proliferation and metabolic fitness. Its knockout impairs mTORC1 signaling, evidenced by reduced phosphorylation of S6K and 4E-BP1, leading to decreased protein synthesis and altered cell growth. This model is particularly relevant for dissecting how TCR and amino acid sensing converge on mTORC1 in leukemia-derived T lymphocytes, and for exploring KIAA1191??s role in oncogenic mTOR pathway dysregulation.
Applications include western blotting for phospho-S6K and phospho-4E-BP1, flow cytometry for cell size and proliferation, lysosomal localization assays of mTOR components, and amino acid starvation/refeeding experiments. The model supports drug discovery for mTOR pathway inhibitors (e.g., rapamycin sensitivity) and metabolic studies in T-cell leukemia. Researchers can combine this knockout with additional perturbations to map functional interactions. For further technical details or customized inquiries, please contact Ascent Research.
