The AMOTL1 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-mediated loss-of-function model of the AMOTL1 gene in the Jurkat human T lymphocyte cell line. This polyclonal knockout population originates from a heterogeneous pool of edited cells, minimizing clonal selection biases and providing a robust tool for investigating AMOTL1-dependent processes. Designed for researchers studying the Hippo pathway, cell polarity, and immune cell migration, the product offers a genetically disrupted T cell background for functional analyses.
Jurkat cells (clone E6-1) are an immortalized human T lymphocyte line derived from acute T cell leukemia. They are widely employed to dissect T cell receptor signaling, activation-induced apoptosis, and cytokine production, owing to their well-characterized signaling networks and rapid suspension growth. This host background enables examination of T cell-specific Hippo pathway functions and the contribution of angiomotin family scaffold proteins to lymphocyte biology.
AMOTL1 (Angiomotin-like 1) functions as a multidomain scaffold protein that integrates inputs from the Hippo pathway, cell polarity cues, and angiogenic signals. It directly interacts with AMOT, LATS1/2 kinases, YAP/TAZ transcriptional co-activators, and tight junction components such as ZO-1 and PALS1. Within the canonical Hippo cascade, MST1/2 kinases phosphorylate and activate LATS1/2, which in turn target AMOTL1 to regulate YAP/TAZ subcellular localization and TEAD-mediated transcription. Upstream regulators including VEGF, hypoxia, and mechanical forces modulate this pathway, while downstream AMOTL1 controls tight junction integrity via occludin and ZO-1, actin remodeling, and cell migration, thus coupling proliferation and polarity signals.
In Jurkat T lymphocytes, disruption of AMOTL1 is predicted to impair Hippo-dependent modulation of migration and polarity. T cells require dynamic cytoskeletal reorganization for chemotaxis and immune synapse assembly; AMOTL1 knockout may alter YAP/TAZ distribution, affect activation marker expression, and modify actin dynamics. Although non-epithelial, Jurkat cells express key junctional and cytoskeletal regulators, rendering them suitable for investigating scaffold-mediated control of immune cell polarity and leukemic progression. This model therefore provides a platform to explore how angiomotin proteins influence T cell behavior and lymphoid malignancy.
This polyclonal knockout population supports diverse applications, including functional dissection of Hippo signaling in T cells, mechanistic analyses of cell migration and invasion in leukemia, and validation of YAP/TAZ-driven transcriptional targets. Researchers can confirm AMOTL1 disruption by Western blotting or RT-qPCR, quantify T cell activation markers (e.g., CD69, CD25) via flow cytometry, and assess migration using transwell assays. YAP/TAZ luciferase reporter systems and immunofluorescence for tight junction proteins (ZO-1, occludin) enable functional and spatial readouts, while co-immunoprecipitation reveals altered protein interaction networks. For further technical information, please contact Ascent Research.
