Description

The TRPV4 Knockout HEK293T Cell Line is a CRISPR/Cas9-edited knockout cell line featuring targeted disruption of the TRPV4 gene. This loss-of-function model enables precise dissection of TRPV4-dependent cellular processes in the widely used HEK293T background, providing a reliable system for mechanistic studies and drug discovery efforts.

HEK293T cells are a human embryonic kidney line transformed with SV40 large T-antigen, facilitating high-level transgene expression and efficient transfection. They serve as a versatile platform for protein expression, ion channel research, and signaling pathway analysis, combining the advantages of renal epithelial origin with robust genetic manipulability.

TRPV4 is a polymodal non-selective cation channel activated by mechanical stretch, hypotonic swelling, heat, and chemical agonists including 4??-PDD and arachidonic acid. It functions as an osmosensor and mechanosensor, mediating calcium influx that triggers calmodulin, calcineurin, and CaMKII signaling, ultimately regulating transcription factors like NFAT and AP-1. The channel interacts with PACSIN2 and caveolin-1 and is modulated by PKA, PKC, and Src kinase. TRPV4-dependent calcium signals intersect with the MAPK/ERK and PI3K-Akt pathways, linking environmental stimuli to gene expression, cell volume control, and inflammatory responses.

Using HEK293T cells as the host provides a simplified, reproducible system to study TRPV4 function in isolation, free from the confounding influence of tissue-specific accessory proteins. This knockout model is particularly advantageous for investigating human TRPV4 mutations linked to skeletal dysplasias and neuropathies, as the human embryonic kidney background supports native-like channel properties while allowing facile transfection for structure-function analysis.

This cell line is ideal for calcium imaging assays using Fluo-4 or Fura-2, patch-clamp electrophysiology, and western blotting for phospho-ERK and other downstream effectors. It supports cell volume regulation and migration studies under mechanical or osmotic challenge and serves as a platform for high-throughput screening of TRPV4 modulators. The model is directly applicable to research on osteoarthritis, pulmonary edema, cardiac fibrosis, and TRPV4-related channelopathies. For more information, contact Ascent Research.