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Fiorio Pla, A., Ong, H.L., Cheng, K.T., Brossa, A., Bussolati, B., Lockwich, T., Paria, B., Munaron, L. and Ambudkar, I.S. (2012) TRPV4 Mediates Tumor-Derived Endothelial Cell Migration via Arachidonic Acid-Activated Actin Remodeling. Oncogene, 31, 200-212.
https://doi.org/10.1038/onc.2011.231

has been cited by the following article:

• TITLE: Ablation of TRPV4 in HepG2 with Its CRISPR/Cas9 Enhances Its Wound Healing

  AUTHORS: Eun Jeoung Lee, Sung Hwa Shin, Sunghee Hyun, Sang Sun Kang

  KEYWORDS: TRPV4, Ca2+ Ion Channel, E-Cadherin, Tubulin, Soft Agar Growth, CRISPR/Cas9 Scissor System

  JOURNAL NAME: American Journal of Molecular Biology, Vol.10 No.1, January 10, 2020

  ABSTRACT: TRPV4 activity modulates cell activities including receptor trafficking and transcriptional or translational regulations. We tested its CRISPR/Cas9 scissor efficacy in HepG2 (HEK293) cell noticed that it worked well in both cell lines to eliminate TRPV4 genome sequences. To confirm TRPV4 functions in the cell morphology maintenance and cell growth (beyond Ca2+ channel), we compared its wound healing, cell surface area, survival property and soft agar growth ability after deletion of TRPV4 gene in the cells with its CRISPR/Cas9 system. With these experiments, we confirmed that TRPV4 is required not only to function as Ca2+ channel but also to maintain its proper cell morphology as a corner stone protein on the cell adhesion junction.