Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 1999 Mar 8;144(5):1019–1031. doi: 10.1083/jcb.144.5.1019

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Gene targeting of the PTP-PEST suppresses fibroblast motility on the extracellular matrix fibronectin. Monolayers of each cell line were wounded (a and b) and maintained at 37°C for 24 h before fixing (c and d). The ability to migrate into the wound was monitored by phase-contrast microscopy of unstained cells which were photographed (×100). The aspect of each wound represents the typical result obtained after five independent experiments. In a chamber-type assay (e), the bottom side of the polycarbonate membrane was coated with fibronectin, and 10⁵ cells were added to the top chamber. After 5 h, the cells that translocated to the bottom side of the membrane were counted and the result is shown as an average of eight fields from four independent experiments (error bars: standard deviation). PTP-PEST (−/−) cells stably overexpressing wild-type PTP-PEST were also tested by the same method. (Inset) Western blotting against PTP-PEST in the two cell lines. The band that appears represents overexpression since the antibody is known not to detect endogenous levels of PTP-PEST. Bar, 200 μm.

Gene targeting of the PTP-PEST suppresses fibroblast motility on the extracellular matrix fibronectin. Monolayers of each cell line were wounded (a and b) and maintained at 37°C for 24 h before fixing (c and d). The ability to migrate into the wound was monitored by phase-contrast microscopy of unstained cells which were photographed (×100). The aspect of each wound represents the typical result obtained after five independent experiments. In a chamber-type assay (e), the bottom side of the polycarbonate membrane was coated with fibronectin, and 10⁵ cells were added to the top chamber. After 5 h, the cells that translocated to the bottom side of the membrane were counted and the result is shown as an average of eight fields from four independent experiments (error bars: standard deviation). PTP-PEST (−/−) cells stably overexpressing wild-type PTP-PEST were also tested by the same method. (Inset) Western blotting against PTP-PEST in the two cell lines. The band that appears represents overexpression since the antibody is known not to detect endogenous levels of PTP-PEST. Bar, 200 μm.