Skip to Main Content
Article navigation

The H. pylori CagA protein disrupts cell–cell contacts among normally adherent epithelial cells.

The ulcer-inducing bacterium Helicobacter pylori busts through the cells that line the stomach by hijacking a host protein, suggest Suzuki and colleagues on page 1235. The co-opted protein turns on multiple signaling pathways in gastric cells that cause the normally adhesive cells to pull apart from their neighbors.

Roughly half of all people worldwide have H. pylori living in their stomachs. Most people host the infection without consequence but, in some, H. pylori infection triggers peptic ulcers and gastric cancer. H. pylori encodes a set of proteins that allows it to adhere to and thrive in the stomach and to avoid immune attack. One of these proteins—CagA (cytotoxin-associated antigen-A)—helps ward off immune cells but also disrupts the epithelial cells that line the stomach.

Many studies have investigated how CagA, which is...

You do not currently have access to this content.
Don't already have an account? Register

or Create an Account

Close Modal
Close Modal

Gift article access

As a benefit of your subscription, you can share temporary access to restricted articles.

Each link will stop working after 30 days or 10 uses. You may create up to 10 links in a 30 day period.

Please sign in to your personal account to gift article access.

Register

Gift article access

As a benefit of your subscription, you can share temporary access to restricted articles.

Each link will stop working after 30 days or 10 uses. You may create up to 10 links in a 30 day period.

Gift articles remaining: --

Gift article access

Each link will stop working after 30 days or 10 uses. You may create up to 10 links in a 30 day period.

Gift articles remaining: --

Gift article access

As a benefit of your subscription, you can share temporary access to restricted articles.

Each link will stop working after 30 days or 10 uses.

You have reached the limit of 10 links within a 30 day period.