Once the bacterial cell signaling protein cagA reaches
the host cytosol, it is capable of altering subsequent generations of progenitor cells, leading to the development of cancer through changes in mitotic activity, apoptosis, cellular assembly, and signaling.26 Although it should be noted that while the presence of the cagA protein doubles the risk of gastric cancer, cagA - negative strands also increase the risk of distal gastric cancer.27 Additional H pylori virulence factors include babA2, which encodes bacterial adhesion with gastric epithelial cells, and vacuolating cytotoxin A, which is encoded by the gene vacA.28, 29 H pylori strains carrying some combination of the babA2, cagA, and vacA genes were associated with the highest risk of developing intestinal metaplasia.
Not exact matches
LLO lacking the PEST - like sequence accumulated in the
host - cell
cytosol, suggesting that this sequence targets LLO for degradation.
One essential virulence mechanism constitutes the specialized secretion systems that are designed to penetrate
host - cell membranes and insert pathogen proteins directly into the
host cell's
cytosol.
These cells relied on a protein called cyclic GMP - AMP synthase (cGAS) to sense the viral DNA in the
cytosol before the foreign DNA became integrated into the
host genome.
Perforin - 2 protects
host cells and mice by restricting the vacuole to
cytosol transitioning of a bacterial pathogen.