Atm) depends on a set of repair factors...

Bacterial pathogen Helicobacter Pylori chronically affects human gastric mucosa and is a major risk factor for development of stomach cancer. Molecular mechanisms

-H. pylori associated gastric carcinogenesis remains poorly defined. In this study we examined the possibility that H. pylori

directly threatens the integrity of the genome of its host cell. We provide evidence that infection is DNA dvunitevy

breaks (DSBs) in primary and transformed mouse and human epithelial and mesenchymal cells. Induction of AS depends on

direct contact with live bacteria, mammalian cells. Infections can cause DNA damage, probably termination

nuclear DNA gel electrophoresis pulse field and high magnification microscope metaphase chromosomes. Bacterial >> << adhesion (eg, through blood group antigen-binding adhezyny) needed to induce DSBs, unlike

pylorus H.

Virulence factors vakuolizuyetsya cytotoxin, γ-hlutamiltranspeptydazy and cytotoxin associated gene (CAG) pathogenicity island

optional for induction of DSBs. DNA breaks damage signaling and repair response involving

ataxia telangiectasia mutated serial (ATM) depends on a set of repair factors p53-binding protein (53BP1) and

mediator of DNA damage checkpoint protein 1 (MDC1) and N2A histone variant X (H2AX) phosphorylation. While most breaks

repaired effectively in stopping infection, we note that the continued active infection leads to saturation

cell repair capabilities. Thus, we can conclude that DNA damage, then potentially inaccurate repair complies with >>

<< carcinogenic properties of H. pylori

, and mutagenic properties in vitro and in vivo and can buy strattera lead to genetic instability and frequent chromosomal aberrations

which is a sign of stomach cancer. . << >>