What does CagA protein do?
Through the interaction, CagA disrupts adherens junctions by perturbing the adaptor function of Crk in cell signaling. CagA binds to Grb2 via the EPIYA-containing region and thus aberrantly activates the Ras signaling pathway to stimulate abnormal cell proliferation.
What is CagA gene?
Helicobacter pylori virulence factor CagA (cytotoxin-associated gene A) is a 120–145kDa protein encoded on the 40kb cag pathogenicity island (PAI). H. pylori strains can be divided into CagA positive or negative strains.
How does CagA cause gastric cancer?
When delivered into gastric epithelial cells, the CagA oncoprotein perturbs multiple intracellular signaling pathways and then promotes malignant transformation of the host cells by providing cancer-hallmark capabilities.
What is CagA and VacA?
Two of the virulence factors that have been implicated in this process are cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA), which are cytotoxins that are injected and secreted by H. pylori, respectively.
What does CagA H. pylori do?
Helicobacter pylori CagA Protein Negatively Regulates Autophagy and Promotes Inflammatory Response via c-Met-PI3K/Akt-mTOR Signaling Pathway. Cytotoxin-associated-gene A (CagA) of Helicobacter pylori (H. pylori) is a virulence factor that plays critical roles in H. pylori-induced gastric inflammation.
What toxins Does H. pylori produce?
At the epithelial cell level H. pylori enzymes generate toxic molecules: ammonia (urease), lysolecithin (phospholipases) and acetaldehyde (alcohol dehydrogenase). The harmful effects of ammonia have been studied the most intensively and seem to be a likely mechanism of pathogenicity.
What is H. pylori CagA?
What type of exotoxin action does Helicobacter pylori take?
H. pylori produces an exotoxin, vacuolating cytotoxin (VacA), which is an important virulence factor associated with gastritis and ulceration. Indeed, oral administration of VacA to mice caused severe gastric damage.
How does H. pylori CagA protein contribute to tumorigenesis?
pylori-induced tumorigenesis of gastric cancer. CagA acts as an initiator that activates multiple host cell signaling pathways via direct or indirect impacts on vital signaling proteins, thereby leading to signaling pathway-dependent oncogene upregulation (Table 1).
What are the virulence factors of Helicobacter pylori?
The virulence factors of H. pylori can be categorized to be related with 3 major pathogenic processes, including colonization, immune escape and disease induction (Table 1). The virulence factors responsible for establishing colonization include urease, flagella, chemotaxis system, and adhesins [2, 3].
Is CagA a virulence factor?
Abstract. Background—VacA and CagA proteins have been reported to be major virulence factors of Helicobacter pylori.
What is the pathogenesis of Helicobacter pylori?
The pathogenesis of Helicobacter pylori infection in humans can be described in three steps: (1) entry to, adherence to, and colonization of the human gastric mucosa; (2) avoidance, subversion, or exploitation of the human immune system; and (3) multiplication, tissue damage, and transmission to a new susceptible host …
What is the CagA protein?
The CagA protein is the 4 th most abundant protein produced by H. pylori strain 26695, ranging behind GroEL (Hp0010), UreB (Hp0072) and TsaA (Hp1563) 11.
What is CagA in Helicobacter pylori?
CagA is one of the most studied pathogenicity factors of the bacterial pathogen Helicobacter pylori. It is injected into host cells via the H. pylori cag -Type IV secretion system.
What is the role of cagA in stem cell differentiation?
CagA activates the caudal-related homeobox 1 (CDX1) transcription factor that induces KLF5 and SALL4 expression ( Fujii et al., 2012 ). KLF5 and SALL4 maintain the stem cell pluripotent marker expression ( Zhang et al., 2006 ).
What is the role of cagA in the pathophysiology of acute myeloid leukemia?
Presence of cag is a major determinant of disease outcome due to expression of the CagA protein, which is able to interact with a wide range of host signaling proteins and undergo tyrosine phosphorylation modifications.