Linked Life Data

14646585

Source:http://linkedlifedata.com/resource/pubmed/id/14646585

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2003-12-3
pubmed:abstractText
Phagocytosis by inflammatory cells is an essential step and a part of innate immunity for protection against foreign pathogens, microorganism or dead cells. Phagocytosis, endocytotic events sequel to binding particle ligands to the specific receptors on phagocyte cell surface such as Fcgamma recptor (FcgammaR), complement receptor (CR), beta-glucan receptor, and phosphatidylserine (PS) receptor, require actin assembly, pseudopod extension and phagosome closure. Rho GTPases (RhoA, Cdc42, and Rac1) are critically involved in these processes. Abrupt superoxide formation, called as oxidative burst, occurs through NADPH oxidase complex in leukocytes following phagocytosis. NADPH oxidase complex is composed of membrane proteins, p22PHOX and gp91PHOX, and cytosolic proteins, p40PHOX, p47PHOX and p67PHOX. The cytosolic subunits and Rac-GTP are translocated to the membrane, forming complete NADPH oxidase complex with membrane part subunits. Binding of imunoglobulin G (IgG)- and complement-opsonized particles to FcgammaR and CR of leukocytes induces apoptosis of the cells, which may be due to oxidative burst and accompanying cytochrome c release and casapase-3 activation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1226-3613
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
325-35
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Phagocytosis induces superoxide formation and apoptosis in macrophages.
pubmed:affiliation
Department of Biochemistry, College of Medicine, Hallym University, Ockchon 1, Kangwon-do 200-702, Korea. jbpark@hallym.ac.kr
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't