Linked Life Data

17765974

Source:http://linkedlifedata.com/resource/pubmed/id/17765974

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-11-5
pubmed:abstractText
Natural killer (NK) cells are the effectors of innate immunity to act as the first line of defense against viruses and tumors. Granzyme H (GzmH) is predicted to evolve from GzmB and constitutively expressed at a high level in human NK cells. It indicates GzmH plays a pivotal role in NK cell mediated cytolysis. However GzmH is defined as an orphan granzyme and its function has less been defined. Here we demonstrate GzmH can induce rapid apoptosis of target cells, which is dependent on caspase activation and mitochondrial damage. GzmH-induced death is characterized by phophatidylserine externalization, nuclear condensation, DNA fragmentation, caspase activation and cytochrome c release that are hallmarks of typical apoptosis. GzmH can directly cleave ICAD to unleash CAD for DNA fragmentation. Moreover, GzmH directly processes Bid to produce the active form tBid leading to cytochrome c release. Therefore, GzmH may play an essential role in caspase-dependent pathogen clearance in the innate immunity that may complement the proapoptotic function of GzmB in human NK cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0161-5890
pubmed:author
pubmed:issnType
Print
pubmed:volume
45
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1044-55
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Granzyme H induces apoptosis of target tumor cells characterized by DNA fragmentation and Bid-dependent mitochondrial damage.
pubmed:affiliation
National Laboratory of Biomacromolecules, Center for Infection and Immunity, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't