Linked Life Data

15032688

Source:http://linkedlifedata.com/resource/pubmed/id/15032688

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2004-3-22
pubmed:abstractText
B-lymphocytes are exposed to a reduction/oxidation environment during activation or inflammatory process, and the antioxidant systems are functional to protect themselves against harmful reactive oxygen species (ROS). The crucial roles of thioredoxin-2 (Trx-2) and a DNA repair enzyme APE/Ref-1 in mitochondria are reported in B-lymphocytes. Furthermore, ROS stimulate different signaling pathways in many cellular responses. Their effects often cause some diseases or are utilized for the treatment of other diseases. For example, the cells derived from Fanconi anemia (FA) patients are intolerant of oxidative stress and the therapeutic effect of anti-CD20 monoclonal antibody rituximab on B cell lymphoproliferative disorders is due to the generation of ROS. To clarify the oxidative stress-induced signaling pathways, we stimulated a B cell line with various concentrations of H(2)O(2). As a result, a protein tyrosine kinase, Syk was involved in the induction of G2/M arrest and protection of cells from apoptosis. Syk might inhibit the activation of caspase-9 through Akt thereby protecting cells from oxidative stress-induced apoptosis. On the other hand, Syk-dependent PLC-gamma2 activation was required for acceleration towards apoptosis following oxidative stress. These findings suggest that oxidative stress-induced Syk activation triggers the activation of different pathways, such as pro-apoptotic or survival pathways, and that the balance of these pathways is a key factor in determining the fate of the cells exposed to oxidative stress. In contrast, the stimulation with the millimolar concentrations of H(2)O(2) rapidly led to necrosis in which tyrosine phosphorylation of FAK was involved at the downstream of Lyn and Syk.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1381-6128
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
835-9
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:15032688-Antibodies, Monoclonal, pubmed-meshheading:15032688-Antibodies, Monoclonal, Murine-Derived, pubmed-meshheading:15032688-Antineoplastic Agents, pubmed-meshheading:15032688-Antioxidants, pubmed-meshheading:15032688-Apoptosis, pubmed-meshheading:15032688-B-Lymphocytes, pubmed-meshheading:15032688-Enzyme Precursors, pubmed-meshheading:15032688-Fanconi Anemia, pubmed-meshheading:15032688-Humans, pubmed-meshheading:15032688-Hydrogen Peroxide, pubmed-meshheading:15032688-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:15032688-Lymphocyte Activation, pubmed-meshheading:15032688-Lymphoma, B-Cell, pubmed-meshheading:15032688-Necrosis, pubmed-meshheading:15032688-Oxidative Stress, pubmed-meshheading:15032688-Protein-Tyrosine Kinases, pubmed-meshheading:15032688-Reactive Oxygen Species, pubmed-meshheading:15032688-Signal Transduction
pubmed:year
2004
pubmed:articleTitle
B cell responses to oxidative stress.
pubmed:affiliation
Department of Genome Sciences, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
pubmed:publicationType
Journal Article, Review