Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1995-11-28
pubmed:abstractText
The induction of apoptosis via surface IgM (sIgM) in immature B cells requires de novo transcription. To investigate the regulation of activation-induced cell death (AICD) in B cells we used a cell line model consisting of an Epstein-Barr virus-negative Burkitt lymphoma cell line (BL41), which is highly sensitive, and a subclone which is resistant to sIgM-mediated apoptosis (BL41/B5). Resistance in this cell line was not due to down-regulation of sIgM or functional impairment in signal transduction of the surface Ig complex. The zinc finger transcription factor nur77 has been implicated to play an important role in CD3-mediated apoptosis in murine T cells. We were able to demonstrate that surface IgM ligation and subsequent apoptosis in BL41 cells is associated with a concomitant induction of NAK-1, the human nur77 homologue. Induction of NAK-1 mRNA and DNA binding activity in the nucleus could be readily observed by means of Northern blot and electrophoretic mobility shift assay, respectively. In contrast, the resistant clone BL41/B5 did not show any NAK-1 expression upon stimulation. This suggests a role for NAK-1 in sIgM-mediated apoptosis of immature B cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2506-10
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Involvement of NAK-1, the human nur77 homologue, in surface IgM-mediated apoptosis in Burkitt lymphoma cell line BL41.
pubmed:affiliation
Humboldt University, Virchow Klinikum, Robert Rössle Klinik, Department of Internal Medicine (Medical Oncology and Tumorimmunology) Berlin-Buch, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't