◀ Back to BCL2
BCL2 — IL1B
Text-mined interactions from Literome
Kühn et al., J Immunol 2000
:
In addition,
IL-1 beta significantly
increased the expression of
Bcl-2
Marselli et al., J Clin Endocrinol Metab 2001
:
IL-1beta , interferon gamma, and TNF alpha
caused no major change in either islet cell survival or
Bcl-2 and Bax mRNA expression after a 12-h incubation ; however, a marked increase in the amount of dead cells, with a major decrease of Bcl-2 mRNA expression, was observed after 72 h
Chandrasekar et al., J Biol Chem 2004
(Inflammation) :
Treatment of HCMEC with IL-18 increases 1 ) NF-kappaB DNA binding activity ; 2 ) induces kappaB-driven luciferase activity ; 3 ) induces
IL-1beta and TNF-alpha expression via NF-kappaB activation ; 4 )
inhibits antiapoptotic
Bcl-2 and Bcl-X ( L ) ; 5 ) up-regulates proapoptotic Fas, Fas-L, and Bcl-X ( S ) expression ; 6 ) induces fas and Fas-L promoter activities via NF-kappaB activation ; 7 ) activates caspases-8, -3, -9, and BID ; 8 ) induces cytochrome c release into the cytoplasm ; 9 ) inhibits FLIP ; and 10 ) induces HCME cell death by apoptosis as seen by increased annexin V staining and increased levels of mono- and oligonucleosomal fragmented DNA
Cooke et al., Transplantation 2005
:
Overexpression of human
Bcl-2 in syngeneic rat donor lungs preserves posttransplant function and
reduces intragraft caspase activity and
interleukin-1beta production ... The authors investigated whether gene transfer of the human antiapoptotic protein
Bcl-2 by means of intratracheal adenoviral administration would preserve posttransplant lung function and
reduce intragraft activated caspase activity and
IL-1beta production in syngeneic rat donor lung grafts
Lizard et al., FEBS Lett 1997
(Leukemia) :
7Beta-hydroxycholesterol and 7-ketocholesterol
induced nuclear condensation and/or fragmentation, internucleosomal DNA fragmentation, and
IL-1beta secretion, which were partially inhibited by
Bcl-2 overexpression
Lee et al., Mol Genet Metab 1998
:
Bcl-2 regulates nonapoptotic signal transduction : inhibition of c-Jun N-terminal kinase (JNK) activation by
IL-1 beta and hydrogen peroxide