Linked Life Data

9729279

Source:http://linkedlifedata.com/resource/pubmed/id/9729279

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1999-5-12
pubmed:abstractText
The proto-oncogene product Bcl-2 is unique in that it inhibits apoptosis rather than promoting cell proliferation. In the present study, we encountered a new possible role of Bcl-2 in the neuronal differentiation. Rat pheochromocytoma PC12 cells have been known as the model of neuronal differentiation by the stimulation of NGF. Bcl-2 transfected PC12 (MB2) cells showed the accelerated neuronal differentiation, as compared with control PC12 (V4) cells. In addition, chemotherapeutic agents Taxol which has been known as neurotoxic compound, induced the acute neuronal cell atrophy and suppressed neuronal differentiation. This neuronal cell atrophy and suppression of neuronal differentiation were not due to apoptotic cell death. Interestingly, Bcl-2 rescued PC12 cells from both neuronal cell atrophy and suppression of neuronal differentiation. Taxol suppressed polymerization between neurofilament light and heavy (NF-L and NF-H), and MB2 cell extract rescued it. We, therefore, suggest the acceleration of polymerization between NF-L and NF-H as the new possible role of Bcl-2.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0006-8993
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Elsevier Science B.V.
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
801
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59-66
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
Bcl-2 accelerates the neuronal differentiation: new evidence approaching to the biofunction of bcl-2 in the neuronal system.
pubmed:affiliation
Drug Safety Research Laboratory, Daiichi Pharmaceutical Co. Ltd., Tokyo R&D Center 16-13, Kiatakasai-1, Edogawa-ku, Tokyo 134, Japan. LEBOO373@niftyserve.or.jp
pubmed:publicationType
Journal Article