Linked Life Data

11291051

Source:http://linkedlifedata.com/resource/pubmed/id/11291051

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-4-6
pubmed:abstractText
Five Epstein-Barr virus (EBV)-positive human lymphoma cell lines maintained in severe combined immune deficiency (SCID) mice were used to investigate the role of G1 cyclins in EBV-induced lymphomagenesis. All the primary tumors had been negative for EBV but became positive after establishment in SCID mice, with monoclonal immunoglobulin gene rearrangement and EBV monoclonality. To compare the expression status of G1 cyclins, these EBV-associated lymphoma lines (6 EBV[-] human SCID mouse lymphoma lines, 13 human B cell lymphomas and 8 samples of human tonsil tissue) were examined by reverse transcription-polymerase chain reaction-Southern blotting, Western blotting and immunohistochemistry. mRNA expression of cyclin D1 (CCND1), cyclin D2 (CCND2), cyclin E (CCNE), cyclin-dependent kinase 2 (CDK2) and 4 (CDK4) was found in all 3 types of lymphomas. Western blotting demonstrated identical results. Immunohistochemistry revealed CCND1 to be negative in all lymphomas. CCND2 was positive and restricted to the nuclei in all EBV(+) SCID mouse lymphoma lines, whereas it was limited to the cytoplasm in half of the EBV(-) counterparts. CCNE was positive in the nuclei in all EBV(+) but negative in all EBV(-) SCID mouse lymphoma lines. Immunoprecipitation of EBV(+) and (-) SCID mouse lymphomas for CCND1, CCND2 and CCNE vs. p21, PCNA and CDK2 or CDK4 demonstrated that, in EBV(+) SCID lines, CCND2/CDK4 complexes were present without binding to p21, suggesting independence from p21 regulation. In EBV(-) SCID mouse lymphomas, half of the cases showed complex formation of CCND2/CDK4 without binding of p21. In contrast, CCND1/CDK4 and CCNE/CDK2 were under regulation of p21 in both EBV(+) and (-) lymphomas. These results suggest that differential expression of CCNDs, CCNE and CDKs, as well as variation in their subcellular localization and association with CDK-inhibitor protein, could explain differences in cell proliferation between EBV(+) and EBV(-) lymphomas.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0020-7136
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
92
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
232-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11291051-Animals, pubmed-meshheading:11291051-Blotting, Southern, pubmed-meshheading:11291051-Blotting, Western, pubmed-meshheading:11291051-Cell Line, Transformed, pubmed-meshheading:11291051-Cell Transformation, Viral, pubmed-meshheading:11291051-Cyclin-Dependent Kinase Inhibitor p21, pubmed-meshheading:11291051-Cyclin-Dependent Kinases, pubmed-meshheading:11291051-Cyclins, pubmed-meshheading:11291051-Epstein-Barr Virus Infections, pubmed-meshheading:11291051-G1 Phase, pubmed-meshheading:11291051-Humans, pubmed-meshheading:11291051-Immunohistochemistry, pubmed-meshheading:11291051-Lymphoma, B-Cell, pubmed-meshheading:11291051-Mice, pubmed-meshheading:11291051-Mice, SCID, pubmed-meshheading:11291051-Neoplasm Transplantation, pubmed-meshheading:11291051-Precipitin Tests, pubmed-meshheading:11291051-RNA, Viral, pubmed-meshheading:11291051-Reverse Transcriptase Polymerase Chain Reaction
pubmed:year
2001
pubmed:articleTitle
Study on the role of G1 cyclins in Epstein-Barr virus-associated human lymphomas maintained in severe combined immune deficiency (SCID) mice.
pubmed:affiliation
First Department of Pathology, Toyama Medical and Pharmaceutical University, Sugitani 2630, Toyama 930-0194, Japan. ymp@ms.toyama-mpu.ac.jp
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't