|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
10
|
|
pubmed:dateCreated |
1995-6-9
|
|
pubmed:abstractText |
The p210bcr/abl chimeric protein is considered to be implicated in the pathogenesis of Philadelphia chromosome-positive human leukemias. To investigate its biologic function in vivo, we generated transgenic mice expressing p210bcr/abl driven by the metallothionein enhancer/promoter. Two of six founder mice and the transgenic progeny developed leukemias several months after birth. In the leukemic tissues, the expression of the p210bcr/abl transgene product was detected and the increased tyrosine-phosphorylation of cellular proteins was observed. The expressed p210bcr/abl transgene product was shown to possess an enhanced kinase activity. The leukemic cells showed rearrangements in the T-cell receptor loci, indicating that the leukemic cells were monoclonal and committed to the T-cell lineage. Polymerase chain reaction analysis for tissue distribution of p210bcr/abl expression showed that, in the transgenic line that reproducibly developed leukemias, p210bcr/abl was expressed in the hematopoietic tissues such as thymus and spleen; on the other hand, in the transgenic lines that have not developed leukemias, p210bcr/abl expression was detected only in the nonhematopoietic tissues such as the brain and kidney. These results suggest that the tumorigenicity of the p210bcr/abl chimeric protein is restricted to the hematopoietic tissues in vivo and that an event enhancing p210bcr/abl expression contributed a proliferative advantage to hematopoietic precursor cells and eventually developed T-cell leukemia in transgenic mice.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/Fusion Proteins, bcr-abl,
http://linkedlifedata.com/resource/pubmed/chemical/Metallothionein,
http://linkedlifedata.com/resource/pubmed/chemical/Phosphotyrosine,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...,
http://linkedlifedata.com/resource/pubmed/chemical/Tyrosine
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
May
|
|
pubmed:issn |
0006-4971
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
15
|
|
pubmed:volume |
85
|
|
pubmed:geneSymbol |
ABL,
BCR
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
2853-61
|
|
pubmed:dateRevised |
2008-11-21
|
|
pubmed:meshHeading |
pubmed-meshheading:7537982-Animals,
pubmed-meshheading:7537982-Base Sequence,
pubmed-meshheading:7537982-Clone Cells,
pubmed-meshheading:7537982-DNA Primers,
pubmed-meshheading:7537982-Female,
pubmed-meshheading:7537982-Fusion Proteins, bcr-abl,
pubmed-meshheading:7537982-Gene Expression Regulation, Neoplastic,
pubmed-meshheading:7537982-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor,
pubmed-meshheading:7537982-Gene Rearrangement, gamma-Chain T-Cell Antigen Receptor,
pubmed-meshheading:7537982-Genes, abl,
pubmed-meshheading:7537982-Leukemia, Myelogenous, Chronic, BCR-ABL Positive,
pubmed-meshheading:7537982-Leukemia, T-Cell,
pubmed-meshheading:7537982-Male,
pubmed-meshheading:7537982-Metallothionein,
pubmed-meshheading:7537982-Mice,
pubmed-meshheading:7537982-Mice, Transgenic,
pubmed-meshheading:7537982-Molecular Sequence Data,
pubmed-meshheading:7537982-Pedigree,
pubmed-meshheading:7537982-Phosphotyrosine,
pubmed-meshheading:7537982-Promoter Regions, Genetic,
pubmed-meshheading:7537982-RNA, Messenger,
pubmed-meshheading:7537982-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:7537982-Receptors, Antigen, T-Cell, gamma-delta,
pubmed-meshheading:7537982-Tissue Distribution,
pubmed-meshheading:7537982-Tyrosine
|
|
pubmed:year |
1995
|
|
pubmed:articleTitle |
Expression of p210bcr/abl by metallothionein promoter induced T-cell leukemia in transgenic mice.
|
|
pubmed:affiliation |
Department of Molecular Biology, Jichi Medical School, Tochigi-ken, Japan.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
