rdf:type |
|
lifeskim:mentions |
umls-concept:C0023487,
umls-concept:C0040624,
umls-concept:C0040715,
umls-concept:C0079411,
umls-concept:C0140278,
umls-concept:C0162768,
umls-concept:C0205419,
umls-concept:C0599718,
umls-concept:C0599813,
umls-concept:C0599893,
umls-concept:C1515708,
umls-concept:C1522702,
umls-concept:C2003941
|
pubmed:issue |
3
|
pubmed:dateCreated |
1994-3-8
|
pubmed:abstractText |
Recently, we described a recurrent variant translocation, t(11;17)(q23;q21), in acute promyelocytic leukemia (APL) which juxtaposes PLZF, a gene encoding a zinc finger protein, to RARA, encoding retinoic acid receptor alpha (RAR alpha). We have now cloned cDNAs encoding PLZF-RAR alpha chimeric proteins and studied their transactivating activities. In transient-expression assays, both the PLZF(A)-RAR alpha and PLZF(B)-RAR alpha fusion proteins like the PML-RAR alpha protein resulting from the well-known t(15;17) translocation in APL, antagonized endogenous and transfected wild-type RAR alpha in the presence of retinoic acid. Cotransfection assays showed that a significant repression of RAR alpha transactivation activity was obtained even with a very low PLZF-RAR alpha-expressing plasmid concentration. A "dominant negative" effect was observed when PLZF-RAR alpha fusion proteins were cotransfected with vectors expressing RAR alpha and retinoid X receptor alpha (RXR alpha). These abnormal transactivation properties observed in retinoic acid-sensitive myeloid cells strongly implicate the PLZF-RAR alpha fusion proteins in the molecular pathogenesis of APL.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1310153,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1311253,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1314166,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1333659,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1375719,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1650447,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1652368,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1652369,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1668609,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1720570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1850498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1957167,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-1988151,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2153268,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2170850,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2173802,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2175343,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2218500,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2224119,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2440339,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2825025,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-2825036,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-3165295,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-3185736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-3821727,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-6586073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-6939451,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-8384553,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8302850-8387545
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Feb
|
pubmed:issn |
0027-8424
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
91
|
pubmed:geneSymbol |
PLZF,
RARA
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1178-82
|
pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8302850-Amino Acid Sequence,
pubmed-meshheading:8302850-Animals,
pubmed-meshheading:8302850-Cell Line,
pubmed-meshheading:8302850-Chromosomes, Human, Pair 11,
pubmed-meshheading:8302850-Chromosomes, Human, Pair 17,
pubmed-meshheading:8302850-Cloning, Molecular,
pubmed-meshheading:8302850-Genetic Variation,
pubmed-meshheading:8302850-Haplorhini,
pubmed-meshheading:8302850-Humans,
pubmed-meshheading:8302850-Leukemia, Promyelocytic, Acute,
pubmed-meshheading:8302850-Molecular Sequence Data,
pubmed-meshheading:8302850-Neoplasm Proteins,
pubmed-meshheading:8302850-Receptors, Retinoic Acid,
pubmed-meshheading:8302850-Recombinant Fusion Proteins,
pubmed-meshheading:8302850-Transcriptional Activation,
pubmed-meshheading:8302850-Transfection,
pubmed-meshheading:8302850-Translocation, Genetic,
pubmed-meshheading:8302850-Tretinoin,
pubmed-meshheading:8302850-Zinc Fingers
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pubmed:year |
1994
|
pubmed:articleTitle |
PLZF-RAR alpha fusion proteins generated from the variant t(11;17)(q23;q21) translocation in acute promyelocytic leukemia inhibit ligand-dependent transactivation of wild-type retinoic acid receptors.
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pubmed:affiliation |
Shanghai Institute of Hematology, Samuel Waxman Cancer Research Foundation Laboratory of Shanghai Second Medical University, Rui-Jin Hospital, China.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|