rdf:type |
|
lifeskim:mentions |
umls-concept:C0009013,
umls-concept:C0017428,
umls-concept:C0080194,
umls-concept:C0086418,
umls-concept:C0205145,
umls-concept:C0205147,
umls-concept:C0282523,
umls-concept:C0376298,
umls-concept:C0600401,
umls-concept:C0600472,
umls-concept:C1158478,
umls-concept:C1167395,
umls-concept:C1444754,
umls-concept:C1527075,
umls-concept:C1705422
|
pubmed:issue |
9
|
pubmed:dateCreated |
1991-7-5
|
pubmed:databankReference |
|
pubmed:abstractText |
Efficient recovery of clones from the 5' end of the human L1 dispersed repetitive elements necessitates the use of deletion mcr- host strains since this region contains a CpG island which is hypermethylated in vivo. Clones recovered with conventional mcr+ hosts seem to have been derived preferentially from L1 members which have accumulated mutations that have removed sites of methylation. We present a revised consensus from the 5' presumptive control region of these elements. This revised consensus contains a consensus RNA polymerase III promoter which would permit the synthesis of transcripts from the 5' end of full length L1 elements. Such potential transcripts are likely to exhibit a high degree of secondary structure. In addition, we have determined the flanking sequences for 6 full length L1 elements. The majority of full length L1 clones show no convincing evidence for target site duplication in the insertion site as commonly observed with truncated L1 elements. These data would be consistent with two mechanisms of integration of transposing L1 elements with different mechanisms predominating for full length and truncated elements.
|
pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-1698287,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-1849497,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2111008,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2161558,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2165587,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2165863,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2339059,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2423876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2423883,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2430722,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2454389,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2459662,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2538469,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2546156,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2552406,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2555370,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2837736,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2842063,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-2845369,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3023821,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3023904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3035487,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3277717,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3593377,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3656447,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3692483,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-3934392,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-6163133,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-6299899,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-6325709,
http://linkedlifedata.com/resource/pubmed/commentcorrection/1710354-7312050
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
0305-1048
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
11
|
pubmed:volume |
19
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2395-401
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:1710354-Base Sequence,
pubmed-meshheading:1710354-Cloning, Molecular,
pubmed-meshheading:1710354-Consensus Sequence,
pubmed-meshheading:1710354-DNA,
pubmed-meshheading:1710354-DNA Transposable Elements,
pubmed-meshheading:1710354-Dinucleoside Phosphates,
pubmed-meshheading:1710354-Humans,
pubmed-meshheading:1710354-Methylation,
pubmed-meshheading:1710354-Molecular Sequence Data,
pubmed-meshheading:1710354-Nucleic Acid Conformation,
pubmed-meshheading:1710354-Promoter Regions, Genetic,
pubmed-meshheading:1710354-RNA,
pubmed-meshheading:1710354-RNA Polymerase III
|
pubmed:year |
1991
|
pubmed:articleTitle |
Revised genomic consensus for the hypermethylated CpG island region of the human L1 transposon and integration sites of full length L1 elements from recombinant clones made using methylation-tolerant host strains.
|
pubmed:affiliation |
Peter MacCallum Cancer Institute, Melbourne, Victoria, Australia.
|