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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
1990-12-7
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pubmed:databankReference | |
pubmed:abstractText |
The protein sequence deduced from the open reading frame of a human placental cDNA encoding a cAMP-responsive enhancer (CRE)-binding protein (CREB-327) has structural features characteristic of several other transcriptional transactivator proteins including jun, fos, C/EBP, myc, and CRE-BP1. Results of Southwestern analysis of nuclear extracts from several different cell lines show that there are multiple CRE-binding proteins, which vary in size in cell lines derived from different tissues and animal species. To examine the molecular diversity of CREB-327 and related proteins at the nucleic acid level, we used labeled cDNAs from human placenta that encode two different CRE-binding proteins (CREB-327 and CRE-BP1) to probe Northern and Southern blots. Both probes hybridized to multiple fragments on Southern blots of genomic DNA from various species. Alternatively, when a human placental c-jun probe was hybridized to the same blot, a single fragment was detected in most cases, consistent with the intronless nature of the human c-jun gene. The CREB-327 probe hybridized to multiple mRNAs, derived from human placenta, ranging in size from 2-9 kilobases. In contrast, the CRE-BP1 probe identified a single 4-kilobase mRNA. Sequence analyses of several overlapping human genomic cosmid clones containing CREB-327 sequences in conjunction with polymerase chain reaction indicates that the CREB-327/341 cDNAs are composed of at least eight or nine exons, and analyses of human placental cDNAs provide direct evidence for at least one alternatively spliced exon. Analyses of mouse/hamster-human hybridoma DNAs by Southern blotting and polymerase chain reaction localizes the CREB-327/341 gene to human chromosome 2. The results indicate that there is a dichotomy of CREB-like proteins, those that are related by overall structure and DNA-binding specificity as well as those that are related by close similarities of primary sequences.
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pubmed:grant | |
pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/DNA,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0888-8809
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
4
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
|
pubmed:pagination |
920-30
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:2146494-Amino Acid Sequence,
pubmed-meshheading:2146494-Animals,
pubmed-meshheading:2146494-Base Sequence,
pubmed-meshheading:2146494-Chromosome Mapping,
pubmed-meshheading:2146494-Chromosomes, Human, Pair 2,
pubmed-meshheading:2146494-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:2146494-DNA,
pubmed-meshheading:2146494-DNA-Binding Proteins,
pubmed-meshheading:2146494-Exons,
pubmed-meshheading:2146494-Female,
pubmed-meshheading:2146494-Genetic Variation,
pubmed-meshheading:2146494-Humans,
pubmed-meshheading:2146494-Molecular Sequence Data,
pubmed-meshheading:2146494-Peptide Fragments,
pubmed-meshheading:2146494-Placenta,
pubmed-meshheading:2146494-Pregnancy,
pubmed-meshheading:2146494-RNA, Messenger,
pubmed-meshheading:2146494-RNA Splicing,
pubmed-meshheading:2146494-Rats,
pubmed-meshheading:2146494-Transcription, Genetic
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pubmed:year |
1990
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pubmed:articleTitle |
Multiple adenosine 3',5'-cyclic [corrected] monophosphate response element DNA-binding proteins generated by gene diversification and alternative exon splicing.
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pubmed:affiliation |
Massachusetts General Hospital, Howard Hughes Medical Institute, Harvard Medical School, Boston 02114.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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