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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
5
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pubmed:dateCreated |
2008-3-10
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pubmed:abstractText |
To explore the role of Dicer-dependent control mechanisms in B lymphocyte development, we ablated this enzyme in early B cell progenitors. This resulted in a developmental block at the pro- to pre-B cell transition. Gene-expression profiling revealed a miR-17 approximately 92 signature in the 3'UTRs of genes upregulated in Dicer-deficient pro-B cells; a top miR-17 approximately 92 target, the proapoptotic molecule Bim, was highly upregulated. Accordingly, B cell development could be partially rescued by ablation of Bim or transgenic expression of the prosurvival protein Bcl-2. This allowed us to assess the impact of Dicer deficiency on the V(D)J recombination program in developing B cells. We found intact Ig gene rearrangements in immunoglobulin heavy (IgH) and kappa chain loci, but increased sterile transcription and usage of D(H) elements of the DSP family in IgH, and increased N sequence addition in Igkappa due to deregulated transcription of the terminal deoxynucleotidyl transferase gene.
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pubmed:grant |
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
1097-4172
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pubmed:author |
pubmed-author:ChakrabortyTirthaT,
pubmed-author:CobbBradley SBS,
pubmed-author:GallerGunther RGR,
pubmed-author:JensenKariK,
pubmed-author:KanellopoulouChryssaC,
pubmed-author:KoralovSergei BSB,
pubmed-author:KrekAzraA,
pubmed-author:MerkenschlagerMatthiasM,
pubmed-author:MuljoStefan ASA,
pubmed-author:RajewskyKlausK,
pubmed-author:RajewskyNikolausN
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pubmed:issnType |
Electronic
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pubmed:day |
7
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pubmed:volume |
132
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
860-74
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:18329371-3' Untranslated Regions,
pubmed-meshheading:18329371-Animals,
pubmed-meshheading:18329371-Antibody Diversity,
pubmed-meshheading:18329371-B-Lymphocytes,
pubmed-meshheading:18329371-Blotting, Northern,
pubmed-meshheading:18329371-Cell Survival,
pubmed-meshheading:18329371-DEAD-box RNA Helicases,
pubmed-meshheading:18329371-Endoribonucleases,
pubmed-meshheading:18329371-Gene Expression Profiling,
pubmed-meshheading:18329371-Gene Rearrangement, B-Lymphocyte,
pubmed-meshheading:18329371-Immunoglobulins,
pubmed-meshheading:18329371-Mice,
pubmed-meshheading:18329371-Mice, Knockout,
pubmed-meshheading:18329371-MicroRNAs,
pubmed-meshheading:18329371-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:18329371-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18329371-Ribonuclease III,
pubmed-meshheading:18329371-Specific Pathogen-Free Organisms
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pubmed:year |
2008
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pubmed:articleTitle |
Dicer ablation affects antibody diversity and cell survival in the B lymphocyte lineage.
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pubmed:affiliation |
Immune Disease Institute and Department of Pathology, Harvard Medical School, 200 Longwood Avenue, Boston, MA 02115, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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