pubmed-article:15860505 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0026339 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0024660 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0085187 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C0936012 | lld:lifeskim |
pubmed-article:15860505 | lifeskim:mentions | umls-concept:C1956267 | lld:lifeskim |
pubmed-article:15860505 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:15860505 | pubmed:dateCreated | 2005-8-24 | lld:pubmed |
pubmed-article:15860505 | pubmed:abstractText | Critical telomere shortening in the absence of telomerase in late generation Terc-/- mice (G3 Terc-/-) or loss of telomere capping due to abrogation of the DNA repair/telomere binding protein Ku86 (Ku86-/- mice) results in telomere dysfunction and organismal premature aging. Here, we report on genome-wide transcription in mouse G3 Terc-/-, Ku86-/- and G3 Terc-/-/Ku86-/- germ cells using high-density oligonucleotide microarrays. Although a few transcripts are modulated specifically in Ku86- or Terc-deficient cells, the observed transcriptional response is mainly inductive and qualitatively similar for all three genotypes, with highest transcriptional induction observed in double mutant G3 Terc-/-/Ku86-/- cells compared with either single mutant. Analysis of 92 known genes induced in G3 Terc-/-/Ku86-/- germ cells compared with wild-type cells shows predominance of genes involved in cell adhesion, cell-to-cell and cell-to-matrix communication, as well as increased metabolic turnover and augmented antioxidant responses. In addition, the data presented in this study support the view that telomere dysfunction induces a robust compensatory response to rescue impaired germ cell function through the induction of survival signals related to the PI3-kinase pathway, as well as by the coordinated upregulation of transcripts that are essential for mammalian spermatogenesis. | lld:pubmed |
pubmed-article:15860505 | pubmed:language | eng | lld:pubmed |
pubmed-article:15860505 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860505 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:15860505 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860505 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860505 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860505 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:15860505 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:15860505 | pubmed:month | Sep | lld:pubmed |
pubmed-article:15860505 | pubmed:issn | 0143-3334 | lld:pubmed |
pubmed-article:15860505 | pubmed:author | pubmed-author:FrancoSoniaS | lld:pubmed |
pubmed-article:15860505 | pubmed:author | pubmed-author:BlascoMaría... | lld:pubmed |
pubmed-article:15860505 | pubmed:author | pubmed-author:KlattPeterP | lld:pubmed |
pubmed-article:15860505 | pubmed:author | pubmed-author:CanelaAndrésA | lld:pubmed |
pubmed-article:15860505 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:15860505 | pubmed:volume | 26 | lld:pubmed |
pubmed-article:15860505 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:15860505 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:15860505 | pubmed:pagination | 1613-26 | lld:pubmed |
pubmed-article:15860505 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
pubmed-article:15860505 | pubmed:meshHeading | pubmed-meshheading:15860505... | lld:pubmed |
pubmed-article:15860505 | pubmed:meshHeading | pubmed-meshheading:15860505... | lld:pubmed |
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pubmed-article:15860505 | pubmed:meshHeading | pubmed-meshheading:15860505... | lld:pubmed |
pubmed-article:15860505 | pubmed:meshHeading | pubmed-meshheading:15860505... | lld:pubmed |
pubmed-article:15860505 | pubmed:meshHeading | pubmed-meshheading:15860505... | lld:pubmed |
pubmed-article:15860505 | pubmed:meshHeading | pubmed-meshheading:15860505... | lld:pubmed |
pubmed-article:15860505 | pubmed:meshHeading | pubmed-meshheading:15860505... | lld:pubmed |
pubmed-article:15860505 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:15860505 | pubmed:articleTitle | Effectors of mammalian telomere dysfunction: a comparative transcriptome analysis using mouse models. | lld:pubmed |
pubmed-article:15860505 | pubmed:affiliation | Telomeres and Telomerase Group, Molecular Oncology Program, Spanish National Cancer Center (CNIO), Melchor Fernández Almagro 3, 28029 Madrid, Spain. | lld:pubmed |
pubmed-article:15860505 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:15860505 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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