| pubmed-article:8267619 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C0338106 | lld:lifeskim |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C0007589 | lld:lifeskim |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C1510779 | lld:lifeskim |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C0017968 | lld:lifeskim |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C0205615 | lld:lifeskim |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C0699900 | lld:lifeskim |
| pubmed-article:8267619 | lifeskim:mentions | umls-concept:C0243125 | lld:lifeskim |
| pubmed-article:8267619 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:8267619 | pubmed:dateCreated | 1994-1-25 | lld:pubmed |
| pubmed-article:8267619 | pubmed:abstractText | The aim of the present study was to elucidate the mechanism responsible for the high mannose glycoprotein instability in undifferentiated HT-29 cells (a human colon cancer cell line) reported previously. The results presented here are consistent with lysosomal degradation of these molecular species. In addition inhibitors of the autophagic-lysosomal degradative pathway (3-methyladenine, okadaic acid and asparagine) dramatically block the degradation of proteins and N-linked glycoproteins in undifferentiated HT-29 cells. The main conclusions of this work are: 1- the autophagic-lysosomal pathway is responsible for the high mannose glycoprotein degradation in undifferentiated HT-29 cells; 2- this degradative pathway exists in differentiated cells but is greatly reduced (3.5-4 fold); 3- the HT-29 cell line is a new model to investigate the molecular regulation of autophagy. | lld:pubmed |
| pubmed-article:8267619 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8267619 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8267619 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8267619 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:8267619 | pubmed:issn | 0006-291X | lld:pubmed |
| pubmed-article:8267619 | pubmed:author | pubmed-author:CodognoPP | lld:pubmed |
| pubmed-article:8267619 | pubmed:author | pubmed-author:TrugnanGG | lld:pubmed |
| pubmed-article:8267619 | pubmed:author | pubmed-author:Ogier-DenisEE | lld:pubmed |
| pubmed-article:8267619 | pubmed:author | pubmed-author:HouriJ JJJ | lld:pubmed |
| pubmed-article:8267619 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8267619 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:8267619 | pubmed:volume | 197 | lld:pubmed |
| pubmed-article:8267619 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8267619 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8267619 | pubmed:pagination | 805-11 | lld:pubmed |
| pubmed-article:8267619 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:8267619 | pubmed:meshHeading | pubmed-meshheading:8267619-... | lld:pubmed |
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| pubmed-article:8267619 | pubmed:meshHeading | pubmed-meshheading:8267619-... | lld:pubmed |
| pubmed-article:8267619 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8267619 | pubmed:articleTitle | Autophagic degradation of N-linked glycoproteins is downregulated in differentiated human colon adenocarcinoma cells. | lld:pubmed |
| pubmed-article:8267619 | pubmed:affiliation | INSERM U239, Unité de Recherche sur la Biologie et la Physiopathologie des Cellules Digestives, Paris, France. | lld:pubmed |
| pubmed-article:8267619 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8267619 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:8267619 | lld:pubmed |
