pubmed-article:10571777 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C0022663 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C0011881 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C0919418 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C0020564 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C0249197 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C1556066 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
pubmed-article:10571777 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
pubmed-article:10571777 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:10571777 | pubmed:dateCreated | 1999-12-10 | lld:pubmed |
pubmed-article:10571777 | pubmed:abstractText | Diabetic nephropathy is characterized by glomerular hypertrophy. We have recently shown that experimental diabetes mellitus is associated with an increase in glomerular expression of the cyclin kinase inhibitor p21WAF1/CIP1 (p21). Furthermore, in vitro glucose-induced mesangial cell hypertrophy is also associated with an up-regulated expression of p21. In this study, we tested the hypothesis that p21 mediates diabetic glomerular hypertrophy in vivo. | lld:pubmed |
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pubmed-article:10571777 | pubmed:language | eng | lld:pubmed |
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pubmed-article:10571777 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:10571777 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10571777 | pubmed:month | Nov | lld:pubmed |
pubmed-article:10571777 | pubmed:issn | 0085-2538 | lld:pubmed |
pubmed-article:10571777 | pubmed:author | pubmed-author:BrownP APA | lld:pubmed |
pubmed-article:10571777 | pubmed:author | pubmed-author:AlpersC ECE | lld:pubmed |
pubmed-article:10571777 | pubmed:author | pubmed-author:BrugarolasJJ | lld:pubmed |
pubmed-article:10571777 | pubmed:author | pubmed-author:ShanklandS... | lld:pubmed |
pubmed-article:10571777 | pubmed:author | pubmed-author:Stehman-Breen... | lld:pubmed |
pubmed-article:10571777 | pubmed:author | pubmed-author:Al-DouahjiMM | lld:pubmed |
pubmed-article:10571777 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:10571777 | pubmed:volume | 56 | lld:pubmed |
pubmed-article:10571777 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10571777 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10571777 | pubmed:pagination | 1691-9 | lld:pubmed |
pubmed-article:10571777 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:10571777 | pubmed:year | 1999 | lld:pubmed |
pubmed-article:10571777 | pubmed:articleTitle | The cyclin kinase inhibitor p21WAF1/CIP1 is required for glomerular hypertrophy in experimental diabetic nephropathy. | lld:pubmed |
pubmed-article:10571777 | pubmed:affiliation | Department of Medicine, University of Washington, School of Medicine, Seattle, Washington, USA. | lld:pubmed |
pubmed-article:10571777 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10571777 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:10571777 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
entrez-gene:12575 | entrezgene:pubmed | pubmed-article:10571777 | lld:entrezgene |
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