| pubmed-article:19722195 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19722195 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:19722195 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:19722195 | lifeskim:mentions | umls-concept:C0001047 | lld:lifeskim |
| pubmed-article:19722195 | lifeskim:mentions | umls-concept:C0030817 | lld:lifeskim |
| pubmed-article:19722195 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:19722195 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:19722195 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:19722195 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:19722195 | pubmed:dateCreated | 2009-12-28 | lld:pubmed |
| pubmed-article:19722195 | pubmed:abstractText | N-acetyl cysteine (NAC) and penicillamine (PEN) have been shown to induce apoptosis in multiple types of human cancer cells; however, the molecular mechanism underlying this activity is unclear. This study was designed to identify the genes responsible for apoptosis induction by NAC and PEN. We found that glucose-regulated protein 78 (GRP78) was upregulated in HeLa cells following treatment with NAC or PEN. GRP78 is a central regulator of endoplasmic reticulum (ER) stress and has been used as a marker of ER stress. Additionally, both the activating transcription factor 6 (ATF6) protein and X box-binding protein 1 (XBP1) mRNA were processed, which facilitates the expression of C/EBP homologous protein (CHOP), a key-signaling component of ER stress-induced apoptosis. Furthermore, the PERK-ATF4 pathway, which also induces the expression of CHOP, was activated in NAC-treated cells. The role of the ER stress pathway was further confirmed through the small interfering RNA (siRNA)-mediated knockdown of CHOP, which attenuated NAC and PEN-induced apoptosis. These results demonstrate that NAC- and PEN-induced apoptosis in HeLa cells is mediated by the ER stress pathway. | lld:pubmed |
| pubmed-article:19722195 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19722195 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19722195 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19722195 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:19722195 | pubmed:issn | 1098-2744 | lld:pubmed |
| pubmed-article:19722195 | pubmed:author | pubmed-author:YangMinM | lld:pubmed |
| pubmed-article:19722195 | pubmed:author | pubmed-author:WangHaoH | lld:pubmed |
| pubmed-article:19722195 | pubmed:author | pubmed-author:WangXiaomingX | lld:pubmed |
| pubmed-article:19722195 | pubmed:author | pubmed-author:ShenZonghouZ | lld:pubmed |
| pubmed-article:19722195 | pubmed:author | pubmed-author:XuYingyingY | lld:pubmed |
| pubmed-article:19722195 | pubmed:author | pubmed-author:GuanDongyinD | lld:pubmed |
| pubmed-article:19722195 | pubmed:copyrightInfo | 2009 Wiley-Liss, Inc. | lld:pubmed |
| pubmed-article:19722195 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19722195 | pubmed:volume | 49 | lld:pubmed |
| pubmed-article:19722195 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19722195 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19722195 | pubmed:pagination | 68-74 | lld:pubmed |
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| pubmed-article:19722195 | pubmed:meshHeading | pubmed-meshheading:19722195... | lld:pubmed |
| pubmed-article:19722195 | pubmed:year | 2010 | lld:pubmed |
| pubmed-article:19722195 | pubmed:articleTitle | N-acetyl cysteine and penicillamine induce apoptosis via the ER stress response-signaling pathway. | lld:pubmed |
| pubmed-article:19722195 | pubmed:affiliation | Department of Biochemistry and Molecular Biology, Fudan University, Shanghai, China. | lld:pubmed |
| pubmed-article:19722195 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:19722195 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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