pubmed-article:17909036 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:17909036 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
pubmed-article:17909036 | lifeskim:mentions | umls-concept:C0035335 | lld:lifeskim |
pubmed-article:17909036 | lifeskim:mentions | umls-concept:C0021376 | lld:lifeskim |
pubmed-article:17909036 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:17909036 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:17909036 | pubmed:issue | 19 | lld:pubmed |
pubmed-article:17909036 | pubmed:dateCreated | 2007-10-2 | lld:pubmed |
pubmed-article:17909036 | pubmed:abstractText | Patients with chronic inflammatory bowel disease have a high risk of colon cancer. The molecules that initiate and promote colon cancer and the cancer pathways altered remain undefined. Here, using in vitro models and a mouse model of colitis, we show that nitric oxide (NO) species induce retinoblastoma protein (pRb) hyperphosphorylation and inactivation, resulting in increased proliferation through the pRb-E2F1 pathway. NO-driven pRb hyperphosphorylation occurs through soluble guanylyl cyclase/guanosine 3',5'-cyclic monophosphate signaling and is dependent on the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase MEK/ERK and phosphatidylinositol 3-kinase/AKT pathways. Our results reveal a link between NO and pRb inactivation and provide insight into molecules that can be targeted in the prevention of the inflammation-to-cancer sequence. | lld:pubmed |
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pubmed-article:17909036 | pubmed:language | eng | lld:pubmed |
pubmed-article:17909036 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:17909036 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:17909036 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:17909036 | pubmed:month | Oct | lld:pubmed |
pubmed-article:17909036 | pubmed:issn | 0008-5472 | lld:pubmed |
pubmed-article:17909036 | pubmed:author | pubmed-author:LeiYingY | lld:pubmed |
pubmed-article:17909036 | pubmed:author | pubmed-author:NagarkattiPra... | lld:pubmed |
pubmed-article:17909036 | pubmed:author | pubmed-author:NagarkattiMit... | lld:pubmed |
pubmed-article:17909036 | pubmed:author | pubmed-author:HofsethLorne... | lld:pubmed |
pubmed-article:17909036 | pubmed:author | pubmed-author:BrowningDarre... | lld:pubmed |
pubmed-article:17909036 | pubmed:author | pubmed-author:HofsethAnne... | lld:pubmed |
pubmed-article:17909036 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:17909036 | pubmed:day | 1 | lld:pubmed |
pubmed-article:17909036 | pubmed:volume | 67 | lld:pubmed |
pubmed-article:17909036 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:17909036 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:17909036 | pubmed:pagination | 9286-93 | lld:pubmed |
pubmed-article:17909036 | pubmed:dateRevised | 2011-8-1 | lld:pubmed |
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