| pubmed-article:10913157 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C0248266 | lld:lifeskim |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C0007595 | lld:lifeskim |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C1171362 | lld:lifeskim |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C0205177 | lld:lifeskim |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C1527249 | lld:lifeskim |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:10913157 | lifeskim:mentions | umls-concept:C1515670 | lld:lifeskim |
| pubmed-article:10913157 | pubmed:issue | 41 | lld:pubmed |
| pubmed-article:10913157 | pubmed:dateCreated | 2000-11-13 | lld:pubmed |
| pubmed-article:10913157 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:abstractText | Although ectopic expression of the cholecystokinin B/gastrin receptor (CCK-BR) is widely reported in human colorectal cancers, its role in mediating the proliferative effects of gastrin1-17 (G-17) on these cancers is unknown. Here we report the isolation of a novel splice variant of CCK-BR that exhibits constitutive (ligand-independent) activation of pathways regulating intracellular free Ca(2+) ([Ca(2+)](i)) and cell growth. The splice variant (designated CCK-BRi4sv for intron 4-containing splice variant) is expressed in colorectal cancers but not in normal colonic mucosa adjacent to the cancer. Balb3T3 cells expressing CCK-BRi4sv exhibited spontaneous, ligand-independent, oscillatory increases in [Ca(2+)](i), whereas cells expressing wild-type CCK-BR did not. Primary cultures of cells isolated from resected colorectal cancers also exhibited a similar pattern of spontaneous [Ca(2+)](i) oscillations. For both Balb3T3 and primary tumor cells, application of G-17 (10 and 200 nm, respectively) caused an increase in [Ca(2+)](i). Selective CCK-BR antagonists blocked the G-17-stimulated Ca(2+) responses but not the spontaneous [Ca(2+)](i) oscillations. Cells expressing CCK-BRi4sv exhibited an increased growth rate ( approximately 2.5-fold), in the absence of G-17, compared with cells expressing wild-type CCK-BR. The selective pattern of expression, constitutive activity, and trophic action associated with CCK-BRi4sv suggest that this variant may regulate colorectal cancer cell proliferation though a gastrin-independent mechanism. | lld:pubmed |
| pubmed-article:10913157 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10913157 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10913157 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10913157 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10913157 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:10913157 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:10913157 | pubmed:author | pubmed-author:TownsendC... | lld:pubmed |
| pubmed-article:10913157 | pubmed:author | pubmed-author:SunW WWW | lld:pubmed |
| pubmed-article:10913157 | pubmed:author | pubmed-author:HellmichM RMR | lld:pubmed |
| pubmed-article:10913157 | pubmed:author | pubmed-author:EversB MBM | lld:pubmed |
| pubmed-article:10913157 | pubmed:author | pubmed-author:FlemingR YRY | lld:pubmed |
| pubmed-article:10913157 | pubmed:author | pubmed-author:HellmichH LHL | lld:pubmed |
| pubmed-article:10913157 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10913157 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:10913157 | pubmed:volume | 275 | lld:pubmed |
| pubmed-article:10913157 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10913157 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10913157 | pubmed:pagination | 32122-8 | lld:pubmed |
| pubmed-article:10913157 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:10913157 | pubmed:meshHeading | pubmed-meshheading:10913157... | lld:pubmed |
| pubmed-article:10913157 | pubmed:meshHeading | pubmed-meshheading:10913157... | lld:pubmed |
| pubmed-article:10913157 | pubmed:meshHeading | pubmed-meshheading:10913157... | lld:pubmed |
| pubmed-article:10913157 | pubmed:meshHeading | pubmed-meshheading:10913157... | lld:pubmed |
| pubmed-article:10913157 | pubmed:meshHeading | pubmed-meshheading:10913157... | lld:pubmed |
| pubmed-article:10913157 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:10913157 | pubmed:articleTitle | Human colorectal cancers express a constitutively active cholecystokinin-B/gastrin receptor that stimulates cell growth. | lld:pubmed |
| pubmed-article:10913157 | pubmed:affiliation | Departments of Surgery, Physiology and Biophysics, and Internal Medicine, the University of Texas Medical Branch, Galveston, Texas 77555, USA. mhellmic@utmb.edu | lld:pubmed |
| pubmed-article:10913157 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10913157 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10913157 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:887 | entrezgene:pubmed | pubmed-article:10913157 | lld:entrezgene |
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