| pubmed-article:20130090 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:20130090 | lifeskim:mentions | umls-concept:C0056889 | lld:lifeskim |
| pubmed-article:20130090 | lifeskim:mentions | umls-concept:C0699900 | lld:lifeskim |
| pubmed-article:20130090 | lifeskim:mentions | umls-concept:C0380202 | lld:lifeskim |
| pubmed-article:20130090 | lifeskim:mentions | umls-concept:C1425021 | lld:lifeskim |
| pubmed-article:20130090 | lifeskim:mentions | umls-concept:C0243125 | lld:lifeskim |
| pubmed-article:20130090 | lifeskim:mentions | umls-concept:C1556156 | lld:lifeskim |
| pubmed-article:20130090 | lifeskim:mentions | umls-concept:C0086597 | lld:lifeskim |
| pubmed-article:20130090 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:20130090 | pubmed:dateCreated | 2010-3-31 | lld:pubmed |
| pubmed-article:20130090 | pubmed:abstractText | The PDZ domain-containing protein CAL mediates lysosomal trafficking and degradation of CFTR. Here we demonstrate the involvement of a CAL-binding SNARE protein syntaxin 6 (STX6) in this process. Overexpression of STX6, which colocalizes and coimmunoprecipitates with CAL, dramatically reduces the steady-state level and stability of CFTR. Conversely, overexpression of a STX6 dominant-negative mutant increases CFTR. Silencing endogenous STX6 increases CFTR but has no effect on DeltaTRL-CFTR, which cannot bind to CAL. Silencing CAL eliminates the effect of STX6 on CFTR. Both results suggest a dependence of CAL on STX6 function. Consistent with its Golgi localization, STX6 does not bind to ER-localized DeltaF508-CFTR. Silencing STX6 has no effect on DeltaF508-CFTR expression. However, overexpression of STX6 coimmunoprecipitates with and reduces temperature-rescued DeltaF508-CFTR that escapes ER degradation. Conversely, silencing STX6 enhances the effect of low temperature in rescuing DeltaF508-CFTR. Finally, in human bronchial epithelial cells, silencing endogenous STX6 leads to increases in protein levels and Cl(-) currents of both wild-type and temperature-rescued CFTR. We have identified STX6 as a new component of the CAL complex that regulates the abundance and function of CFTR at the post-ER level. Our results suggest a therapeutic role of STX6 in enhancing rescued DeltaF508-CFTR. | lld:pubmed |
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| pubmed-article:20130090 | pubmed:language | eng | lld:pubmed |
| pubmed-article:20130090 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:20130090 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:20130090 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:20130090 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:20130090 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:20130090 | pubmed:issn | 1939-4586 | lld:pubmed |
| pubmed-article:20130090 | pubmed:author | pubmed-author:ChengJieJ | lld:pubmed |
| pubmed-article:20130090 | pubmed:author | pubmed-author:GugginoWillia... | lld:pubmed |
| pubmed-article:20130090 | pubmed:author | pubmed-author:CebotaruValer... | lld:pubmed |
| pubmed-article:20130090 | pubmed:author | pubmed-author:CebotaruLiudm... | lld:pubmed |
| pubmed-article:20130090 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:20130090 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:20130090 | pubmed:volume | 21 | lld:pubmed |
| pubmed-article:20130090 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:20130090 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:20130090 | pubmed:pagination | 1178-87 | lld:pubmed |
| pubmed-article:20130090 | pubmed:dateRevised | 2010-9-28 | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
| pubmed-article:20130090 | pubmed:meshHeading | pubmed-meshheading:20130090... | lld:pubmed |
