Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
41
pubmed:dateCreated
2008-10-16
pubmed:abstractText
Polycystin-2 (PC2), the gene product of one of two genes mutated in dominant polycystic kidney disease, is a member of the transient receptor potential cation channel family and can function as intracellular calcium (Ca(2+)) release channel. We performed a yeast two-hybrid screen by using the NH(2) terminus of PC2 and identified syntaxin-5 (Stx5) as a putative interacting partner. Coimmunoprecipitation studies in cell lines and kidney tissues confirmed interaction of PC2 with Stx5 in vivo. In vitro binding assays showed that the interaction between Stx5 and PC2 is direct and defined the respective interaction domains as the t-SNARE region of Stx5 and amino acids 5 to 72 of PC2. Single channel studies showed that interaction with Stx5 specifically reduces PC2 channel activity. Epithelial cells overexpressing mutant PC2 that does not bind Stx5 had increased baseline cytosolic Ca(2+) levels, decreased endoplasmic reticulum (ER) Ca(2+) stores, and reduced Ca(2+) release from ER stores in response to vasopressin stimulation. Cells lacking PC2 altogether had reduced cytosolic Ca(2+) levels. Our data suggest that PC2 in the ER plays a role in cellular Ca(2+) homeostasis and that Stx5 functions to inactivate PC2 and prevent leaking of Ca(2+) from ER stores. Modulation of the PC2/Stx5 interaction may be a useful target for impacting dysregulated intracellular Ca(2+) signaling associated with polycystic kidney disease.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-10414292, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-10497221, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-10990372, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-11245681, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-11359862, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-11687880, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-11854751, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12062060, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12062067, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12239239, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12407099, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12514735, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12532278, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12562778, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12874107, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-12920399, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-14742446, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-15123714, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-15843396, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-16077087, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-16223735, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-16316413, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-16537653, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-16565726, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-17008358, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-17404231, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-17581879, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-17620407, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-17725325, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-18388856, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-18483626, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-8144041, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-8334704, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-8524397, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-9307973, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-9384384, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-9445473, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-9647643, http://linkedlifedata.com/resource/pubmed/commentcorrection/18836075-9724814
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1091-6490
pubmed:author
pubmed:issnType
Electronic
pubmed:day
14
pubmed:volume
105
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
15920-5
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Syntaxin 5 regulates the endoplasmic reticulum channel-release properties of polycystin-2.
pubmed:affiliation
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural