Linked Life Data

8756555

Source:http://linkedlifedata.com/resource/pubmed/id/8756555

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1996-11-13
pubmed:databankReference
pubmed:abstractText
An extracellular Ca(2+)-sensing mechanism consisting of a G protein-coupled receptor linked to phosphoinositide turnover and inhibition of PTH secretion, has recently been identified in bovine parathyroid cells. In C cells, voltage-dependent L-type calcium channels are thought to be involved in calcium-sensing mechanisms, but evidence exists for additional calcium-sensing mechanisms, such as via a calcium-sensing receptor (CaSR). Using the human medullary C cell carcinoma cell line TT, which lacks L-type calcium channels, we found that Ca2+ or cations specific for the CaSR lead to the release of calcium ions from intracellular stores and to an increase in calcitonin secretion. By molecular cloning we isolated the complete protein-coding complementary DNA of a CaSR from human TT cells, which are derived from a human medullary thyroid carcinoma. The CaSR is derived from the same CaSR gene expressed in the parathyroid gland. In addition, TT cells contain an alternative receptor form of CaSR, CaSRb. These findings provide strong evidence for the presence of a functional CaSR in the human C cell line TT. This receptor contributes not only to the inhibition of PTH secretion in the parathyroid, but also to the stimulation of calcitonin secretion in C cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
137
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3842-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Expression of a calcium-sensing receptor in a human medullary thyroid carcinoma cell line and its contribution to calcitonin secretion.
pubmed:affiliation
Pharmakologisches Institut, Universität Heidelberg, Mannheim, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't