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LGR7‐Truncate Is a Splice Variant of the Relaxin Receptor LGR7 and Is a Relaxin Antagonist in Vitro
Author(s) -
SCOTT D J,
TREGEAR G W,
BATHGATE R A D
Publication year - 2005
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1282.005
Subject(s) - relaxin , biology , microbiology and biotechnology , hek 293 cells , exon , alternative splicing , receptor , signal transduction , complementary dna , gene , biochemistry
A bstract : The relaxin receptor (LGR7) and the insulin‐like peptide 3 (INSL3) receptor (LGR8) are unique LGR family members in possessing a single, functionally important amino terminal LDL‐A module.1 Mouse and rat cDNA was screened for LGR7 and LGR7 splice variant expression. A uterus‐specific exon 4 deleted variant was identified and named LGR7‐Truncate. Deletion of exon 4 results in a premature stop codon and a transcript that putatively encodes a secreted protein containing LGR7's LDL‐A module. Expression of LGR7‐Truncate with LGR7 in HEK‐293T cells resulted in decreased relaxin‐induced signaling of LGR7. LGR7‐Truncate is potentially an endogenous regulator of LGR7 signaling.