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Rescue of defective...
Rescue of defective G protein-coupled receptor function in vivo by intermolecular cooperation
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Rivero-Muller, A (författare)
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Chou, YY (författare)
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Ji, I (författare)
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- Lajic, S (författare)
- Karolinska Institutet
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Hanyaloglu, AC (författare)
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Jonas, K (författare)
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Rahman, N (författare)
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Ji, TH (författare)
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Huhtaniemi, I (författare)
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(creator_code:org_t)
- 2010-01-11
- 2010
- Engelska.
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 1091-6490. ; 107:5, s. 2319-2324
- Relaterad länk:
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http://www.pnas.org/...
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http://kipublication...
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https://doi.org/10.1...
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Abstract
Ämnesord
Stäng
- G protein–coupled receptors (GPCRs) are ubiquitous mediators of signaling of hormones, neurotransmitters, and sensing. The old dogma is that a one ligand/one receptor complex constitutes the functional unit of GPCR signaling. However, there is mounting evidence that some GPCRs form dimers or oligomers during their biosynthesis, activation, inactivation, and/or internalization. This evidence has been obtained exclusively from cell culture experiments, and proof for the physiological significance of GPCR di/oligomerization in vivo is still missing. Using the mouse luteinizing hormone receptor (LHR) as a model GPCR, we demonstrate that transgenic mice coexpressing binding-deficient and signaling-deficient forms of LHR can reestablish normal LH actions through intermolecular functional complementation of the mutant receptors in the absence of functional wild-type receptors. These results provide compelling in vivo evidence for the physiological relevance of intermolecular cooperation in GPCR signaling.
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- ref (ämneskategori)
- art (ämneskategori)
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