Evidence map›Paper›PMID 27330080›Full record

ArticleThe Journal of biological chemistry2016

Structure and Function of Cross-class Complexes of G Protein-coupled Secretin and Angiotensin 1a Receptors.

Kaleeckal G Harikumar, Mary Lou Augustine, Leo T O Lee, Billy K C Chow, Laurence J Miller

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 24% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

Kaleeckal G HarikumarFrom the Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Scottsdale, Arizona 85259.
Mary Lou AugustineFrom the Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Scottsdale, Arizona 85259.
Leo T O Leethe Centre of Reproduction, Development and Aging, University of Macau, Taipa, Macau, and.
Billy K C Chowthe School of Biological Sciences, The University of Hong Kong, Pokfulam Road, Hong Kong.
Laurence J MillerFrom the Department of Molecular Pharmacology and Experimental Therapeutics, Mayo Clinic, Scottsdale, Arizona 85259, miller@mayo.edu.
Mayo Clinic in Arizona · USUniversity of Hong Kong · HKUniversity of Macau · MO

Funding

SECRETIN RECEPTOR STRUCTURE, FUNCTION, AND REGULATIONR01DK046577 · NIDDK · MAYO CLINIC COLL OF MED, MAYO CLINIC AZ · PI MILLER, LAURENCE J · 1995 to 2013
$4.9M
Secretin Receptor Structure, Function and RegulationR56DK046577 · NIDDK · MAYO CLINIC ARIZONA · PI MILLER, LAURENCE J · 2014 to 2014
$154k
NIDDK NIH HHS R01 DK046577NIDDK NIH HHS R56 DK046577
6 · The paper itself

Abstract

Complexes of secretin (SecR) and angiotensin 1a (Atr1a) receptors have been proposed to be functionally important in osmoregulation, providing an explanation for overlapping and interdependent functions of hormones that bind and activate different classes of GPCRs. However, the nature of these cross-class complexes has not been well characterized and their signaling properties have not been systematically explored. We now use competitive inhibition of receptor bioluminescence resonance energy transfer and bimolecular fluorescence complementation to establish the dominant functionally important state as a symmetrical homodimeric form of SecR decorated by monomeric Atr1a, interacting through lipid-exposed faces of Atr1a TM1 and TM4. Conditions increasing prevalence of this complex exhibited negative allosteric modulatory impact on secretin-stimulated cAMP responses at SecR. In contrast, activating Atr1a with full agonist in such a complex exhibited a positive allosteric modulatory impact on the same signaling event. This modulation was functionally biased, with secretin-stimulated calcium responses unaffected, whereas angiotensin-stimulated calcium responses through the complex were reduced or absent. Further supporting this interpretation, Atr1a with mutations of lipid-exposed faces of TM1 and TM4 that did not affect its ability to bind or signal, could be expressed in the same cell as SecR, yet not exhibit either the negative or positive allosteric impact on cAMP observed with the inactive or activated states of wild type Atr1a on function, and not interfere with angiotensin-stimulated calcium responses like complexes with Atr1a. This may provide a more selective means of exploring the physiologic functional impact of this cross-class receptor complex without interfering with the function of either component receptor.

Indexed as

AnimalsCalcium SignalingChlorocebus aethiopsCHO CellsCOS CellsCricetinaeCricetulusHEK293 CellsHumansMiceMutationProtein DomainsProtein Structure, QuaternaryRatsReceptor, Angiotensin, Type 1Receptors, Gastrointestinal HormoneReceptor, Angiotensin, Type 1Receptors, Gastrointestinal HormoneReceptors, G-Protein-Coupledsecretin receptorallosteric regulationangiotensinbioluminescence resonance energy transfer (BRET)calciumdimerizationG protein-coupled receptor (GPCR)

Identifiers

PMID27330080
PMCPMC5016131
OpenAlexW2465117129

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.