Evidence map›Paper›PMID 28656888›Full record

ArticleeLife2017

The complex of TRIP-Br1 and XIAP ubiquitinates and degrades multiple adenylyl cyclase isoforms.

Wenbao Hu, Xiaojie Yu, Zhengzhao Liu, Ying Sun, Xibing Chen, Xin Yang, Xiaofen Li, Wai Kwan Lam, Yuanyuan Duan, Xu Cao and 3 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  4. KCTD1 regulation of Adenylyl cyclase type 5 adjusts striatal cAMP signaling.Proceedings of the National Academy of Sciences of the United States of America · 2024
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  10. Deafness mutation D572N of TMC1 destabilizes TMC1 expression by disrupting LHFPL5 binding.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Review
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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

13 authors at 3 institutions in 3 countries.

Wenbao HuDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Xiaojie YuDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Zhengzhao LiuDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Ying SunDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Xibing ChenDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Xin YangDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Xiaofen LiDivision of Biomedical Engineering, Hong Kong University of Science and Technology, Hong Kong, China.
Wai Kwan LamDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Yuanyuan DuanDivision of Biomedical Engineering, Hong Kong University of Science and Technology, Hong Kong, China.
Xu CaoDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Hermann StellerStrang Laboratory of Apoptosis and Cancer Biology, Howard Hughes Medical Institute, The Rockefeller University, New York, United States.
Kai LiuDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.
Pingbo HuangDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, China.ORCID 0000-0002-4560-8760
Hong Kong University of Science and Technology · HKHoward Hughes Medical Institute · USJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Adenylyl cyclases (ACs) generate cAMP, a second messenger of utmost importance that regulates a vast array of biological processes in all kingdoms of life. However, almost nothing is known about how AC activity is regulated through protein degradation mediated by ubiquitination or other mechanisms. Here, we show that transcriptional regulator interacting with the PHD-bromodomain 1 (TRIP-Br1, Sertad1), a newly identified protein with poorly characterized functions, acts as an adaptor that bridges the interaction of multiple AC isoforms with X-linked inhibitor of apoptosis protein (XIAP), a RING-domain E3 ubiquitin ligase. XIAP ubiquitinates a highly conserved Lys residue in AC isoforms and thereby accelerates the endocytosis and degradation of multiple AC isoforms in human cell lines and mice. XIAP/TRIP-Br1-mediated degradation of ACs forms part of a negative-feedback loop that controls the homeostasis of cAMP signaling in mice. Our findings reveal a previously unrecognized mechanism for degrading multiple AC isoforms and modulating the homeostasis of cAMP signaling.

Indexed as

ProteolysisUbiquitinationAdenylyl CyclasesAnimalsCell LineHumansMiceNuclear ProteinsProtein IsoformsTrans-ActivatorsTranscription FactorsX-Linked Inhibitor of Apoptosis ProteinAdenylyl CyclasesNuclear ProteinsProtein IsoformsSERTAD1 protein, humanTrans-ActivatorsTranscription FactorsXIAP protein, humanX-Linked Inhibitor of Apoptosis Proteinadenylyl cyclasecAMPcell biologydegradationmouseTRIP-Br1ubiquitinationXIAP

Identifiers

PMID28656888
PMCPMC5503512
OpenAlexW2726110196

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.