Evidence map›Paper›PMID 38183076›Full record

ArticleCell communication and signaling : CCS2024

R-spondin-1 induces Axin degradation via the LRP6-CK1ε axis.

Lifeng Tan, Mengfang Yan, Zijie Su, Hanbin Wang, Huan Li, Xibao Zhao, Shanshan Liu, Long Zhang, Qi Sun, Desheng Lu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

3 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. A novel variation inFrontiers in pediatrics · 2025
    Article
  3. R Spondin in Cancer: Inducer or Impeder?Technology in cancer research & treatment
    Article
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

10 authors at 2 institutions in 1 country.

Lifeng Tan *Guangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Mengfang Yan *Guangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Zijie SuGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Hanbin WangGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Huan LiGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Xibao ZhaoGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Shanshan LiuGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China.
Long ZhangMOE Laboratory of Biosystems Homeostasis & Protection and Innovation Center for Cell Signaling Network, Life Sciences Institute, Zhejiang University, Hangzhou, 310058, China.
Qi SunGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China. sunqi@szu.edu.cn.
Desheng LuGuangdong Provincial Key Laboratory of Regional Immunity and Disease, International Cancer Center, Marshall Laboratory of Biomedical Engineering, Department of Pharmacology, Shenzhen University Medical School, Shenzhen University, Shenzhen, 518055, Guangdong, China. delu@szu.edu.cn.
Shenzhen University Health Science Center · CNZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

R-spondins (RSPOs) are secreted signaling molecules that potentiate the Wnt/β-catenin pathway by cooperating with Wnt ligands. RSPO1 is crucial in tissue development and tissue homeostasis. However, the molecular mechanism by which RSPOs activate Wnt/β-catenin signaling remains elusive. In this study, we found that RSPOs could mediate the degradation of Axin through the ubiquitin-proteasome pathway. The results of Co-IP showed that the recombinant RSPO1 protein promoted the interaction between Axin1 and CK1ε. Either knockout of the CK1ε gene or treatment with the CK1δ/CK1ε inhibitor SR3029 caused an increase in Axin1 protein levels and attenuated RSPO1-induced degradation of the Axin1 protein. Moreover, we observed an increase in the number of associations of LRP6 with CK1ε and Axin1 following RSPO1 stimulation. Overexpression of LRP6 further potentiated Axin1 degradation mediated by RSPO1 or CK1ε. In addition, recombinant RSPO1 and Wnt3A proteins synergistically downregulated the protein expression of Axin1 and enhanced the transcriptional activity of the SuperTOPFlash reporter. Taken together, these results uncover the novel mechanism by which RSPOs activate Wnt/β-catenin signaling through LRP6/CK1ε-mediated degradation of Axin.

Indexed as

Axin ProteinThrombospondinsWnt Signaling Pathwaybeta CateninBiological TransportHumansR-SpondinsWnt3A ProteinAXIN1 protein, humanAxin Proteinbeta CateninRSPO1 protein, humanR-SpondinsThrombospondinsWnt3A ProteinAxinCK1εLRP6RSPO1Wnt/β-catenin signaling

Identifiers

PMID38183076
PMCPMC10768284
OpenAlexW4390613726

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.