Evidence map›Paper›PMID 37153740›Full record

ArticleTheranostics2023

Gαi1/3 mediate Netrin-1-CD146-activated signaling and angiogenesis.

Ya Li, Jin-Long Chai, Xin Shi, Yu Feng, Jia-Jun Li, Li-Na Zhou, Cong Cao, Ke-Ran Li

Open access · goldAbstract read
In one paragraph

Article in Theranostics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 34 citations in OpenAlex.

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  8. Endothelial UNC5B regulates blood‑retinal barrier homeostasis.International journal of molecular medicine · 2026
    Article
  9. Gαi1/3 Is a Novel Regulatory Target for RANKL Signal Transduction and Osteoporosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    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

8 authors at 5 institutions in 1 country.

Ya LiClinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University and North District, The Municipal Hospital of Suzhou, Gusu School, Nanjing Medical University, Suzhou, China.
Jin-Long ChaiClinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University and North District, The Municipal Hospital of Suzhou, Gusu School, Nanjing Medical University, Suzhou, China.
Xin ShiClinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University and North District, The Municipal Hospital of Suzhou, Gusu School, Nanjing Medical University, Suzhou, China.
Yu FengDepartment of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, China.
Jia-Jun LiThe Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Li-Na ZhouDepartment of Radiotherapy and Oncology, Kunshan First People's Hospital Affiliated to Jiangsu University, Kunshan, China.
Cong CaoClinical Research Center of Neurological Disease, The Second Affiliated Hospital of Soochow University and North District, The Municipal Hospital of Suzhou, Gusu School, Nanjing Medical University, Suzhou, China.
Ke-Ran LiThe Affiliated Eye Hospital, Nanjing Medical University, Nanjing, China.
Soochow University · CNSecond Affiliated Hospital of Soochow University · CNJiangsu University · CNNanjing Medical University · CNSecond Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Netrin-1 binds to the high-affinity receptor CD146 to activate downstream signaling and angiogenesis. Here, we examine the role and underlying mechanisms of G protein subunit alpha i1 (Gαi1) and Gαi3 in Netrin-1-induced signaling and pro-angiogenic activity. In mouse embryonic fibroblasts (MEFs) and endothelial cells, Netrin-1-induced Akt-mTOR (mammalian target of rapamycin) and Erk activation was largely inhibited by silencing or knockout of Gαi1/3, whereas signaling was augmented following Gαi1/3 overexpression. Netrin-1 induced Gαi1/3 association with CD146, required for CD146 internalization, Gab1 (Grb2 associated binding protein 1) recruitment and downstream Akt-mTOR and Erk activation. Netrin-1-induced signaling was inhibited by CD146 silencing, Gab1 knockout, or Gαi1/3 dominant negative mutants. Netrin-1-induced human umbilical vein endothelial cell (HUVEC) proliferation, migration and tube formation were inhibited by Gαi1/3 short hairpin RNA (shRNA), but were potentiated by ectopic Gαi1/3 overexpression.

Indexed as

Diabetic RetinopathyProto-Oncogene Proteins c-aktAnimalsCarrier ProteinsCD146 AntigenFibroblastsHumansHuman Umbilical Vein Endothelial CellsMammalsMiceNetrin-1RNA, Small InterferingTOR Serine-Threonine KinasesCarrier ProteinsCD146 AntigenNetrin-1Proto-Oncogene Proteins c-aktRNA, Small InterferingTOR Serine-Threonine KinasesAngiogenesisCD146Diabetic RetinopathyGαi1 and Gαi3Netrin-1

Identifiers

PMID37153740
PMCPMC10157725
OpenAlexW4375954995

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.