Evidence map›Paper›PMID 40954218›Full record

ArticleEMBO reports2025

CDC42 supports HBV entry by NTCP translocation to the plasma membrane and macropinocytosis.

Shuzhi Cui, Wei Gao, Yuxin Chen, Yi Xu, Zhifang Li, Yu Wei, Yaming Jiu

Abstract read
In one paragraph

Article in EMBO reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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

7 authors.

Shuzhi Cui *Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, 510623, Guangzhou, China.
Wei Gao *Unit of Cell Biology and Imaging Study of Pathogen Host Interaction, Key Laboratory of Molecular Virology and Immunology, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, 200031, Shanghai, China.
Yuxin Chen *Department of Laboratory Medicine, Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, 210008, Nanjing, China.
Yi XuGuangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, 510623, Guangzhou, China.
Zhifang LiUnit of Cell Biology and Imaging Study of Pathogen Host Interaction, Key Laboratory of Molecular Virology and Immunology, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, 200031, Shanghai, China.
Yu WeiUniversity of Chinese Academy of Sciences, Yuquan Road No. 19(A), Shijingshan District, 100049, Beijing, China. yu.wei@pasteur.fr.ORCID 0000-0002-0020-6549
Yaming JiuUnit of Cell Biology and Imaging Study of Pathogen Host Interaction, Key Laboratory of Molecular Virology and Immunology, Shanghai Institute of Immunity and Infection, Chinese Academy of Sciences, 200031, Shanghai, China. ymjiu@siii.cas.cn.ORCID 0000-0002-8601-8820

Funding

MOST | National Key Research and Development Program of China (NKPs) 2022YFC2303502MOST | National Natural Science Foundation of China (NSFC) 32222022MOST | National Natural Science Foundation of China (NSFC) 92054104MOST | National Natural Science Foundation of China (NSFC) 92354301R&D Program of Guangzhou National Laboratory GZNL2023A03004STCSM | Natural Science Foundation of Shanghai Municipality ( ) 23ZR1470900
6 · The paper itself

Abstract

CDC42 is a member of Rho GTPase family that regulates various biological processes and its activity can be hijacked by invading pathogens. Here, we discovered that the level of active CDC42 in hepatocytes positively correlates with the entry capacity of hepatitis B virus (HBV). Mechanistically, CDC42 activation effectively promotes the transport of the viral receptor sodium taurocholate co-transporting polypeptide (NTCP) to the plasma membrane via Rab11 dependent recycling endosomal pathway. NTCP interacts with Rab11 and activation of CDC42 signaling reinforces the interaction between NTCP and Rab11. We further show that clathrin mediated endocytosis (CME), the known HBV entry pathway, is independent of CDC42 activity. Intriguingly, we reveal that CDC42 dependent macropinocytosis is a route for HBV entry, which is equally essential for viral infection as CME. Together, our findings uncover new mechanisms for HBV entry that involve unrecognized functions of CDC42 and suggest that Rho GTPase signaling might represent a potential target for antiviral therapy.

Indexed as

cdc42 GTP-Binding ProteinCell MembraneHepatitis B virusOrganic Anion Transporters, Sodium-DependentPinocytosisSymportersVirus InternalizationEndocytosisEndosomesHepatitis BHepatocytesHep G2 CellsHumansProtein Transportrab11 GTP-Binding Proteinsrab GTP-Binding Proteinscdc42 GTP-Binding ProteinCDC42 protein, humanOrganic Anion Transporters, Sodium-Dependentrab11 GTP-Binding Proteinsrab GTP-Binding Proteinssodium-bile acid cotransporterSymportersCDC42Hepatitis B VirusMacropinocytosisSodium Taurocholate Cotransporting PolypeptideVirus Entry

Identifiers

PMID40954218
PMCPMC12592336

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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.