ArticleJournal of virology2026
PPP2R5B regulates ANPEP expression and TGEV entry via dephosphorylation of HSF1 at Ser304/Ser308.
Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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.
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.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Transmissible gastroenteritis virus (TGEV) is an enteric coronavirus responsible for severe gastrointestinal disease in swine; however, the host determinants and mechanisms underlying viral entry remain poorly defined. This study systematically examines the role of the serine/threonine protein phosphatase 2A (PP2A) regulatory subunit B'β (PPP2R5B) during TGEV infection. Genetic ablation of PPP2R5B in PK-15 cells significantly reduced TGEV infectivity. Stage-specific analyses revealed that loss of PPP2R5B selectively impaired viral entry, while viral replication and release were unaffected. Transcriptomic profiling and functional validation identified the TGEV receptor aminopeptidase N (ANPEP) as a critical downstream effector of PPP2R5B. PPP2R5B-mediated regulation of ANPEP expression was independent of the AMPK, PI3K/AKT, ERK, and WNT/β-catenin signaling pathways. Instead, PPP2R5B directly interacted with heat shock factor 1 (HSF1) and promoted dephosphorylation of HSF1 at Ser304 and Ser308, thereby reducing HSF1-dependent transcriptional activation of ANPEP. These findings reveal a previously unrecognized PPP2R5B-HSF1-ANPEP regulatory axis that governs TGEV cellular entry and suggest that host dephosphorylation-dependent regulation may represent a potential target for antiviral intervention.IMPORTANCECoronavirus entry is a critical determinant of viral tropism and pathogenicity. This study identifies PPP2R5B, a regulatory subunit of the PP2A phosphatase complex, as a host factor that facilitates TGEV entry by controlling the expression of the cellular receptor ANPEP. We demonstrate that PPP2R5B regulates ANPEP transcription through modulation of HSF1 phosphorylation, independent of several canonical signaling pathways. These findings uncover a host phosphatase-dependent regulatory mechanism underlying coronavirus entry and highlight host signaling components as potential targets for antiviral intervention.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.