GEO series

Glucosidase Alpha Neutral C Promotes Influenza Virus Replication by Inhibiting Proteosome-Dependent Degradation of Hemagglutinin

GSE291573 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2025/03/24 Platform GPL24676

At a glance

RNA-seq (gene expression) · human · 12 samples

What it is: RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism: Homo sapiens (human)
Samples: 12 samples: 12 samples, each with a distinct title — no replicated groupsGroups are read from the sample names, not from the paper. Check the list below.
Data you can get: A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper: Glucosidase alpha neutral C promotes influenza virus replication by inhibiting proteosome-dependent degradation of hemagglutininSignal transduction and targeted therapy · 2025

Summary (written by the submitters)

The H7N9 influenza virus poses a significant threat to human health, and the mechanism by which it infects humans remains incompletely understood. Our investigation has unveiled significant insights into the role of glucosidase alpha, neutral C (ganc) gene in human H7N9 infections. Through whole genome sequencing (WGS), we identified five low-frequency functional and heterozygous variants of ganc strongly associated with human H7N9 infections compared to healthy controls.

Read the full summary ↓

Furthermore, we observed a reduction in mRNA and protein expression of GANC following H7N9 virus infection in vitro and in vivo. Subsequent experiments involving GANC demonstrated promotion of H7N9 virus replication in a stable strain with GANC overexpression. Conversely, GANC knockdown exhibited the ability to restrict influenza A virus (IAV) replication, including H7N9, H9N2 and H1N1, both in vitro and in vivo. This inhibition was mediated by GANC's ability to promote the degradation of H7N9 hemagglutinin (HA). Moreover, we discovered that GANC knockdown facilitated the degradation of HA in a proteasome-dependent manner. The inhibition caused by GANC knockdown was mediated by promoting direct binding of HA with the proteasome 26S subunit, non-ATPase, 1 (PSMD1) and PSMD2. All the five variants in the ganc gene reduced its ability to promote H7N9 virus replication, and also diminished the levels of GANC-induced HA protein expression. Our findings revealed a novel mechanism by which GANC inhibited the proteasome-dependent degradation of HA to promote H7N9 virus replication. These results suggest that GANC may play an important role in IAV replication.

Published in

Glucosidase alpha neutral C promotes influenza virus replication by inhibiting proteosome-dependent degradation of hemagglutinin

Liao X, Xie Q, Liang M et al. · Signal transduction and targeted therapy 2025 · PMID 40263249 · doi:10.1038/s41392-025-02227-6

This dataset

Open GSE291573 in finder → Find more human RNA-seq datasets →

Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓

2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE291573_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓

3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1234177 and SRA study SRP569285. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40263249) ↗

Study design

12 samples, each with a distinct title — no replicated groups

Any grouping that defines a comparison lives in the sample characteristics, which GEO records separately from the titles.

How we read this: Read from 12 sample titles: 12 distinct titles with little repetition. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study

GSM8837860 A549 cells,si-GANC-1(siGANC-1),36h
GSM8837861 A549 cells,si-GANC-1+MOI of 0.1 virus(siGANC-1+),36h
GSM8837862 A549 cells,si-GANC-2(siGANC-2),36h
GSM8837863 A549 cells,si-GANC-2+MOI of 0.1virus(siGANC-2+),36h
GSM8837864 A549 cells,si-GANC-3(siGANC-3),36h
GSM8837865 A549 cells,si-GANC-3+MOI of 0.1virus(siGANC-3+),36h
GSM8837866 A549 cells,si-NC-1(NC-1),36h
GSM8837867 A549 cells,si-NC-1+MOI of 0.1 virus(NC-1+),36h
GSM8837868 A549 cells,si-NC-2(NC-2),36h
GSM8837869 A549 cells,si-NC-2+MOI of 0.1 virus(NC-2+),36h
GSM8837870 A549 cells,si-NC-3(NC-3),36h
GSM8837871 A549 cells,si-NC-3+MOI of 0.1 virus(NC-3+),36h

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