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ACC1 regulates plasma membrane cholesterol levels by controlling lipid droplet catabolism

GSE298034 Homo sapiens (human) RNA-seq (gene expression) 16 samples Submitted 2026/05/23 Platform GPL34284
At a glance

RNA-seq (gene expression) · human · 16 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
16 samples: 4 × HAP1 cells, untreated control, biol vs 4 × HAP1 cells, Firsocostat 6 hours, biol vs 4 × HAP1 cells, Triacsin C 6 hours, biol vs 4 × HAP1 cells, Firsocostat 24 hours, biolGroups 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.
Summary (written by the submitters)
Cholesterol constitutes ~30% of the lipids in the vertebrate cell plasma membrane (PM), where it plays indispensable roles in membrane trafficking and receptor signaling. Despite this, how PM cholesterol levels are sensed and regulated remains incompletely understood. Using a genome-wide screen we found that ACC1, the rate-limiting enzyme in fatty acid biosynthesis, is required to maintain PM cholesterol homeostasis.
Read the full summary ↓
ACC1 loss causes a ~10-fold increase in PM cholesterol in cells and a mouse model. We find evidence that ACC1 controls PM cholesterol indirectly through regulating lipid droplet (LD) abundance. LD depletion blocks cholesterol trafficking out of the PM in unstimulated cells and in response to 25-hydroxycholesterol, an immune signaling molecule. Conversely, when LD numbers are elevated, PM cholesterol levels decrease. These findings uncover a previously unrecognized role for ACC1 and LDs in PM cholesterol regulation, which has implications for diseases where LD numbers are altered, from metabolic syndromes to neurodegeneration.
This dataset
Open GSE298034 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 GSE298034_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 PRJNA1267140 and SRA study SRP587283. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
4 × HAP1 cells, untreated control, biol vs 4 × HAP1 cells, Firsocostat 6 hours, biol vs 4 × HAP1 cells, Triacsin C 6 hours, biol vs 4 × HAP1 cells, Firsocostat 24 hours, biol

Supports a between-group comparison across 16 samples.

How we read this: 4 replicated groups read from 16 sample titles; they account for 16 of them. 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
Datasets on a similar topic

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Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.