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Transcriptomic changes assoicated with hepatic AHR or ARNT loss in female mice challenged with high-fat diet

GSE161147 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2024/06/08 Platform GPL21626
At a glance

RNA-seq (gene expression) · mouse · 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
Mus musculus (mouse)
Samples
12 samples: 3 × ARNT KO vs 3 × ARNT Flox vs 3 × AHR Flox vs 3 × AHR KOGroups 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)
The aryl hydrocarbon receptor (AHR) is an important hepatic transcription factor that appears to have a role in regulating endogenous liver metabolism. Canonical AHR-mediated regulation of transcription requires AHR binding to its DNA-binding partner, the AHR nuclear translocator (ARNT). We previously demonstrated that the AHR can regulate transcription independent of ARNT via “non-canonical” interactions with Kruppel-like factor 6, and that hepatic AHR loss can protect against high-fat diet (HFD) challenge.
Read the full summary ↓
In this study, we examined the effects of hepatic AHR or ARNT loss in HFD-fed mice to determine whether AHR regulation of liver metabolism might partially occur independent of ARNT. The data show that similar to AHR loss, ARNT loss reduces HFD-driven hepatic lipid deposition, but does not recapitulate the diminished weight gain and adiposity observed in AHR KO animals. Utilizing transcriptomic sequencing analyses, we uncovered specific gene pathways that likely account for these phenotypic differences/similarities associated with AHR or ARNT loss. Together, these data highlight the physiological significance of ARNT-independent AHR activity, and identify discrete aspects of liver metabolism likely regulated via canonical AHR action.
This dataset
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.

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 GSE161147_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA675758 and SRA study SRP291913. Searching any of these in the dataset finder brings you back here.

Study design
3 × ARNT KO vs 3 × ARNT Flox vs 3 × AHR Flox vs 3 × AHR KO

Supports a between-group comparison across 12 samples.

How we read this: 4 replicated groups read from 12 sample titles; they account for 12 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
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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.