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DNA-binding protein-A promotes renal ischemia/reperfusion injury and participates in mitochondrial function

GSE264448 Mus musculus (mouse) RNA-seq (gene expression) 12 samples Submitted 2024/04/26 Platform GPL24247
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
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)
DNA-binding protein-A (DbpA; gene: Ybx3) belongs to the cold shock protein family with known functions in cell cycling, transcription, translation and tight junction communication. In chronic nephritis DbpA is upregulated, however its activities in acute injury models, such as renal ischemia/reperfusion injury (IRI), are unclear. Mice harboring Ybx3+/+, Ybx3+/- or Ybx3-/- genotype were characterized over a period of 24 months and following experimental renal IRI.
Read the full summary ↓
Mitochondrial function, number and integrity were analyzed by mito stress tests, MitoTracker staining and electron microscopy. Immunohistochemistry, Western blotting and flow cytometry were performed to quantify tubular cell damage and immune cell infiltration. DbpA is dispensable for kidney development and tissue homeostasis under healthy conditions. Furthermore, endogenous DbpA protein localizes within mitochondria in primary tubular epithelial cells (TECs). Genetic deletion of Ybx3 elevates the mitochondrial membrane potential, the lipid uptake and metabolism, the oxygen consumption rates (OCR) and glycolytic activities of TECs. Ybx3-/- mice demonstrate protection from IRI with less immune cell infiltration, ER stress and tubular cell damage. A putative protective mechanism is identified via upregulated antioxidant activities and reduced ferroptosis, when Ybx3 is deleted. Here, experimental evidences reveal DbpA acts as a mitochondrial protein with profound adverse effects on cell metabolism and highlights a protective effect against IRI when Ybx3 is genetically deleted.
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 GSE264448_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 PRJNA1102427 and SRA study SRP505695. Searching any of these in the dataset finder brings you back here.

Samples in this study

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