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DNA-PK Mediated CRTC2 Phosphorylation Promotes CRTC2 Relocation from Transcription to Repair Complexes Enhancing NHEJ and Suppressing Abscopal Effect

GSE307028 Mus musculus (mouse) RNA-seq (gene expression) 2 samples Submitted 2026/04/20 Platform GPL13112
At a glance

RNA-seq (gene expression) · mouse · 2 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
2 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.
Paper
DNA-PK-mediated CRTC2 phosphorylation promotes NHEJ and suppresses antitumor immunity via relocation to repair complexesNature communications · 2026
Summary (written by the submitters)
DNA damage repair and transcription are antagonistic cellular processes that require precise spatiotemporal coordination to maintain genomic integrity. Transcriptional silencing at DSB sites is essential for efficient repair, mediated through localized histone modifications and direct inhibition of RNA polymerase II (Pol II). However, the role of transcriptional activators in coordinating DSB repair with transcriptional silencing remains elusive.
Read the full summary ↓
Here, we identify the transcriptional coactivator CRTC2 as a key coordinator of DNA repair and transcriptional regulation. We demonstrate that CRTC2 promotes canonical non-homologous end joining (c-NHEJ) both in vitro and in vivo. Mechanistically, PARP1 activation recruits CRTC2 to DNA breaks, where it facilitates DNA-PKcs recruitment and assembly of the DNA-PK holoenzyme, thereby driving c-NHEJ. DNA-PK–mediated phosphorylation of CRTC2 at Ser433 dissociates it from transcriptional complexes, suppressing target gene transcription, and promoting its incorporation into DNA repair complexes. Thus, establishing a positive feedback loop that enhances NHEJ efficiency. CRTC2 loss radiosensitizes cancer cells, potentiates irradiation-induced cGAS–STING activation, promotes cytotoxic CD8⁺ T cell infiltration, and enhances the abscopal effect. Furthermore, AAV8-mediated targeting of CRTC2 sensitizes tumors to radioimmunotherapy. Our results reveal CRTC2 as bifunctional nodal effector coupling transcriptional silencing to DNA repair and propose its inhibition as a promising strategy for radioimmunotherapy sensitization in resistant malignancies.
Published in
DNA-PK-mediated CRTC2 phosphorylation promotes NHEJ and suppresses antitumor immunity via relocation to repair complexes
Zou F, Yao Z, Dong X et al. · Nature communications 2026 · PMID 42151152 · doi:10.1038/s41467-026-73228-4
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 GSE307028_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 PRJNA1314142 and SRA study SRP616611. Searching any of these in the dataset finder brings you back here.

Samples in this study

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