GEO series

Transcriptomic profiling of AML cell lines MV4-11 and Kasumi-1 treated with CK1α degrader PinA1

GSE326946 Homo sapiens (human) RNA-seq (gene expression) 12 samples Submitted 2026/07/28 Platform GPL34281

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)
Topic: Acute myeloid leukemiaThis series is part of our curated briefing on it.
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.

Summary (written by the submitters)

Acute myeloid leukemia (AML) is characterized by dysregulated transcriptional programs that support malignant proliferation and survival. Casein kinase 1 alpha (CK1α) has been implicated in the regulation of p53 signaling and represents a potential therapeutic target. In this study, we aimed to investigate whether CK1α degradation induces broad transcriptomic changes in a p53-dependent manner.

Read the full summary ↓

To address this, we performed RNA sequencing (RNA-seq) in two human AML cell lines with distinct TP53 status: MV4-11 (TP53 wild-type) and Kasumi-1 (TP53 mutant). Cells were treated with a CK1α degrader (PinA1) or vehicle control, followed by transcriptomic profiling. Comparative analysis was conducted to assess the extent and nature of gene expression changes induced by CK1α degradation. Notably, this study was designed to evaluate whether CK1α targeting leads to more pronounced transcriptional alterations in TP53 wild-type cells compared to TP53-mutant contexts. Our data provide insights into the p53-dependent transcriptional consequences of CK1α degradation and support its potential as a therapeutic strategy in AML.

This dataset

Open GSE326946 in finder → Find more human RNA-seq datasets → Acute myeloid leukemia landscape →

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 GSE326946_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 PRJNA1446174 and SRA study SRP688643. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

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

GSM9644126 MV4-11, DMSO Control #1, 24h
GSM9644127 MV4-11, DMSO Control #2, 24h
GSM9644128 MV4-11, DMSO Control #3, 24h
GSM9644129 MV4-11, PinA1 #1, 24h
GSM9644130 MV4-11, PinA1 #2, 24h
GSM9644131 MV4-11, PinA1 #3, 24h
GSM9644132 Kasumi-1, DMSO Control #1, 24h
GSM9644133 Kasumi-1, DMSO Control #2, 24h
GSM9644134 Kasumi-1 DMSO Control #3, 24h
GSM9644135 Kasumi-1, PinA1 #1, 24h
GSM9644136 Kasumi-1, PinA1 #2, 24h
GSM9644137 Kasumi-1, PinA1 #3, 24h

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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.