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Series GSE126302 Query DataSets for GSE126302
Status Public on Aug 02, 2020
Title Loss of Setd2 promote Kras-induced acinar-to-ductal metaplasia and epitheliamesenchymal transition during pancreatic carcinogenesis
Organism Mus musculus
Experiment type Expression profiling by high throughput sequencing
Genome binding/occupancy profiling by high throughput sequencing
Summary TCGA(PAAD) public database and PDAC tissue array with SETD2/H3K36me3 staining was used to investigate the clinical relevance of SETD2 in PDAC. Furthermore, to define the role of SETD2 in the carcinogenesis of PDAC, we crossed conditional Setd2 knockout mice (PdxcreSetd2flox/flox) together with with KrasG12D mice. Moreover, to examine the role of SETD2 after ductal metaplasia, Crisp/cas9 was used to deplete Setd2 in PDAC cells. RNA-seq and H3K36me3 Chip-seq were performed to uncover the mechanism.
Overall design RNA-seq and H3K36me3 Chip-seq were performed in mouse acinar cell and KPC1199 cell line.
Contributor(s) Xue J
Citation(s) 32739869, 36453584
Submission date Feb 08, 2019
Last update date Feb 06, 2023
Contact name Ningning Niu
Phone 86-21-68382281
Organization name Shanghai Jiao Tong University School of Medicine Affiliated Renji Hospital
Department Clinical Stem Cell Research Center
Street address 160 Pu Jian Road, Shanghai
City Shanghai
ZIP/Postal code 200127
Country China
Platforms (1)
GPL21273 HiSeq X Ten (Mus musculus)
Samples (10)
GSM3595860 KO1-1
GSM3595861 KO1-2
GSM3595862 KO2-1
BioProject PRJNA521511
SRA SRP184682

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Supplementary file Size Download File type/resource
GSE126302_KO_IPvsKO_input_peaks.bed.gz 1.5 Kb (ftp)(http) BED
GSE126302_WT_IPvsWT_input_peaks.bed.gz 30.1 Kb (ftp)(http) BED
GSE126302_all.counts.txt.gz 362.0 Kb (ftp)(http) TXT
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Raw data are available in SRA
Processed data are available on Series record

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