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Sex-biased ZRSR2 mutations in myeloid malignancies impair plasmacytoid dendritic cell activation and apoptosis
PubMed Full text in PMC Similar studies
Sex-biased ZRSR2 mutations in myeloid malignancies impair plasmacytoid dendritic cell activation and apoptosis [cell line]
PubMed Full text in PMC Similar studies Analyze with GEO2RSRA Run Selector
Sex-biased ZRSR2 mutations in myeloid malignancies impair plasmacytoid dendritic cell activation and apoptosis [patients]
Expression data from 12 BPDCN samples, 35 T-ALL samples, and 65 AML samples
PubMed Full text in PMC Similar studies Analyze with GEO2R
RNA-seq analysis after GSK595 treatment in CAL-1 cells
PubMed Full text in PMC Similar studies SRA Run Selector
Single-cell Multiomics Reveals Clonal T-cell Expansions and Exhaustion in Blastic Plasmacytoid Dendritic Cell Neoplasm
Aberrant splicing of U12-type introns is the hallmark of ZRSR2 mutant myelodysplastic syndrome
RUNX2 promotes the development of Blastic plasmacytoid dendritic cell neoplasm (BPDCN)
ZRSR1 cooperates with ZRSR2 in regulating splicing of U12-type introns in murine hematopoietic cells
ZRSR1 cooperates with ZRSR2 in regulating splicing of U12-type introns in murine hematopoietic cells I
Ultraviolet radiation shapes dendritic cell leukaemia transformation in the skin
A Druggable TCF4- and BRD4-dependent Transcriptional Network Sustains Malignancy in Blastic Plasmacytoid Dendritic Cell Neoplasm (ATAC-Seq)
A Druggable TCF4- and BRD4-dependent Transcriptional Network Sustains Malignancy in Blastic Plasmacytoid Dendritic Cell Neoplasm (RNA-Seq)
A druggable TCF4- and BRD4-dependent transcriptional network sustains malignancy in blastic plasmacytoid dendritic cell neoplasm (ChIP-Seq)
A druggable TCF4- and BRD4-dependent transcriptional network sustains malignancy in blastic plasmacytoid dendritic cell neoplasm
Molecular profiling of blastic plasmacytoid dendritic cell neoplasm reveals a unique pattern and suggests selective sensitivity to nf-kb pathway inhibition
Blastic plasmacytoid dendritic cell neoplasm: genomics mark epigenetic dysregulation as a primary therapeutic target
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