Mir142 loss unlocks IDH2R140-dependent leukemogenesis through antagonistic regulation of HOX genes

ChEBI2020-06-05 更新2026-07-12 收录

白血病发病机制

基因调控与功能

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https://www.ebi.ac.uk/biostudies/ArrayExpress/studies/E-MTAB-8042 数据链接链接失效反馈

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Mir142 loss unlocks IDH2R140-dependent leukemogenesis through antagonistic regulation of HOX genes

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2020-06-05

Phf6 restricts the self-renewal of hematopoietic stem cells via regulation of Nr4a1 expression

造血干细胞调控

白血病发病机制

Recurrent inactivating mutations have been identified in various hematological malignancies in the X-linked PHF6 gene. However, it is currently unknown how PHF6 regulates normal hematopoiesis and how

NIAID Data Ecosystem120

Two mutations associated with leukemia that change a single tyrosine residue in the STAT5B SH2 domain have opposite effects on the transcriptional programs controlling hematopoiesis [ChIP-seq]

白血病发病机制

细胞转录调控

Normal hematopoiesis is regulated by various cytokines via the JAK-STAT signaling pathway. Gene deletion studies in mice have demonstrated the crucial role of STAT5B in the proliferation, differentiat

NIAID Data Ecosystem50

Transcriptional profiling (SMARTer-Seq) has been performed on CD48-/CD48+ LSK hematopoietic cells to determine the effect introduced by the abrogation of Sbds within mesenchymal cells.

白血病发病机制

间质-造血细胞互作

Mesenchymal niche cells may drive tissue failure and malignant transformation in the hematopoietic system but the molecular mechanisms and their relevance to human disease remain poorly defined Here,

NIAID Data Ecosystem30

Hematopoietic stem cell-restricted Cdx2 expression induces transformation to myelodysplasia and acute leukemia [RNASeq_Cdx2_secondaryAML]

白血病发病机制

造血干细胞

The caudal-related homeobox transcription factor CDX2 is ectopically expressed in the majority of patients with acute myeloid leukemia (AML). We generated an inducible transgenic mouse model whereby C

NIAID Data Ecosystem70

Functional Characterization of Cooperating MGA Mutations in RUNX1::RUNX1T1 Acute Myeloid Leukemia [ATAC-seq]

白血病发病机制

表观遗传调控

MGA (Max-gene associated) is a dual-specificity transcription factor that negatively regulates MYC-target genes to inhibit proliferation and promote differentiation. Loss-of-function mutations in MGA

NIAID Data Ecosystem30

Mir142 loss unlocks IDH2R140-dependent leukemogenesis through antagonistic regulation of HOX genes

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