HMGA1 Chromatin Regulators Drive MPN Progression
收藏NIAID Data Ecosystem2026-05-01 收录
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This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
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2024-01-08
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Physical interaction between mutant calreticulin and the thrombopoietin receptor is required for transformation of hematopoietic cells. Mus musculus
Somatic mutations in calreticulin (CALR) are present in approximately 40% of patients with myeloproliferative neoplasms (MPN). However, the mechanism by which mutant CALR is oncogenic is unknown. Here
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JAK2 Naive and Persitent Murine BaF3 cells infected with MPLW515L. Mus musculus
Transcriptional profiling of Murine BaF3 cells infected with MPLW515L grown under either normal conditions (Naive) or in 0.8 uM INCB18424 for 4-6 weeks (Persistent). Naive and Persistent cells were th
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ZRSR2-loss causes aberrant splicing in a JAK2V617F-driven myeloproliferative neoplasm but is not sufficient to drive disease progression. ZRSR2-loss causes aberrant splicing in a JAK2V617F-driven myeloproliferative neoplasm but is not sufficient to drive disease progression
This SuperSeries is composed of the SubSeries listed below. Overall design: Refer to individual Series
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Jak2V617F Reversible Activation Shows an Essential Requirement for Jak2V617F in Myeloproliferative Neoplasms. Jak2V617F Reversible Activation Shows an Essential Requirement for Jak2V617F in Myeloproliferative Neoplasms
Janus kinases (JAKs) mediate cytokine signaling, cell growth and hematopoietic differentiation. Gain-of-function mutations activating JAK2 signaling are seen in the majority of myeloproliferative neop
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Fibroblast growth factor receptor 1 is fused to FIM in stem-cell myeloproliferative disorder with t(8;13)(p12;q12)
Chromosome 8p11–12 is the site of a recurrent breakpoint in a myeloproliferative disorder that involves lymphoid (T- or B-cell), myeloid hyperplasia and eosinophilia, and evolves toward acute leukemia
PubMed Central1998-05-12 更新40
