Goro Sashida
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View article: TYK2 is essential for the therapeutic effect of IFN-α in Jak2V617F-induced murine myeloproliferative neoplasms
TYK2 is essential for the therapeutic effect of IFN-α in Jak2V617F-induced murine myeloproliferative neoplasms Open
Interferon-α (IFN-α) exhibits antiviral and antiproliferative effects on normal and neoplastic cells. Intracellular signaling of IFN-α is mediated by tyrosine kinase 2 (TYK2) and janus kinase 1 (JAK1), followed by signal transducers and ac…
View article: Chromatin Modifier Hmga1 Maintains Hematopoietic Stem Cell Integrity in Stress Conditions
Chromatin Modifier Hmga1 Maintains Hematopoietic Stem Cell Integrity in Stress Conditions Open
Hematopoietic stem cells (HSCs) respond to various stresses, such as inflammation, and expand hematopoietic stem and progenitor cells (HSPCs) to produce mature blood cells; however, the mechanisms by which HSCs maintain hematopoiesis in di…
View article: Multiple myeloma–associated DIS3 gene is essential for hematopoiesis, but loss of DIS3 is insufficient for myelomagenesis
Multiple myeloma–associated DIS3 gene is essential for hematopoiesis, but loss of DIS3 is insufficient for myelomagenesis Open
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View article: HAPLOINSUFFICIENCY OF TIE2 IN MUTATED BLOOD CELLS SUPPRESS ANGIOGENESIS IN THE BONE MARROW AND INHIBIT PROGRESSION OF MDS
HAPLOINSUFFICIENCY OF TIE2 IN MUTATED BLOOD CELLS SUPPRESS ANGIOGENESIS IN THE BONE MARROW AND INHIBIT PROGRESSION OF MDS Open
Introduction: Tie2 is a receptor tyrosine kinase and regulates angiogenesis and vascular quiescence. Given that Tie2 modulates microvascular density in cancer, we hypothesized that deletion of Tie2 in blood cells can inhibit progression of…
View article: Late B Cell-Specific Dis3-Knockout Mice Do Not Develop Plasma Cell Neoplasm
Late B Cell-Specific Dis3-Knockout Mice Do Not Develop Plasma Cell Neoplasm Open
Recent advances in next-generation sequencing have unveiled genetic abnormalities associated with multiple myeloma (MM). Of note, DIS3 mutations have been observed in ~10% of MM patients, and 13q deletion including the DIS3 gene locus are …
View article: Exposure to microbial products followed by loss of Tet2 promotes myelodysplastic syndrome via remodeling HSCs
Exposure to microbial products followed by loss of Tet2 promotes myelodysplastic syndrome via remodeling HSCs Open
Aberrant innate immune signaling in myelodysplastic syndrome (MDS) hematopoietic stem/progenitor cells (HSPCs) has been implicated as a driver of the development of MDS. We herein demonstrated that a prior stimulation with bacterial and vi…
View article: Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic disorders that are incurable with conventional therapy. Their incidence is increasing with global population aging. Although many genetic, epigenetic, splicing, and metabolic …
View article: Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Figure S1-13 and Table S1,3
View article: Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Supplementary Methods
View article: Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Supplementary Methods
View article: Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Figure S1-13 and Table S1,3
View article: Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Table S2
View article: Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Table S2
View article: Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes Open
Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic disorders that are incurable with conventional therapy. Their incidence is increasing with global population aging. Although many genetic, epigenetic, splicing, and metabolic …
View article: Data from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Data from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
RUNX3, a RUNX family transcription factor, regulates normal hematopoiesis and functions as a tumor suppressor in various tumors in humans and mice. However, emerging studies have documented increased expression of RUNX3 in hematopoietic st…
View article: Supplementary Data 3 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 3 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Runx1 target genes
View article: Supplementary Table 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Table 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
RUNX3 IHC and clinical data of MDS patients
View article: Supplementary Data 3 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 3 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Runx1 target genes
View article: Supplementary Data 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
GO analysis of RUNX3-Tet2 KO MDS
View article: Supplementary Data 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Up- and down-regulated genes
View article: Supplementary Data 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
GO analysis of RUNX3-Tet2 KO MDS
View article: Supplementary Table 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Table 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Primers for q-RT-PCR
View article: Supplementary Table 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Table 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Primers for q-RT-PCR
View article: Supplementary Data 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Up- and down-regulated genes
View article: Supplementary Data 4 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 4 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Motif enrichment analysis
View article: Supplementary Figure 1-11 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Figure 1-11 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Supplementary Figure 1-11
View article: Supplementary Data 4 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Supplementary Data 4 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
Motif enrichment analysis
View article: Data from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
Data from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome Open
RUNX3, a RUNX family transcription factor, regulates normal hematopoiesis and functions as a tumor suppressor in various tumors in humans and mice. However, emerging studies have documented increased expression of RUNX3 in hematopoietic st…