Ai Hamashima
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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: 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 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 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 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 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…
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 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: The acidic domain of Hmga2 and the domain’s linker region are critical for driving self-renewal of hematopoietic stem cell
The acidic domain of Hmga2 and the domain’s linker region are critical for driving self-renewal of hematopoietic stem cell Open
High mobility group AT-hook 2 (Hmga2) is a chromatin modifier protein that plays a critical role in fetal development and leukemia propagation by binding to chromatin and DNA via its AT-hook domains. However, the molecular mechanisms by wh…