Daichi Inoue
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View article: BRD4 and MYB inhibition overcomes venetoclax resistance in EVI1-rearranged acute myeloid leukemia
BRD4 and MYB inhibition overcomes venetoclax resistance in EVI1-rearranged acute myeloid leukemia Open
EVI1-rearranged acute myeloid leukemia (AML) with inv(3)(q21q26) or t(3;3)(q21q26) represents a distinct and aggressive subtype characterized by poor prognosis and limited treatment options. However, the optimal strategy to overcome resist…
View article: In-depth functional analysis of BRD9 in fetal hematopoiesis reveals context-dependent roles
In-depth functional analysis of BRD9 in fetal hematopoiesis reveals context-dependent roles Open
The hierarchical organization of hematopoietic stem cells (HSCs) governing adult hematopoiesis has been extensively investigated. However, the dynamic epigenomic transition from fetal to adult hematopoiesis remains incompletely understood,…
View article: Photochemical Transformations of Glycosyl Bromides in the Presence of Amines
Photochemical Transformations of Glycosyl Bromides in the Presence of Amines Open
View article: Examining the Connection Between the Color Scheme of Event Announcement Images and View Counts on Social Media Through Machine Learning Models
Examining the Connection Between the Color Scheme of Event Announcement Images and View Counts on Social Media Through Machine Learning Models Open
View article: Photochemical Transformations of Glycosyl Bromides in the Presence of Amines
Photochemical Transformations of Glycosyl Bromides in the Presence of Amines Open
View article: BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state
BRD9 determines the cell fate of hematopoietic stem cells by regulating chromatin state Open
ATP-dependent chromatin remodeling SWI/SNF complexes exist in three subcomplexes: canonical BAF (cBAF), polybromo BAF (PBAF), and a newly described non-canonical BAF (ncBAF). While cBAF and PBAF regulate fates of multiple cell types, roles…
View article: Systematic evaluation of AML-associated antigens identifies anti-U5 SNRNP200 therapeutic antibodies for the treatment of acute myeloid leukemia
Systematic evaluation of AML-associated antigens identifies anti-U5 SNRNP200 therapeutic antibodies for the treatment of acute myeloid leukemia Open
View article: SETBP1 is dispensable for normal and malignant hematopoiesis
SETBP1 is dispensable for normal and malignant hematopoiesis Open
View article: Extracellular vesicle-mediated remodeling of the bone marrow microenvironment in myeloid malignancies
Extracellular vesicle-mediated remodeling of the bone marrow microenvironment in myeloid malignancies Open
View article: Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation Open
Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
View article: Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation Open
Supplementary Figure from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
View article: Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation Open
Recently, screens for mediators of resistance to FLT3 and ABL kinase inhibitors in leukemia resulted in the discovery of LZTR1 as an adapter of a Cullin-3 RING E3 ubiquitin ligase complex responsible for the degradation of RAS GTPases. In …
View article: Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation
Data from Impaired Proteolysis of Noncanonical RAS Proteins Drives Clonal Hematopoietic Transformation Open
Recently, screens for mediators of resistance to FLT3 and ABL kinase inhibitors in leukemia resulted in the discovery of LZTR1 as an adapter of a Cullin-3 RING E3 ubiquitin ligase complex responsible for the degradation of RAS GTPases. In …
View article: Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Supplementary Table Captions for Tables S1-S6
View article: Table S3 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S3 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Fold-change in abundance and statistical significance of proteins in XPO1E571K/WT versus XPO1WT NALM-6 cells detected by SILAC analysis of cytoplasmic fractions
View article: Table S2 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S2 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
578 genes sequenced in mouse genomic DNA.
View article: Table S3 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S3 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Fold-change in abundance and statistical significance of proteins in XPO1E571K/WT versus XPO1WT NALM-6 cells detected by SILAC analysis of cytoplasmic fractions
View article: Table S1 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S1 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Number and frequency of XPO1 hotspot mutations found across cancer types.
View article: Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Supplementary Methods
View article: Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Altered expression of XPO1, the main nuclear export receptor in eukaryotic cells, has been observed in cancer, and XPO1 has been a focus of anticancer drug development. However, mechanistic evidence for cancer-specific alterations in XPO1 …
View article: Supplementary Figures from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Supplementary Figures from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Supplementary Figures S1-S12
View article: Table S2 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S2 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
578 genes sequenced in mouse genomic DNA.
View article: Table S4 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S4 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Fold-change in abundance and statistical significance of proteins in XPO1E571K/WT versus XPO1WT NALM-6 cells detected by SILAC analysis of nuclear fractions
View article: Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Proteins with predicted or known nuclear export signals and significantly enhanced or reduced in nuclear export in XPO1 mutant versus wild-type from SILAC analysis.
View article: Table S6 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S6 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Characteristics of XPO1 mutant and wild-type CLL patients that underwent RNA-sequencing analysis.
View article: Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Supplementary Table Captions from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Supplementary Table Captions for Tables S1-S6
View article: Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Supplementary Methods from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Supplementary Methods
View article: Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S5 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Proteins with predicted or known nuclear export signals and significantly enhanced or reduced in nuclear export in XPO1 mutant versus wild-type from SILAC analysis.
View article: Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Data from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Altered expression of XPO1, the main nuclear export receptor in eukaryotic cells, has been observed in cancer, and XPO1 has been a focus of anticancer drug development. However, mechanistic evidence for cancer-specific alterations in XPO1 …
View article: Table S6 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis
Table S6 from Altered Nuclear Export Signal Recognition as a Driver of Oncogenesis Open
Characteristics of XPO1 mutant and wild-type CLL patients that underwent RNA-sequencing analysis.