Ella M. Melnik
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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.
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 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 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