Wei‐Xing Zong
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View article: Supplementary Table S2 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition
Supplementary Table S2 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition Open
Supplementary Table S2
View article: Supplementary Data from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition
Supplementary Data from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition Open
Supplementary Figs. S1-S6
View article: Supplementary Table S5 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition
Supplementary Table S5 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition Open
Supplementary Table S5
View article: Supplementary Table S4 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition
Supplementary Table S4 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition Open
Supplementary Table S4
View article: Supplementary Table S3 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition
Supplementary Table S3 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition Open
Supplementary Table S3
View article: Supplementary Table S1 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition
Supplementary Table S1 from <i>RBM10</i> Loss Promotes <i>EGFR</i>-Driven Lung Cancer and Confers Sensitivity to Spliceosome Inhibition Open
Supplementary Table S1
View article: Supplementary Table 2 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency
Supplementary Table 2 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency Open
Prevalent IgH VDJ sequences of MLN B cells in aging M-Traf3-/- mice
View article: Figures S1-S9 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency
Figures S1-S9 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency Open
Supplementary Figure S1. Analysis of ERV reactivation in aging M-Traf3-/- mice with BCL and WT mice. Supplementary Figure S2. Assessment of gut barrier integrity and commensal bacterial transmigration in aging WT and MTraf3-/- mice. Supple…
View article: Supplementary Table 1 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency
Supplementary Table 1 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency Open
IgH VDJ sequence characteristics of dominant malignant B-cell clones spontaneously developed in aging M-Traf3-/- mice
View article: Data from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency
Data from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency Open
Myeloid cells are central players in innate immunity and inflammation. Their function is regulated by the adapter protein TRAF3. We previously reported that aging myeloid cell–specific TRAF3-deficient (M-Traf3−/−) mice sp…
View article: Figures S1-S9 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency
Figures S1-S9 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency Open
Supplementary Figure S1. Analysis of ERV reactivation in aging M-Traf3-/- mice with BCL and WT mice. Supplementary Figure S2. Assessment of gut barrier integrity and commensal bacterial transmigration in aging WT and MTraf3-/- mice. Supple…
View article: Supplementary Table 2 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency
Supplementary Table 2 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency Open
Prevalent IgH VDJ sequences of MLN B cells in aging M-Traf3-/- mice
View article: Supplementary Table 1 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency
Supplementary Table 1 from Commensal Bacteria Drive B-cell Lymphomagenesis in the Setting of Innate Immunodeficiency Open
IgH VDJ sequence characteristics of dominant malignant B-cell clones spontaneously developed in aging M-Traf3-/- mice
View article: Splicing Shift of <i>RAC1</i> Accelerates Tumorigenesis and Defines a Potent Therapeutic Target in Lung Cancer
Splicing Shift of <i>RAC1</i> Accelerates Tumorigenesis and Defines a Potent Therapeutic Target in Lung Cancer Open
Dysregulated RNA splicing has emerged as a pervasive yet understudied feature of cancer. The small GTPase RAC1 undergoes splicing changes in multiple cancers. However, the in vivo functional disparities between the two major RAC1 isoforms,…
View article: Author response: Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse model
Author response: Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse model Open
View article: Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse model
Propionyl-CoA carboxylase subunit B regulates anti-tumor T cells in a pancreatic cancer mouse model Open
Most human pancreatic ductal adenocarcinoma (PDAC) are not infiltrated with cytotoxic T cells and are highly resistant to immunotherapy. Over 90% of PDAC have oncogenic KRAS mutations, and phosphoinositide 3-kinases (PI3Ks) are direct effe…
View article: Disruption of Mitochondrial Dynamics and Stasis Leads to Liver Injury and Tumorigenesis
Disruption of Mitochondrial Dynamics and Stasis Leads to Liver Injury and Tumorigenesis Open
Background & Aims Mitochondrial dysfunction has been implicated in aging and various cancer development. As highly dynamic organelles, mitochondria constantly undergo fission, mediated by dynamin-related protein 1 (DRP1, gene name Dnm1l ),…
View article: Data from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Data from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
In lung adenocarcinoma (LUAD), loss-of-function mutations in the splicing factor RBM10 frequently co-occur with oncogenic EGFR mutations. A detailed understanding of the functional consequences and therapeutic impact of RBM10 loss in EGFR-…
View article: Supplementary Table S3 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S3 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S3
View article: Supplementary Table S1 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S1 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S1
View article: Supplementary Table S1 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S1 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S1
View article: Supplementary Table S2 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S2 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S2
View article: Supplementary Table S4 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S4 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S4
View article: Supplementary Table S5 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S5 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S5
View article: Supplementary Table S2 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S2 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S2
View article: Supplementary Data from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Data from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Figs. S1-S6
View article: Supplementary Table S3 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S3 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S3
View article: Supplementary Data from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Data from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Figs. S1-S6
View article: Supplementary Table S5 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S5 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S5
View article: Supplementary Table S4 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition
Supplementary Table S4 from RBM10 loss promotes EGFR-driven lung cancer and confers sensitivity to spliceosome inhibition Open
Supplementary Table S4