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View article: The kinase domain of RIPK3 tunes its scaffolding functions
The kinase domain of RIPK3 tunes its scaffolding functions Open
The pro-inflammatory programmed cell death pathway, necroptosis, relies on phosphorylation of the terminal effector, MLKL, by RIPK3. RIPK3-deficient mice or those harboring the kinase-inactivating mutation, RIPK3 K51A , are ostensibly norm…
View article: Supplementary Figures from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Figures from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Supplementary Figures 1-23 including results for fine mapping of MACROD2 deletions, xenograft assay, immunofluoresence, comet assays, western blots, PARP1 activity assays, clonogenic assays, apoptosis assays, metaphase spreads and chromoso…
View article: Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
ADP-ribosylation is an important posttranslational protein modification that regulates diverse biological processes, controlled by dedicated transferases and hydrolases. Here, we show that frequent deletions (∼30%) of the MACROD2 mono-ADP-…
View article: Identification of Serum Biomarkers to Monitor Therapeutic Response in Intestinal-Type Gastric Cancer
Identification of Serum Biomarkers to Monitor Therapeutic Response in Intestinal-Type Gastric Cancer Open
There are a limited number of clinically useful serum biomarkers to predict tumor onset or treatment response in gastric cancer (GC). For this reason, we explored the serum proteome of the gp130Y757F murine model of intestinal-type gastric…
View article: Figure S2 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Figure S2 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Adenoma tumour development in Apcmin/+ and Dclk1Cre/+;Apcfl/fl mice
View article: Data from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Data from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Adenomatous polyposis coli (APC) truncations occur in many colorectal cancers and are often associated with immune infiltration. The aim of this study was to determine whether a combination of Wnt inhibition with anti-inflammatory (sulinda…
View article: Figure S1 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Figure S1 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Xgal and DCLK1 staining of colon crypts from DCLK1-CreERT2 BAC transgenic mice
View article: Figure S3 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Figure S3 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Histology and immunohistochemical analysis of beta-catenin in adenomas from treated Dclk1Cre/+;Apcfl/fl mice.
View article: Figure S2 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Figure S2 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Adenoma tumour development in Apcmin/+ and Dclk1Cre/+;Apcfl/fl mice
View article: Data from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Data from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Adenomatous polyposis coli (APC) truncations occur in many colorectal cancers and are often associated with immune infiltration. The aim of this study was to determine whether a combination of Wnt inhibition with anti-inflammatory (sulinda…
View article: Figure S3 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Figure S3 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Histology and immunohistochemical analysis of beta-catenin in adenomas from treated Dclk1Cre/+;Apcfl/fl mice.
View article: Figure S1 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC
Figure S1 from Combined Treatment with a WNT Inhibitor and the NSAID Sulindac Reduces Colon Adenoma Burden in Mice with Truncated APC Open
Xgal and DCLK1 staining of colon crypts from DCLK1-CreERT2 BAC transgenic mice
View article: Supplementary Figures from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Figures from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Supplementary Figures 1-23 including results for fine mapping of MACROD2 deletions, xenograft assay, immunofluoresence, comet assays, western blots, PARP1 activity assays, clonogenic assays, apoptosis assays, metaphase spreads and chromoso…
View article: Supplementary Tables from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Tables from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Supplementary Tables 1-11 includes GISTIC results, clinical characteristics, details on cell lines and MACROD2 deletions, pathogenicity predictions, metaphase chromosomes anomalies, multivariate analyses and primer sequences.
View article: Supplementary Figures from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Figures from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Supplementary Figures 1-23 including results for fine mapping of MACROD2 deletions, xenograft assay, immunofluoresence, comet assays, western blots, PARP1 activity assays, clonogenic assays, apoptosis assays, metaphase spreads and chromoso…
View article: Supplementary Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Mouse phenotyping data
View article: Supplementary Methods from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Methods from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Supplementary Methods for generation of CRISPR and stable cell lines, MACROD2 mutation detection, QRT-PCR, phenotyping of MACROD2/APCmin mice, IHC, WB, TCF reporter assay, RNAseq analysis, generation of MACROD2 antibody, clonogenic assay, …
View article: Supplementary Methods from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Methods from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Supplementary Methods for generation of CRISPR and stable cell lines, MACROD2 mutation detection, QRT-PCR, phenotyping of MACROD2/APCmin mice, IHC, WB, TCF reporter assay, RNAseq analysis, generation of MACROD2 antibody, clonogenic assay, …
View article: Supplementary Tables from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Tables from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Supplementary Tables 1-11 includes GISTIC results, clinical characteristics, details on cell lines and MACROD2 deletions, pathogenicity predictions, metaphase chromosomes anomalies, multivariate analyses and primer sequences.
View article: Supplementary Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Supplementary Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
Mouse phenotyping data
View article: Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors
Data from <i>MACROD2</i> Haploinsufficiency Impairs Catalytic Activity of PARP1 and Promotes Chromosome Instability and Growth of Intestinal Tumors Open
ADP-ribosylation is an important posttranslational protein modification that regulates diverse biological processes, controlled by dedicated transferases and hydrolases. Here, we show that frequent deletions (∼30%) of the MACROD2 mono-ADP-…
View article: Supplementary Methods from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model
Supplementary Methods from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model Open
Extended methods and materials are provided as a supplement to the methods section in the main manuscript and to describe additional methods from the supplementary data.
View article: Supplementary Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism
Supplementary Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism Open
The content of this file containing Supplementary Figures (and a Supplementary Table) provides additional (and essential) data supporting our conclusions that the ASC inflammasome/caspase-1/IL-18 axis promotes gastric tumorigenesis.
View article: Supplementary Figure Legends from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model
Supplementary Figure Legends from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model Open
Supplementary Figure Legends
View article: Supplementary Methods from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model
Supplementary Methods from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model Open
Extended methods and materials are provided as a supplement to the methods section in the main manuscript and to describe additional methods from the supplementary data.
View article: Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism
Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism Open
Inflammasomes are key regulators of innate immunity in chronic inflammatory disorders and autoimmune diseases, but their role in inflammation-associated tumorigenesis remains ill-defined. Here we reveal a protumorigenic role in gastric can…
View article: Supplementary Figures 1 through 7 and Supplementary Table 1 from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model
Supplementary Figures 1 through 7 and Supplementary Table 1 from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model Open
Additional supportive data is provided as Fig S1 (Generation and validation of Tg(Tff1-CreERT2)mice), Fig. S2 (Tff1-CreERT2 transgene, endogenous Tff1, and Lgr5 expression in the stomach), Fig. S3 (Tff1-CreERT2-mediated I2-galactosidase re…
View article: Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism
Data from Inflammasome Adaptor ASC Suppresses Apoptosis of Gastric Cancer Cells by an IL18-Mediated Inflammation-Independent Mechanism Open
Inflammasomes are key regulators of innate immunity in chronic inflammatory disorders and autoimmune diseases, but their role in inflammation-associated tumorigenesis remains ill-defined. Here we reveal a protumorigenic role in gastric can…
View article: Data from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model
Data from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model Open
About 5% to 10% of human gastric tumors harbor oncogenic mutations in the KRAS pathway, but their presence alone is often insufficient for inducing gastric tumorigenesis, suggesting a requirement for additional mutagenic events or microenv…
View article: Supplementary Figures 1 through 7 and Supplementary Table 1 from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model
Supplementary Figures 1 through 7 and Supplementary Table 1 from Stomach-Specific Activation of Oncogenic KRAS and STAT3-Dependent Inflammation Cooperatively Promote Gastric Tumorigenesis in a Preclinical Model Open
Additional supportive data is provided as Fig S1 (Generation and validation of Tg(Tff1-CreERT2)mice), Fig. S2 (Tff1-CreERT2 transgene, endogenous Tff1, and Lgr5 expression in the stomach), Fig. S3 (Tff1-CreERT2-mediated I2-galactosidase re…