Thomas C. Smyrk
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View article: Correction: Quantitative assessment of ultrasound microvessel imaging in Crohn’s disease: correlation with pathological inflammation
Correction: Quantitative assessment of ultrasound microvessel imaging in Crohn’s disease: correlation with pathological inflammation Open
View article: Supplementary Figure 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 1 shows correlation of SNP rs1992901 and GLI2 Transcript Expression.
View article: Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 9 shows that Gli2 does not change H3K27Ac enrichment at Ccnd1 promoter downstream of oncogenic KRAS.
View article: Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 10 shows not differences in H3K4me1 enrichment at Ccnd1 promoter in mutant KRAS cells.
View article: Supplementary Table 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 3 includes the sequence of the primers used in our study.
View article: Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 6 describes RNA-seq shows differential gene expression induced by oncogenic KRAS.
View article: Supplementary Figure 5 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 5 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 5 shows the IHC results looking at CD4 and CD8 expression in KC and KCRG mice. The results show no difference in the immune landscape between these mouse models.
View article: Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 8 shows the expression of GLI target genes in all experimental groups.
View article: Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 4 shows the validation of Kras signaling activation and chronic pancreatitis phenotypic examples in KC and KCRG mice.
View article: Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 2 includes the SNP analysis of components of the Hedgehog pathway.
View article: Supplementary Figure 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 2 describes the characterization of the impact Gli2 overexpression in pancreas development. showing that Gli2 loss has no impact on pancreas development or survival in vivo.
View article: Supplementary Figure 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 3 shows Gli2 expression in CRG and KCRG mice and Gli luciferase activity in ΔNGli2-transfected cells.
View article: Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 7 shows how oncogenic KRAS modulates GLI target gene expression.
View article: Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 1 describes the characteristics of the patients used in our study.
View article: Clinical Characteristics and Outcomes of Small Bowel Neoplasms in Crohn’s Disease: A Case-Control Study
Clinical Characteristics and Outcomes of Small Bowel Neoplasms in Crohn’s Disease: A Case-Control Study Open
Background Patients with Crohn’s disease (CD) who have ileal or any small bowel (SB) involvement are at increased risk of developing SB cancer. Due to the rarity of this complication of CD, we aimed to describe the clinical features, prese…
View article: Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 1 describes the characteristics of the patients used in our study.
View article: Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 1 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 1 describes the characteristics of the patients used in our study.
View article: Data from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Data from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Aberrant activation of GLI transcription factors has been implicated in the pathogenesis of different tumor types including pancreatic ductal adenocarcinoma. However, the mechanistic link with established drivers of this disease remains in…
View article: Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 2 includes the SNP analysis of components of the Hedgehog pathway.
View article: Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 8 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 8 shows the expression of GLI target genes in all experimental groups.
View article: Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 7 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 7 shows how oncogenic KRAS modulates GLI target gene expression.
View article: Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 6 describes RNA-seq shows differential gene expression induced by oncogenic KRAS.
View article: Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 4 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 4 shows the validation of Kras signaling activation and chronic pancreatitis phenotypic examples in KC and KCRG mice.
View article: Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 9 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 9 shows that Gli2 does not change H3K27Ac enrichment at Ccnd1 promoter downstream of oncogenic KRAS.
View article: Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 6 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 6 describes RNA-seq shows differential gene expression induced by oncogenic KRAS.
View article: Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Table 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Table 2 includes the SNP analysis of components of the Hedgehog pathway.
View article: Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 10 shows not differences in H3K4me1 enrichment at Ccnd1 promoter in mutant KRAS cells.
View article: Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 10 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 10 shows not differences in H3K4me1 enrichment at Ccnd1 promoter in mutant KRAS cells.
View article: Supplementary Figure 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 2 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 2 describes the characterization of the impact Gli2 overexpression in pancreas development. showing that Gli2 loss has no impact on pancreas development or survival in vivo.
View article: Supplementary Figure 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis
Supplementary Figure 3 from KRAS Promotes GLI2-Dependent Transcription during Pancreatic Carcinogenesis Open
Supplementary Figure 3 shows Gli2 expression in CRG and KCRG mice and Gli luciferase activity in ΔNGli2-transfected cells.