Ashley N. Sigafoos
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View article: Nuclear VAV1 increases GLI1-dependent transcription in pancreatic cancer cells
Nuclear VAV1 increases GLI1-dependent transcription in pancreatic cancer cells Open
The oncogenic role of VAV1, a GTPase guanine nucleotide exchange factor (GEF) with cytoplasmic and nuclear localizations, has been previously reported in multiple malignancies. Most of the mechanisms underlying this pro-tumoral activity ha…
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Supp Fig 3
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Supp Table 1
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Supp Table 2
View article: Figure 1 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Figure 1 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
SNX10 genetic alterations and expression in human PDAC. A, Interrogation of PDAC from ICGC (https://dcc.icgc.org) and COSMIC (https://cancer.sanger.ac.uk/cosmic), showing mutations in the SNX10 gene. B, A schematic of the SNX…
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Supp Fig 1
View article: Figure 5 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Figure 5 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Depletion of Snx10 enhances malignancy markers in PDAC mice: A–D, Number of mice per group: P48 Cre (control mouse, n = 4), KPC (n = 4), KPCSfl/fl (n = 4), KC (n = 4), and KCSfl/fl (…
View article: Figure 4 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Figure 4 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Loss of Snx10 leads to adverse outcomes in PDAC. Kaplan–Meier curves of (A) KC (n = 12) and KCSfl/fl (n = 12) group (P = 0.0016). B, KPC (n = 12) and KPCSfl/fl (n = 14)…
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
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View article: Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Pancreatic ductal adenocarcinoma (PDAC), one of the most aggressive forms of pancreatic cancer, is associated with poor survival outcomes and currently ranks as the third leading cause of cancer-related death in the United States. Despite …
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Supp Table 4
View article: Figure 2 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Figure 2 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
OE of SNX10 decreased cell proliferation in AsPC1 and HPAF-II PDAC cell lines. A, SNX10 transfection confirmation in AsPC1 and HPAF-II cells by qPCR fold change expression. Actin was used as a reference gene. B, Western blot …
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
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View article: Figure 3 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Figure 3 from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
OE of SNX10 participated in regulating the protumorigenic protein expression. A, Western blot of control vs. SNX10 OE in AsPC1 and HPAF-II cell lines probing for the expression of protumorigenic markers. Protumorigenic markers probe…
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Supp Fig 2
View article: Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Supplementary Data from Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Supp Fig 4
View article: Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis
Loss of Sorting Nexin 10 Accelerates KRAS-Induced Pancreatic Tumorigenesis Open
Pancreatic ductal adenocarcinoma (PDAC), one of the most aggressive forms of pancreatic cancer, is associated with poor survival outcomes and currently ranks as the third leading cause of cancer-related death in the United States. Despite …
View article: Emerin is an effector of oncogenic KRAS-driven nuclear dynamics in pancreatic cancer
Emerin is an effector of oncogenic KRAS-driven nuclear dynamics in pancreatic cancer Open
For over a century, scientists reported the disruption of normal nuclear shape and size in cancer. These changes have long been used as tools for diagnosis and staging of malignancies. However, to date, the mechanisms underlying these aber…
View article: Paracrine regulation of pancreatic cancer cell response to chemotherapy by GLI2–collagen I signaling
Paracrine regulation of pancreatic cancer cell response to chemotherapy by GLI2–collagen I signaling Open
Despite the well-described role of noncellular components of the tumor microenvironment (TME) in regulating tumor growth, the molecular events dictating expression and biological functions of key components of the TME remain elusive. Here,…
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.