Matthew Jennis
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View article: Supplemental Figure 5 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 5 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S5. TRIML2 regulates a subset of p53 target genes.
View article: Supplemental Figure 4 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 4 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S4. Effect of TRIML2 knockdown on p53 target gene expression.
View article: Supplemental Table 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Table 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Table S2. Primers used for qRT-PCR and ChIP assays.
View article: Supplemental Figure legends from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure legends from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Supplemental Figure legends
View article: Supplemental Figure 4 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 4 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S4. Effect of TRIML2 knockdown on p53 target gene expression.
View article: Supplemental Table 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Table 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Table S2. Primers used for qRT-PCR and ChIP assays.
View article: Supplemental Figure 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S2. p53-dependent TRIML2 induction is increased in R72 cells and positively regulates p53 activation and apoptosis.
View article: Supplemental Figure 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S1. Identification of differentially-regulated p53 target genes between P72 and R72 NHFs using microarray experiment.
View article: Supplemental Figure 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S1. Identification of differentially-regulated p53 target genes between P72 and R72 NHFs using microarray experiment.
View article: Supplemental Table 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Table 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Table S1. Genes specifically upregulated by P72 or R72 p53 in microarray analysis.
View article: Supplemental Figure 6 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 6 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S6. TRIML2 does not affect SUMO1- or Ubiquitin modification of p53; TRIML2 is the only TRIM protein differentially regulated by codon 72 polymorphism of p53.
View article: Supplemental Figure legends from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure legends from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Supplemental Figure legends
View article: Data from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Data from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
The tumor-suppressor protein p53, encoded by TP53, inhibits tumorigenesis by inducing cell-cycle arrest, senescence, and apoptosis. Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino…
View article: Supplemental Table 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Table 1 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Table S1. Genes specifically upregulated by P72 or R72 p53 in microarray analysis.
View article: Supplemental Figure 3 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 3 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S3. TRIML2 contributes to the different apoptotic potential between P72 and R72.
View article: Supplemental Figure 5 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 5 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S5. TRIML2 regulates a subset of p53 target genes.
View article: Supplemental Figure 6 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 6 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S6. TRIML2 does not affect SUMO1- or Ubiquitin modification of p53; TRIML2 is the only TRIM protein differentially regulated by codon 72 polymorphism of p53.
View article: Data from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Data from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
The tumor-suppressor protein p53, encoded by TP53, inhibits tumorigenesis by inducing cell-cycle arrest, senescence, and apoptosis. Several genetic polymorphisms exist in TP53, including a proline to arginine variant at amino…
View article: Supplemental Figure 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 2 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S2. p53-dependent TRIML2 induction is increased in R72 cells and positively regulates p53 activation and apoptosis.
View article: Supplemental Figure 3 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes
Supplemental Figure 3 from Identification of TRIML2, a Novel p53 Target, that Enhances p53 SUMOylation and Regulates the Transactivation of Proapoptotic Genes Open
Figure S3. TRIML2 contributes to the different apoptotic potential between P72 and R72.
View article: Suppl. Figure 5 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 5 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Impact of PET-16 on melanoma in vivo A. Cell viability analysis of B16-F10 cell line treated with DMSO or the indicated doses of PES-Cl or PET-16 for 72 hours.
View article: Suppl. Figure 3 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 3 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
RPPA Analysis of Melanoma cell lines treated with PET-16 WM793 and 1205Lu cells were treated with DMSO or with the indicated concentrations of PET-16 for 24 hours and then subjected to RPPA analysis.
View article: Suppl. Figure 3 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 3 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
RPPA Analysis of Melanoma cell lines treated with PET-16 WM793 and 1205Lu cells were treated with DMSO or with the indicated concentrations of PET-16 for 24 hours and then subjected to RPPA analysis.
View article: Suppl. Figure 4 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 4 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Impact of PET-16 on melanoma in vitro A. Immunoprecipitation-western analysis in the H1299 cell line using antisera to HSP70 and IgG, followed by Western blot analysis for the associated total and phosphorylated FAK. B. 1205Lu and WM852 ce…
View article: Suppl. Figure 1 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 1 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Chemical structures of the HSP70 inhibitors used in this study
View article: Suppl. Figure 7 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 7 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Impact of PET-16 on the level of HSP70 client proteins in vivo A. Immunofluorescence analysis for phospho-FAK (pTyr-397) in the tumors from mice described in (6G). Scale bar = 15 μm B
View article: Suppl. Figure 4 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 4 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Impact of PET-16 on melanoma in vitro A. Immunoprecipitation-western analysis in the H1299 cell line using antisera to HSP70 and IgG, followed by Western blot analysis for the associated total and phosphorylated FAK. B. 1205Lu and WM852 ce…
View article: Suppl. Table 1 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Table 1 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Coefficient of interaction (CI) values for PET-16 and targeted therapeutic agent PLX4032 in BRAF V600E melanoma cell lines.
View article: Suppl. Figure 7 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 7 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Impact of PET-16 on the level of HSP70 client proteins in vivo A. Immunofluorescence analysis for phospho-FAK (pTyr-397) in the tumors from mice described in (6G). Scale bar = 15 μm B
View article: Suppl. Figure 8 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors
Suppl. Figure 8 from HSP70 Inhibition Limits FAK-Dependent Invasion and Enhances the Response to Melanoma Treatment with BRAF Inhibitors Open
Melanoma cell lines with acquired resistance to BRAF inhibitors Cell viability analysis of the Yumm1.7 and WM983 melanoma cells treated with DMSO or the indicated doses of PLX4032 for 72 hours.