John Bechill
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View article: Efficient and durable gene activation by Cas9-mediated epigenome editing in vivo
Efficient and durable gene activation by Cas9-mediated epigenome editing in vivo Open
Epigenome editing technology holds great promise for treating diverse genetic disorders. While a series of advances has been made on epigenetic silencing using programmable editors, little progress has been made in leveraging epigenetic ac…
View article: Supplementary Figure 1 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 1 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 1 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: Supplementary Figure 3 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 3 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 3 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Viral oncogene expression is insufficient for neoplastic transformation of human cells, so human papillomavirus (HPV)–associated cancers will also rely upon mutations in cellular oncogenes and tumor suppressors. However, it has been diffic…
View article: Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Data from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Viral oncogene expression is insufficient for neoplastic transformation of human cells, so human papillomavirus (HPV)–associated cancers will also rely upon mutations in cellular oncogenes and tumor suppressors. However, it has been diffic…
View article: Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Supplemental Methods, Tables 1-9 and Figures 1-9. Supplemental Methods: Animals; Sleeping Beauty transposon mapping; Reagents and antibodies; HPV recombination, T2/Onc excision and Hras mutation specific PCRs. Supplemental Table 1: Mouse s…
View article: Supplementary Figure 4 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 4 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 4 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: Data from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Data from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
In the earliest stages of metastasis, breast cancer cells must reorganize the cytoskeleton to affect cell shape change and promote cell invasion and motility. These events require the cytoskeletal regulators Cdc42 and Rho, their effectors …
View article: Supplementary Figure 2 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 2 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 2 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Supplemental Methods, Tables 1-9, and Figures 1-9 from Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Supplemental Methods, Tables 1-9 and Figures 1-9. Supplemental Methods: Animals; Sleeping Beauty transposon mapping; Reagents and antibodies; HPV recombination, T2/Onc excision and Hras mutation specific PCRs. Supplemental Table 1: Mouse s…
View article: Data from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Data from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
In the earliest stages of metastasis, breast cancer cells must reorganize the cytoskeleton to affect cell shape change and promote cell invasion and motility. These events require the cytoskeletal regulators Cdc42 and Rho, their effectors …
View article: Supplementary Figure 3 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 3 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 3 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: Supplementary Figure 1 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 1 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 1 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: Supplementary Figure 2 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 2 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 2 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: Supplementary Figure 4 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
Supplementary Figure 4 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp Open
Supplementary Figure 4 from Cdc42-Interacting Protein 4 Promotes Breast Cancer Cell Invasion and Formation of Invadopodia through Activation of N-WASp
View article: A High-Throughput Cell-Based Screen Identified a 2-[(E)-2-Phenylvinyl]-8-Quinolinol Core Structure That Activates p53
A High-Throughput Cell-Based Screen Identified a 2-[(E)-2-Phenylvinyl]-8-Quinolinol Core Structure That Activates p53 Open
p53 function is frequently inhibited in cancer either through mutations or by increased degradation via MDM2 and/or E6AP E3-ubiquitin ligases. Most agents that restore p53 expression act by binding MDM2 or E6AP to prevent p53 degradation. …
View article: Loss of E2F1 Extends Survival and Accelerates Oral Tumor Growth in HPV-Positive Mice
Loss of E2F1 Extends Survival and Accelerates Oral Tumor Growth in HPV-Positive Mice Open
The Human Papillomavirus (HPV) is associated with several human cancers, including head and neck squamous cell carcinomas (HNSCCs). HPV expresses the viral oncogene E7 that binds to the retinoblastoma protein (RB1) in order to activate the…
View article: Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis
Notch1 Activation or Loss Promotes HPV-Induced Oral Tumorigenesis Open
Viral oncogene expression is insufficient for neoplastic transformation of human cells, so human papillomavirus (HPV)–associated cancers will also rely upon mutations in cellular oncogenes and tumor suppressors. However, it has been diffic…