Area of research
Molecular Biology · Genetics
Research interest
Research interests include Receptor Mechanisms and Signaling, Estrogen and related hormone effects, Cancer, Hypoxia, and Metabolism, and Growth Hormone and Insulin-like Growth Factors.
G Protein-coupled and Membrane Tyrosine Kinase Receptor Relationships Yield Therapeutic Opportunities.
Supplementary Figure 1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Data from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 4 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 3 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Data from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 7 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S1 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 5 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 6 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Table S2 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Supplementary Figure 8 from Competing engagement of β-arrestin isoforms balances IGF1R/p53 signaling and controls melanoma cell chemotherapeutic responsiveness
Competing Engagement of β-arrestin Isoforms Balances IGF1R/p53 Signaling and Controls Melanoma Cell Chemotherapeutic Responsiveness.
Editorial: DNA damage response pathways meet endocrine systems.
Correction: IGF-1R is a molecular determinant for response to p53 reactivation therapy in conjunctival melanoma.
Supplementary Figure 5 from Competing Engagement of β-arrestin Isoforms Balances IGF1R/p53 Signaling and Controls Melanoma Cell Chemotherapeutic Responsiveness
Supplementary Figure 3 from Competing Engagement of β-arrestin Isoforms Balances IGF1R/p53 Signaling and Controls Melanoma Cell Chemotherapeutic Responsiveness
Table S1 from Competing Engagement of β-arrestin Isoforms Balances IGF1R/p53 Signaling and Controls Melanoma Cell Chemotherapeutic Responsiveness
Table S1 from Competing Engagement of β-arrestin Isoforms Balances IGF1R/p53 Signaling and Controls Melanoma Cell Chemotherapeutic Responsiveness