- Computational Drug Discovery Methods
- Cancer-related Molecular Pathways
- Malaria Research and Control
- Mosquito-borne diseases and control
- Ubiquitin and proteasome pathways
- DNA Repair Mechanisms
- Genetics and Neurodevelopmental Disorders
Optibrium (United Kingdom)
2022
Newcastle University
2020-2021
A central challenge of antimalarial therapy is the emergence resistance to components artemisinin-based combination therapies (ACTs) and urgent need for new drugs acting through novel mechanism action. Over last decade, compounds identified in phenotypic high throughput screens (HTS) have provided starting point six candidate currently Medicines Malaria Venture (MMV) clinical development portfolio. However, published screening data which much chemical matter malaria drug discovery projects...
The SCFSKP2 ubiquitin ligase relieves G1 checkpoint control of CDK-cyclin complexes by promoting p27KIP1 degradation. We describe reconstitution stable containing SKP1-SKP2 and CDK1-cyclin B or CDK2-cyclin A/E, mediated the CDK regulatory subunit CKS1. further show that a direct interaction between SKP2 N-terminal motif cyclin A can stabilize SKP1-SKP2-CDK2-cyclin in absence identify binding site on demonstrate is not present E. This distinct from but overlapping with features mediate other...
Abstract A central challenge of antimalarial therapy is the emergence resistance to components artemisinin-based combination therapies (ACTs) and urgent need for new drugs acting through novel mechanism action. Over last decade, compounds identified in phenotypic high throughput screens (HTS) have provided starting point six candidate currently Medicines Malaria Venture (MMV) clinical development portfolio. However, published screening data which much chemical matter malaria drug discovery...
Abstract The SCF SKP2 ubiquitin ligase relieves G1 checkpoint control of CDK-cyclin complexes by promoting p27KIP1 degradation. We describe reconstitution stable containing SKP1-SKP2 and CDK1-cyclin B or CDK2-cyclin A/E, mediated the CDK regulatory subunit CKS1. further show that a direct interaction between N-terminal motif cyclin A can stabilize SKP1-SKP2-CDK2-cyclin in absence identify binding site on demonstrate is not present E. This distinct from but overlapping with features mediate...