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- A new regulator of 'stemness' to create dendritic cell factories for immunotherapy
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- Deciphering the heterogeneity of breast cancer at the epigenetic and genetic levels
- Developing drugs to block malaria transmission
- Developing new computational tools for CRISPR genomics to advance cancer research
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- Discovering novel paradigms to cure viral and bacterial infections
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- Dissecting host cell invasion by the diarrhoeal pathogen Cryptosporidium
- Do membrane forces govern assembly of the deadly apoptotic pore?
- Doublecortin-like kinases, drug targets in cancer and neurological disorders
- E3 ubiquitin ligases in neurodegeneration, autoinflammation and cancer
- Engineering improved CAR-T cell therapies
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- Exploiting cell death pathways in regulatory T cells for cancer immunotherapy
- Finding treatments for chromatin disorders of intellectual disability
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- How does DNA damage shape disease susceptibility over a lifetime?
- How does DNA hypermutation shape the development of solid tumours?
- How platelets prevent neonatal stroke
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- Interaction with Toxoplasma parasites and the brain
- Interactions between tumour cells and their microenvironment in non-small cell lung cancer
- Investigating the role of dysregulated Tom40 in neurodegeneration
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- Malaria: going bananas for sex
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- Understanding how malaria parasites sabotage acquisition of immunity
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- Understanding the mechanism of type I cytokine receptor activation
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- Using alpaca antibodies to understand malaria invasion and transmission
- Using combination immunotherapy to tackle heterogeneous brain tumours
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- Using structural biology to understand programmed cell death
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David Vaux - Research Projects
Researcher:
Determining the mechanism of lymphocyte apoptosis induced by glucocorticoids
In the mouse thymoma cell line WEHI-7, Flomerfelt and Miesfeld (JCB 1994) showed that there are at least six unique genes required for them to undergo apoptosis following treatment with dexamethasone. While they showed that the first gene in the path was the glucocorticoid receptor, they were not able to identify the other genes. We are re-visiting this system, using CrispR technology to identify the genes involved.
Regulation of autophagy by Bcl-2
We found that Bcl-2 is unable to inhibit autophagy in cells that lacked Bax and Bak, but when Bax and Bak were present, autophagy occurred as cells underwent apoptosis. This indicates that when activated, Bax and Bak can directly or indirectly promote autophagy.
We are seeking to determine the molecular pathway by which autophagy is induced in cells undergoing apoptosis.
Regulation of cell size and proliferation in the absence of apoptosis
Unlike their wild type parents, lymphoid (WEHI-7) and myeloid (FDM) cell lines lacking genes for Bax and Bak do not undergo apoptosis when treated with steroids or starved of IL-3. They shrink, arrest, and persist for weeks in a quiescent state.
These cells do not require autophagy, proteasome activity or protein synthesis to survive.
We wish to determine the mechanism for this arrest using CrispR screens, RNAseq, and CHIPseq.
These arrested cells are resistant to many chemotherapeutic agents. A drug that blocked this arrest might restore sensitivity to allow chemotherapeutic agents to kill cancer cells.
How does dexamethasone block cytokine growth signals?
Normally, factor starved arrested Bax/Bak deleted FDMs grow and proliferate as soon as IL-3 is added.
In contrast, FDMs arrested with dexamethasone do not grow and proliferate when IL-3 is added.
We wish to determine the mechanism by which the glucocorticoid receptor blocks signaling pathways activated by cytokines.