Mapping the integration of T cell fate control across time and space. This project aims to apply new methods to determine how coordination of signalling complexes impacts upon the fate of cells of the adaptive immune system. It expects to determine how the context of signallng orchestrates cell fates such as differentiation, death and proliferation. The project is expected to yield an experimental and analytical platform for further investigations into a broad range of biological questions, and ....Mapping the integration of T cell fate control across time and space. This project aims to apply new methods to determine how coordination of signalling complexes impacts upon the fate of cells of the adaptive immune system. It expects to determine how the context of signallng orchestrates cell fates such as differentiation, death and proliferation. The project is expected to yield an experimental and analytical platform for further investigations into a broad range of biological questions, and to provide new knowledge of this fundamental problem. This platform should support further work that ultimately provides new models for tissue and immune cell regeneration, and new manufacturing platforms for therapies for humans and livestock, among other benefits.Read moreRead less
Chemical staples and chemical probes to dissect dynamins cellular roles. Modulation of protein structure drives cellular function. Dynamin GTPase forms at least two macromolecular structures with different cellular functions. The drivers behind these different structures is unknown. In this project we will leverage our discoveries, and planned enhancements, of chemical biology probes that will modulate dynamin activity by inhibiting at three distinct sites, and one site that stimulates dynamin a ....Chemical staples and chemical probes to dissect dynamins cellular roles. Modulation of protein structure drives cellular function. Dynamin GTPase forms at least two macromolecular structures with different cellular functions. The drivers behind these different structures is unknown. In this project we will leverage our discoveries, and planned enhancements, of chemical biology probes that will modulate dynamin activity by inhibiting at three distinct sites, and one site that stimulates dynamin activity. It is known that Dynamin helices and rings are believed responsible for at least three in cell biological functions: in hormone, neutral and receptor internalisation; cellular mitosis and in actin dynamics. Prior to this work we have lacked the tools to understand the role of shape modulation of protein function.Read moreRead less
Discovery Early Career Researcher Award - Grant ID: DE240100707
Funder
Australian Research Council
Funding Amount
$450,926.00
Summary
Towards a molecular fingerprint for human-specific endogenous retroviruses. This project aims to understand how ancient viral sequences resident in the human genome can contribute to cellular processes. Using a novel molecular toolbox that combines affinity-directed proximity labelling mass spectrometry and single molecule microscopy, this project will characterise the cellular fingerprint of a human endogenous retrovirus family HERV-K (HML-2). This fingerprint will comprehensively describe how ....Towards a molecular fingerprint for human-specific endogenous retroviruses. This project aims to understand how ancient viral sequences resident in the human genome can contribute to cellular processes. Using a novel molecular toolbox that combines affinity-directed proximity labelling mass spectrometry and single molecule microscopy, this project will characterise the cellular fingerprint of a human endogenous retrovirus family HERV-K (HML-2). This fingerprint will comprehensively describe how expressed HERV-K loci engage with the homeostasis network in human cells. This will provide significant benefits in the form of new knowledge concerning fundamental aspects of cellular homeostasis, and a state-of-the-art molecular biology toolbox ready to explore quantitatively the role of HERV-K in human health and disease.Read moreRead less