@BabrahamInst, Cambridge, UK. Main funding @BBSRC
Views are our own.
Great work Neesha and thanks to our collaborators and our funders
Great work Neesha and thanks to our collaborators and our funders
• Provides far better data from mammalian cells
• Includes multiplexing for higher throughput
TrAEL-seq reveals replication patterns and fork progression in unsynchronised, unlabelled and unsorted cells
www.biorxiv.org/content/10.1...
• Provides far better data from mammalian cells
• Includes multiplexing for higher throughput
TrAEL-seq reveals replication patterns and fork progression in unsynchronised, unlabelled and unsorted cells
www.biorxiv.org/content/10.1...
Hanane's work shows that we can acheive excellent healthy ageing through metabolic rewiring, even on an unrestricted diet
Profile:
whova.com/embedded/spe...
Preprint:
www.biorxiv.org/content/10.1...
Hanane's work shows that we can acheive excellent healthy ageing through metabolic rewiring, even on an unrestricted diet
Profile:
whova.com/embedded/spe...
Preprint:
www.biorxiv.org/content/10.1...
Babraham Institute @babrahaminst.bsky.social
#BBSRC @ukri.org
Babraham Institute @babrahaminst.bsky.social
#BBSRC @ukri.org
…including regulation of fatty acid synthesis through phosphorylation of the same enzyme
This highly conserved regulatory system presents a promising and unexplored target for healthy ageing research across Eukaryotes
…including regulation of fatty acid synthesis through phosphorylation of the same enzyme
This highly conserved regulatory system presents a promising and unexplored target for healthy ageing research across Eukaryotes
Acetyl coenzyme A is the building block for fatty acids but excess acetyl coenzyme A availability is detrimental
A2A cells make the fatty acid they need but get rid of excess acetyl coenzyme A into mitochondria
Acetyl coenzyme A is the building block for fatty acids but excess acetyl coenzyme A availability is detrimental
A2A cells make the fatty acid they need but get rid of excess acetyl coenzyme A into mitochondria
Our A2A mutant combines AMPK activation with a mutation that allows continued fatty acid synthesis
The majority of A2A cells maintain fitness very late in life even though they don't live any longer
Our A2A mutant combines AMPK activation with a mutation that allows continued fatty acid synthesis
The majority of A2A cells maintain fitness very late in life even though they don't live any longer
We show that AMPK activation in budding yeast allows some cells to age without senescence on a normal diet...
We show that AMPK activation in budding yeast allows some cells to age without senescence on a normal diet...
Our latest Preprint describes metabolic re-engineering of yeast to avoid senescence
The A2A mutant we created is super-fit late in life even on a rich high glucose diet
www.biorxiv.org/content/10.1...
Our latest Preprint describes metabolic re-engineering of yeast to avoid senescence
The A2A mutant we created is super-fit late in life even on a rich high glucose diet
www.biorxiv.org/content/10.1...
Amy's poster showed that circular DNAs providing copper resistance can be stably transmitted for hundreds of generations in yeast
Amy's poster showed that circular DNAs providing copper resistance can be stably transmitted for hundreds of generations in yeast