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@ELSpharma
#MolecularBiology#CallForPapers#BiomedicalResearch#Elsevier
We are excited to share our latest work on mechanisms that protect from mitochondrial dysfunction. Thank you to all collaborators and the 4th anonymous reviewer for supporting us. @labs_mann@NatureComms@metaboflo
https://t.co/xLNyW00oil
New study from us:
https://t.co/GioeqFmsKo
High mtDNA copy number promotes lung cancer growth in the mouse, whereas mtDNA depletion in tumor cells reduces tumor growth. This tumor-intrinsic role for mtDNA can be exploited for development of future lung cancer therapies.
Inspiring science at the Postdoc Networking Day yesterday at @AstraZeneca. Happy to have contributed to this wonderful event with the Cambridge Biomedical Campus and @AstraZeneca. Huge thanks to Jonathan Lawson for organising this gathering.
The MBU Postdoc Society
A small gift to celebrate the Postdoc Appreciation Week!! 😊
Thank you all for your great work and commitment to science! 🔬
The MBU Postdoc Society @MBU_postdocs@MRC_MBU
(thank you @MariangelaDiony for your help 😉)
Thrilled to announce that our project has been published in @CellCellPress. In this work, we link mitochondrial dynamics to mitochondrial quality control and mtDNA maintenance by characterizing the molecular function of MTFP1. Please DM; happy to discuss! https://t.co/uZqi9Fc8PM
We’re hiring! The Whitworth lab (Mitochondrial Neurodegeneration) is recruiting a postdoc to work on mechanisms of #calcium and #iron handling on #mitophagy in mouse or iNeuron models of neurodegeneration. https://t.co/3Qukb9HE6x
https://t.co/Caw6CKTW4K
Delighted to share the last study of the lab led by the fantastic postdoc @Tabara_LC out in @CellCellPress !!!
We show how MTFP1 controls mitochondrial fusion to regulate inner membrane quality control and maintain mtDNA levels.
@MRC_MBU@Cambridge_Uni
https://t.co/xM0vjtReOW
Read our new study: https://t.co/o6WNyQI38n
Treatment of obese mice with small molecule inhibitors of mtDNA transcription (IMTs) leads to marked beneficial metabolic effects. The weight is normalized, the fat deposition in liver disappears and glucose homeostasis is normalized.
Our study is finally out! https://t.co/RYUgW9J8ow
We here show that PARKIN is dispensable for OXPHOS function in adult mouse tissues and in skeletal muscle from a PD-patient.
Thanks to @mitopinionated , @LabMotori, @perlmannlab and Per Svenningsson for the great collaboration!
Our new review exploring how CRISPRi can and will be used in iPSC models to understand neurodegeneration is available now in Biochemical Society Transactions https://t.co/uN3dOAuEcT