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RT @AndyHogan82
Delighted to see our latest paper out in @scisignal - led by @KediaMehta & Marta Pisarska with superstar collaborator @LindaVSinclair - we go deeper on metabolism and the impact of obesity - science.org/doi/10.1126/scisig

RT @NgordonNeil
⁦@tcddublin⁩ research from Matt Campbell and Jeff O’Callaghan glaucoma gene therapy that can change peoples lives ⁦@TCD_Innovation⁩ ⁦@scienceirel⁩ ⁦@Entirl⁩ ⁦@KTIconnect⁩ science.org/doi/10.1126/sciadv

A great opportunity here to do a PhD working on immunometabolism during viral infection. @tcdTBSI @tcdbi @BiochemSocTCD
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RT @LittwitzSalomon
Are you looking for a PhD position in the field of virology and immunology as well as immunometabolism? Please apply here:
karriere.ume.de/job-finder/?ge
twitter.com/LittwitzSalomon/st

RT @MiriamMerad
Excited to share our new paper in @NatImmunol on how TREM2+ monocyte-derived macrophages in lung cancer reduce activity of natural killer cells that fight tumors. We provide potential dual targeting strategies to improve antitumor immunity. Read here: rdcu.be/damS8

RT @McLoughlin_Lab
Fantastic research on show today @tcdTBSI for our annual celebration of Postgraduate research @tcdbi Congratulations to Roisin Lynch from @EdLavellee lab this years winner of the Tipton medal for postgraduate research also Erika Stewart from @TJRyan_77 lab a worthy runner up.

RT @LindaVSinclair
So happy and proud to see this paper out now! Big collaborative effort - well done @KediaMehta @AndyHogan82
“The proliferation of human mucosal-associated invariant T cells requires a MYC-SLC7A5-glycolysis metabolic axis” science.org/doi/10.1126/scisig

This is why ye want to release those cytotoxic granules directly at a target cell! 🤷‍♂️

NK cell-derived extracellular granzyme B drives epithelial ulceration during HSV-2 genital infection

doi.org/10.1016/j.celrep.2023.

RT @LNivisonSmith
Did you just tweet about your new paper? 🥳

Does it feel like no-one heard you? 😞

How to use the Twitter algorithm to maximise the reach of your tweets 😎

@AcademicChatter @OpenAcademics

RT @ImmunoSens
👩‍🔬👨‍🔬Two Open (s) in Immunometabolism available at
👉immunosensation.de/opportuniti

Join the great team of @surace_laura @UniklinikBonn who recently recieved the prestigous MaxEder Grant by @Krebshilfe_Bonn! 👉immunosensation.de/news/fighti

RT @WHO
Pharaoh Ramses V comes to life. Watch this fascinating story about the eradication of a deadly disease. !

Did you know?
Following an ambitious 12-year global vaccination campaign led by WHO, smallpox is finally eradicated in 1980. 🙌

RT @ImmPRes_
We are delighted to see this write up now being officially out in @NatImmunol @AJ_Brenes
@LabDac

If you were looking for a reference to cite when using data, this is the one.

nature.com/articles/s41590-023

What would I do without @RyanLab_MBU ‘s weekly roundup of the new papers? Thank you Dylan for making it so easy to keep up to date. You’re an absolute ⭐️.

Mitochondrial H2O2 release does not directly cause genomic DNA damage

biorxiv.org/content/10.1101/20

Mitochondrial H2O2 release does not directly cause genomic DNA damage

Reactive Oxygen Species (ROS) derived from mitochondrial respiration are frequently cited as a major source of genomic DNA damage and subsequent mutations that contribute to cancer development and aging. However, experimental evidence showing that ROS released by mitochondrial can directly damage nuclear DNA under (patho)physiological conditions has been largely lacking. In this study we modeled the effects of mitochondrial H2O2 release and compared this to H2O2 production at the nucleosomes in an untransformed human cell line. We used a chemogenetic approach to produce localized H2O2 and combined it with a new method we developed to directly quantify the amount of H2O2 produced. This enabled us to precisely investigate to what extent DNA damage occurs downstream of near- and supraphysiological amounts of localized H2O2 generation. Nuclear H2O2 production gives rise to DNA strand breaks, subsequent activation of the DNA damage response, cell cycle arrest and eventually senescence. Release of H2O2 from mitochondria on the other hand shows none of these effects, even at levels that are orders of magnitude higher than what mitochondria normally produce. Artificially high levels of mitochondrial H2O2 release do result in DNA strand breaks, but in parallel invariably cause ferroptosis-mediated cell death, preventing propagation of DNA damage-induced mutations. This study shows that H2O2 released from mitochondria is unlikely to directly damage genomic DNA, limiting its contribution to oncogenic transformation and aging. ### Competing Interest Statement The authors have declared no competing interest.

www.biorxiv.org

RT @FrezzaLab
Triglyceride cycling enables modification of stored fatty acids | Nature Metabolism nature.com/articles/s42255-023

RT @NatImmunol
Interested in ? Check out a new community resource ImmPRes immpres.co.uk/ ImmPRes was created with the aim to provide an in-depth, high quality, quantitative map of the immuno proteome. See doi.org/10.1038/s41590-023-014

RT @DrSTANtheMAN
The NK cell receptor NKp46 recognizes ecto-calreticulin on ER-stressed cells ⁦@Nature⁩ nature.com/articles/s41586-023

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