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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

RT @RafaJArguello
📢🙏 share and help us to find a motivated PhD candidate for an 🤯🤓🤩 opportunity at @CancerImmunoAMU

🧪🧠 Exciting call in ! to advance research using innovative single-cell metabolomic profiling! @SCENITHmetab

1/

An interesting new double act!!

immunotherapies engage to eliminate tumor antigen escape variants

doi.org/10.1016/j.cell.2023.03

I never thought I would be a nerd, but here we are 🤷‍♂️🤣. Gonna enjoy reading doing of these articles.
---
RT @CellPressNews
'The new @Molecular_Cell special issue focuses on the . The review articles in this issue focus on the diverse cellular processes involving mitochondria and the approaches used to study them. Take a look. hubs.li/Q01J2qN20
twitter.com/CellPressNews/stat

RT @Morganti_Lab
Loss of fatty acid degradation by astrocytic mitochondria triggers neuroinflammation and neurodegeneration | Nature Metabolism nature.com/articles/s42255-023

RT @RyanLabTCD
New Ryan Lab preprint on the adaptive properties of forgetting - featuring the PhD research of Livia Autore, with @jamesoleary & @Clrar.

Adaptive Expression of Engrams by Retroactive Interference biorxiv.org/content/10.1101/20

Adaptive Expression of Engrams by Retroactive Interference

Long-term memories are stored as stable configurations of neuronal ensembles, termed engrams. While investigation of engram cell properties and functionality in memory recall has been extensive, less is known about how engram cells are affected by forgetting. We describe a form of interference-based forgetting using an object memory behavioral paradigm. By using activity-dependent cell labelling, we show that although retroactive interference results in decreased engram cell reactivation during recall trials, optogenetic stimulation of the labelled engram cells is sufficient to induce memory retrieval. Forgotten engrams may also be reinstated via the presentation of similar or related environmental information. Furthermore, we demonstrate that engram activity is necessary for interference to occur. Taken together, these findings indicate that retroactive interference modulates engram expression in a manner that is both reversible and updatable. Retroactive inference may constitute a form of adaptive forgetting, where in everyday life new perceptual and environmental inputs modulate the natural forgetting process. ### Competing Interest Statement The authors have declared no competing interest.

www.biorxiv.org

RT @biorxiv_cellbio
Hexokinase 1 forms rings that constrict mitochondria during energy stress biorxiv.org/cgi/content/short/

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