Coskun Lipid Cellar @ ZML Dresden

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Coskun Lipid Cellar @ ZML Dresden

Coskun Lipid Cellar @ ZML Dresden

@CoskunPLID

Membrane lipids in health and disease, Structure Bio, Cell signaling, Cellular Metabolism, @lipid for tooth and blue place

Dresden, Germany Katılım Aralık 2017
593 Takip Edilen1.2K Takipçiler
Misha Kudryashev 🔬 ❄🕊️
Misha Kudryashev 🔬 ❄🕊️@MishaKudryashev·
That's quite interesting.... Adding a 300 USD per review per round will make the reviewing faster and better. Also seems like a fair things to do to compensate for the time (??) And will also add a 2k price tag for a publication paid by the research budgets.
nature@Nature

A biology journal trialled paying their reviewers and found it led to faster first editorial decisions – and increased review quality. go.nature.com/4v7XkSv

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Veijo Salo
Veijo Salo@VeijoS·
How does a cell remodel the ER membrane into a lipid droplet? Excited to share our new preprint. We find that regulated opening of the seipin ring defines a functional ER–lipid droplet interface — and identify SMLR1 as a regulator of this transition. biorxiv.org/content/10.648…
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Coskun Lipid Cellar @ ZML Dresden retweetledi
Lipotype
Lipotype@Lipotype_Global·
Lipids at Dresden Science Night on 26th of June! --- The Fedorova Lab, the Coskun group, and Lipotype are at Stand 1.08, CRTD, Fetscherstraße 105. Try thin-layer chromatography, play a lipid game, see a Science Slam and more. More: wissenschaftsnacht-dresden.de/en/events/deta…
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Svetlana Dodonova
Svetlana Dodonova@Sveta_Dodonova·
Excited to share our new preprint!🧬❄️ by brilliant Max Dreimann & Co! Using cryo-ET&EM, we reveal archaeal chromatin in a near-native state: variable-beads-on-a-string fibers shaped by growth phase and histone composition tinyurl.com/TkChrom
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Bostina Lab
Bostina Lab@mihnea_bostina·
How does mitosis look in its native environment? New article from our group where we used volume EM to describe the 3D ultrastructure of dividing cells in a real tissue context. Congratulations to Nick, Sai and all the collaborators. journals.biologists.com/jcs/article/13…
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Coskun Lipid Cellar @ ZML Dresden
@DanielJDrucker On can discuss (in)sanity of using a dual chamber syringe, different buffer conditions and a lot more. But about few % difference? My bet anyway is Cagri in its current form will be discontinued.
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Coskun Lipid Cellar @ ZML Dresden
@DanielJDrucker It is so crazy how badly things a communicated. We are comparing 2.5 mg vs 15 mg! dose. One should discuss how Cagri-Sema can be increased before having problems in terms of biochemistry as well as side-effects.
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Coskun Lipid Cellar @ ZML Dresden
Ups we did it again! Please mark you calendar: EMBO Workshop “Lipid Code to Life”, taking place September 7–11, 2026, in Dresden, organized by Maria Fedorova, @CoskunPLID , Valerie O'Donnell, Joost Holthuis, Liana C Silva. More details where the Skies are blue!
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Michael Bronstein
Michael Bronstein@mmbronstein·
Garibaldi and his mount. I was once bullied by a horse aptly named after the famous revolutionary.
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Derya Unutmaz, MD
Derya Unutmaz, MD@DeryaTR_·
In my opinion, this is the most important aging-related paper of the year! It identifies a critical protein that could eventually extend lifespan by many years. Not surprisingly, it involves DNA repair and regulation of the immune response. Below is a breakdown of the key points (via GPT-5): What did they find and why important? •Naked mole-rats live a very long time and rarely get cancer. •A key reason is a tiny change in a cell sensor called cGAS. This sensor usually detects stray DNA inside cells and sounds an alarm to the immune system. •In humans, cGAS can drift into the nucleus and get in the way of one of our best DNA repair tools (called homologous recombination). That means more un-fixed DNA damage over time. •In naked mole-rats, four small amino acid changes in cGAS flip the script. Their version does not block repair. Instead, it helps the high-fidelity repair process work better. Why is this big for aging? •Aging is partly the story of accumulating DNA damage. Better repair means fewer mutations, less cellular dysfunction, and a slower march toward age-related diseases. •If we can make human cGAS behave more like the mole-rat version, we might reduce the daily damage load, which could: •Lower cancer risk •Preserve tissue function longer •Delay multiple age-related declines at once How could this translate to people? 1.Drug design: Create small molecules that keep human cGAS from interfering with DNA repair inside the nucleus, while still letting it do its normal immune-sensing job in the cytosol. 2.Protein engineering or gene therapy: Introduce cGAS variants that mimic the mole-rat’s four changes in high-risk tissues, carefully and locally. 3.Biomarkers and screening: Use cGAS activity and DNA repair efficiency as readouts to find who might benefit and to measure whether a therapy is working. 4.Combination strategies: Pair cGAS-tuning with other repair boosters and senescence-reducers for a bigger effect. Bottom line: A few precise tweaks to one protein can shift the balance from ongoing damage toward cleaner, faster DNA repair. That is exactly the kind of leverage aging research needs: change a small control knob, get system-wide benefits. The naked mole-rat just showed us one such knob. Paper link in the thread.
Derya Unutmaz, MD tweet media
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