George Walters-Marrah

the job market is looking abysmal, I'm gnna have to lock in

EndoMAP.v1 charts the structural landscape of human early endosome complexes The following chemicals and reagents were used: Dounce homogenizer (DWK Life Sciences, 885302-0002); Pierce anti-HA magnetic beads (Thermo Scientific, 88837); Pierce anti-Flag magnetic agarose (Thermo Scientific, A36797); anti-Flag M2 magnetic beads (Sigma Millipore, M8823); Pierce protein A/G magnetic beads (Thermo...

EndoMAP.v1 charts the structural landscape of human early endosome complexes
->Nature | #Landscape | More info from EcoSearch

EndoMAP.v1 Reveals Human Early Endosome Structure In a groundbreaking study published in Nature, researchers have unveiled a comprehensive structural and functional map of human early endosome complexes, shedding new light on the dynamic interplay of ion transporters and their accessory proteins within this critical cellular compartment. This study notably identifies TMEM9 and TMEM9B as essential core subunits of the endosomal chloride/proton antiporters CLCN3, CLCN4, and CLCN5, reshaping our understanding of endosomal ion homeostasis and its implications in neuronal health and disease.

EndoMAP.v1 Reveals Human Early Endosome Structure

In a groundbreaking study published in Nature, researchers have unveiled a comprehensive structural and functional map of human early endosome complexes, shedding new light on the dynamic interplay of ion transporters and their accessory proteins…

IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes https://www.biorxiv.org/content/10.1101/2025.06.01.657267v1

IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes https://www.biorxiv.org/content/10.1101/2025.06.01.657267v1

IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes Interferon-induced transmembrane (IFITM) proteins are potent innate immune factors that restrict an array of viruses at the entry stage of infection. We previously characterized a GxxxG motif in the CD225 domain of human IFITM3 that mediates its multimerization, which is essential for the reduction of membrane fluidity by IFITM3 and for its antiviral activity against Influenza A virus. Here, using an unbiased approach coupling immunoprecipitation with mass spectrometry, we show that the GxxxG motif is also important for the interaction of IFITM3 with other proteins, including IFITM1. While IFITM1 is primarily regarded as a cell surface protein that restricts the entry of viruses fusing at the plasma membrane, this model is based mostly on overexpression studies and is at odds with some studies showing that it can restrict endocytic viruses. Here, we show that endogenous IFITM1 and IFITM3 co-reside in membranes of acidic late endosomes and lysosomes (endolysosomes) and form a protein-protein complex as determined by co-immunoprecipitation and proximity ligation assay. Knockdown of endogenous IFITM3 resulted in enhanced localization of IFITM1 at the plasma membrane, indicating that IFITM3 promotes IFITM1 localization to endolysosomes. To assess the antiviral protection conferred by endogenous IFITM1 and IFITM3 against viruses fusing at endolysosomal membranes, we measured cell entry mediated by the Influenza A fusogen hemagglutinin (HA). While knockdown of IFITM3 significantly boosted HA-mediated entry, combined knockdown of both IFITM3 and IFITM1 boosted entry even further. These results suggest that endogenous IFITM1 restricts Influenza A virus entry in a manner that is non-redundant with IFITM3, and that IFITM1 and IFITM3 inhibit virus entry in a cooperative manner.

(BioRxiv All) IFITM1 and IFITM3 cooperate to restrict virus entry in endolysosomes: Interferon-induced transmembrane (IFITM) proteins are potent innate immune factors that restrict an array of viruses at the entry stage of infection. We previously characterized a GxxxG motif… #BioRxiv #MassSpecRSS

ATG9A and ARFIP2 cooperate to control PI4P levels for lysosomal repair Lysosome damage activates multiple pathways to prevent lysosome-dependent cell death, including a repair mechanism involving endoplasmic reticulum (ER…

Excited to share our newly published work on ATG9A — this time focusing on its role at the lysosome. Discover how ARFIP2 and ATG9A coordinate PI4P regulation during lysosomal repair!

Congrats to all the authors, and special thanks to @stedet.bsky.social & @satooze.bsky.social !!

📜 bit.ly/43EbrDo

Endosome map reveals v-ATPase IS the ultimate connector!

The biological pathways or functions these proteins influence may ultimately have a more significant impact!

Article here: www.nature.com/articles/s41...

yea man, this isn't normal

PAIR-UP/MBL Microscopy Boot Camp Workshop Optical imaging is central to biomedical research. We will host a weeklong microscopy bootcamp training at the Marine Biological Laboratory. This bootcamp is planned to train graduate students and pos...

PAIR-UP is partnering with the MBL to host an intensive Imaging Boot Camp. This workshop is free to those selected. APPLY NOW! forms.gle/DDWmQq8ogk2h...

Just made a Pinksky account and this is my first post! Had a great time at #KSHostMicrobe25 conference in Canada it was beautiful

Plane

Day 1 mixer

Day 2

Currently in Banff for #KSHostMicrobe25 these are the fits so far, already learned a ton of cool stuff 😁

Trump Administration Halts H.I.V. Drug Distribution in Poor Countries PEPFAR’s computer systems also are being taken offline, a sign that the program may not return, as Republican critics had hoped.

The shortsighted new US regime stopped HIV funding to poor countries. This prevented 26 million deaths and the global spread of AIDS.

Humanitarian aid is the groundwork of global stability.

They've also removed us from the WHO, and instructed the NIH to halt all travel and communications.

Why?

US health officials ordered to stop working with WHO immediately US experts said the sudden pause came as a surprise and would set back efforts to contain health threats abroad.

Trump has ordered an abrupt end on all U.S health officials that work with the World Health Organization (WHO).

The CDC staff involved have to stop their work immediately and are not allowed to visit WHO offices.

Will bird flu spark a human pandemic? Scientists say the risk is rising H5N1 is adapting to new mammal hosts, raising the possibility of the virus spreading between humans.

The risk of bird flu continues to rise as it spreads in herds &flock around the country. This is the absolute worst time for health communications the CDC to be muzzled. If we have another pandemic we will be even more vulnerable than the last time around. #h5n1
www.nature.com/articles/d41...

Lysosomes finely control macrophage inflammatory function via regulating the release of lysosomal Fe2+ through TRPML1 channel - Nature Communications Lysosomes are best known for their roles in inflammatory responses via autophagy. Here, Xing et al., find that lysosomes regulate macrophage inflammatory responses by finely controlling interleukin-1β...

Lysosomes finely control macrophage inflammatory function via regulating the release of lysosomal Fe2+ through TRPML1 channel #MECFS #LongCovid

www.nature.com/articles/s41...

An optimized macrophage-specific transfection strategy supports in vivo CRISPR editing of mRNAs to facilitate phagocytosis
www.science.org/doi/10.1126/...

Menaquinone-specific turnover by Mycobacterium tuberculosis cytochrome bd is redox regulated by the Q-loop disulfide bond Cytochrome bd from Mycobacterium tuberculosis (Mtbd) is a menaquinol oxidase that has gained interest as an antibiotic target because of its importance in survival under infectious conditions. Mtbd co...

Great paper by the group of @larsjeuken.bsky.social in J. Biol. Chem. with first author Tijn van der Velden. Cytochrome bd of M. tuberculosis is RedOx-regulated through a disulfide with potential important implications for survival in the phagosome #chemsky #ChemBio (1/2)
www.jbc.org/article/S002...

Programmed ribosomal frameshifting during PLEKHM2 mRNA decoding generates a constitutively active mediator of kinesin-1-dependent lysosome transport Programmed ribosomal frameshifting is a process where a proportion of ribosomes change their reading frame on an mRNA, rephasing the ribosome relative to the mRNA. While frameshifting is commonly employed by viruses, very few phylogenetically conserved examples are known in nuclear encoded genes and some of the evidence is controversial. Here we report a +1 frameshifting event during decoding of the human gene PLEKHM2. This frameshifting occurs at the sequence UCC\_UUU\_CGG, which is conserved in vertebrates and is similar to an influenza virus sequence that frameshifts with similar efficiency. The new C-terminal domain generated by this frameshift forms an α-helix, which relieves PLEKHM2 from autoinhibition and allows it to move to the tips of cells via association with kinesin-1 without requiring activation by ARL8. Reintroducing both the canonically-translated and frameshifted protein are necessary to restore normal contractile function of PLEKHM2-knockout cardiomyocytes, demonstrating the necessity of frameshifting for normal cardiac activity. ### Competing Interest Statement The authors have declared no competing interest.

Programmed ribosomal frameshifting during PLEKHM2 mRNA decoding generates a constitutively active mediator of kinesin-1-dependent lysosome transport [NEW RESULTS]
http://biorxiv.org/cgi/content/short/2024.08.30.610563v2?rss=1

A new study uses a cutting-edge technology to explore how faulty lysosomes cause problems in cells, especially affecting cholesterol buildup and mitochondrial health in certain mutants. The findings highlight a useful tool for discovering how these issues play out in various genetic disorders.

NIH appears to have canceled/postponed all of its study sections—the independent review panels that approve federal grants for health research.

Such grants fund the work/salaries of 300k people at more than 2,500 institutions

Hey Roger!

I just spoke to @wang.social and he suggested I reach out to you since you are interested in building geographic tools into the AT Protocol. I would love to dm you a google doc with some ideas for an app that can be built on top of that, and I'm happy to discuss more!

I sent a similar reply to Skyseed and would love to hear any thoughts or if anyone is working on something like that!

The reason I ask is that with several crises potentially brewing (health system stress, climate change and natural disasters, policy uncertainty leading to economic issues) local leaders will probably need to spearhead local solution based initiatives and the AT protocol could serve as a catalyst.

Hey Peter! I was interested in how the AT protocol could be used to strengthen local communities and
combat misinformation and potentially catalyze grassroots driven, bottom up governance. Are there any proposals that suggest using the AT protocol to develop decentralized truth seeking platforms?

I wonder if the potential decentralization of social media through the AT protocol could be used to catalyze local bottom-up influence and combat top down misinformation. Is anyone working on stuff like that?

I'd love to hear any thoughts about this!

The reason I ask is that with several crises potentially brewing (health system stress, climate change and natural disasters, policy uncertainty leading to economic issues) local leaders will probably need to spearhead local solution based initiatives and the AT protocol could serve as a catalyst

Hey Skyseed! I was interested in how AT protocol could be used to strengthen local communities and
combat misinformation and potentially catalyze grassroots driven bottom up governance. Are there any proposals that suggest using the AT protocol to develop local decentralized truth seeking platforms?