Have you wondered what the wet lab success rates are for current AI-driven protein design models? Look no further!
In our new review, @kevinkaichuang.bsky.social
@avapamini.bsky.social, @sarahalamdari.bsky.social, and I report wet lab success rates for *over 200* different protein design tasks 🧬💻
That's a lovely perspective. Thanks so much, Aanchal!
The culmination of a fantastic collaboration between our lab and Bob Yauch’s lab that resulted in the uncovering of a proteosomal regulatory mechanism for PP2A. Congratulations to all the authors!
www.nature.com/articles/s41...
Great to see @agwrobel.bsky.social there. In parallel to our individual LS1-panel grants, we work together on an HFSP grant on a side topic.
Last Friday I had the HUGE pleasure of visiting LS1 @erc.europa.eu grantees based at the University of Oxford and to give an info session on all the changes implemented in the 2026 WP. Thanks so much for the warm welcome @agwrobel.bsky.social, @georgiaisom.bsky.social and @achilleskap.bsky.social!
🎉 As we celebrate #TIBS50, we're highlighting #CitedClassics and revisiting the top cited article from each of the last 50 years!
Check out this one from 1989!
Read it here 👉 www.sciencedirect.com/science/arti...
Congratulations to our Head of Department, @mjafreeman.bsky.social, awarded the @biochemsoc.bsky.social Centenary Award!
This recognises his contributions in the field of intramembrane proteases and pseudoproteases, and his commitment to supporting talent within the scientific community.
* By the way, if you heard about Top7 (Nobel prize, Science paper, >2000 citations), but not Top7-cfr (JMB paper, 36 citations), you are in for a treat.
When Top7 is expressed in E coli, a fraction of it is mistranslated into a 49 residue C-terminal fragment. 4/n
doi.org/10.1016/j.jm...
@lukekennard.bsky.social is a legend.
CDK1-dependent N-terminal NuMA phosphorylation promotes dynein-dynactin-NuMA assembly for accurate chromosome segregation
Data. A mouse model of glioblastoma leads to inevitable death within 50 days. Delivery of HSV+TK plus IL2, driven by a strong and specific synthetic superenhancer, allows almost all mice to survive even after nearly 150 days. From Fig5 of Koeber et al 2026
Just look at this graph (Fig 5A,B from Koeber et al).
Amazing.
Congratulations to the Pollard lab and all authors.
www.nature.com/articles/s41...
We show that the E3 ubiquitin ligase DTX2 creates a dual hybrid ADP-ribosyl-ubiquitin mark (ADPr-Ub) at DNA damage sites, driving the recruitment of RNF114, RNF138, and RNF166 proteins independently of HPF1.
journals.plos.org/plosbiology/...
🥁 New insights alert! Today, we take you into the fascinating world of RING-type E3 ubiquitin ligases through this article from our #Highlights2025 collection.
📕 RING dimerisation drives higher-order organisation of SINA/SIAH E3 ubiquitin ligases
➡️ buff.ly/rIErxm1
#ubiquitin #E3ligase #RING #SIAH1
Une soirée, 2 prix, et une immense fierté pour le CBM.
Félicitations à nos #doctorants !
Le 30/03/26, à l’occasion de la 13ᵉ de la 1/2 finale locale de #MT180 par @cnrs.fr, @franceuniversites.bsky.social et l’ @univorleans.bsky.social, au Bouillon, 2 de nos docs ont brillé:
"C'est un choix pour nos sociétés, pour l'avenir", les chercheurs du CNRS protestent après l'annonce d'une nouvelle coupe budgétaire par le gouvernement pour 2026.
www.francebleu.fr/emissions/l-...
I wrote an essay. It’s about gain-of-function mutations. And penguins. Also ion channels, chihuahuas, the film Alien, recycled cardboard, and the Apollonian mind. Oh, and muffins.
Thanks to the editors of #GENETICS @genetics-gsa.bsky.social for letting me take some stylistic liberties. 1/2
The paper describing our sensitive poly-ADPr antibodies and a few other things is now out in Nature Communications. Congrats to all the authors!!
www.nature.com/articles/s41...
Hyperosmotic stress induces PARP1-mediated HPF1-dependent mono(ADP-ribosyl)ation:
febs.onlinelibrary.wiley.com/doi/10.1002/...
A cool new study from @ahellab.bsky.social showing clear in vitro ADP-ribosylation of uridine. With contributions - amlong others - from our colleagues @ucagne.bsky.social and Guillaume @cbm-upr4301.bsky.social and a tiny bit from us.
Out now in @science.org
Pearling drives mitochondrial DNA nucleoid distribution | Science www.science.org/doi/10.1126/...
So such features (exposed beta sheet, a pocket for an aromatic) are advantages but also vulnerabilities, as they can both attract positive evolution and attract hijacking. You would expect such features to exist in those proteins where expanding the network justifies the risk.
And structurally this seems to often involve beta augmentation: adding an extra beta strand to your exposed beta sheet. Which makes sense, because strand-strand interactions are partly main chain-mediated and thus more loosely dependent on sequence. Plus in ATG8: a deep pocket for an aromatic 'hook'
So if the binding pocket has weak but appreciable affinity for simple motifs that occur frequently by chance, specific substrates can then optimise those if advantageous. At least that's how I think about it, though this assumes that having the initial rudimentary affinity is the kinetic bottleneck
I wonder what is the main feature of such pockets that makes them 'sticky'. Perhaps it is about being able to show meaningful affinity even to redimentary motifs encountered in proteins by chance: in some sense, you can only optimise in evolution what you already have at least in a rudimentary form.
We study SIMs which are one such example, and AIM/LIR motifs are another, perhaps a better one. By the way, SUMO, which binds to SIMs, and ATG8 proteins, which bind to AIMs, are evolutionarily related. Perhaps there used to a be a proto-SUMO/ATG8 protein binding to protoSIM/AIMs in the distant past.
Having a pocket for which simple binding motifs emerge readily de novo gives an advantage to a system dependent on that pocket - you can easily expand an interaction network in evolution - but also creates a vulnerability vis a vis pathogens hijacking those pockets (and perhaps cancer could too?).
New PI presenting to senior PIs at faculty mtg
