Billy Li
@RNAedit
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Leading RNA editing to treating disease
Stanford, CA
Joined August 2015
3/3 I’d be also happy to meet and discuss what ADAR can do as a novel modality for therapeutic RNA base editing and how human genetics plays a crucial role for the target discovery etc. (Disclosure: I co-founded AIRNA, a company in this exciting space.) .
airna.com
A bold visionfor genetic medicines AIRNA is committed to delivering the promise of RNA editing to people with rare diseases and common conditions The
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2/3 I look forward to meeting old and new friends! If you are interested in our work (exemplified by this paper) and seeking postdoc or collaboration opportunities, please feel free to DM or email me to schedule time to meet up! .
nature.com
Nature - cis-RNA editing quantitative trait loci, which are associated with immunogenic double-stranded RNAs, underlie genome-wide association study variants in common autoimmune and inflammatory...
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1/3 Super excited to present our work on RNA editing and sensing through the lens of human genetics of autoimmune and inflammatory diseases at #ASHG2024 in the Featured Symposium of #ADAR #RNAediting, Thursday Nov 7th 8:00-9:30am. #ASHG24.
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Excited about the additional $60M raise of AIRNA - kudos to the team! I never expected the amazing potential to help patients when I encountered this bizarre biology many years ago. More to come about ADAR, a truly one of its kind enzyme!.
businesswire.com
AIRNA announces the successful closing of an oversubscribed $60 million financing round, which brings the total Series A funding to $90 million.
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Congratulations Xiaojing and the team! It’s amazing to watch all the ADAR-related developments. I cannot wait to see how things unfold and what the next ADAR-related invention will be! #ADAR #RNAediting.
Radar Tx is de-stealthed today! It's been so great working (or rather, tagging along) with co-founders, @EerikKaseniit, Sophia Lugo, and Jim Collins. We've assembled a stellar research team, forging ahead with new designs. We are still hiring more.
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Excited to be part of this symposium to celebrate the extraordinary career of my PhD co-advisor Gary Stormo @gdstormo! I look forward to seeing Gary and other mentors and friends!.
The Stormo Symposium on Computational Biology is open for registration! Join us and our exceptional group of speakers on “History and Current Developments in Computational Biology”. Don't miss this incredible event @WashUGenetics Please share and register!
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Honored to be part of this exciting webinar organized by Bryan Harada @structural_biol. I will focus on dsRNA editing mediated by ADAR1 and dsRNA sensing mediated by MDA5 and PKR. #ADAR.
Free Cell Press webinar, RNA sensing in immunity, w/ speakers Sun Hur @harvardmed @BostonChildrens, Stacy Horner @DukeMedSchool @TheHornerLab & Jin Billy Li @Stanford, Nov 15, 12:00 pm ET.
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RT @MolecularCell: Online Now: ADAR1p150 prevents MDA5 and PKR activation via distinct mechanisms to avert fatal autoinflammation https://t….
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I cannot ask for a better collaborator than Carl Walkley @SVIResearch and a nicer team spearheaded by Shibin Hu and @jacki_hf.
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This preprint finds a nice home @MolecularCell. We hope that the mechanistic understanding of how ADAR1 safeguards cellular dsRNAs will provide insights for therapeutic developments. #RNAediting #ADAR .
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Thank you Rohini for the heavy lifting of writing this nice review! A lot has been happening in the RNA editing field.
Greatly enjoyed writing this advanced review on the therapeutic potential of #RNA #editing, ranging from #cancer #immunotherapy to #viral (focusing on #SARSCoV2) #infections. Part of #postdoc research at #Stanford. Congratulations to all the co-authors!
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Thrilled to be on this exciting journey! It is surreal to have this opportunity to translate the fundamental discoveries (that my co-founder Thorsten Stafforst pioneered), with the help from a passionate team of executives, scientists, and investors.
endpoints.news
The race to develop new therapies that precisely edit short-lived RNA molecules instead of making irreversible changes to DNA is heating up. A new entrant to the growing field emerged ...
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Huge congratulations to Qin for the incredible milestone! Feeling really proud! Penn is lucky to have you!.
Feeling incredibly thrilled to announce that in January 2024, I'll be joining @PennGenetics and @UPenn_I3H as an Assistant Professor! My lab will study the genetic basis of immune recognition of RNA and its role in health and disease. Please reach out or DM if you are interested.
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Congratulations Jacki, Carl and the team! As many pay attention to the role of ADAR1 in cancer, this is a very important message showing that ADAR1 upregulation in cancers is not causal, but correlative.
Happy to share the new preprint from the Walkley lab where we directly tested whether increasing levels of #ADAR1 and A-to-I editing levels in vivo could promote #cancer formation or progression. (1/n). @SVIResearch @AlistairChalk .
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This is indeed THE result worth emphasizing @jacki_hf . It is the type of “black & white” experiments we seem to see less as biology appears more complex.
Just in case you missed it in the twitter thread. Full rescue of Adar1p150 KOs by loss of MDA5 and PKR!.
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Finally, I’d like to thank Carl for the long-time collaboration that has has made me a better scientist. He is the dream collaborator one can hope for! I truly appreciate the tremendous efforts from very talented Shi-Bin and Jacki, along with many other members of our labs.
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MDA5 and PKR are unequivocally the primary in vivo effectors of fatal autoinflammation following the loss of ADAR1p150. Other dsRBPs such as ZBP1 also play functional roles in the context of ADAR1, but future work is needed to dissect the mechanisms to reveal a full picture.
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To summarize: we demonstrate that discrete functions of ADAR1p150 determines MDA5 or PKR engagement: A-to-I.editing of endogenous dsRNA specifically prevents MDA5 activation, while PKR activation is prevented by editing-independent, competitive dsRNA binding in the cytoplasm.
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Subsequently, we attempted to rescue the Adar1p150-/- mice by knocking out both MDA5 and PKR. Long story short, it is a FULL rescue - at the Mendelian ratio! The oldest Adar1p150-/-Ifih1-/-Eif2ak2-/- mice are >42 weeks old now.
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Key findings: The activation of PKR is independent of RNA editing, but dependent on RNA binding activities of ADAR1. It is the RNA binding of the cytoplasmic ADAR1p150 isoform that suppresses PKR activation.
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