Sumin Feng

Postdoc @durocherlab. Interested in genome stability, DNA repair

[andre nussenzweig lab @nussenza]

A high-resolution view of how replication-coupled DNA breaks are generated, processed and repaired. Congrats to @pavani_raphael, @TripathiVeenu, and many terrific collaborators including @FrogWalterLab, @CejkaLab, @weiwsmiling. See https://t.co/HjXVyHWIWE

[Sumin Feng @Sumin_666]

@AmelieFT So shocked and sad to hear this! Wei was so passionate about life and science💔

[Roger Greenberg @RogerRogergr]

We're excited to report a new mechanism of replisome proteostasis https://t.co/IjX0wEHkK5. 55LCC ATPase/unfoldase complex dependent replisome turnover prevents chromosome instability. Great collaboration by @vidhya_k7 and @RobertLDilley with @FoglizzoMartina and @zeqiraj.

[Dheva Setiaputra @biochemDheva]

Very excited to share a new preprint from the @durocherlab! We used AlphaFold2 to exhaustively map the 53BP1-RIF1-shieldin-CST pathway and found a novel RIF1-SHLD3 binding interface essential for pathway function. 🧵below 1/6
https://t.co/LKdKE9zayI

[Sumin Feng @Sumin_666]

the screaming nuclear

[durocherlab @durocherlab]

🚨Job alert🚨 Our lab is looking for a bioinformatics associate to support our work using functional genomic/proteomic approaches (CRISPR screens, proximity proteomics, various Seq approaches).

👇
https://t.co/HQ4Szipij8

[Sumin Feng @Sumin_666]

Thanks Dongyi and collaboraters!

[Dongyi Xu @Dongyixu1]

Our final version came out with new data. Happy to share our study linking DNA repair and dynamic changes of high-order chromatin structure to suppress initiation of resection. Thanks to Sumin Feng, Sai Ma & Kejiao Li in my lab and our collaborators!
https://t.co/yhXjm7WO3E

[Dheva Setiaputra @biochemDheva]

Honored and looking forward to presenting my postdoctoral work on the 53BP1-RIF1-shieldin pathway as part of the ECS3 seminar at @ircm_mtl!

[Dongyi Xu @Dongyixu1]

Happy to share our new work that RIF1 forms a complex with histone chaperone ASF1, which condenses adjacent chromatin by heterochromatinization to protect broken DNA ends and promote NHEJ. https://t.co/Q4dr3wYVVS

[Dongyi Xu @Dongyixu1]

We found that the Fanconi anemia pathway is intrinsically a BIR pathway and persistent replication stress is a potential offending cause of disease symptoms in Fanconi anemia. https://t.co/q3BWbIxjQY