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Reposted by H. Courtney Hodges

From the Labs at Baylor College of Medicine @bcmfromthelabs.bsky.social · Jul 30

Drs. HC Hodges @hodgeshc.bsky.social, #chanyuensan, K Cermakova @cermakova.bsky.social et al discovered a molecular bridge that facilitates interactions among disordered proteins involved in regulating #geneExpression. #BetaCatenin @bcmhouston.bsky.social #MolecularCell blogs.bcm.edu/2025/07/24/f...

A molecular bridge helps disordered proteins work properly

The findings reveal that despite their disordered nature, the protein interactions that drive gene expression are surprisingly modular and even have an underlying organization.

blogs.bcm.edu

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H. Courtney Hodges @hodgeshc.bsky.social · Jul 24

Thanks a lot!

H. Courtney Hodges @hodgeshc.bsky.social · Jul 23

Thanks a lot Ariel. We hope it may increase focus on IDR-domain interactions, we think there’s a lot to do in that space. Hope you’re doing great!

H. Courtney Hodges @hodgeshc.bsky.social · Jul 23

Thank you so much!

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H. Courtney Hodges @hodgeshc.bsky.social · Jul 22

We were very lucky to have so many amazing collaborators on this paper, including @vaclav-veverka.bsky.social, @cermakova.bsky.social, and many others, including Yuen San Chan as first author. Please check out our paper for more information!

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H. Courtney Hodges @hodgeshc.bsky.social · Jul 22

Excitingly, β-catenin links cBAF not only to SF-1, but also to YAP1, SOX2, FOXO3, and CBP/p300, highlighting its critical role in chromatin remodeling across diverse cellular processes

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H. Courtney Hodges @hodgeshc.bsky.social · Jul 22

Dissection of interactions revealed that intrinsically disordered regions (IDRs) of ARID1A bind directly to the structured Armadillo domain of β-catenin

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H. Courtney Hodges @hodgeshc.bsky.social · Jul 22

Sustained inhibition leads to loss of steroid production, positioning cBAF as a key steroidogenic dependency

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H. Courtney Hodges @hodgeshc.bsky.social · Jul 22

We show that BAF inhibition disrupts the ability of the TF known as steroidogenic factor 1 (SF-1) and β-catenin to bind at enhancers targeted by ARID1A

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H. Courtney Hodges @hodgeshc.bsky.social · Jul 22

How do chromatin remodelers use #IDRs to find TF binding partners? In our new Molecular Cell paper, we show that β-catenin is an adaptor that links SWI/SNF (cBAF) subunit ARID1A with binding partners via IDR-domain interactions.
www.cell.com/molecular-ce...

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H. Courtney Hodges @hodgeshc.bsky.social · Nov 28

We also show that neural crest cells and NCC-derived neurons tolerate SWI/SNF inhibition. I anticipate that non-cycling cells are frequently independent, and cycling cells with different circuitries have alternatives or plasticity to activate Cyclin D

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H. Courtney Hodges @hodgeshc.bsky.social · Nov 28

Thanks Hiten, it is surprising that SWI/SNF inhibition is well tolerated, and we've seen very good therapeutic window in vivo. Not all cycling cells need SWI/SNF, it's dispensable for example in HEK293Ts

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H. Courtney Hodges @hodgeshc.bsky.social · Nov 27

What do SWI/SNF-addicted cancers have in common? And when are they most sensitive to SWI/SNF inhibition? Check out Katka’s thread highlighting our most recent paper

Katerina Cermakova @cermakova.bsky.social · Nov 27

For the first time, we find a common mechanism for SWI/SNF addiction in cancer! Our paper reveals that G1 phase is a critical junction for SWI/SNF activity in several addicted cancers, including neuroblastoma, AML, prostate cancer, and uveal melanoma academic.oup.com/nar/advance-... (1/6)

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Reposted by H. Courtney Hodges

Alex Holehouse @alexholehouse.bsky.social · Nov 13

A labor of love - our review on why IDRs matter for cellular function is live in Nat. Rev. Mol. Cell. Biol:
www.nature.com/articles/s41...

Working with Birthe Kraglund on this was such a pleasure, and we hope this review will be helpful to a broad audience!

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