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This Review examines how transcriptional or co-transcriptional processes become dysregulated in cancer cells, and how this dysfunction might create targetable vulnerabilities, and summarizes advances in therapeutic strategies targeting transcriptional CDKs.
This work presents a scalable mammalian cell-display workflow to identify AI-designed minibinders against cancer surface targets and identifies biochemical optimization beyond the binding interface as a critical requirement for translating AI-minibinders into functional applications.
This work proposes FAM222B as a novel candidate gene for cardiovascular laterality defects, described as a substrate of Nemo-like kinase (NLK), associated with left–right body axis determination in zebrafish homologues, fam222ba/bb, and fam222aa.
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