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cs.AI, q-bio.NC updates on arXiv.org
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Co-Designing Quantum Codes with Transversal Diagonal Gates via Multi-Agent Systems
arXiv:2510.20728v3 Announce Type: replace-cross Abstract: Exact scientific discovery requires more than heuristic search: candidate constructions must be turned into exact objects and checked independently. We address this gap by extending TeXRA with an independent Lean 4 verification layer, turning it into a human-guided multi-agent platform for exact scientific discovery. The platform couples symbolic synthesis, combinatorial and linear-programming search, exact reconstruction of numerical ca
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(Multiomics OR Omics) AND (Lung OR gastric OR Hepatocellular)
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RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy
Nat Commun. 2026 Mar 23. doi: 10.1038/s41467-026-70798-1. Online ahead of print.ABSTRACTGlioblastoma (GBM) remains a lethal brain tumor due to therapy resistance. While autophagy contributes to temozolomide (TMZ) resistance, its regulation is incompletely understood. This study investigates the role of replication factor RFC4, which is associated with poor prognosis and TMZ resistance in GBM. Multi-omics analyses and molecular experiments reveal that TMZ-induced chromatin accessibility enables t
RFC4 drives temozolomide resistance in glioblastoma by activating STK38-BECN1-dependent autophagy
Nat Commun. 2026 Mar 23. doi: 10.1038/s41467-026-70798-1. Online ahead of print.
ABSTRACT
Glioblastoma (GBM) remains a lethal brain tumor due to therapy resistance. While autophagy contributes to temozolomide (TMZ) resistance, its regulation is incompletely understood. This study investigates the role of replication factor RFC4, which is associated with poor prognosis and TMZ resistance in GBM. Multi-omics analyses and molecular experiments reveal that TMZ-induced chromatin accessibility enables transcription factor YY1 to bind the RFC4 promoter and upregulate its expression. RFC4, in turn, stabilizes the kinase STK38, which is essential for autophagosome formation. The RFC4-STK38 interaction facilitates BECN1 recruitment, thereby activating autophagy. Phosphorylation of STK38 at T444 stabilizes this complex, whereas a phospho-deficient mutant impairs autophagy. In vivo, RFC4 overexpression confers TMZ resistance, reversible by autophagy inhibition. Thus, our findings identify the RFC4-STK38-BECN1 axis as a mechanism underlying TMZ resistance and a potential target for precision therapy in GBM.
PMID:41872171 | DOI:10.1038/s41467-026-70798-1
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cs.AI, q-bio.NC updates on arXiv.org
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Adaptation of Agentic AI: A Survey of Post-Training, Memory, and Skills
arXiv:2512.16301v3 Announce Type: replace Abstract: Large language model (LLM) agents are moving beyond prompting alone. ChatGPT marked the rise of general-purpose LLM assistants, DeepSeek showed that on-policy reinforcement learning with verifiable rewards can improve reasoning and tool use, and OpenClaw highlights a newer direction in which agents accumulate persistent memory and reusable skills. Yet the research landscape remains fragmented across post-training, retrieval, memory, and skill