> 매일 아침 research-watcher가 27개 query family × PubMed/GEO를 스캔해서, Brown Biotech 파이프라인 관점에서 decision-ready 인사이트로 정리합니다. 매일 06:00 KST 자동 생성. **Category focus:** Bioinformatics & Multi-Omics **Published:** 2026-07-25 06:15 KST **Entry ID:** 52 **Tags:** #Nr4a1 #NR4A1 #intestinal stem cells #immune homeostasis #fibroblast #macrophage #single-cell RNA-seq #gene regulatory network #single-cell entropy #GSE306798 #Hutchinson-Gilford progeria syndrome #HGPS --- ## 🔬 Today's Top Findings ### 1. Nr4a1 knockout reshapes colonic stem and immune-cell homeostasis (GSE306798, score 7, n=8, Mus musculus, single-cell RNA-seq, pdat 2026/07/07) ### 2. Single-cell atlas of progeric vascular aging reveals ER-stress and mutation trajectories (GSE317471, score 4, n=30, Mus musculus, Smart-seq2, pdat 2026/06/30) ### 3. Complement-C3 stromal remodeling is targetable in murine myelofibrosis (GSE336713, score 4, n=5, Mus musculus, single-cell/spatial context, pdat 2026/07/01) ## 📋 Synthesis 2026-07-25 watcher scan: 105 hits across 27 queries. The score-9 kidney-transplant, mycosis-fungoides, and DMD hits were recycled from the prior digest and excluded. Three novel, actionable signals survived: GSE306798 is a score-7, n=8 single-cell perturbation atlas of Nr4a1-knockout versus wild-type mouse colon, with broad remodeling of intestinal-stem-cell, macrophage, T-cell, B-cell, and fibroblast communication and increased single-cell entropy after deletion. GSE317471 is a score-4, n=30 Smart-seq2 atlas of progeric aortic arch, with ER stress, VSMC-to-fibroblast-like switching, DNA damage, somatic mutations, ROS/p53 activation, and apoptosis by 12 weeks; TUDCA did not prevent the switch. GSE336713 is a score-4, n=5 myelofibrosis spleen atlas in WT, ThPO, and MPLW515L mice; its GEO summary reports complement/TNF-alpha/TGF-beta/ECM/Thbs1-driven stromal remodeling and reduced splenomegaly and marrow fibrosis after stromal C3 deletion or pharmacological inhibition. These are promising research hypotheses, not validated therapies; all three GEO records list no linked PMID or DOI. --- ## 🎯 Highlights ### 1. Regenerative biology + perturbation — GSE306798 (score 7, n=8 Mus musculus, pdat 2026/07/07, CSV/MTX/RDS/TSV) compares whole-body Nr4a1-knockout and wild-type colon by single-cell RNA-seq. The GEO abstract reports remodeled communication among intestinal stem cells, macrophages, T cells, B cells, and fibroblasts, plus increased single-cell entropy and stem-like properties after deletion. Why it matters for BB: a compact perturbation input for NR4A1-dependent regenerative and immune-stromal analysis; small murine study, no chemistry conclusion, and first-time primary feature today. No linked PMID or DOI. ### 2. Longevity + vascular aging — GSE317471 (score 4, n=30 progeria-model and wild-type aortic-arch cells, pdat 2026/06/30, Smart-seq2, TXT) resolves age-dependent VSMC and fibroblast states. The GEO summary reports ER-stress-associated VSMC switching, DNA damage, somatic-mutation accumulation, ROS/p53 activation, and apoptosis by 12 weeks; TUDCA did not block the switch. Why it matters for BB: low-cost vascular-aging target benchmarking plus a negative-result constraint for intervention design; first-time primary feature today. No linked PMID or DOI. ### 3. Fibrosis + targetable axis — GSE336713 (score 4, n=5 Mus musculus spleen samples, pdat 2026/07/01, MTX/TSV) profiles WT, ThPO, and MPLW515L myelofibrosis. Its GEO summary reports pro-fibrotic reticular-cell remodeling driven by complement, TNF-alpha, TGF-beta, ECM, and Thbs1 programs, with reduced splenomegaly and marrow fibrosis after stromal C3 deletion or pharmacological inhibition. Why it matters for BB: a concrete complement-C3 hypothesis for anti-fibrotic and refractory-hematology work; small-n murine evidence needs QC and external validation. No linked PMID or DOI. ### 4. Four-axis gate — GSE306798: peptide 0/3, AI-agent infrastructure 3/3, longevity 1/3, low-cost/ease 3/3 = 7/12; GSE317471: 0/3, 3/3, 3/3, 3/3 = 9/12; GSE336713: 0/3, 2/3, 1/3, 3/3 = 6/12. Combined 22/36; all three are novel versus the retained top-five window. Next: QC and annotate the three files, intersect NR4A1 and C3 immune/fibroblast programs with existing IPF and muscle-aging atlases, and treat TUDCA as a negative-control constraint. --- ## 💼 Next Steps - **[View Nr4a1 knockout colon atlas](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE306798)** - **[View progeria vascular-aging atlas](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE317471)** - **[View myelofibrosis complement-C3 atlas](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE336713)** - **[Request longevity + fibrosis brief](https://brownbio.tech/multiomics#brief)** --- ## 📡 Provenance - **Source:** research-watcher (PubMed/GEO scan, 27 query families × Brown Biotech pipelines) - **Pipeline:** [`brown-biotech-daily-tech-digest`](https://github.com/ohbryt/brown-biotech-platform) — 06:00 KST cron - **Generated:** 2026-07-25 06:15 KST - **Repo:** `ohbryt/brown-biotech-platform` --- _Auto-published by `brown_biotech_research_digest_publisher.py` · [brownbio.tech](https://brownbio.tech) · Decision-ready research, daily._
Brown Biotech Research Digest — 2026-07-25
PubMed/GEO scan · research-watcher · 06:00 KST