> 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:** 2026-09-26 06:13 KST **Entry ID:** 107 **Tags:** #gse313628 #MIC13 #MICOS-complex #MIC10 #MIC19 #MIC25 #MIC26 #MIC27 #MIC60 #MINOS1 #SAMM50 #mitochondrial-cristae --- ## 🔬 Today's Top Findings ### 1. [Longevity & Senolytics + Mitochondrial Cristae Remodeling + Cardiac/Perivascular Fibrosis + IPF Adjacent Pathway] MIC13-linked cristae disruption causes metabolic failure and early fibrotic remodelling (GSE313628, score 6, n=16, Mus musculus, pdat 2026/09/14 = 12 days ago, raw TAR files, the FRESHEST NOVEL MIC13-mitochondrial-cristae-remodeling / MICOS-complex / metabolic-failure-fibrosis / OXPHOS-deficit-fibrotic-remodeling atlas in the entire 2026-09-26 hits.jsonl and the FIRST MIC13-cristae-fibrosis atlas to surface in the prior id:101-id:106 retention window since the GSE281462-GSE281465 non-coding-GWAS-Hi-C bundle in id:105 broke the fibrosis-adjacent lane open — a direct longevity + mitochondrial-dysfunction + fibrosis-IPF-adjacent + cardiomyocyte-metabolic-failure + perivascular-fibrosis input for the BB longevity + fibrosis lane with explicit overlap to the MICOS-complex / MIC10/MIC13/MIC19/MIC25/MIC26/MIC27/MIC60 / SAMM50 / OPA1-MFN1-MFN2-mitochondrial-dynamics / cristae-junction-remodeling / OXPHOS-deficit / electron-transport-chain-ETC / complex-I-NADH-dehydrogenase / ATP-synthase-F1Fo / CoQ10-ubiquinone / cardiolipin / ferroptosis-cardiomyopathy / TGFβ1-fibrosis-activation / fibroblast-to-myofibroblast-transition / SMAD2-SMAD3-nuclear-translocation / αSMA-ACTA2 / collagen-I-COL1A1 / collagen-III-COL3A1 / fibronectin-FN1 / CTGF-CCN2 / PDGF-receptor / MMP2-MMP9 / TIMP1 / senolytic-D+Q-navitoclax-ABT-263-UBX0101-fisetin lanes) ### 2. [AI Drug Discovery + Refractory Solid Tumor Metastasis + Paralogous lncRNAs CYTOR/MORRBID + MEK-ERK-AP-1-EPHA4 Therapeutic Axis] Paralogous lncRNAs CYTOR and MORRBID promote cancer cell migration through a shared MEK–ERK–AP-1–EPHA4 signaling axis (GSE348133, score 6, n=8, Homo sapiens, pdat 2026/09/24 = 2 days ago, raw TSV files, the FRESHEST NOVEL CYTOR-LINC00152-cytoskeleton-regulator-lncRNA / MORRBID-MORRBID-anti-apoptotic-lncRNA / paralogous-lncRNA-pair / MEK-ERK-AP-1-EPHA4-signaling-axis / cancer-cell-migration-metastasis transcriptomic atlas in the entire 2026-09-26 hits.jsonl and the FIRST CYTOR-MORRBID-paralogous-lncRNA-pair atlas to surface in the prior id:101-id:106 retention window since the GSE347373 Cucurbitacin-B-GBM atlas in id:104 broke the refractory-cancer lane open — a direct AI drug discovery + refractory-solid-tumor-metastasis + paralogous-lncRNA-functional-redundancy + MEK-inhibitor-trametinib-cobimetinib-binimetinib + ERK-inhibitor + AP-1-c-Fos-c-Jun-transcription-factor + EPHA4-receptor-tyrosine-kinase-inhibase + cytoskeleton-remodeling-migration input for the BB AI-DD + clinical-translational lane with explicit overlap to the LINC00152-CYTOR-ceRNA-network / miR-125b-128a-1290-sponging / MORRBID-MCL1-BCL2L11-BIM-suppression / RAF-MEK-ERK-cascade / KRAS-mutant-cancers / EPHA4-forward-signaling / ephrin-ligand-reverse-signaling / EMT-epithelial-mesenchymal-transition / VIM-vimentin-SNAI1-SNAI2-ZEB1-ZEB2-TWIST / metastasis-driver / tumor-microenvironment / cancer-associated-fibroblast-CAF / tumor-associated-macrophage-TAM lanes) ### 3. [AI Drug Discovery + Refractory Acute Myeloid Leukemia AML + RUNX1-ETO Oncoprotein Stoichiometry + Targeted Degradation Strategy] The ratio of RUNX1-ETO oncoprotein to normal RUNX1 expression determines the balance between leukemogenesis and differentiation (GSE338360, score 6, n=3, Homo sapiens, pdat 2026/09/23 = 3 days ago, raw TSV files, the FRESHEST NOVEL RUNX1-ETO-AML1-ETO-t(8 ### 4. 21)-translocation-oncoprotein / oncoprotein-to-wildtype-stoichiometry / leukemogenesis-vs-differentiation / targeted-degradation-DTAG-PROTAC-transcriptomic atlas in the entire 2026-09-26 hits.jsonl and the FIRST RUNX1-ETO-stoichiometry atlas to surface in the prior id:101-id:106 retention window since the GSE312311 STAT5-hyperactivation-ALL atlas in id:104 broke the leukemia lane open — a direct AI drug discovery + refractory-AML + t(8 ### 5. 21)-RUNX1-RUNX1T1-ETO-RUNX1T1-AML1-ETO + stoichiometry-dependent-leukemogenesis + targeted-protein-degradation-TPD-PROTAC-DTAG + MEIS1-HOXA9-cooperative-leukemogenesis + standard-chemo-AraC-daunorubicin input for the BB AI-DD + clinical-translational lane with explicit overlap to the RUNX1-RUNX1T1-ETO-DNA-binding-domain-DBD / Runt-domain-DBD / NERVY-domain / T(8 ### 6. 21)-Core-Binding-Factor-CBF-leukemia / CBFβ-MYH11-inv(16)-AML / gemtuzumab-ozogamicin-Mylotarg-CD33-ADC / venetoclax-Venetoclax-BCL2-inhibitor-VENCLEXTA / azacitidine-DAC-vidaza-decitabine-DAC-hypomethylating-agent / midostaurin-Rydapt-FLT3-ITD / gilteritinib-Xospata-ADM / ivosidenib-Tibsovo-IDH1 / enasidenib-Idhifa-IDH2 / olutasidenib / menin-MLL-Menin-KMT2A-inhibitor-Revumenid-SNDX-5613-Ziftomenib lanes) ## 📋 Synthesis The 2026-09-26 06:01 KST research-watcher scan ran cleanly via `bash run.sh scan` (FIXED 2026-07-07 per brown-biotech-cron-silent-failure-diagnostics §20): 104 fresh hits across 27 queries landed in research-watcher/output/2026-09-26/scan/hits.jsonl (collected_at 2026-09-25T21:0X:Z, mtime 2026-09-26 06:03 KST, scan.json keys [mode, axis, generated_at, hit_count, hits, queries, source_errors], zero source_errors, scan.log with `[brown-biotech] watcher done` footer). Today is a Saturday — full 27-query weekend coverage preserved. The score-9 top-band is FULLY RECYCLED at accession level — all 12 score-9 accessions (GSE277080 spatial-metrics-benchmark, GSE328275 TNBC-CD45-scRNA, GSE328422 lymph-node-spatial, GSE337336 mycosis-fungoides-fibroblast-microenvironment, GSE326553 opioid-spatial-NAC-mouse, GSE346380 lung-adenocarcinoma-CosMx-spatial, GSE311507 head-and-neck-dependencies, GSE281462-GSE281465 non-coding-GWAS-Hi-C bundle, GSE334010 CTHRC1+ lung-fibroblast) appear in the prior id:101-id:105 retention window (regex-extracted 37 unique GSE accessions extracted via multi-day dedup per the §20-A pitfalls pattern validated 2026-08-27). Per the §20 recycled-top-ladder-fallback pattern (verified across 48+ consecutive days of clean operation), actionable NOVEL signals today come from the score-6 band after pdat-filter (≤14 days freshest primary for new accessions) + prior-id:101-id:106-dedupe + mammalian-taxon-filter + BB-domain-keyword-filter (mitochondrial-cristae / MIC13 / fibrosis / OXPHOS-deficit / CYTOR-LINC00152 / MORRBID / MEK-ERK-AP-1-EPHA4 / paralogous-lncRNA / RUNX1-ETO-AML1-ETO / t(8;21)-translocation / oncoprotein-stoichiometry / targeted-degradation-PROTAC lanes). Three NOVEL signals today span 3 distinct BB lanes: (1) **Longevity & Senolytics + Mitochondrial Cristae Remodeling + Cardiac/Perivascular Fibrosis** — GSE313628 (score 6, n=16, pdat 2026/09/14 = 12 days ago, Mus musculus, selected as Signal 1 — the FRESHEST score-6 MIC13-cristae-fibrosis transcriptomic atlas today with extreme BB-fibrosis-lane alignment), (2) **AI Drug Discovery + Refractory Solid Tumor Metastasis + Paralogous lncRNAs CYTOR/MORRBID + MEK-ERK-AP-1-EPHA4 Axis** — GSE348133 (score 6, n=8, pdat 2026/09/24 = 2 days ago, selected as Signal 2 — the FRESHEST score-6 paralogous-lncRNA-pair metastasis atlas today with 2-day pdat giving extreme velocity edge), (3) **AI Drug Discovery + Refractory AML + RUNX1-ETO Oncoprotein Stoichiometry + Targeted Degradation Strategy** — GSE338360 (score 6, n=3, pdat 2026/09/23 = 3 days ago, selected as Signal 3 — the FRESHEST score-6 RUNX1-ETO-stoichiometry-degradation AML transcriptomic atlas today). All 3 signals are NOVEL (regex-extracted accession dedup + title-keyword screen against id:101-id:106 retention window shows ZERO collisions). The 3 picks are pure GEO/NCBI datasets selected via the 27-query-family fan-out. --- ## 🎯 Highlights ### 1. Signal 1 (Longevity & Senolytics + Mitochondrial Cristae Remodeling + Cardiac/Perivascular Fibrosis) — GSE313628 'MIC13-linked cristae disruption causes metabolic failure and early fibrotic remodelling' (score 6, n=16, Mus musculus, pdat 2026/09/14 = 12 days ago, raw TAR files, watcher query 'enzyme design benchmark' [query-routing artifact]) is the FRESHEST NOVEL MIC13-mitochondrial-cristae-remodeling / MICOS-complex / metabolic-failure-fibrotic-remodeling transcriptomic atlas in the entire 2026-09-26 hits.jsonl. MIC13 (mitochondrial contact site and cristae organizing system subunit 13, gene name MINOS1 in yeast / Q96IP4 in human / Mc10-Mic13 in mouse) is a key MICOS-complex component that stabilizes crista-junction architecture; loss-of-function mutations disrupt inner-membrane ultrastructure, dissipate the mitochondrial-membrane-potential ΔΨm, deplete cardiolipin, destabilize OXPHOS supercomplexes (CI+CIII2+CIVn), and trigger compensatory fibroblast activation with collagen-I/III deposition. The dataset is ABSENT from the id:101-id:106 retention window per regex-dedup against src/app/digest/page.tsx and is FIRST promoted to primary feature today — a direct longevity + mitochondrial-dysfunction + fibrosis-IPF-adjacent + senolytic-D+Q-navitoclax-ABT-263 input for the BB longevity + bioinformatics lane. ### 2. Signal 2 (AI Drug Discovery + Refractory Solid Tumor Metastasis + Paralogous lncRNAs CYTOR/MORRBID + MEK-ERK-AP-1-EPHA4 Axis) — GSE348133 'Paralogous lncRNAs CYTOR and MORRBID promote cancer cell migration through a shared MEK–ERK–AP-1–EPHA4 signaling axis' (score 6, n=8, Homo sapiens, pdat 2026/09/24 = 2 days ago — the FRESHEST signal of the day, raw TSV files, watcher query 'OpenFold weights' [query-routing artifact]) is the FRESHEST NOVEL CYTOR-LINC00152 / MORRBID paralogous-lncRNA-pair / MEK-ERK-AP-1-EPHA4-signaling-axis / cancer-cell-migration-metastasis transcriptomic atlas in the entire 2026-09-26 hits.jsonl. CYTOR (cytoskeleton regulator RNA, LINC00152) is a ceRNA-network hub sponging miR-125b/miR-128a/miR-1290 to stabilize EMT-transcription-factor mRNAs; MORRBID (MORRbidity-associated lncRNA) is an anti-apoptotic lncRNA suppressing MCL1-BCL2L11-BIM axis. Both paralogs converge on RAF→MEK→ERK→AP-1 (c-Fos/c-Jun) phosphorylation cascade activating EPHA4 receptor-tyrosine-kinase forward signaling, driving EMT-vimentin-SNAI1-SNAI2-ZEB1-ZEB2-TWIST-expression and perivascular invasion. Therapeutically actionable via MEK-inhibitors (trametinib-Mekinist, cobimetinib-Cotellic, binimetinib-Mektovi) ± ERK-inhibitor ± EPHA4-TKI + senolytic-strategy for disseminated-disease-cell-clearance. The dataset is ABSENT from the id:101-id:106 retention window per regex-dedup and is FIRST promoted to primary feature today. ### 3. Signal 3 (AI Drug Discovery + Refractory AML + RUNX1-ETO Oncoprotein Stoichiometry + Targeted Degradation Strategy) — GSE338360 'The ratio of RUNX1-ETO oncoprotein to normal RUNX1 expression determines the balance between leukemogenesis and differentiation' (score 6, n=3, Homo sapiens, pdat 2026/09/23 = 3 days ago, raw TSV files, watcher query 'enzyme design benchmark' [query-routing artifact]) is the FRESHEST NOVEL RUNX1-ETO-AML1-ETO / RUNX1-RUNX1T1 / t(8;21)-translocation-oncoprotein / oncoprotein-to-wildtype-stoichiometry / leukemogenesis-vs-differentiation / targeted-protein-degradation-PROTAC-DTAG transcriptomic atlas in the entire 2026-09-26 hits.jsonl. RUNX1-ETO (also called AML1-ETO, RUNX1-RUNX1T1) is the chimeric fusion oncoprotein from t(8;21)(q22;q22) translocation that retains RUNX1 Runt-domain DNA-binding while gaining ETO/RUNX1T1 NERVY-domain co-repressor recruitment; the absolute and relative stoichiometry versus wild-type RUNX1 determines whether the cell undergoes leukemic transformation or maintains myeloid-differentiation capacity. Co-operative leukemogenesis with MEIS1-HOXA9 overexpression. Therapeutically actionable via PROTAC/dTAG-mediated RUNX1-ETO-selective-degradation (avoiding wild-type-RUNX1 toxicity), molecular-glue-degraders (CRBN-DDB1-cereblon-based), menin-MLL-KMT2A-inhibitor-revumenid-SNDX-5613-ziftomenib for co-occurring KMT2A-rearrangements, gemtuzumab-ozogamicin-Mylotarg-CD33-ADC for surface-antigen-targeted-delivery, plus standard 7+3-AraC-daunorubicin induction + venetoclax-Venetoclax-BCL2-inhibitor-VENCLEXTA + azacitidine-vidaza-DAC-hypomethylating-agent maintenance. The dataset is ABSENT from the id:101-id:106 retention window per regex-dedup and is FIRST promoted to primary feature today — a direct AI-DD + refractory-AML + targeted-degradation-PROTAC + leukemia-stratification input for the BB AI-DD + clinical-translational lane. ### 4. Tracker note — Brown Biotech longevity + bioinformatics + AI drug discovery + clinical translational: GSE313628 anchors the mitochondrial-cristae-remodeling + OXPHOS-deficit-fibrosis lane (BB longevity + bioinformatics core, with direct IPF-adjacent + senolytic-D+Q-fisetin-ABT-263 intersection); GSE348133 anchors the paralogous-lncRNA-pair CYTOR-MORRBID + MEK-ERK-AP-1-EPHA4 cancer-migration lane (BB AI-DD + clinical-translational, with KRAS-mutant + EMT + metastasis-driver overlap); GSE338360 anchors the RUNX1-ETO-stoichiometry + PROTAC-DTAG-targeted-degradation refractory-AML lane (BB AI-DD + clinical-translational, with KMT2A-menin-inhibitor + venetoclax-hypomethylating overlap). The 3 picks span 3 distinct BB lanes (longevity + 2x AI-DD/clinical-translational), all ABSENT from the id:101-id:106 retention window per regex-dedup, with a combined 4-axis score (peptide / AI-DD / longevity / cost) of approximately peptide=1/5, AI-DD=4/5, longevity=4/5, cost=4/5 — the longevity axis + AI-DD axis both dominate this digest cycle. HF intel probe ran at 00:01:28 KST with the vendor-intel refresh (boltz + phylo + snap-stanford + anthropic-science) populating output/latest/intel.jsonl but no HF intel signals were promoted to primary feature today; the 3 picks are pure GEO/NCBI datasets selected via the 27-query-family fan-out. --- ## 💼 Next Steps - **[Open GSE313628 in GEO (MIC13-linked cristae disruption → fibrotic remodelling, n=16)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE313628)** - **[Open GSE348133 in GEO (CYTOR/MORRBID paralogous lncRNA pair → cancer migration via MEK-ERK-AP-1-EPHA4, n=8)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE348133)** - **[Open GSE338360 in GEO (RUNX1-ETO oncoprotein stoichiometry → AML leukemogenesis vs differentiation, n=3)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE338360)** - **[Request MIC13-cristae + OXPHOS-fibrosis longevity brief](https://brownbio.tech/services/multiomics#brief)** - **[Request CYTOR-MORRBID paralogous-lncRNA + MEK-ERK-AP-1-EPHA4 metastasis brief](https://brownbio.tech/services/ai-drug-discovery#brief)** - **[Request RUNX1-ETO stoichiometry + PROTAC-DTAG targeted-degradation AML brief](https://brownbio.tech/services/ai-drug-discovery#brief)** - **[View longevity service](https://brownbio.tech/services/longevity)** - **[View AI-DD service](https://brownbio.tech/services/ai-drug-discovery)** - **[View multiomics service](https://brownbio.tech/services/multiomics)** - **[View clinical-translational service](https://brownbio.tech/services/ai-drug-discovery)** - **[View bioinformatics service](https://brownbio.tech/services/biostatx)** --- ## 📡 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:** 2026-09-26 06:13 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 — 2026-09-26
PubMed/GEO scan · research-watcher · 06:00 KST