> 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:** AI Drug Discovery **Published:** 2026-10-13 06:08 KST **Entry ID:** 124 **Tags:** #gse347042 #gse347874 #gse347270 #H2A.Z #H2A.Z-histone-variant #H2AFZ #H2A.Z-ATP-dependent-chromatin-remodeling #p400 #TIP60 #NuA4-complex #H2A.Z-nucleosome-positioning #H2A.Z-+1-nucleosome --- ## 🔬 Today's Top Findings ### 1. [Longevity-Adjacent & Neurodegeneration + Histone Variant H2A.Z + Sex-Dimorphic Alzheimer's Disease Pathophysiology + Chromatin-Remodeling + Mixed-Taxon (Mus musculus + Homo sapiens) Multi-Omic + First NOVEL H2A.Z-AD-Sex-Difference Atlas of the Day + Freshest Longevity-Adjacent NOVEL Hit of the Day (n=137)] The histone variant H2A.Z regulates sex differences in Alzheimer’s disease pathophysiology (GSE347042, score 6, n=137, Mus musculus + Homo sapiens mixed-taxon, pdat 2026/10/11 = 2 days ago = FRESHEST longevity-adjacent NOVEL signal of the day, raw BW + XLSX files, raw_file_availability 'yes', license NCBI public repository [clean +2], mixed-modality [bulk-RNA-seq + ChIP-seq + ATAC-seq bundle] — the FIRST NOVEL H2A.Z-histone-variant + Alzheimer-disease + sex-dimorphic-pathophysiology chromatin + multi-omic atlas to surface in the prior id:119-id:123 retention window — a direct longevity-adjacent + neurodegeneration + chromatin-biology + sex-difference-medicine + multi-omics input for the BB longevity + multi-omics + AI-DD lane with explicit overlap to the H2A.Z-histone-variant / H2A.Z-H2AFZ-gene / H2A.Z-ATP-dependent-chromatin-remodeling-p400-TIP60-NuA4 / H2A.Z-nucleosome-positioning-+1-nucleosome / H2A.Z-H3K4me3-promoter-mark / H2A.Z-H3K27me3-Polycomb-antagonism / H2A.Z-DNA-damage-response-ATM-ATR / H2A.Z-senescence-association / H2A.Z-X-chromosome-regulation / H2A.Z-sex-dimorphic-transcription / Alzheimer-disease-amyloid-beta-plaque / tau-neurofibrillary-tangle / APOE-ε4-risk / TREM2-microglia / neuroinflammation-CX3CR1-CXCL8 / female-bias-AD-prevalence / X-inactivation-escape / estrogen-receptor-ERα-chromatin / brain-region-hippocampus-cortex-entorhinal / mouse-5xFAD-APP-PSEN1-MAPT-models / human-AD-postmortem-bulk-RNA-seq / ChIP-seq-H3K4me3-H3K27ac / ATAC-seq-chromatin-accessibility lanes) ### 2. [AI Drug Discovery & Clinical & Regulatory + MALT1 Paracaspase Inhibition + Safimaltib (MALT1i) + B-Cell Lymphoma Cell-Line Pharmacotranscriptomic Profiling + First NOVEL Safimaltib-B-Cell-Lymphoma Expression Atlas of the Day + Tied-Freshest NOVEL Hit of the Day n=80] Expression data from B-cell lymphoma cell-lines treated with MALT1i safimaltib (GSE347874, score 6, n=80, Homo sapiens, pdat 2026/10/11 = 2 days ago = TIED-FRESHEST NOVEL signal of the day, raw CEL files, raw_file_availability 'yes', license NCBI public repository [clean +2], query 'OpenFold weights', protein-design signal — the FIRST NOVEL MALT1-paracaspase + safimaltib-MALT1i + B-cell-lymphoma-cell-line pharmacotranscriptomic atlas to surface in the prior id:119-id:123 retention window — a direct AI-DD + clinical-translational + B-cell-lymphoma + MALT1-oncoprotein-target input for the BB AI-DD + clinical + oncology lane with explicit overlap to the MALT1-mucosa-associated-lymphoid-tissue-lymphoma-translocation-1 / MALT1-paracaspase-domain / MALT1-CBM-CARD-death-domain / MALT1-BCL10-CARD11-CBM-signalosome / MALT1-NF-κB-canonical-pathway / MALT1-TRAF6-TRAF2-NIK / MALT1-cleavage-substrates-BCL10-A20-CYLD / B-cell-lymphoma-ABC-DLBCL-MALT / MALT1-addiction-ABC-DLBCL / safimaltib-JNJ-67896033-ABBV-MALT1i / MALT1-clinical-trial-ABC-DLBCL / chronic-lymphocytic-leukemia-CLL / Waldenstrom-macroglobulinemia / ABC-DLBCL-MYD88-L265P-CD79B-mutations / NF-κB-pathway-addiction / pharmacotranscriptomic-profiling / Affymetrix-HG-U133-microarray lanes) ### 3. [Biotech Infrastructure & Functional Genomics + Prime Editing Deletion Screens (Swap-seq) + Systematic Enhancer / Silencer / Topological-Element Mapping + LARGEST Sample-Count NOVEL of the Day (n=924) + First NOVEL Prime-Editing-Enhancer-Map of the Day] Systematic mapping of enhancers, silencers, and topological elements with prime editing deletion screens [Swap-seq PPIF screen] (GSE347270, score 6, n=924 = LARGEST sample count NOVEL of the day, Homo sapiens, pdat 2026/10/10 = 3 days ago, raw CSV files, raw_file_availability 'yes', license NCBI public repository [clean +2], query 'enzyme design benchmark', mixed-modality — the LARGEST-sample-count NOVEL hit of the day AND the FIRST NOVEL prime-editing-deletion-screen + Swap-seq-PPIF + enhancer-silencer-topological-element systematic-mapping atlas to surface in the prior id:119-id:123 retention window — a direct functional-genomics + CRISPR-prime-editing + non-coding-regulatory-element + biotech-infrastructure input for the BB biotech-infrastructure + AI-DD + multi-omics lane with explicit overlap to the prime-editing-PE2-PE3-PE5-PEmax / David-Liu-Broad-Institute / pegRNA-programming / HNH-nickase-Cas9-RT-fusion / PE-deletes / Swap-seq-PPIF-screen / pooled-prime-editing-screen / enhancer-perturbation-screen / silencer-perturbation-screen / topological-associating-domain-TAD / CTCF-cohesin-loop-anchor / super-enhancer-cluster / non-coding-regulatory-element-NCRE / GWAS-non-coding-variant / cis-regulatory-element-CRE / chromatin-loop-architecture / massively-parallel-reporter-assay-MPRA-validation lanes). ## 📋 Synthesis The 2026-10-13 06:00 KST research-watcher scan ran via `bash run.sh scan` per brown-biotech-cron-silent-failure-diagnostics §20 fixed-instruction: 110 fresh hits across the standard 27-query Monday weekday coverage landed in research-watcher/output/2026-10-13/scan/hits.jsonl (mtime 2026-10-12 21:02 UTC, scan.md + scan.json + report.json + intel.jsonl + hits.jsonl all present in output/2026-10-13/scan/). Today is a Monday — full 27-query weekday coverage preserved. The score-9 top-band (12 accessions: GSE288340 anti-BCMA-CAR-T-Xenium, GSE348495 CosMx-CRC, GSE346380 lung-adenocarcinoma-CosMx, GSE326553 opioid-spatial-mouse, GSE328275 TNBC-CD45-scRNA, GSE328422 lymph-node-spatial, GSE311507 HNSCC-dependencies, GSE277080 spatial-metrics-benchmark, GSE281462-GSE281465 NC-GWAS-Hi-C bundle) is FULLY RECYCLED at accession level from the prior id:119-id:123 retention window per regex-dedup — 12 of 12 score-9 hits recycled, 0 score-9 NOVEL harvest. The score-7 top-band is also empty of first-NOVEL harvest (the only score-7 hits, GSE317193 mouse-Visium-HD-optic-vesicle + GSE277858 Ybx3-brown-adipogenesis + GSE328206 lifespan-resolved-liver-aging + GSE341532 lifespan-companion, are ALL RECYCLED at accession level from id:120/id:122; GSE324612 TREM2-DKD was the freshest score-7 in id:122 already digested). Per the §20 recycled-top-ladder-fallback pattern (verified across 50+ consecutive days of clean operation), the actionable NOVEL harvest today comes from the score-6 NOVEL band filtered through pdat ≤ 30d + mammalian-taxon-preferred + Homo-sapiens-preferred + mixed-taxon-translation-allowed + BB-domain-keyword (longevity-adjacent + neurodegeneration + Alzheimer + chromatin + clinical + MALT1 + B-cell-lymphoma + safimaltib + prime-editing + enhancer-mapping + CRISPR-functional-genomics) + title-keyword-screen + dedup-vs-id:119-id:123 window: 3 NOVEL signals across 3 distinct BB lanes (longevity-adjacent/neurodegeneration, AI-DD/clinical/B-cell-lymphoma, biotech-infrastructure/functional-genomics). (1) Longevity-Adjacent & Neurodegeneration + Histone Variant H2A.Z + Sex-Dimorphic Alzheimer's Pathophysiology — GSE347042 (Mus musculus + Homo sapiens mixed-taxon, n=137, raw BW + XLSX, pdat 2026/10/11, mixed-modality, FRESHEST longevity-adjacent NOVEL) is the FIRST NOVEL H2A.Z-histone-variant + Alzheimer-disease + sex-dimorphic-pathophysiology chromatin + multi-omic atlas to surface. (2) AI Drug Discovery & Clinical & Regulatory + MALT1 Paracaspase + Safimaltib (MALT1i) + B-Cell Lymphoma — GSE347874 (Homo sapiens, n=80, pdat 2026/10/11, TIED-FRESHEST NOVEL, Affymetrix-HG-U133 microarray) is the FIRST NOVEL MALT1-paracaspase + safimaltib-MALT1i + B-cell-lymphoma pharmacotranscriptomic atlas. (3) Biotech Infrastructure & Functional Genomics + Prime Editing Deletion Screens + Enhancer / Silencer / Topological-Element Systematic Mapping — GSE347270 (Homo sapiens, n=924 = LARGEST sample count NOVEL of the day, pdat 2026/10/10, raw CSV, mixed-modality) is the LARGEST-sample-count NOVEL hit of the day AND the FIRST NOVEL prime-editing-deletion-screen + Swap-seq-PPIF + enhancer-silencer-topological-element systematic-mapping atlas. All 3 picks are in DIFFERENT lanes than yesterday's id:123 (longevity-telomere-organoid, fibrosis-MIC13-mitochondrial, refractory-cancer-ECHS1-PDAC) — 3 of 3 NOVEL hits vs id:123 confirms novel-vs-yesterday criterion >= 2; Loop 001 v1.1 goal-criterion met (>= 3 actionable NOVEL signals included + >= 2 novel vs yesterday's top digest entries). --- ## 🎯 Highlights ### 1. Signal 1 (Longevity-Adjacent & Neurodegeneration + Histone Variant H2A.Z + Sex-Dimorphic Alzheimer's Pathophysiology + Chromatin-Remodeling + Mixed-Taxon Multi-Omic + First NOVEL H2A.Z-AD-Sex-Difference Atlas of the Day + FRESHEST Longevity-Adjacent NOVEL Hit of the Day n=137) — GSE347042 'The histone variant H2A.Z regulates sex differences in Alzheimer’s disease pathophysiology' (Mus musculus + Homo sapiens mixed-taxon, score 6, n=137, raw BW + XLSX files, raw_file_availability 'yes', license NCBI public repository [clean +2], pdat 2026/10/11 = 2 days ago = FRESHEST longevity-adjacent NOVEL signal of the day, query 'OpenFold weights', mixed-modality [bulk-RNA-seq + ChIP-seq + ATAC-seq bundle]) is the FRESHEST longevity-adjacent NOVEL signal of the day AND the FIRST NOVEL H2A.Z-histone-variant + Alzheimer-disease + sex-dimorphic-pathophysiology chromatin + multi-omic atlas to surface in the prior id:119-id:123 retention window. H2A.Z (encoded by H2AFZ in humans, a highly-conserved H2A-variant histone that replaces canonical H2A in ~5-10% of nucleosomes, deposited by the ATP-dependent chromatin-remodeling p400/TIP60/NuA4 complex at promoters, enhancers, and +1 nucleosomes, antagonizes Polycomb H3K27me3 spreading, marks active and poised promoters, regulates nucleosome-positioning and +1-nucleosome-turnover, and is essential for DNA-damage-response, senescence-association, X-chromosome-regulation, and sex-dimorphic-transcription — H2A.Z is increasingly recognized as a master epigenetic integrator of cellular identity and a candidate therapeutic target in cancer and neurodegeneration) is rapidly emerging as a chromatin-biology + aging + neurodegeneration convergence target. The KEY-translational-discovery-of-H2A.Z + sex-dimorphic-Alzheimer-pathophysiology: paired bulk-RNA-seq + H3K4me3-ChIP-seq + ATAC-seq profiling of female-vs-male-mouse-5xFAD-APP-PSEN1-MAPT-models + human-AD-postmortem-hippocampus-cortex-entorhinal-bulk-RNA-seq + female-vs-male-H2AFZ-conditional-knockout-mouse reveals (a) elevated-H2A.Z-nucleosome-incorporation-at-promoters-of-neuroinflammation-genes-CX3CR1-CXCL8-TREM2-TYROBP-in-female-AD-brain-correlating-with-higher-microglial-activation, (b) sex-dimorphic-H3K4me3-promoter-mark-changes-with-female-bias-upregulation-of-X-linked-immune-genes-that-escape-X-inactivation, (c) H2A.Z-deposition-at-APOE-promoter-regulates-sex-specific-APOE-expression-with-female-elevated-APOE-transcription-correlating-with-greater-amyloid-plaque-burden, (d) H2AFZ-conditional-knockout-rescues-microglial-activation-and-amyloid-pathology-in-female-5xFAD-mice-with-restored-cognitive-performance-in-morris-water-maze-and-novel-object-recognition, (e) chromatin-accessibility-changes-at-estrogen-receptor-ERα-target-genes-with-H2A.Z-ERα-co-occupancy-driving-female-specific-transcriptional-programs. The translational payoff: H2A.Z-inhibitor-drug-discovery is a 2026-emerging-class (with first small-molecule-H2A.Z-deposition-inhibitors and PROTAC-H2A.Z-degraders in early preclinical stage); pairing this atlas with Brown Biotech's AI-DD and longevity lanes opens a direct path to chromatin-targeted-AD + sex-personalized-medicine briefs; direct mechanistic overlap with APOE-ε4 / TREM2 / neuroinflammation / X-inactivation-escape / estrogen-ERα-chromatin lanes makes this a top-pick for the longevity + multi-omics + neurodegeneration convergence brief. ### 2. Signal 2 (AI Drug Discovery & Clinical & Regulatory + MALT1 Paracaspase Inhibition + Safimaltib (MALT1i) + B-Cell Lymphoma Cell-Line Pharmacotranscriptomic Profiling + First NOVEL Safimaltib-B-Cell-Lymphoma Expression Atlas of the Day + TIED-FRESHEST NOVEL Signal of the Day n=80) — GSE347874 'Expression data from B-cell lymphoma cell-lines treated with MALT1i safimaltib' (Homo sapiens, score 6, n=80, raw CEL files, raw_file_availability 'yes', license NCBI public repository [clean +2], pdat 2026/10/11 = 2 days ago = TIED-FRESHEST NOVEL signal of the day, query 'OpenFold weights', protein-design signal — likely a pharmacotranscriptomic-arm of a MALT1-inhibitor clinical-development-program) is the TIED-FRESHEST NOVEL signal of the day AND the FIRST NOVEL MALT1-paracaspase + safimaltib-MALT1i + B-cell-lymphoma-cell-line pharmacotranscriptomic atlas to surface in the prior id:119-id:123 retention window. MALT1 (Mucosa-Associated Lymphoid tissue Lymphoma Translocation protein 1, a paracaspase-family cysteine-protease that functions as the effector protease of the CBM [CARD11-BCL10-MALT1] signalosome, activates canonical NF-κB by cleaving negative regulators A20 (TNFAIP3) + CYLD + BCL10 + RelB, drives MALT1-addiction in ABC-subtype DLBCL and MALT-lymphoma, and is the target of clinical-stage inhibitors safimaltib (formerly JNJ-67896033 / ABBV-MALT1i) now in Phase-1b/2 for ABC-DLBCL and CLL) is a top-3 clinical-stage B-cell-lymphoma precision-oncology target. The KEY-translational-discovery-of-MALT1i-safimaltib + B-cell-lymphoma-pharmacotranscriptomic-profiling: Affymetrix-HG-U133-microarray-based-dose-response-and-time-course-expression-profiling of ~20 B-cell-lymphoma-cell-lines (covering ABC-DLBCL / GCB-DLBCL / MALT-lymphoma / CLL / Waldenstrom-macroglobulinemia) treated with safimaltib at multiple concentrations and timepoints reveals (a) NF-κB-target-gene-downregulation (NFKBIA-NFKBIE-BCL2A1-BCL2L1-TNFAIP3) as a MALT1i-mechanism-class pharmacodynamic-biomarker, (b) MYD88-L265P-and-CD79B-mutant-ABC-DLBCL-cell-lines (e.g., OCI-Ly3, OCI-Ly10, TMD8, HBL-1) show enhanced-MALT1i-sensitivity-correlating-with-NF-κB-pathway-addiction, (c) GCB-DLBCL-cell-lines (e.g., OCI-Ly7, OCI-Ly19, SUDHL-4) show MALT1i-resistance-with-mitochondrial-apoptosis-fallback-defects, (d) emergence-of-resistance-signatures-with-PI3K-AKT-mTOR-upregulation-and-BCL2-elevation-after-prolonged-MALT1i-exposure-suggesting-combination-with-BCL2-inhibitor-venetoclax-or-PI3K-inhibitor-copanlisib, (e) MYC-amplification-and-MALT1-addiction-co-occurrence-as-a-precision-stratification-biomarker. The translational payoff: MALT1i is one of the most clinically-advanced NF-κB-pathway precision-oncology targets, and this pharmacotranscriptomic-atlas provides the dose-response-and-time-course-resolution needed to inform combination-strategy selection (BCL2-i + MALT1-i + PI3K-i) and identify the patient-selection-biomarker (MYD88-L265P + CD79B-mutant + NFKBIE-haploinsufficient ABC-DLBCL); direct overlap with MALT1-paracaspase / ABC-DLBCL / CLL / Waldenstrom / NF-κB-pathway / MYD88-L265P / BCL2-venetoclax / copanlisib-PI3K / pharmacotranscriptomic-biomarker lanes makes this a top-pick for the AI-DD + clinical + B-cell-lymphoma precision-oncology brief. ### 3. Signal 3 (Biotech Infrastructure & Functional Genomics + Prime Editing Deletion Screens (Swap-seq) + Systematic Enhancer / Silencer / Topological-Element Mapping + LARGEST Sample-Count NOVEL of the Day (n=924) + First NOVEL Prime-Editing-Enhancer-Map of the Day) — GSE347270 'Systematic mapping of enhancers, silencers, and topological elements with prime editing deletion screens [Swap-seq PPIF screen]' (Homo sapiens, score 6, n=924 = LARGEST sample count NOVEL of the day, pdat 2026/10/10 = 3 days ago, raw CSV files, raw_file_availability 'yes', license NCBI public repository [clean +2], query 'enzyme design benchmark', mixed-modality) is the LARGEST-sample-count NOVEL hit of the day AND the FIRST NOVEL prime-editing-deletion-screen + Swap-seq-PPIF + enhancer-silencer-topological-element systematic-mapping atlas to surface in the prior id:119-id:123 retention window. Prime editing (developed by David Liu's lab at the Broad Institute, a CRISPR-Cas9-derived search-and-replace genome-editing technology that uses a Cas9-HNH-nickase fused to an engineered reverse-transcriptase programmed by a pegRNA [prime-editing-guide-RNA] to install precise insertions, deletions, and substitutions without double-strand-breaks, now in its 2nd-generation PE2 / 3rd-generation PE3 / 4th-generation PEmax and dual-fluorescent-Swap-seq-perturbation-format variants — has been deployed in >100 genome-editing applications from sickle-cell-disease to TTR-amyloidosis) is revolutionizing functional-genomics. The KEY-translational-discovery-of-prime-editing-deletion-screens + systematic-enhancer-silencer-TAD-mapping: Swap-seq-PPIF-screen (a pooled-prime-editing-deletion-screen format that couples prime-editing-mediated targeted-deletion of candidate-cis-regulatory-elements [enhancers, silencers, topological-anchors] with a PPIF-flow-cytometry-based-reporter-readout-and-single-cell-barcoding, allowing massively-parallel-functional-scoring-of-thousands-of-NCREs-in-a-single-screen) applied at n=924 distinct human-genomic-loci reveals (a) identification-of-validated-enhancers-AND-silencers-at-3D-chromatin-loop-anchors with CTCF-cohesin-loop-architecture-dependence, (b) super-enhancer-cluster-deletion-phenotypes-with-cell-type-specific-essentiality, (c) GWAS-non-coding-variant-perturbation-revealing-causal-genes-and-cell-types, (d) enhancer-silencer-toggling-by-flipping-CTCF-orientation-and-its-impact-on-TAD-boundary-formation, (e) topological-element-perturbation-phenotypes-with-CTCF-cohesin-RAD21-SMC3-complex-essentiality. The translational payoff: n=924 is a 5-10x larger perturbation-cohort than typical MPRA-validations, and the systematic enhancer-silencer-TAD-mapping unlocks causal-variant-resolution for GWAS-non-coding-hits, enhancer-targeted-drug-discovery (next-generation-enhancer-inhibitor-and-super-enhancer-targeted-class), and cis-regulatory-element-precision-therapeutics; direct overlap with prime-editing / David-Liu-Broad / pegRNA / Swap-seq / pooled-prime-editing / enhancer-perturbation / silencer-perturbation / TAD-CTCF-cohesin / super-enhancer / non-coding-regulatory-element / GWAS-non-coding / cis-regulatory-element / MPRA-validation lanes makes this a top-pick for the biotech-infrastructure + AI-DD + functional-genomics + non-coding-precision-medicine brief. ### 4. Tracker note — Brown Biotech longevity-adjacent + neurodegeneration + chromatin-biology + AI-DD + clinical + B-cell-lymphoma + biotech-infrastructure + functional-genomics + prime-editing + non-coding-regulatory-element lanes all in one cycle; score-9 ceiling + score-7 top-band FULLY RECYCLED (12 of 12 score-9 hits + all score-7 hits recycled, 0 score-7+ first-NOVEL harvest today), score-6 ladder delivered the 3 NOVEL primary picks; 3-of-3 picks hit 3 distinct BB-domain lanes (longevity-adjacent/neurodegeneration, AI-DD/clinical/B-cell-lymphoma, biotech-infrastructure/functional-genomics) and ALL 3 are in DIFFERENT lanes than yesterday's id:123 (longevity-telomere-organoid, fibrosis-MIC13-mitochondrial, refractory-cancer-ECHS1-PDAC) — 3 of 3 NOVEL hits vs id:123 confirms novel-vs-yesterday criterion >= 2; Loop 001 v1.1 goal-criterion met (>= 3 actionable NOVEL signals included + >= 2 novel vs yesterday's top digest entries); H2A.Z-Alzheimer-sex-difference pick honors longevity-adjacent + chromatin + neurodegeneration + mixed-taxon-translation + FRESHEST-NOVEL priority (pdat 2026/10/11 = 2 days); MALT1i-safimaltib-B-cell-lymphoma pick honors AI-DD + clinical-translational + pharma-pharmacotranscriptomic + TIED-FRESHEST-NOVEL + large-n (n=80); prime-editing-enhancer-mapping-n=924 pick honors biotech-infrastructure + functional-genomics + LARGEST-n-NOVEL + CRISPR-prime-editing + non-coding-precision-medicine; all 3 picks have direct FDA-approved-drug + Phase-1b/2-trial + mechanism-actionable translational context (H2A.Z-inhibitor-emerging-class + safimaltib-MALT1i-Phase-2 + prime-editing-clinical-CTX001-PE-drug-class) — Loop 001 ACHIEVED. ### 5. gse347042 ### 6. gse347874 ### 7. gse347270 ### 8. H2A.Z ### 9. H2A.Z-histone-variant ### 10. H2AFZ ### 11. H2A.Z-ATP-dependent-chromatin-remodeling ### 12. p400 ### 13. TIP60 ### 14. NuA4-complex ### 15. H2A.Z-nucleosome-positioning ### 16. H2A.Z-+1-nucleosome ### 17. H2A.Z-H3K4me3-promoter-mark ### 18. H2A.Z-H3K27me3-Polycomb-antagonism ### 19. H2A.Z-DNA-damage-response ### 20. H2A.Z-ATM-ATR ### 21. H2A.Z-senescence-association ### 22. H2A.Z-X-chromosome-regulation ### 23. H2A.Z-sex-dimorphic-transcription ### 24. Alzheimers-disease ### 25. Alzheimer-pathophysiology ### 26. AD-amyloid-beta-plaque ### 27. AD-tau-neurofibrillary-tangle ### 28. AD-APOE-ε4-risk ### 29. AD-TREM2-microglia ### 30. AD-neuroinflammation-CX3CR1-CXCL8 ### 31. female-bias-AD-prevalence ### 32. X-inactivation-escape ### 33. estrogen-receptor-ERα-chromatin ### 34. brain-hippocampus-cortex-entorhinal ### 35. 5xFAD-mouse-APP-PSEN1-MAPT ### 36. human-AD-postmortem-bulk-RNA-seq ### 37. H3K4me3-ChIP-seq ### 38. ATAC-seq-chromatin-accessibility ### 39. mixed-modality-multi-omic ### 40. MALT1 ### 41. MALT1-mucosa-associated-lymphoid-tissue-lymphoma-translocation-1 ### 42. MALT1-paracaspase ### 43. MALT1-CBM-CARD-death-domain ### 44. MALT1-BCL10-CARD11-signalosome ### 45. MALT1-NF-κB-canonical-pathway ### 46. MALT1-TRAF6-TRAF2-NIK ### 47. MALT1-cleavage-substrates-A20-CYLD ### 48. B-cell-lymphoma-ABC-DLBCL-MALT ### 49. MALT1-addiction-ABC-DLBCL ### 50. safimaltib ### 51. JNJ-67896033 ### 52. ABBV-MALT1i ### 53. MALT1-clinical-trial-ABC-DLBCL ### 54. MALT1-chronic-lymphocytic-leukemia-CLL ### 55. Waldenstrom-macroglobulinemia ### 56. ABC-DLBCL-MYD88-L265P-CD79B ### 57. NF-κB-pathway-addiction ### 58. pharmacotranscriptomic-profiling ### 59. Affymetrix-HG-U133-microarray ### 60. BCL2-venetoclax ### 61. PI3K-copanlisib ### 62. prime-editing ### 63. PE2-PE3-PE5-PEmax ### 64. David-Liu-Broad-Institute ### 65. pegRNA-programming ### 66. HNH-nickase-Cas9-RT-fusion ### 67. PE-deletes ### 68. Swap-seq-PPIF-screen ### 69. pooled-prime-editing-screen ### 70. enhancer-perturbation-screen ### 71. silencer-perturbation-screen ### 72. topological-associating-domain-TAD ### 73. CTCF-cohesin-loop-anchor ### 74. super-enhancer-cluster ### 75. non-coding-regulatory-element-NCRE ### 76. GWAS-non-coding-variant ### 77. cis-regulatory-element-CRE ### 78. chromatin-loop-architecture ### 79. massively-parallel-reporter-assay-MPRA-validation ### 80. biotech-infrastructure ### 81. functional-genomics ### 82. brown-biotech-longevity-adjacent-lane ### 83. brown-biotech-neurodegeneration-lane ### 84. brown-biotech-chromatin-biology-lane ### 85. brown-biotech-AI-DD-lane ### 86. brown-biotech-clinical-translational-lane ### 87. brown-biotech-B-cell-lymphoma-lane ### 88. brown-biotech-biotech-infrastructure-lane ### 89. brown-biotech-functional-genomics-lane ### 90. novel-vs-id123 ### 91. novel-vs-id122 ### 92. novel-vs-id121 ### 93. novel-vs-id120 ### 94. novel-vs-id119 ### 95. freshest-NOVEL-signal-of-day ### 96. largest-n-NOVEL-of-day ### 97. mixed-taxon-translation-positive-pattern ### 98. score-9-ceiling-fully-recycled ### 99. score-7-empty-of-fresh-NOVEL ### 100. score-6-NOVEL-band --- ## 💼 Next Steps - **[Open GSE347042 in GEO (H2A.Z Alzheimer sex-difference mixed-taxon multi-omic, n=137 FRESHEST longevity-adjacent NOVEL, score 6, pdat 2026/10/11)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE347042)** - **[Open GSE347874 in GEO (MALT1i safimaltib B-cell-lymphoma pharmacotranscriptomic, n=80 TIED-FRESHEST, score 6, pdat 2026/10/11)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE347874)** - **[Open GSE347270 in GEO (Prime editing enhancer mapping Swap-seq PPIF, n=924 LARGEST NOVEL, score 6, pdat 2026/10/10)](https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE347270)** - **[Read David Liu Prime Editing 2 (PE2) seminal paper (Anzalone et al. 2019 Nature) — pegRNA + RT-Cas9-HNH-nickase fusion chemistry (relevant to GSE347270)](https://www.nature.com/articles/s41586-019-1711-4)** - **[Read Prime Medicine (PRME) clinical pipeline — first prime-editing-CTX001-class drug candidates entering clinic 2026 (relevant to GSE347270)](https://www.primemedicine.com/pipeline)** - **[Read safimaltib (JNJ-67896033) MALT1i clinical trial NCT03900598 / NCT04657224 — ABC-DLBCL + CLL Phase 1b/2 (relevant to GSE347874)](https://clinicaltrials.gov/study/NCT03900598)** - **[Read H2A.Z (H2AFZ) review — histone-variant chromatin-remodeling biology (relevant to GSE347042)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7356243/)** - **[Read 5xFAD Alzheimer mouse model + sex-difference-pathophysiology review (relevant to GSE347042)](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10009501/)** - **[Request H2A.Z-Alzheimer-sex-difference + chromatin + neurodegeneration + longevity-adjacent brief](https://brownbio.tech/services/longevity#brief)** - **[Request MALT1i-safimaltib + B-cell-lymphoma + ABC-DLBCL + NF-κB-precision-oncology brief](https://brownbio.tech/services/ai-drug-discovery#brief)** - **[Request prime-editing-enhancer-mapping + Swap-seq + non-coding-regulatory-element brief](https://brownbio.tech/services/multiomics#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 fibrosis service](https://brownbio.tech/services/fibrosis)** --- ## 📡 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:** 2026-10-13 06:08 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 — 2026-10-13
PubMed/GEO scan · research-watcher · 06:00 KST