{"id":919,"date":"2022-01-24T12:28:30","date_gmt":"2022-01-24T03:28:30","guid":{"rendered":"https:\/\/shibataxlab.com\/english\/?page_id=919"},"modified":"2025-07-26T12:03:47","modified_gmt":"2025-07-26T03:03:47","slug":"check-papers","status":"publish","type":"page","link":"https:\/\/shibataxlab.com\/english\/?page_id=919","title":{"rendered":"Pickup Papers"},"content":{"rendered":"

2025\u5e74\uff0d\uff0d\uff0d\uff0d
\n<\/strong>Comprehensive whole-genome sequencing reveals origins of mutational signatures associated with aging, mismatch repair deficiency and temozolomide chemotherapy,\u00a0<\/span>NAR<\/strong><\/p>\n

<\/strong>Spatial transcriptomic analysis of immune checkpoint blockade response in triple negative breast cancers containing tertiary lymphoid structures,\u00a0<\/span>iScience<\/strong><\/p>\n

Transcriptional repression facilitates RNA:DNA hybrid accumulation at DNA double-strand break,\u00a0<\/span>NCB<\/strong><\/p>\n

CTC1-STN1-TEN1 controls DNA break repair pathway choice via DNA end resection blockade,\u00a0<\/span>Science<\/strong><\/p>\n

Ku limits RNA-induced innate immunity to allow Alu-expansion in primates,\u00a0<\/span>Nature<\/strong><\/p>\n

A dual role of Cohesin in DNA DSB repair,Nat Comm<\/strong><\/p>\n

ARID1A stabilises non-homologous end joining factors at DNA breaks induced by the G4 ligand pyridostatin,bioRxiv<\/strong><\/p>\n

LC8 enhances 53BP1 foci through heterogeneous bridging of 53BP1 oligomers,\u00a0<\/span>eLife<\/strong><\/p>\n

Fluorescence recovery in the Super-Resolution regime reveals subcompartments of 53BP1 foci,\u00a0<\/span>bioRxiv<\/strong><\/p>\n

Nuclear accumulation of YTHDF1 regulates mRNA splicing in the DNA damage response,\u00a0<\/span>Sci Adv<\/strong><\/p>\n

Histone H1 deamidation facilitates chromatin relaxation for DNA repair,\u00a0<\/span>Nature<\/strong><\/p>\n

Mechanism of DNA replication fork breakage and PARP1 hyperactivation during replication catastrophe,\u00a0<\/span>Sci Adv<\/strong><\/p>\n

Mitochondrial DNA released by senescent tumor cells enhances PMN-MDSC-driven immunosuppression through the cGAS-STING pathway,\u00a0<\/span>Immunity<\/strong><\/p>\n

SRSF2 overexpression induces transcription-\/replication-dependent DNA double-strand breaks and interferes with DNA repair pathways to promote lung tumor progression,\u00a0<\/span>NAR Cancer<\/strong><\/p>\n

Mechanisms and regulation of DNA end resection in the maintenance of genome stability,\u00a0<\/span>Nature Reviews Molecular Cell Biology<\/span><\/strong><\/p>\n

Temporal and spatial dynamics of DNA double-strand break repair centers,\u00a0<\/span>DNA Repair<\/strong><\/p>\n

Lipoylation inhibition enhances radiation control of lung cancer by suppressing homologous recombination DNA damage repair,\u00a0<\/span>Sci Adv<\/strong><\/p>\n

WEE1 inhibitors synergise with mRNA translation defects via activation of the kinase GCN2,\u00a0<\/span>bioRxiv<\/strong><\/p>\n

WEE1 inhibitors trigger GCN2-mediated activation of the integrated stress response,\u00a0<\/span>bioRxiv<\/strong><\/p>\n

Engineering mtDNA deletions by reconstituting end joining in human mitochondria,\u00a0<\/span>Cell<\/strong><\/p>\n

Uracil processing by SMUG1 in the absence of UNG triggers homologous recombination and selectively kills BRCA1\/2-deficient tumors,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Mechanism for local attenuation of DNA replication at double-strand breaks,\u00a0<\/span>Nature<\/strong><\/p>\n

Endogenous DNA damage at sites of terminated transcripts,\u00a0<\/span>Nature<\/strong><\/p>\n

DNA break induces rapid transcription repression mediated by proteasome-dependent RNAPII removal,\u00a0<\/span>Cell Rep 2024<\/strong><\/p>\n

Spatial Chromosome Folding and Active Transcription Drive DNA Fragility and Formation of Oncogenic MLL Translocations,\u00a0<\/span>Mol Cell 2019<\/strong><\/p>\n

CHD6 has poly (ADP-ribose)-and DNA-binding domains and regulates PARP1\/2-trapping inhibitor sensitivity via abasic site repair,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Homologous recombination promotes non-immunogenic mitotic cell death upon DNA damage,\u00a0<\/span>NCB<\/strong><\/p>\n

KLF5 loss sensitizes cells to ATR inhibition and is synthetic lethal with ARID1A deficiency,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Inflammatory macrophage dependence on NAD+ salvage is a consequence of reactive oxygen species\u2013mediated DNA damage,\u00a0<\/span>Nat Immunology 2019
\n<\/strong><\/p>\n

2024\u5e74\uff0d\uff0d\uff0d\uff0d<\/strong>
\nExploration of histone protein \u03b3-H2AX as a prognostic factor in soft tissue sarcomas and its association with biological behavior, immune cell environment and survival in leiomyosarcoma,\u00a0<\/span>Int J of Cancer<\/strong><\/p>\n

CXCL12 restricts tumor growth by suppressing the Ras, ERK1\/2, c-Myc, and the immune checkpoint PD-L1 pathways,\u00a0<\/span>PNAS<\/strong><\/p>\n

High expression of H2AX\/\u03b3-H2AX is associated with distinct biological pathway alterations and shorter survival in oropharyngeal squamous cell carcinoma,\u00a0<\/span>Oral Oncolgy<\/strong><\/p>\n

Nuclear PD-L1 triggers tumour-associated inflammation upon DNA damage,\u00a0<\/span>EMBO Rep<\/strong>\uff08\u8056\u30de\u30ea\u30a2\u30f3\u30ca\u533b\u79d1\u5927\u5b66\u306e\u592a\u7530\u5148\u751f\u3068\u4ec1\u5e73\u5148\u751f\u306e\u8ad6\u6587\u3067\u3059\uff09<\/span><\/p>\n

RNA sensing induced by chromosome missegregation augments anti-tumor immunity,\u00a0<\/span>Mol Cell<\/strong>\uff08\u30aa\u30b9\u30b9\u30e1\uff01\u304c\u3093\u7814\u306e\u5317\u5d8b\u4fca\u8f14\u5148\u751f\u304ccorresponding author\u306e\u8ad6\u6587\u3067\u3059\uff09<\/span><\/strong><\/p>\n

Antigen-presenting cell activation requires intrinsic and extrinsic STING signaling after the phagocytosis of DNA-damaged cells,\u00a0<\/span>Science Immunology<\/strong><\/p>\n

Bi-phasic DNA damage and non-canonical replication stress response govern radiation-induced senescence in Glioblastoma,\u00a0<\/span>JCS
\n<\/strong><\/p>\n

ATR inhibition radiosensitizes cells through augmented DNA Damage and G2 cell cycle arrest abrogation,\u00a0<\/span>JCI insight<\/strong><\/p>\n

Identification of the main barriers to Ku accumulation in chromatin,\u00a0<\/span>Cell Rep<\/strong>\u00a0<\/span>(\u5967\u6751\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/strong><\/p>\n

Non-homologous end joining shapes the genomic rearrangement landscape of chromothripsis from mitotic errors,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Unprocessed genomic uracil as a source of DNA replication stress in cancer cells,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

ATR inhibition induces synthetic lethality in mismatch repair-deficient cells and augments immunotherapy,\u00a0<\/span>Gene&Dev<\/strong><\/p>\n

Widespread chromatin context-dependencies of DNA double-strand break repair proteins,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Strand asymmetry in the repair of replication dependent double-strand breaks,\u00a0<\/span>preprint<\/strong><\/p>\n

Evolved histone tail regulates 53BP1 recruitment at damaged chromatin,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

UBE2D3 facilitates NHEJ by orchestrating ATM signalling through multi-level control of RNF168,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Ubiquitin-induced RNF168 condensation promotes DNA double-strand break repair,\u00a0<\/span>PNAS<\/strong><\/p>\n

ATM inhibition exploits checkpoint defects and ATM-dependent double strand break repair in TP53-mutant glioblastoma,\u00a0<\/span>Nat Comm<\/strong><\/strong><\/p>\n

Base excision repair and double strand break repair cooperate to modulate the formation of unrepaired double strand breaks in mouse brain,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

High-complexity of DNA double-strand breaks is key for alternative end-joining choice, Comm Biol<\/strong><\/p>\n

Lamin A\/C facilitates DNA damage response by modulating ATM signaling and homologous recombination pathways,\u00a0<\/span>Anim Cells Syst (Seoul)<\/strong><\/p>\n

DNA double-strand break\u2013capturing nuclear envelope tubules drive DNA repair,\u00a0<\/span>NSMB<\/strong>
\n<\/strong><\/p>\n

HLTF resolves G4s and promotes G4-induced replication fork slowing to maintain genome stability,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Guidelines for minimal information on cellular senescence experimentation in vivo,\u00a0<\/span>Cell<\/strong><\/p>\n

mTORC2-driven chromatin cGAS mediates chemoresistance through epigenetic reprogramming in colorectal cancer,\u00a0<\/span>NCB<\/strong><\/p>\n

NBS1 lactylation is required for efficient DNA repair and chemotherapy resistance,\u00a0<\/span>Nature<\/strong><\/p>\n

Systematic investigation of BRCA1-A, -B, and -C complexes and their functions in DNA damage response and DNA repair,\u00a0<\/span>Oncogene<\/strong><\/p>\n

A non-canonical role for a small nucleolar RNA in ribosome biogenesis and senescence,\u00a0<\/span>Cell<\/strong><\/p>\n

SMARCAL1 is a dual regulator of innate immune signaling and PD-L1 expression that promotes tumor immune evasion,\u00a0<\/span>Cell<\/strong><\/p>\n

DNA break induces rapid transcription repression mediated by proteasome-dependent RNAPII removal,\u00a0<\/span>Cell Reports<\/strong><\/p>\n

CCAR1 promotes DNA repair via alternative splicing,\u00a0<\/span>Molecular Cell<\/strong><\/p>\n

Circadian PERIOD proteins regulate TC-DSB repair through 2 anchoring to the nuclear envelope,\u00a0<\/span>bioRxiv<\/strong><\/p>\n

Structure and repair of replication-coupled DNA breaks,\u00a0<\/span>Science<\/strong>\u00a0(\u2190\u8ab0\u304b\u8ad6\u6587\u7d39\u4ecb\u3057\u3066\u304f\u308c\u307e\u3059\u304b\u306d\u3001\u3001)<\/span>
\n<\/strong>
\nInherited C-terminal TREX1 variants disrupt homology-directed repair to cause senescence and DNA damage phenotypes in Drosophila, mice, and humans,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Tumor-associated neutrophil precursors impair homologous DNA repair and promote sensitivity to PARP-inhibition,\u00a0<\/span>Preprint (Research Square)<\/strong><\/p>\n

Heterochromatic 3D genome organization is directed by HP1a- and H3K9-dependent and independent mechanisms,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Micronuclei induced by radiation, replication stress, or chromosome segregation errors do not activate cGAS-STING, Mol Cell<\/strong>\u00a0<\/span>(\u9928\u91ce\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/p>\n

Homologous recombination promotes mitotic death to suppress the innate immune response,\u00a0<\/span>bioRxiv<\/strong><\/p>\n

The CRL5\u2013SPSB3 ubiquitin ligase targets nuclear cGAS for degradation,\u00a0<\/span>Nature<\/strong><\/p>\n

DNA-PK participates in pre-rRNA biogenesis independent of DNA double-strand break repair,\u00a0<\/span>NAR<\/strong><\/p>\n

ARID1A regulates DNA repair through chromatin organization and its deficiency triggers DNA damage-mediated anti-tumor immune response,\u00a0<\/span>NAR<\/strong><\/p>\n

Passive smoking-induced mutagenesis as a promoter of lung carcinogenesis,\u00a0<\/span>Journal of Thoracic Oncology<\/strong><\/p>\n

PARP1-DNA co-condensation drives DNA repair site assembly to prevent disjunction of broken DNA ends,\u00a0<\/span>Cell<\/strong><\/p>\n

Irradiated Tumour Cell-Derived Microparticles Upregulate MHC-I Expression in Cancer Cells via DNA Double-Strand Break Repair Pathway,\u00a0<\/span>Cancer Letters<\/strong><\/p>\n

Formation of memory assemblies through the DNA-sensing TLR9 pathway,\u00a0<\/span>Nature<\/strong>\u00a0(\u6d45\u7530\u5148\u751f\u3001GDN journal\u3067\u306e\u3054\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/p>\n

Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration,\u00a0<\/span>Cell<\/strong>\u00a0(\u6797\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/p>\n

Mitochondrial DNA damage triggers spread of Parkinson\u2019s disease-like pathology,\u00a0<\/span>Molecular Psychiatry<\/strong><\/p>\n

Transcription-coupled repair of DNA\u2013protein cross-links depends on CSA and CSB,\u00a0<\/span>NCB<\/strong><\/p>\n

BLM helicase unwinds lagging strand substrates to assemble the ALT telomere damage response,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

The SPATA5-SPATA5L1 ATPase complex directs replisome proteostasis to ensure genome integrity,\u00a0<\/span>Cell<\/strong><\/p>\n

NFATC2IP is a mediator of SUMO-dependent genome integrity,\u00a0<\/span>Genes & Development<\/strong><\/p>\n

VCF1 is a p97\/VCP cofactor promoting recognition of ubiquitylated p97-UFD1-NPL4 substrates,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

SMARCAL1 ubiquitylation controls its association with RPA-coated ssDNA and promotes replication fork stability,\u00a0<\/span>PLOS Biology<\/strong><\/p>\n

Genetic determinants of micronucleus formation in vivo,\u00a0<\/span>Nature<\/strong>\u00a0(\u5965\u7530\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/p>\n

Mechanisms of RNF168 nucleosome recognition and ubiquitylation,\u00a0<\/span>Mol Cell
\n<\/strong><\/p>\n

Chromatin Organization after High-LET Irradiation Revealed by Super-Resolution STED Microscopy,\u00a0<\/span>IJMS<\/strong><\/p>\n

Single-cell and spatial profiling identify three response trajectories to pembrolizumab and radiation therapy in triple negative breast cancer,\u00a0<\/span>Cancer Cell<\/strong><\/p>\n

Tumor- and circulating-free DNA methylation identifies clinically relevant small cell lung cancer subtypes,\u00a0<\/span>Cancer Cell<\/strong><\/p>\n

EXO1-mediated ssDNA gap expansion is essential for ATR activation and to maintain viability in BRCA1-deficient cells,\u00a0<\/span>bioRxiv<\/strong><\/p>\n

EXO1 protects BRCA1-deficient cells against toxic DNA lesions,\u00a0<\/span>Molecular Cell<\/strong><\/p>\n

APOBEC3A induces DNA gaps through PRIMPOL and confers gap-associated therapeutic vulnerability,\u00a0<\/span>Sci Adv<\/strong>\u00a0(\u2190\u8ab0\u304b\u8ad6\u6587\u7d39\u4ecb\u3057\u3066\u304f\u308c\u307e\u3059\u304b\u306d\u3001\u3001)<\/span><\/p>\n

Aberrant DNA repair reveals a vulnerability in histone H3.3-mutant brain tumors,\u00a0<\/span>NAR<\/strong><\/p>\n

2023\u5e74\uff0d\uff0d\uff0d\uff0d
\n<\/strong>CDC7 inhibition induces replication stress-mediated aneuploid cells with an inflammatory phenotype sensitizing tumors to immune checkpoint blockade,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

DNA double-strand break end synapsis by DNA loop extrusion,\u00a0<\/span>Nat Comm
\n<\/strong>
\nGenome-wide analysis of DNA-PK-bound MRN cleavage products supports a sequential model of DSB repair pathway choice,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Visualization of direct and diffusion-assisted RAD51 nucleation by full-length human BRCA2 protein,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

MutS\u03b2 protects common fragile sites by facilitating homology-directed repair at DNA double-strand breaks with secondary structures,\u00a0<\/span>NAR<\/strong><\/p>\n

Metabolic regulation of homologous recombination repair by MRE11 lactylation,\u00a0<\/span>Cell<\/strong>\u00a0(\u6797\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/p>\n

iMUT-seq: high-resolution DSB-induced mutation profiling reveals prevalent homologous-recombination dependent mutagenesis,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Unrepaired base excision repair intermediates in template DNA strands trigger replication fork collapse and PARP inhibitor sensitivity,\u00a0<\/span>EMBO J<\/strong><\/p>\n

Quantitative, titratable and high-throughput reporter assays to measure DNA double strand break repair activity in cells,\u00a0<\/span>NAR<\/strong><\/p>\n

Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration,\u00a0<\/span>Cell<\/strong><\/p>\n

The chromatin network helps prevent cancer-associated mutagenesis at transcription-replication conflicts,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Chromatin compartmentalization regulates the response to DNA damage,\u00a0<\/span>Nature<\/strong>\u00a0(\u5965\u6751\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span>
\n<\/span>
\n<\/strong>ATR promotes clearance of damaged DNA and damaged cells by rupturing micronuclei,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

DNA damage induces nuclear envelope rupture through ATR-mediated phosphorylation of lamin A\/C,\u00a0<\/span>Mol Cell<\/strong>\u00a0<\/span><\/p>\n

DICER ribonuclease removes harmful R-loops,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Antagonistic roles of canonical and Alternative-RPA in disease-associated tandem CAG repeat instability,\u00a0<\/span>Cell<\/strong><\/p>\n

Pol\u03b8 is phosphorylated by PLK1 to repair double-strand breaks in mitosis,\u00a0<\/span>Nature<\/strong><\/p>\n

MSH2-MSH3 promotes DNA end resection during homologous recombination and blocks polymerase theta-mediated end-joining through interaction with SMARCAD1 and EXO1,\u00a0<\/span>NAR<\/strong><\/p>\n

RAP80 phase separation at DNA double-strand break promotes BRCA1 recruitment,\u00a0<\/span>NAR<\/strong><\/p>\n

GAPDH facilitates homologous recombination repair by stabilizing RAD51 in an HDAC1-dependent manner,\u00a0<\/span>EMBO Rep<\/strong><\/p>\n

ZEB1 promotes non-homologous end joining double-strand break repair,\u00a0<\/span>NAR<\/strong><\/p>\n

DNA-PK is activated by SIRT2 deacetylation to promote DNA double-strand break repair by non-homologous end joining,\u00a0<\/span>NAR<\/strong><\/p>\n

Immunotherapy targeting different immune compartments in combination with radiation therapy induces regression of resistant tumors,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Short Double-Stranded DNA (\u226440-bp) Affects Repair Pathway Choice,\u00a0<\/span>IJMS<\/strong><\/p>\n

Unrepaired base excision repair intermediates in template DNA strands trigger replication fork collapse and PARP inhibitor sensitivity,\u00a0<\/span>EMBO J<\/strong><\/p>\n

The complementarity of DDR, nucleic acids and anti-tumour immunity,\u00a0<\/span>Nature<\/strong><\/p>\n

The interplay between the DNA damage response and ectonucleotidases modulates tumor response to therapy,\u00a0<\/span>Science Immunology<\/strong><\/p>\n

Break-induced replication orchestrates resection-dependent template switching,\u00a0<\/span>Nature<\/strong><\/p>\n

DNA double-strand break end synapsis by DNA loop extrusion,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

ATM phosphorylates the FATC domain of DNA-PKcs at threonine 4102 to promote non-homologous end joining,\u00a0<\/span>NAR<\/strong><\/p>\n

SLFN5-mediated chromatin dynamics sculpt higher-order DNA repair topology,\u00a0<\/span>Mol Cell<\/strong>\u00a0(\u6797\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/p>\n

Sequence and chromatin features guide DNA double-strand break resection initiation,\u00a0<\/span>Mol Cell<\/strong>\u00a0[<\/span>\u304a\u3059\u3059\u3081] (\u5965\u6751\u3055\u3093\u3001\u8b1b\u5ea7\u8ad6\u6587\u7d39\u4ecb\u3067\u306e\u7d39\u4ecb\u3042\u308a\u304c\u3068\u3046\u3054\u3056\u3044\u307e\u3057\u305f)<\/span><\/strong><\/p>\n

Polymerase \u03b8 inhibition activates the cGAS-STING pathway and cooperates with immune checkpoint blockade in models of BRCA-deficient cancer,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

SARS-CoV-2 infection induces DNA damage, through CHK1 degradation and impaired 53BP1 recruitment, and cellular senescence,\u00a0<\/span>NCB<\/strong>\u00a0<\/span>[<\/span>\u304a\u3059\u3059\u3081]<\/span><\/p>\n

Phase separation properties of RPA combine high-affinity ssDNA binding with dynamic condensate functions at telomeres,\u00a0<\/span>NSMB\u00a0<\/span><\/strong>[<\/span>\u304a\u3059\u3059\u3081]<\/span><\/p>\n

DDX47, MeCP2, and other functionally heterogeneous factors protect cells from harmful R loops,\u00a0<\/span>Cell Rep<\/strong><\/p>\n

Antecedent chromatin organization determines cGAS recruitment to ruptured micronuclei,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Metabolic enzyme UAP1 mediates IRF3 pyrophosphorylation to facilitate innate immune response,\u00a0<\/span>Molecular Cell<\/strong><\/p>\n

2022\u5e74\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d
\nHeterochromatic repeat clustering imposes a physical barrier on homologous recombination to prevent chromosomal translocations,\u00a0<\/span>Molecular Cell<\/strong><\/p>\n

ATR-mediated CD47 and PD-L1 up-regulation restricts radiotherapy-induced immune priming and abscopal responses in colorectal cancer,\u00a0<\/span>Science Immunology<\/strong>\u00a0<\/span>[<\/span>\u304a\u3059\u3059\u3081]<\/span><\/p>\n

Single-nucleosome imaging reveals steady-state motion of interphase chromatin in living human cells,\u00a0<\/span>Science Advances<\/strong><\/p>\n

Radiotherapy in combination with CD47 blockade elicits a macrophage-mediated abscopal effect,\u00a0<\/span>Nature Cancer<\/strong><\/p>\n

Tissue fluidification promotes a cGAS\u2013STING cytosolic DNA response in invasive breast cancer,\u00a0<\/span>Nature Materials<\/strong><\/p>\n

R-loop-derived cytoplasmic RNA\u2013DNA hybrids activate an immune response,\u00a0<\/span>Nature<\/strong><\/p>\n

Predicting tumour radiosensitivity to deliver precision radiotherapy,\u00a0<\/span>Nature Reviews Clinical Oncology<\/strong><\/p>\n

The BRCA1 BRCT promotes antisense RNA production and double-stranded RNA formation to suppress ribosomal R-loops,\u00a0<\/span>PNAS<\/strong><\/p>\n

Active DNA demethylation promotes cell fate specification and the DNA damage response,\u00a0<\/span>Science<\/strong><\/p>\n

DNA double-strand break-derived RNA drives TIRR\/53BP1 complex dissociation,\u00a0<\/span>Cell Rep<\/strong><\/p>\n

Blocking PD-L1\u2013PD-1 improves senescence surveillance and ageing phenotypes,\u00a0<\/span>Nature<\/strong><\/p>\n

CtIP-dependent nascent RNA expression flanking DNA breaks guides the choice of DNA repair pathway,\u00a0Nat Comm.<\/strong><\/p>\n

Precision digital mapping of endogenous and induced genomic DNA breaks by INDUCE-seq,\u00a0<\/span>Nat Comm.<\/strong><\/p>\n

Formation of clustered DNA damage in vivo upon irradiation with ionizing radiation: Visualization and analysis with atomic force microscopy,\u00a0<\/span>PNAS<\/strong><\/p>\n

CDYL1-dependent decrease in lysine crotonylation at DNA double-strand break sites functionally uncouples transcriptional silencing and repair,\u00a0<\/span>Mol Cell<\/strong><\/strong><\/p>\n

A POLD3\/BLM dependent pathway handles DSBs in transcribed chromatin upon excessive RNA:DNA hybrid accumulation,\u00a0<\/span>Nat Comm.<\/strong><\/strong><\/p>\n

Bloom helicase mediates formation of large single-stranded DNA loops during DNA end processing,\u00a0<\/span>Nat Comm.<\/strong><\/p>\n

BRD4 promotes resection and homology-directed repair of DNA double-strand breaks,\u00a0<\/span>Nat Comm.<\/strong><\/p>\n

Targeting replication stress in cancer therapy,\u00a0<\/span>Nature Reviews Drug Discovery<\/strong><\/p>\n

Cyclin J\u2013CDK complexes limit innate immune responses by reducing proinflammatory changes in macrophage metabolism,\u00a0<\/span>Science Signaling<\/strong><\/p>\n

S1-END-seq reveals DNA secondary structures in human cells,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

RAD51 protects human cells from transcription-replication conflicts,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Mitotic DNA synthesis is caused by transcription-replication conflicts in BRCA2-deficient cells,\u00a0<\/span>Mol Cell<\/strong>
\n
\n<\/strong>Increasing cell size remodels the proteome and promotes senescence,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Structural mechanism of endonucleolytic processing of blocked DNA ends and hairpins by Mre11-Rad50,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Autologous K63 deubiquitylation within the BRCA1-A complex licenses DNA damage recognition,\u00a0<\/span>JCB<\/strong><\/p>\n

Deciphering the immunopeptidome in vivo reveals new tumour antigens,\u00a0<\/span>Nature<\/strong><\/p>\n

Cancer cells use self-inflicted DNA breaks to evade growth limits imposed by genotoxic stress,\u00a0<\/span>Science<\/strong><\/p>\n

Stalled replication fork protection limits cGAS\u2013STING and P-body-dependent innate immune signalling,\u00a0<\/span>NCB<\/strong><\/p>\n

RIF1-ASF1-mediated high-order chromatin structure safeguards genome integrity,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

Histone chaperone ASF1 acts with RIF1 to promote DNA end joining in BRCA1-deficient cells,\u00a0<\/span>JBC<\/strong><\/p>\n

BRD4 promotes resection and homology-directed repair of DNA double-strand breaks MARCH8 attenuates cGAS-mediated innate immune responses through ubiquitylation,\u00a0<\/span>Science Signaling<\/strong><\/p>\n

STING agonism reprograms tumor-associated macrophages and overcomes resistance to PARP inhibition in BRCA1-deficient models of breast cancer,\u00a0<\/span>Nature Communications<\/strong><\/p>\n

Mre11-Rad50 oligomerization promotes DNA double-strand break repair,\u00a0<\/span>Nature Communications<\/strong><\/p>\n

The use of machine learning to discover regulatory networks controlling biological systems,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Cancer cells use self-inflicted DNA breaks to evade growth limits imposed by genotoxic stress,\u00a0<\/span>Science<\/strong><\/p>\n

H3K4 methylation by SETD1A\/BOD1L facilitates RIF1-dependent NHEJ,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Human topoisomerases and their roles in genome stability and organization,\u00a0<\/span>Nature Review<\/strong>
\n
\n<\/strong>NBS1-CtIP\u2013mediated DNA end resection suppresses cGAS binding to micronuclei,\u00a0<\/span>NAR<\/strong>\u00a0<\/span>[<\/span>\u304a\u3059\u3059\u3081]<\/span><\/p>\n

RIF1 acts in DNA repair through phosphopeptide recognition of 53BP1,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

Telomere dysfunction in ageing and age-related diseases,\u00a0<\/span>Nat Cell Biol, review<\/strong><\/p>\n

The threat of programmed DNA damage to neuronal genome integrity and plasticity,\u00a0<\/span>Nature Genetics<\/strong><\/p>\n

Genetic analysis of cancer drivers reveals cohesin and CTCF as suppressors of PD-L1,\u00a0<\/span>PNAS<\/strong><\/p>\n

BRD4-IRF1 axis regulates chemoradiotherapy-induced PD-L1 expression and immune evasion in non-small cell lung cancer,\u00a0<\/span>Clin. Transl. Med.<\/strong><\/p>\n

Mutations in the adenosine deaminase ADAR1 that prevent endogenous Z-RNA binding induce Aicardi-Gouti\u00e8res syndrome\u2013like encephalopathy,\u00a0<\/span>Immunity<\/strong><\/p>\n

ResOU\u3000https:\/\/resou.osaka-u.ac.jp\/ja<\/a><\/span><\/p>\n

53BP1 regulates heterochromatin through liquid phase separation,\u00a0<\/span>Nat Comm<\/strong><\/p>\n

53BP1\u2013shieldin-dependent DSB processing in BRCA1-deficient cells requires CST\u2013Pol\u03b1\u2013primase fill-in synthesis,\u00a0<\/span>Nature\u00a0<\/span><\/strong>[<\/span>\u304a\u3059\u3059\u3081]<\/span><\/p>\n

cGAS recruitment to micronuclei is dictated by pre-existing nuclear chromatin status,\u00a0<\/span>bioRxiv<\/strong><\/p>\n

Demethylase JMJD2D induces PD-L1 expression to promote colorectal cancer immune escape by enhancing IFNGR1-STAT3-IRF1 signaling,\u00a0<\/span>Oncogene<\/strong><\/p>\n

DNA-PK inhibitor peposertib amplifies radiation-induced inflammatory micronucleation and enhances TGF\u03b2\/PD-L1 targeted cancer immunotherapy,\u00a0<\/span>Mol Can Res<\/strong><\/p>\n

DNA-PK promotes activation of the survival kinase AKT in response to DNA damage through an mTORC2-ECT2 pathway\u00a0<\/span>Science Signaling<\/strong><\/p>\n

EMSY inhibits homologous recombination repair and the interferon response, promoting lung cancer immune evasion,\u00a0<\/span>Cell<\/strong><\/p>\n

Assessing kinetics and recruitment of DNA repair factors using high content screens,\u00a0<\/span>Cell Reports<\/strong><\/p>\n

2021\u5e74\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d
\n<\/strong>Impact of chromatin context on Cas9-induced DNA double-strand break repair pathway balance,\u00a0<\/span>Mol Cell<\/strong>\u00a0[<\/span>\u304a\u3059\u3059\u3081]<\/span><\/strong><\/p>\n

Cas9 deactivation with photocleavable guide RNAs,\u00a0<\/span>Mol Cell<\/strong>\u00a0[<\/span>\u304a\u3059\u3059\u3081]<\/span><\/p>\n

Microenvironmental IL-6 inhibits anti-cancer immune responses generated by cytotoxic chemotherapy,\u00a0<\/span>Nature Communications<\/strong><\/p>\n

Radiation therapy enhances immunotherapy response in microsatellite stable colorectal and pancreatic adenocarcinoma in a phase II trial,\u00a0<\/span>Nat Cancer<\/strong><\/p>\n

Global burden of cancer in 2020 attributable to alcohol consumption: a population-based study,\u00a0<\/span>The Lancet Oncology<\/strong><\/p>\n

cGAS phase separation inhibits TREX1-mediated DNA degradation and enhances cytosolic DNA sensing,\u00a0<\/span>Mol Cell
\n<\/strong>
\nRadiation Therapy Enhances Immunotherapy Response in Microsatellite-stable Colorectal and Pancreatic Adenocarcinoma in a Phase II Trial,\u00a0<\/span>Nat Cancer<\/strong><\/p>\n

Compromised nuclear envelope integrity drives TREX1-dependent DNA damage and tumor cell invasion,\u00a0<\/span>Cell<\/strong><\/p>\n

ER-directed TREX1 limits cGAS activation at micronuclei,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

HELQ is a dual-function DSB repair enzyme modulated by RPA and RAD51,\u00a0<\/span>Nature<\/strong><\/p>\n

RPA phosphorylation facilitates RAD52 dependent homologous recombination in BRCA-deficient cells,\u00a0<\/span>MCB<\/strong><\/p>\n

IFI16 inhibits DNA repair that potentiates type-I interferon-induced antitumor effects in triple negative breast cancer,\u00a0<\/span>Cell Reports
\n<\/strong>
\nGenome instability independent of type I interferon signaling drives neuropathology caused by impaired ribonucleotide excision repair,\u00a0<\/span>Neuron<\/strong>
\nDNA damage rather than type I IFN signaling is the primary mediator of neural dysfunction in Aicardi-Goutie`res syndrome after RNASEH2 disruption,\u00a0<\/span>Neuron (review)<\/strong><\/p>\n

FAM72A antagonizes UNG2 to promote mutagenic repair during antibody maturation,\u00a0<\/span>Nature<\/strong><\/p>\n

The effect of hypoxia on PD-L1 expression in bladder cancer,\u00a0<\/span>BMC Cancer
\n<\/strong>
\nR-loops trigger the release of cytoplasmic ssDNAs leading to chronic inflammation upon DNA damage,\u00a0<\/span>Sci Adv<\/strong><\/p>\n

The ubiquitin E3 ligase FBXO22 degrades PD-L1 and sensitizes cancer cells to DNA damage,\u00a0<\/span>PNAS<\/strong><\/p>\n

DUSP6 regulates radio-sensitivity in glioblastoma by modulating the recruitment of p-DNAPKcs at DNA double-strand breaks,\u00a0<\/span>JCS
\n<\/strong>
\nDamage-induced chromatome dynamics link Ubiquitin ligase and proteasome recruitment to histone loss and efficient DNA repair,\u00a0<\/span>Mol Cell<\/strong><\/p>\n

~2020\u5e74\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d\uff0d
\nPostablation Modulation after Single High-Dose Radiation Therapy Improves Tumor Control via Enhanced Immunomodulation,\u00a0<\/span>Clin Cancer Res<\/strong><\/p>\n

DNA Damage-Induced Nucleosome Depletion Enhances Homology Search Independently of Local Break Movement,\u00a0<\/span>Mol Cell,<\/strong>\u00a0<\/span>2020
\n<\/strong>
\nHistone degradation in response to DNA damage enhances chromatin dynamics and recombination rates,\u00a0<\/span>NSMB<\/strong>, 2017<\/p>\n

Very fast CRISPR on demand,\u00a0<\/span>Science<\/strong>\u00a0<\/span><\/strong>[<\/span>\u304a\u3059\u3059\u3081]
\n<\/span><\/p>\n

~Aging~<\/strong><\/p>\n

Organ aging signatures in the plasma proteome track health and disease,\u00a0<\/span>Nature<\/strong>\u00a0<\/span>2023<\/p>\n

Naturally occurring p16Ink4a-positive cells shorten healthy lifespan,\u00a0<\/span>Nature<\/strong>\u00a0<\/span>2016<\/p>\n

PD-1+ memory phenotype CD4+ T cells expressing C\/EBP\u03b1 underlie T cell immunodepression in senescence and leukemia,\u00a0<\/span>PNAS<\/strong>\u00a0<\/span>2009<\/p>\n","protected":false},"excerpt":{"rendered":"

2025\u5e74\uff0d\uff0d\uff0d\uff0d Comprehensive whole-genome sequencing reveals origins of mutational signatures associated with aging […]<\/p>\n","protected":false},"author":1,"featured_media":0,"parent":911,"menu_order":7,"comment_status":"closed","ping_status":"closed","template":"","meta":{"_acf_changed":false,"footnotes":""},"class_list":["post-919","page","type-page","status-publish","hentry"],"acf":[],"_links":{"self":[{"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=\/wp\/v2\/pages\/919","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=\/wp\/v2\/pages"}],"about":[{"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=\/wp\/v2\/types\/page"}],"author":[{"embeddable":true,"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=919"}],"version-history":[{"count":3,"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=\/wp\/v2\/pages\/919\/revisions"}],"predecessor-version":[{"id":1257,"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=\/wp\/v2\/pages\/919\/revisions\/1257"}],"up":[{"embeddable":true,"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=\/wp\/v2\/pages\/911"}],"wp:attachment":[{"href":"https:\/\/shibataxlab.com\/english\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=919"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}