Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registry
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what money
Authors and funding
12 authors.
Jessica L KelliherDepartment of Radiation Oncology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Melissa L FolkertsDepartment of Medicine, Division of Hematology/Oncology, University of California, Irvine, Irvine, CA, 92697, USA.ORCID http://orcid.org/0009-0009-9657-6146
Kaiyuan V ShenDepartment of Medicine, Division of Hematology/Oncology, University of California, Irvine, Irvine, CA, 92697, USA.
Wan SongDepartment of Radiation Oncology, University of Texas Health and Science Center, San Antonio, TX, 78229, USA.
Kyle TenglerDepartment of Radiation Oncology, University of Texas Health and Science Center, San Antonio, TX, 78229, USA.
Clara M StiefelDepartment of Radiation Oncology, University of Texas Health and Science Center, San Antonio, TX, 78229, USA.
Seong-Ok LeeDepartment of Radiation Oncology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Eloise DrayDepartment of Biochemistry and Structural Biology, University of Texas Health and Science Center, San Antonio, TX, 78229, USA.ORCID http://orcid.org/0000-0001-6793-9838
Weixing ZhaoDepartment of Biochemistry and Structural Biology, University of Texas Health and Science Center, San Antonio, TX, 78229, USA.ORCID http://orcid.org/0000-0001-5746-3696
Brian KossDepartment of Biochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA.
Nicholas R PannunzioDepartment of Medicine, Division of Hematology/Oncology, University of California, Irvine, Irvine, CA, 92697, USA. nrpann@hs.uci.edu.ORCID http://orcid.org/0000-0002-8290-8236
Justin W LeungDepartment of Radiation Oncology, University of Arkansas for Medical Sciences, Little Rock, AR, 72205, USA. Leungj@uthscsa.edu.ORCID http://orcid.org/0000-0003-4601-390X
Funding
Bladder cancer PD-L1 control of homologous recombination: Basic mechanisms applied to novel treatmentsR01CA268641 · NCI · DARTMOUTH-HITCHCOCK CLINIC · PI Tyler J. Curiel, WEIXING Wilson ZHAO · 2022 to 2026
$2.5M
Rapid detection of CRLF2 rearrangements in Hispanic Ph-like ALL patients to access diagnosis and relapseR37CA266042 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Nicholas Pannunzio · 2022 to 2026
$2.5M
Deciphering the chromatin-based DNA damage response pathwayR35GM137798 · NIGMS · UNIV OF ARKANSAS FOR MED SCIS · PI Justin Wai Chung Leung · 2020 to 2026
$2.4M
Immunology Research Training ProgramT32AI060573 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI PEARLMAN, ERIC · 2005 to 2020
$1.9M
Discovering T cell proteome turnover dynamics to overcome the solid tumor microenvironmentDP5OD031863 · OD · UNIV OF ARKANSAS FOR MED SCIS · PI KOSS, BRIAN · 2021 to 2025
$1.9M
Genome Maintenance via the BRCA-RAD54 Axis.R01GM141091 · NIGMS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ZHAO, WEIXING WILSON · 2021 to 2025
$1.8M
Mechanistic characterization of the cell cycle-dependent DNA repair pathway- ResubmissionR01CA244261 · NCI · UNIV OF ARKANSAS FOR MED SCIS · PI Justin Wai Chung Leung · 2021 to 2026
$1.5M
Aberrant V(D)J recombination in B cells initiates lymphoid malignancyR01CA276470 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Nicholas Pannunzio · 2024 to 2026
$1.0M
Immunology Research Training GrantT32AI177324 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI Eric Pearlman · 2023 to 2026
$735k
Understanding post translational modifiers in DNA damage repairR21ES035997 · NIEHS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DRAY, ELOISE · 2024 to 2025
$426k
DNA-PKcs Regulation of LAT-Mediated Early TCR Signaling in CD4+ and CD8+ T CellsR21AI173759 · NIAID · ARKANSAS CHILDREN'S HOSPITAL RES INST · PI BURDINE, MARIE SCHLUTERMAN, KOSS, BRIAN · 2023 to 2024
$424k
American Cancer Society (American Cancer Society, Inc.) IRG-16-187-13American Cancer Society (American Cancer Society, Inc.) RSG-20-131-01-DMCAmerican Cancer Society (American Cancer Society, Inc.) RSG-22721675-01-DMCAmerican Cancer Society (American Cancer Society, Inc.) TLC-21-164-01-TLCNCI NIH HHS R01 CA244261NCI NIH HHS R01 CA268641NCI NIH HHS R01 CA276470NCI NIH HHS R37 CA266042NIAID NIH HHS R21 AI173759NIAID NIH HHS T32 AI060573NIAID NIH HHS T32 AI177324NIEHS NIH HHS R21 ES035997NIGMS NIH HHS R01 GM141091NIGMS NIH HHS R35 GM137798NIH HHS DP5 OD031863U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA244261U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA268641U.S. Department of Health & Human Services | NIH | National Cancer Institute (NCI) R01CA276470U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases (NIAID) R21AI173759U.S. Department of Health & Human Services | NIH | National Institute of Environmental Health Sciences (NIEHS) 1R21ES035997-01U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R01GM141091U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) R35GM13779U.S. Department of Health & Human Services | NIH | NIH Office of the Director (OD) DP5OD031863
6 · The paper itself
Abstract
The master DNA damage repair histone protein, H2AX, is essential for orchestrating the recruitment of downstream mediator and effector proteins at damaged chromatin. The phosphorylation of H2AX at S139, γH2AX, is well-studied for its DNA repair function. However, the extended C-terminal tail is not characterized. Here, we define the minimal motif on H2AX for the canonical function in activating the MDC1-RNF8-RNF168 phosphorylation-ubiquitination pathway that is important for recruiting repair proteins, such as 53BP1 and BRCA1. Interestingly, H2AX recruits 53BP1 independently from the MDC1-RNF8-RNF168 pathway through its evolved C-terminal linker region with S139 phosphorylation. Mechanistically, 53BP1 recruitment to damaged chromatin is mediated by the interaction between the H2AX C-terminal tail and the 53BP1 Oligomerization-Tudor domains. Moreover, γH2AX-linker mediated 53BP1 recruitment leads to camptothecin resistance in H2AX knockout cells. Overall, our study uncovers an evolved mechanism within the H2AX C-terminal tail for regulating DNA repair proteins at damaged chromatin.
Indexed as
ChromatinDNA DamageHistonesTumor Suppressor p53-Binding Protein 1UbiquitinationAdaptor Proteins, Signal TransducingBRCA1 ProteinCamptothecinCell Cycle ProteinsDNA RepairHEK293 CellsHumansPhosphorylationUbiquitin-Protein LigasesAdaptor Proteins, Signal TransducingBRCA1 ProteinCamptothecinCell Cycle ProteinsChromatinH2AX protein, humanHistonesMDC1 protein, humanTP53BP1 protein, humanTumor Suppressor p53-Binding Protein 1Ubiquitin-Protein Ligases
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.
Evolved histone tail regulates 53BP1 recruitment at damaged chromatin. · full record | OpenQuestion