Evidence map›Paper›PMID 36301493›Full record

ArticleSub-cellular biochemistry2022

Role of the Histone Acetyl Transferase MOF and the Histone Deacetylase Sirtuins in Regulation of H4K16ac During DNA Damage Repair and Metabolic Programming: Implications in Cancer and Aging.

Tej K Pandita, Clayton R Hunt, Vipin Singh, Santanu Adhikary, Shruti Pandita, Siddhartha Roy, Kenneth Ramos, Chandrima Das

Abstract read
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In one paragraph

Article in Sub-cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
1.5field-weighted citation impact, top 17% of its field
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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
  3. Stem Cells in Aging and Anti-Aging.Stem cell reviews and reports · 2026
    Review
  4. Chemoresistance: The hidden barrier in cancer treatment.Cancer pathogenesis and therapy · 2026
    Review
  5. Review
4 · The record

Corrections and comments

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

8 authors at 5 institutions in 2 countries.

Tej K PanditaThe Houston Methodist Research Institute, Houston, TX, USA. tpandita@tamu.edu.
Clayton R Hunt *The Houston Methodist Research Institute, Houston, TX, USA.
Vipin Singh *Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Santanu Adhikary *Biophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Shruti PanditaDepartment of Internal Medicine, Division of Hematology, Oncology and Cellular Therapy, Saint Louis University School of Medicine, St. Louis, MO, USA.
Siddhartha RoyBiophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Kenneth RamosCenter for Genomics and Precision Medicine, Texas A&M College of Medicine, Houston, TX, USA.
Chandrima DasBiophysics and Structural Genomics Division, Saha Institute of Nuclear Physics, Kolkata, India.
Saha Institute of Nuclear Physics · INHouston Methodist · USIndian Institute of Chemical Biology · INSaint Louis University · USTexas A&M Health Science Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The accurate repair of genomic damage mediated by ionizing radiation (IR), chemo- or radiomimetic drugs, or other exogenous agents, is necessary for maintenance of genome integrity, preservation of cellular viability and prevention of oncogenic transformation. Eukaryotes have conserved mechanisms designed to perceive and repair the damaged DNA quite efficiently. Among the different types of DNA damage, double strand breaks (DSB) are the most detrimental. The cellular DNA DSB response is a hierarchical signaling network that integrates damage sensing and repair with chromatin structural changes that involve a range of pre-existing and induced covalent modifications. Recent studies have revealed that pre-existing histone modifications are important contributors within this signaling/repair network. This chapter discusses the role of a critical histone acetyl transferase (HAT) known as MOF (males absent on the first) and the histone deacetylases (HDACs) Sirtuins on histone H4K16 acetylation (H4K16ac) and DNA damage repair. We also discuss the role of this important histone modification in light of metabolic rewiring and its role in regulating human pathophysiologic states.

Indexed as

AgingHistone AcetyltransferasesNeoplasmsSirtuinsAcetylationChromatinDNADNA DamageDNA RepairHistone DeacetylasesHistonesHumansChromatinDNAHistone AcetyltransferasesHistone DeacetylasesHistonesSirtuinsChromatinDNA damage responseHistone H4K16acMOF

Identifiers

PMID36301493
OpenAlexW4307841792

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.