Evidence map›Paper›PMID 29383801›Full record

ReviewOral diseases2018

Preserving salivary gland physiology against genotoxic damage - the Tousled way.

G Sunavala-Dossabhoy

Open access · bronzeAbstract readReview
In one paragraph

Review in Oral diseases, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Targeting Prostate Cancer, the 'Tousled Way'.International journal of molecular sciences · 2023
    Review
  4. Article
  5. Review
  6. Review
  7. Interaction of TLK1 and AKTIP as a Potential Regulator of AKT Activation in Castration-Resistant Prostate Cancer Progression.Pathophysiology : the official journal of the International Society for Pathophysiology · 2021
    Article
  8. Review
  9. Article
  10. Review
  11. Article
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

1 author at 1 institution in 1 country.

G Sunavala-DossabhoyDepartment of Biochemistry and Molecular Biology, Louisiana State University Health Sciences Center, Shreveport, LA, USA.ORCID http://orcid.org/0000-0001-9204-6513
Louisiana State University Health Sciences Center Shreveport · US

Funding

Selective transduction of radioprotector protein, Tousled, for treatment of canceR21CA173162 · NCI · LOUISIANA STATE UNIV HSC SHREVEPORT · PI SUNAVALA-DOSSABHOY, GULSHAN · 2014 to 2015
$340k
National Institute of Health (NIH) R21CA173162NCI NIH HHS R21 CA173162
6 · The paper itself

Abstract

Tousled and its homologs are evolutionarily conserved serine/threonine kinases present in plants and animals. Human Tousled-like kinases, TLK1 and TLK2, are implicated in chromatin assembly during DNA replication, chromosome segregation during mitosis, as well as in DNA damage response and repair. They share a high degree of sequence similarity, but have few non-redundant functions. Our laboratory has studied TLK1 and found that it increases the resistance of cells to ionizing radiation (IR) damage through expedited double-strand break (DSB) repair. DSBs are life-threatening lesions which when repaired restore DNA integrity and promote cell survival. A major focus in our laboratory is to dissect TLK1's role in DSB response and repair and study its usefulness in averting salivary gland hypofunction, a condition that invariably afflicts patients undergoing regional radiotherapy. The identification of anti-silencing factor 1 (ASF1), histone H3, and Rad9 as substrates of TLK1 links the protein to chromatin organization and DNA damage response and repair. However, recent findings of new interacting partners that include NEK1 suggest that TLK1 may play a broader role in DSB repair. This review provides a brief overview of the DNA damage response and DSB repair, and it highlights our current understanding of TLK1 in the process.

Indexed as

AnimalsChromatin Assembly and DisassemblyDNA Breaks, Double-StrandedDNA End-Joining RepairHomologous RecombinationHumansProtein KinasesProtein Serine-Threonine KinasesRadiation, IonizingSalivary GlandsProtein Kinasesprotein kinase UProtein Serine-Threonine KinasesTLK1 protein, humancheckpointDNA repairprotectionradiationTLK1

Identifiers

PMID29383801
PMCPMC6066457
OpenAlexW2792125387

What OpenQuestion holds

Textmetadata
LicenceTDM
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.