Evidence map›Paper›PMID 28811338›Full record

ReviewJournal of cell science2017

Emerging functions of the Fanconi anemia pathway at a glance.

Rhea Sumpter, Beth Levine

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cell science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Altered Mitochondrial Dynamic in Lymphoblasts and Fibroblasts Mutated forInternational journal of molecular sciences · 2023
    Article
  9. Review
  10. [Research progress of Fanconi anemia and DNA interstrand crosslink repair].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2022
    Article
  11. Management of oral leukoplakia in patients with Fanconi anemia.Journal of oral and maxillofacial pathology : JOMFP · 2022
    Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 2 institutions in 1 country.

Rhea SumpterCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA rhea.sumpter@stjude.org.
Beth LevineCenter for Autophagy Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390, USA.
Howard Hughes Medical Institute · USThe University of Texas Southwestern Medical Center · US

Funding

Genetic and Pathway Analysis CoreU19AI109725 · NIAID · WASHINGTON UNIVERSITY · PI VIRGIN, HERBERT W · 2014 to 2018
$32.7M
Beclin 1-Bcl-2 Interactions: Effects on AutophagyR01CA109618 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI LEVINE, BETH C · 2004 to 2014
$3.1M
Novel host factors in selective autophagy of virusesK08AI099150 · NIAID · UT SOUTHWESTERN MEDICAL CENTER · PI SUMPTER, RHEA M · 2012 to 2014
$391k
NCI NIH HHS R01 CA109618NIAID NIH HHS K08 AI099150NIAID NIH HHS U19 AI109725
6 · The paper itself

Abstract

Fanconi anemia (FA) is a rare disease, in which homozygous or compound heterozygous inactivating mutations in any of 21 genes lead to genomic instability, early-onset bone marrow failure and increased cancer risk. The FA pathway is essential for DNA damage response (DDR) to DNA interstrand crosslinks. However, proteins of the FA pathway have additional cytoprotective functions that may be independent of DDR. We have shown that many FA proteins participate in the selective autophagy pathway that is required for the destruction of unwanted intracellular constituents. In this Cell Science at a Glance and the accompanying poster, we briefly review the role of the FA pathway in DDR and recent findings that link proteins of the FA pathway to selective autophagy of viruses and mitochondria. Finally, we discuss how perturbations in FA protein-mediated selective autophagy may contribute to inflammatory as well as genotoxic stress.

Indexed as

AnimalsAutophagyDNA RepairFanconi AnemiaFanconi Anemia Complementation Group ProteinsGenomic InstabilityHumansMutationSignal TransductionFanconi Anemia Complementation Group ProteinsDNA damage responseFanconi anemiaInflammasomeMitophagySelective autophagyVirophagy

Identifiers

PMID28811338
PMCPMC5576063
OpenAlexW2748478517

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.