Evidence map›Paper›PMID 11001585›Full record

ArticleAmerican journal of human genetics2000

Isolation of a cDNA representing the Fanconi anemia complementation group E gene.

J P de Winter, F Léveillé, C G van Berkel, M A Rooimans, L van Der Weel, J Steltenpool, I Demuth, N V Morgan, N Alon, L Bosnoyan-Collins and 10 more

Abstract read
In one paragraph

Article in American journal of human genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing 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.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed.

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  10. Mechanisms of interstrand DNA crosslink repair and human disorders.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2016
    Review
  11. Review
  12. Review
  13. Article
  14. TNF-α signaling in Fanconi anemia.Blood cells, molecules & diseases · 2014
    Review
  15. Article
  16. Article
  17. Review
  18. Article
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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

20 authors.

J P de WinterDepartment of Clinical Genetics and Human Genetics, Free University Medical Center, NL-1081 BT Amsterdam, The Netherlands.
F Léveillé
C G van Berkel
M A Rooimans
L van Der Weel
J Steltenpool
I Demuth
N V Morgan
N Alon
L Bosnoyan-Collins
J Lightfoot
P A Leegwater
Q Waisfisz
K Komatsu
F Arwert
J C Pronk
C G Mathew
M Digweed
M Buchwald
H Joenje

Funding

FAA AND FAD GENES AND PROTEINSR01HL050131 · NHLBI · HOSPITAL FOR SICK CHLDRN (TORONTO) · PI BUCHWALD, MANUEL · 1993 to 1999
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NHLBI NIH HHS HL50131
6 · The paper itself

Abstract

Fanconi anemia (FA) is an autosomal recessive chromosomal instability syndrome with at least seven different complementation groups. Four FA genes (FANCA, FANCC, FANCF, and FANCG) have been identified, and two other FA genes (FANCD and FANCE) have been mapped. Here we report the identification, by complementation cloning, of the gene mutated in FA complementation group E (FANCE). FANCE has 10 exons and encodes a novel 536-amino acid protein with two potential nuclear localization signals.

Indexed as

Genetic Complementation TestAlternative SplicingAmino Acid SequenceBangladeshCloning, MolecularDNA, ComplementaryExonsFanconi AnemiaFanconi Anemia Complementation Group E ProteinHumansIntronsMolecular Sequence DataMutationNuclear Localization SignalsNuclear ProteinsTurkeyDNA, ComplementaryFANCE protein, humanFanconi Anemia Complementation Group E ProteinNuclear Localization SignalsNuclear Proteins

Identifiers

PMID11001585
PMCPMC1288571

What OpenQuestion holds

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Registered trials

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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.