Evidence map›Paper›PMID 9114034›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1997

A variable domain of delayed replication in FRAXA fragile X chromosomes: X inactivation-like spread of late replication.

R S Hansen, T K Canfield, A D Fjeld, S Mumm, C D Laird, S M Gartler

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Different classes of genomic inserts contribute to human antibody diversity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  3. Review
  4. Alternative DNA StructuresMicrobiology and molecular biology reviews : MMBR · 2021
    Review
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  15. Sequencing newly replicated DNA reveals widespread plasticity in human replication timing.Proceedings of the National Academy of Sciences of the United States of America · 2010
    Article
  16. 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

6 authors at 2 institutions in 1 country.

R S HansenDepartment of Medicine, University of Washington, Seattle, WA 98195, USA. shansen@genetics.washington.edu
T K Canfield
A D Fjeld
S Mumm
C D Laird
S M Gartler
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

DOSAGE COMPENSATION IN MAMMALS: X-INACTIVATIONR01HD016659 · NICHD · UNIVERSITY OF WASHINGTON · PI GARTLER, STANLEY · 1996 to 2004
$1.9M
MOLECULAR GENETICS AND EPIGENETICS OF FRAGILE X SYNDROMER01GM053805 · NIGMS · UNIVERSITY OF WASHINGTON · PI LAIRD, CHARLES D · 1995 to 2004
$918k
DOSAGE COMPENSATION IN MAMMALS: X-INACTIVATIONR37HD016659 · NICHD · UNIVERSITY OF WASHINGTON · PI GARTLER, STANLEY · 1986 to 1995
–
NICHD NIH HHS HD16659NICHD NIH HHS R01 HD016659NIGMS NIH HHS GM53805NIGMS NIH HHS R01 GM053805
6 · The paper itself

Abstract

The timing of DNA replication in the Xq27 portion of the human X chromosome was studied in cells derived from normal and fragile X males to further characterize the replication delay on fragile X chromosomes. By examining a number of sequence-tagged sites (STSs) that span several megabases of Xq27, we found this portion of the normal active X chromosome to be composed of two large zones with different replication times in fibroblasts, lymphocytes, and lymphoblastoid cells. The centromere-proximal zone replicates very late in S, whereas the distal zone normally replicates somewhat earlier and contains FMR1, the gene responsible for fragile X syndrome when mutated. Our analysis of the region of delayed replication in fragile X cells indicates that it extends at least 400 kb 5' of FMR1 and appears to merge with the normal zone of very late replication in proximal Xq27. The distal border of delayed replication varies among different fragile X males, thereby defining three replicon-sized domains that can be affected in fragile X syndrome. The distal boundary of the largest region of delayed replication is located between 350 and 600 kb 3' of FMR1. This example of variable spreading of late replication into multiple replicons in fragile X provides a model for the spread of inactivation associated with position-effect variegation or X chromosome inactivation.

Indexed as

DNA ReplicationDosage Compensation, GeneticRNA-Binding ProteinsCell CycleDNA, ComplementaryFibroblastsFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeGene ExpressionGenetic MarkersHematopoietic Stem CellsHumansLymphocytesMaleNerve Tissue ProteinsTime FactorsDNA, ComplementaryFMR1 protein, humanFragile X Messenger Ribonucleoprotein 1Genetic MarkersNerve Tissue ProteinsRNA-Binding Proteins

Identifiers

PMID9114034
PMCPMC20767
OpenAlexW2126555879

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.