Evidence map›Paper›PMID 23656696›Full record

ArticleBMC research notes2013

The wooly mutation (wly) on mouse chromosome 11 is associated with a genetic defect in Fam83g.

Legairre A Radden, Kevin M Child, Elisabeth B Adkins, Damek V Spacek, Aaron M Feliciano, Thomas R King

Open access · goldAbstract read
In one paragraph

Article in BMC research notes, 2013. 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
0.4field-weighted citation impact, top 35% 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, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. FAM83G Is a Novel Inducer of Apoptosis.Molecules (Basel, Switzerland) · 2020
    Article
  4. AGenes · 2020
    Article
  5. PathogenicWellcome open research · 2019
    Article
  6. Review
  7. Article
  8. Article
  9. Expression of human skin-specific genes defined by transcriptomics and antibody-based profiling.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2015
    Article
  10. Article
  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

6 authors at 1 institution in 1 country.

Legairre A RaddenBiomolecular Sciences, Central Connecticut State University, 1615 Stanley Street, New Britain, CT 06053, USA.
Kevin M Child
Elisabeth B Adkins
Damek V Spacek
Aaron M Feliciano
Thomas R King
Central Connecticut State University · US

Funding

Positional cloning of mutations that disrupt hair development in mice.R15AR059572 · NIAMS · CENTRAL CONNECTICUT STATE UNIVERSITY · PI KING, THOMAS R · 2011 to 2011
$288k
NIAMS NIH HHS 1R15AR059572NIAMS NIH HHS R15 AR059572
6 · The paper itself

Abstract

backgroundMice homozygous for the spontaneous wooly mutation (abbreviated wly) are recognized as early as 3-4 weeks of age by the rough or matted appearance of their coats. Previous genetic analysis has placed wly in a 5.9 Mb interval on Chromosome 11 that contains over 200 known genes. Assignment of wly to one of these genes is needed in order to provide probes that would ultimately facilitate a complete molecular analysis of that gene's role in the normal and disrupted development of the mammalian integument.

resultsHere, a large intraspecific backcross family was used to genetically map wly to a smaller (0.8 Mb) span on mouse Chromosome 11 that includes fewer than 20 genes. DNA sequencing of the coding regions in two of these candidates known to be expressed in skin has revealed a 955 bp, wly-specific deletion. This deletion, which lies within the coordinates of both Slc5a10 [for solute carrier family 5 (sodium/glucose cotransporter), member 10] and Fam83g (for family with sequence similarity 83, member G), alters the splicing of mutant Fam83g transcripts only, and is predicted to result in a severely truncated (probably non-functional) protein product.

conclusionWe suggest that this mutation in Fam83g is the likely basis of the mouse wooly phenotype.

Indexed as

Chromosome MappingMutationAmino Acid SequenceAnimalsBase SequenceCrosses, GeneticDNA PrimersMeiosisMiceMolecular ProbesMolecular Sequence DataPhenotypeProteinsSequence Homology, Amino AcidDNA PrimersFAM83g protein, mouseMolecular ProbesProteins

Identifiers

PMID23656696
PMCPMC3663780
OpenAlexW2022838647

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.