Evidence map›Paper›PMID 21777851›Full record

ReviewJournal of genetics and genomics = Yi chuan xue bao2011

Recent progress in the genetics of generalized vitiligo.

Richard A Spritz

Open access · greenAbstract readReview
In one paragraph

Review in Journal of genetics and genomics = Yi chuan xue bao, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

24 citing papers in PubMed, 67 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Granzyme B Gene Polymorphisms Are Associated With Severe Non-segmental Vitiligo.The Journal of clinical and aesthetic dermatology · 2023
    Article
  5. Article
  6. A Rare Case of Congenital Vitiligo in a Neonate.The Journal of clinical and aesthetic dermatology · 2021
    Article
  7. Review
  8. Article
  9. Clinical and Molecular Aspects of Vitiligo Treatments.International journal of molecular sciences · 2018
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The genetics of human skin disease.Cold Spring Harbor perspectives in medicine · 2014
    Review
  17. Current aspects of vitiligo genetics.Postepy dermatologii i alergologii · 2014
    Review
  18. Article
  19. Article
  20. 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.

Richard A SpritzHuman Medical Genetics Program, University of Colorado School of Medicine, Aurora, CO 80045, USA. richard.spritz@ucdenver.edu
University of Colorado Denver · US

Funding

VitGene International Consortium to Identify Susceptibility Genes for GeneralizedR01AR056292 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SPRITZ, RICHARD ANDREW · 2008 to 2016
$6.9M
VitiligoR01AR045584 · NIAMS · UNIVERSITY OF COLORADO DENVER · PI SPRITZ, RICHARD ANDREW · 1999 to 2014
$6.2M
REGULATION OF EPIDERMAL DIFFERENTATION BY PTHRPR01AR045585 · NIAMS · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FOLEY, JOHN GREGORY · 2000 to 2004
$1.4M
NIAMS NIH HHS R01 AR045584NIAMS NIH HHS R01 AR045585NIAMS NIH HHS R01 AR056292NIAMS NIH HHS R01AR45585
6 · The paper itself

Abstract

Vitiligo is an acquired disease characterized principally by patchy depigmentation of skin and overlying hair. Generalized vitiligo (GV), the predominant form of the disorder, results from autoimmune loss of melanocytes from affected regions. GV is a "complex trait", inherited in a non-Mendelian polygenic, multifactorial manner. GV is epidemiologically associated with other autoimmune diseases, both in GV patients and in their close relatives, suggesting that shared genes underlie susceptibility to this group of diseases. Early candidate gene association studies yielded a few successes, such as PTPN22, but most such reports now appear to be false-positives. Subsequent genomewide linkage studies identified NLRP1 and XBP1, apparent true GV susceptibility genes involved in immune regulation, and recent genome-wide association studies (GWAS) of GV in Caucasian and Chinese populations have yielded a large number of additional validated GV susceptibility genes. Together, these genes highlight biological systems and pathways that reach from the immune cells to the melanocyte, and provide insights into both disease pathogenesis and potential new targets for both treatment and even prevention of GV and other autoimmune diseases in genetically susceptible individuals.

Indexed as

Adaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsAutoimmune DiseasesDNA-Binding ProteinsGenetic LinkageGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMelanocytesMetabolic Networks and PathwaysMultifactorial InheritanceNLR ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 22Regulatory Factor X Transcription FactorsTranscription FactorsVitiligoAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsDNA-Binding ProteinsNLRP1 protein, humanNLR ProteinsProtein Tyrosine Phosphatase, Non-Receptor Type 22PTPN22 protein, humanRegulatory Factor X Transcription FactorsTranscription FactorsX-Box Binding Protein 1XBP1 protein, human

Identifiers

PMID21777851
PMCPMC3513342
OpenAlexW2118100696

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.