Evidence map›Paper›PMID 12510981›Full record

ReviewJournal of pediatric endocrinology & metabolism : JPEM2002

Imprinting disorders: non-Mendelian mechanisms affecting growth.

Merlin G Butler

Open access · greenAbstract readReview
In one paragraph

Review in Journal of pediatric endocrinology & metabolism : JPEM, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

9 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Imprinting disorders in humans: a review.Current opinion in pediatrics · 2020
    Review
  6. Gestational overgrowth and undergrowth affect neurodevelopment: similarities and differences from behavior to epigenetics.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2013
    Review
  7. Article
  8. Article
  9. Genomic imprinting disorders in humans: a mini-review.Journal of assisted reproduction and genetics
    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

1 author at 1 institution in 1 country.

Merlin G ButlerSection of Medical Genetics and Molecular Medicine, Children 's Mercy Hospitals and Clinics and The University of Missouri-Kansas City School of Medicine, Kansas City, MO 64108, USA. mgbutler@cmh.edu
Children's Mercy Hospital · US

Funding

COMPULSIVE FOOD-SEEKING &FOOD MOTIVATION IN PWSR01HD041672 · NICHD · UNIVERSITY OF ROCHESTER · PI ZARCONE, JENNIFER R · 2001 to 2005
$1.2M
NICHD NIH HHS R01 HD041672
6 · The paper itself

Abstract

Most autosomal genes are expressed from both maternal and paternal alleles. However, imprinted genes are an example of non-Mendelian genetics, in which only one member of the gene pair is expressed and expression is determined by the parent of origin. Imprinted genes may account for 0.1-1% of all mammalian genes. At least 50 imprinted genes have been identified in humans, and imprinted genes frequently cluster under the control of an imprinting center. Many imprinted genes contribute to growth, either as growth factors, such as insulin-like growth factors (IGF2 in Beckwith-Wiedemann syndrome), or as growth inhibitors, such as the GRB10 gene in Russell-Silver syndrome. Imprinted genes have evolved over time in mammals to fine-tune the growth of the fetus. Paternally expressed genes generally enhance growth, whereas maternally expressed genes appear to suppress growth. In addition, normal and abnormal genomic imprinting and loss of heterozygosity contribute to a wide range of malignancies. A common process for controlling gene activity is methylation, which can be changed during male or female gametogenesis. Examples of classic human disorders related to genomic imprinting are Beckwith-Wiedemann syndrome (chromosome 11), Prader-Willi/Angelman syndromes (chromosome 15), Russell-Silver syndrome (chromosome 7), and Albright hereditary osteodystrophy (chromosome 20). Several of these disorders are discussed and illustrated.

Indexed as

Genomic ImprintingBeckwith-Wiedemann SyndromeDNA MethylationFemaleGRB10 Adaptor ProteinGrowthGrowth DisordersHumansInsulin-Like Growth Factor IIMalePrader-Willi SyndromeProteinsGRB10 Adaptor ProteinInsulin-Like Growth Factor IIProteins

Identifiers

PMID12510981
PMCPMC5178135
OpenAlexW2418455973

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.