Evidence map›Paper›PMID 22391303›Full record

ReviewVitamins and hormones2012

Gli-similar proteins: their mechanisms of action, physiological functions, and roles in disease.

Kristin Lichti-Kaiser, Gary ZeRuth, Hong Soon Kang, Shivakumar Vasanth, Anton M Jetten

Abstract readReview
In one paragraph

Review in Vitamins and hormones, 2012. 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
12.8field-weighted citation impact, top 2% 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, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Transcriptional regulation of Glis2 in hepatic fibrosis.Experimental & molecular medicine · 2023
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Frontiers in endocrinology · 2018
    Article
  20. 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

5 authors at 2 institutions in 1 country.

Kristin Lichti-KaiserCell Biology Section, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina, USA.
Gary ZeRuth
Hong Soon Kang
Shivakumar Vasanth
Anton M Jetten
National Institutes of Health · USNational Institute of Environmental Health Sciences · US

Funding

Mechanism Of Action And Functions Of The Gli-related Proteins Glis 1-3ZIAES100485 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2009 to 2025
$35.9M
Mechanism Of Action And Functions Of The Gli-related Proteins Glis 1-3Z01ES100485 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI JETTEN, ANTON M · 2002 to 2008
$2.3M
Intramural NIH HHS Z01 ES100485
6 · The paper itself

Abstract

Gli-similar (Glis) 1-3 proteins constitute a subfamily of Krüppel-like zinc-finger proteins that are closely related to members of the Gli family. Glis proteins have been implicated in several pathologies, including cystic kidney disease, diabetes, hypothyroidism, fibrosis, osteoporosis, psoriasis, and cancer. In humans, a mutation in the Glis2 gene has been linked to the development of nephronophthisis (NPHP), a recessive cystic kidney disease, while mutations in Glis3 lead to an extended multisystem phenotype that includes the development of neonatal diabetes, polycystic kidneys, congenital hypothyroidism, and facial dysmorphism. Glis3 has also been identified as a risk locus for type-1 and type-2 diabetes and additional studies have revealed a role for Glis3 in pancreatic endocrine development, β-cell maintenance, and insulin regulation. Similar to Gli1-3, Glis2 and 3 have been reported to localize to the primary cilium. These studies appear to suggest that Glis proteins are part of a primary cilium-associated signaling pathway(s). It has been hypothesized that Glis proteins are activated through posttranslational modifications and subsequently translocate to the nucleus where they regulate transcription by interacting with Glis-binding sites in the promoter regions of target genes. This chapter summarizes the current state of knowledge regarding mechanisms of action of the Glis family of proteins, their physiological functions, as well as their roles in disease.

Indexed as

Binding SitesDiabetes MellitusEpithelial-Mesenchymal TransitionHumansKidney Diseases, CysticKruppel-Like Transcription FactorsProtein Processing, Post-TranslationalSignal TransductionTranscriptional ActivationTranscription FactorsZinc Finger Protein GLI1Zinc FingersGLI1 protein, humanKruppel-Like Transcription FactorsTranscription FactorsZinc Finger Protein GLI1

Identifiers

PMID22391303
PMCPMC3799816
OpenAlexW1515897021

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.