Evidence map›Paper›PMID 20357005›Full record

ArticleMolecular biology of the cell2010

Mitf induction by RANKL is critical for osteoclastogenesis.

Ssu-Yi Lu, Mengtao Li, Yi-Ling Lin

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular biology of the cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 22% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Article
  7. SP7: from Bone Development to Skeletal Disease.Current osteoporosis reports · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Vitamin E enriched diet increases the rate of orthodontic tooth movement.American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics · 2022
    Article
  12. 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

3 authors at 1 institution in 1 country.

Ssu-Yi LuSection of Oral Pathology, Department of Diagnostic and Surgical Sciences, School of Dentistry, University of California, Los Angeles, CA 90095, USA.
Mengtao Li
Yi-Ling Lin
University of California, Los Angeles · US

Funding

PROTECTIVE ACTIONS OF ESTRADIOL/SERMS ON BRAIN/HIVP20RR015592 · NCRR · UNIVERSITY OF KENTUCKY · PI KILGORE, MICHAEL · 2000 to 2009
$18.2M
Is Mitf the Missing Puzzle Linking NFATc1 to OsteoclastogenesisR03DE019490 · NIDCR · UNIVERSITY OF KENTUCKY · PI LIN, YI-LING · 2009 to 2010
$226k
NCRR NIH HHS P20 RR015592NCRR NIH HHS P20 RR15592NIDCR NIH HHS R03 DE019490
6 · The paper itself

Abstract

Microphthalmia-associated transcription factor (Mitf) regulates the development and function of several cell lineages, including osteoclasts. In this report, we identified a novel mechanism by which RANKL regulates osteoclastogenesis via induction of Mitf isoform E (Mitf-E). Both Mitf-A and Mitf-E are abundantly present in osteoclasts. Unlike Mitf-A, which is ubiquitously expressed and is present in similar amounts in macrophages and osteoclasts, Mitf-E is almost nondetectable in macrophages, but its expression is significantly up-regulated during osteoclastogenesis. In addition to their different expression profiles, the two isoforms are drastically different in their abilities to support osteoclastogenesis, despite sharing all known functional domains. Unlike Mitf-A, small amounts of Mitf-E are present in nuclear lysates unless chromatin is digested/sheared during the extraction. Based on these data, we propose a model in which Mitf-E is induced during osteoclastogenesis and is closely associated with chromatin to facilitate its interaction with target promoters; therefore, Mitf-E has a stronger osteoclastogenic activity. Mitf-A is a weaker osteoclastogenic factor, but activated Mitf-A alone is not sufficient to fully support osteoclastogenesis. Therefore, this receptor activator for nuclear factor-kappaB ligand (RANKL)-induced Mitf phenomenon seems to play an important role during osteoclastogenesis. Although the current theory indicates that Mitf and its binding partner Tfe3 are completely redundant in osteoclasts, using RNA interference, we demonstrated that Mitf has a distinct role from Tfe3. This study provides the first evidence that RANKL-induced Mitf is critical for osteoclastogenesis and Mitf is not completely redundant with Tfe3.

Indexed as

AnimalsBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCell DifferentiationCell NucleusChromatinLigandsMacrophagesMiceMicrophthalmia-Associated Transcription FactorOsteoclastsProtein BindingRNA InterferenceTranscriptional ActivationBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsChromatinLigandsMicrophthalmia-Associated Transcription FactorTFE3 protein, human

Identifiers

PMID20357005
PMCPMC2869381
OpenAlexW2142330950

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.