Evidence map›Paper›PMID 25152440›Full record

ArticleExperimental cell research2014

Mitf regulates osteoclastogenesis by modulating NFATc1 activity.

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

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Experimental cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 2 pooled it
0.1field-weighted citation impact, top 47% 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

23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.

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  8. Role and Regulation of Transcription Factors in Osteoclastogenesis.International journal of molecular sciences · 2023
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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 2 institutions in 1 country.

Ssu-Yi LuDepartment of Diagnostic and Surgical Sciences, School of Dentistry, University of California, Los Angeles, CA, USA. Electronic address: ssuyilu@yahoo.com.tw.
Mengtao LiDepartment of Diagnostic and Surgical Sciences, School of Dentistry, University of California, Los Angeles, CA, USA; CHS 23-087, 10833 Le Conte Ave., Los Angeles, CA 90095, USA. Electronic address: mli@dentistry.ucla.edu.
Yi-Ling LinDepartment of Diagnostic and Surgical Sciences, School of Dentistry, University of California, Los Angeles, CA, USA; Gene Regulation Program, Jonsson Comprehensive Cancer Center, University of California, Los Angeles, CA, USA. Electronic address: ylin@dentistry.ucla.edu.
University of California, Los Angeles · USUniversity of Southern California · US

Funding

Is Mitf the Missing Puzzle Linking NFATc1 to OsteoclastogenesisR03DE019490 · NIDCR · UNIVERSITY OF KENTUCKY · PI LIN, YI-LING · 2009 to 2010
$226k
NIDCR NIH HHS R03 DE019490NIDCR NIH HHS R03DE019490
6 · The paper itself

Abstract

Transcription factors Mitf and NFATc1 share many downstream targets that are critical for osteoclastogenesis. Since RANKL signals induce/activate both NFATc1 and Mitf isoform-E (Mitf-E), a tissue-restricted Mitf isoform in osteoclasts, it is plausible that the two factors work together to promote osteoclastogenesis. Although Mitf was shown to function upstream of NFATc1 previously, this study showed that expression of Mitf had little effects on NFATc1 and NFATc1 was critical for the induction of Mitf-E. In Mitf(mi/mi) mice, the semi-dominant mutation in Mitf gene leads to arrest of osteoclastogenesis in the early stages. However, when stimulated by RANKL, the Mitf(mi/mi) preosteoclasts responded with a significant induction of NFATc1, despite that the cells cannot differentiate into functional osteoclasts. In the absence of RANKL stimulation, very high levels of NFATc1 are required to drive osteoclast development. Our data indicate that Mitf functions downstream of NFATc1 in the RANKL pathway, and it plays an important role in amplifying NFATc1-dependent osteoclastogenic signals, which contributes to the significant synergy between the two factors during osteoclastogenesis. We propose that Mitf-E functions as a tissue-specific modulator for events downstream of NFATc1 activation during osteoclastogenesis.

Indexed as

Cell DifferentiationGene Expression RegulationAnimalsBlotting, WesternCell ProliferationCells, CulturedMiceMice, Inbred C57BLMicrophthalmia-Associated Transcription FactorNFATC Transcription FactorsOsteoclastsRANK LigandReal-Time Polymerase Chain ReactionReverse Transcriptase Polymerase Chain ReactionRNA, MessengerRNA, Small InterferingMicrophthalmia-Associated Transcription FactorMitf protein, mouseNfatc1 protein, mouseNFATC Transcription FactorsRANK LigandRNA, MessengerRNA, Small InterferingTnfsf11 protein, mouseFusionMitfNFATc1OsteoclastsRANKLTranscription factors

Identifiers

PMID25152440
PMCPMC4177974
OpenAlexW1977742473

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.