Evidence map›Paper›PMID 24961988›Full record

ArticleOncotarget2014

SCFβ-TRCP regulates osteoclastogenesis via promoting CYLD ubiquitination.

Xiaomian Wu, Hidefumi Fukushima, Brian J North, Yoshiyuki Nagaoka, Katsuyuki Nagashima, Feng Deng, Koji Okabe, Hiroyuki Inuzuka, Wenyi Wei

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. RIPK4 activity in keratinocytes is controlled by the SCFCellular and molecular life sciences : CMLS · 2018
    Article
  10. Article
  11. Deubiquitinating Enzymes and Bone Remodeling.Stem cells international · 2018
    Review
  12. 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

9 authors at 5 institutions in 3 countries.

Xiaomian WuChongqing key Laboratory for Oral Diseases and Biomedical Sciences, The Affiliated Hospital of Stomatology, Chongqing Medical University, Chongqing, P.R. China; Department of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Hidefumi Fukushima
Brian J North
Yoshiyuki Nagaoka
Katsuyuki Nagashima
Feng Deng
Koji Okabe
Hiroyuki InuzukaDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Wenyi WeiDepartment of Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA.
Fukuoka Dental College · JPBeth Israel Deaconess Medical Center · USHarvard University · USChongqing Medical University · CNStomatological Hospital of Chongqing Medical University · CN

Funding

Novel regulation of PI3K/Akt to direct targeted breast cancer therapiesR01CA177910 · NCI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2013 to 2023
$3.9M
Functional analysis of beta-TRCP in cell cycle control and DNA damage responseR01GM094777 · NIGMS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI WEI, WENYI · 2012 to 2015
$1.3M
New insights into the role of the Fbw7 tumor suppressor in senescence and agingK01AG041218 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI INUZUKA, HIROYUKI · 2011 to 2015
$621k
NCI NIH HHS CA177910NCI NIH HHS R01 CA177910NIA NIH HHS AG041218NIA NIH HHS K01 AG041218NIGMS NIH HHS GM094777NIGMS NIH HHS R01 GM094777
6 · The paper itself

Abstract

CYLD negatively regulates the NF-κB signaling pathway and osteoclast differentiation largely through antagonizing TNF receptor-associated factor (TRAF)-mediated K63-linkage polyubiquitination in osteoclast precursor cells. CYLD activity is controlled by IκB kinase (IKK), but the molecular mechanism(s) governing CYLD protein stability remains largely undefined. Here, we report that SCFβ-TRCP regulates the ubiquitination and degradation of CYLD, a process dependent on prior phosphorylation of CYLD at Ser432/Ser436 by IKK. Furthermore, depletion of β-TRCP induced CYLD accumulation and TRAF6 deubiquitination in osteoclast precursor cells, leading to suppression of RANKL-induced osteoclast differentiation. Therefore, these data pinpoint the IKK/β-TRCP/CYLD signaling pathway as an important modulator of osteoclastogenesis.

Indexed as

AnimalsDeubiquitinating Enzyme CYLDHeLa CellsHumansMaleMiceOsteoclastsSignal TransductionSKP Cullin F-Box Protein LigasesTransfectionTumor Suppressor ProteinsUbiquitinationCYLD protein, humanDeubiquitinating Enzyme CYLDSKP Cullin F-Box Protein LigasesTumor Suppressor Proteins

Identifiers

PMID24961988
PMCPMC4147317
OpenAlexW2119847256

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.