Evidence map›Paper›PMID 35733270›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2022

IFT80 negatively regulates osteoclast differentiation via association with Cbl-b to disrupt TRAF6 stabilization and activation.

Vishwa Deepak, Shu-Ting Yang, Ziqing Li, Xinhua Li, Andrew Ng, Ding Xu, Yi-Ping Li, Merry Jo Oursler, Shuying Yang

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
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

20 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Primary cilia dysfunction: A critical driver of metabolic diseases (Review).International journal of molecular medicine · 2026
    Review
  4. Article
  5. Article
  6. Article
  7. MST4 as a key driver of osteoclast activation in osteoporosis.Journal of pharmaceutical analysis · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. REGγ is essential to maintain bone homeostasis by degrading TRAF6, preventing osteoporosis.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. KIAA0753 enhances osteoblast differentiation suppressed by diabetes.Journal of cellular and molecular medicine · 2024
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Vishwa DeepakDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Shu-Ting YangDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Ziqing LiDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Xinhua LiDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104.
Andrew NgDepartment of Oral Biology, School of Dental Medicine, State University of New York at Buffalo, Buffalo, NY 14214.
Ding XuDepartment of Oral Biology, School of Dental Medicine, State University of New York at Buffalo, Buffalo, NY 14214.ORCID 0000-0001-9380-2712
Yi-Ping LiDepartment of Pathology and Laboratory Medicine, Tulane University School of Medicine, New Orleans, LA 70112.
Merry Jo OurslerRobert and Arlene Kogod Center on Aging, Mayo Clinic College of Medicine, Rochester, MN 55905.
Shuying YangDepartment of Basic and Translational Sciences, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19104.ORCID 0000-0002-7126-6901
University of Pennsylvania · USCenter for Innovation · USUniversity at Buffalo, State University of New York · USMayo Clinic · USTulane University · US

Funding

Overall: Resource-based Center for Musculoskeletal Disorders Research (Overall Application)P30AR069619 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI LOUIS J SOSLOWSKY · 2016 to 2026
$9.1M
Inhibiting Periodontitis by Targeting Cathepsin K and Attenuating TLR SignalingR01DE023813 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2014 to 2023
$3.9M
Mechanistic basis of the role of Cbx3 in negatively regulating osteoclast differentiation through epigenetic modificationR01AR075735 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2019 to 2024
$2.4M
Regulation of skeletal development and homeostasis by IFT proteinR01DE023105 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$2.0M
Role of RGS12, a Regulator of G protein Signaling, in Bone RemodelingR01AR066101 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.8M
Gα13 signaling attenuates periodontal inflammation and alveolar bone loss in the mouse model of age-associated periodontitisR01DE028264 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2018 to 2022
$1.8M
Function of Regulator of G protein signaling in aging skeletonR01AG048388 · NIA · UNIVERSITY OF PENNSYLVANIA · PI YANG, SHUYING · 2014 to 2018
$1.7M
Characterizing the negative signaling in dendritic cells and macrophages to attenuate inflammation and bone destruction in Rheumatoid arthritisR01AR074954 · NIAMS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LI, YI-PING · 2020 to 2024
$1.6M
NIAMS NIH HHS P30 AR069619NIAMS NIH HHS R01 AR066101NIAMS NIH HHS R01 AR074954NIAMS NIH HHS R01 AR075735NIA NIH HHS R01 AG048388NIDCR NIH HHS R01 DE023105NIDCR NIH HHS R01 DE023813NIDCR NIH HHS R01 DE028264
6 · The paper itself

Abstract

Excess bone loss due to increased osteoclastogenesis is a significant clinical problem. Intraflagellar transport (IFT) proteins have been reported to regulate cell growth and differentiation. The role of IFT80, an IFT complex B protein, in osteoclasts (OCs) is completely unknown. Here, we demonstrate that deletion of IFT80 in the myeloid lineage led to increased OC formation and activity accompanied by severe bone loss in mice. IFT80 regulated OC formation by associating with Casitas B-lineage lymphoma proto-oncogene-b (Cbl-b) to promote protein stabilization and proteasomal degradation of tumor necrosis factor (TNF) receptor-associated factor 6 (TRAF6). IFT80 knockdown resulted in increased ubiquitination of Cbl-b and higher TRAF6 levels, thereby hyperactivating the receptor activator of nuclear factor-κβ (NF-κβ) ligand (RANKL) signaling axis and increased OC formation. Ectopic overexpression of IFT80 rescued osteolysis in a calvarial model of bone loss. We have thus identified a negative function of IFT80 in OCs.

Indexed as

Adaptor Proteins, Signal TransducingBone ResorptionCarrier ProteinsOsteoclastsOsteogenesisProto-Oncogene Proteins c-cblTNF Receptor-Associated Factor 6AnimalsCell DifferentiationDisease Models, AnimalGene DeletionMiceProteolysisRANK LigandUbiquitinationAdaptor Proteins, Signal TransducingCarrier ProteinsCblb protein, mouseIFT80 protein, mouseProto-Oncogene Proteins c-cblRANK LigandTNF Receptor-Associated Factor 6TRAF6 protein, mouseboneIFT80osteoblastosteoclast

Identifiers

PMID35733270
PMCPMC9245634
OpenAlexW4283310721

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.