Evidence map›Paper›PMID 38989661›Full record

ArticleGlia2024

Loss of YAP in Schwann cells improves HNPP pathophysiology.

Seth M Moore, Eunbi Jeong, Muhammad Zahid, Joseph Gawron, Simar Arora, Sophie Belin, Fraser Sim, Yannick Poitelon, M Laura Feltri

Abstract read
In one paragraph

Article in Glia, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Review
  2. High-Fat Diet Disrupt Nerve Function by Targeting Schwann Cells.Journal of the peripheral nervous system : JPNS · 2025
    Article
  3. Low-Intensity Ultrasound Stimulates TAZ in Schwann cells.bioRxiv : the preprint server for biology · 2025
    Article
  4. Article
  5. Article
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.

Seth M MooreDepartment of Biochemistry, University at Buffalo, Buffalo, New York, USA.ORCID 0000-0001-9488-3905
Eunbi JeongDepartment of Biochemistry, University at Buffalo, Buffalo, New York, USA.
Muhammad ZahidInstitute for Myelin and Glia Exploration, Jacob's School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA.
Joseph GawronDepartment of Biochemistry, University at Buffalo, Buffalo, New York, USA.
Simar AroraAlbany Medical College, Department of Neuroscience and Experimental Therapeutics, Albany, New York, USA.
Sophie BelinAlbany Medical College, Department of Neuroscience and Experimental Therapeutics, Albany, New York, USA.
Fraser SimDepartment of Pharmacology and Toxicology, University at Buffalo, Buffalo, New York, USA.ORCID 0000-0002-3942-6637
Yannick PoitelonAlbany Medical College, Department of Neuroscience and Experimental Therapeutics, Albany, New York, USA.ORCID 0000-0001-9868-1569
M Laura FeltriDepartment of Biochemistry, University at Buffalo, Buffalo, New York, USA.ORCID 0000-0002-2276-9182

Funding

Laminin Receptors and Signals in Schwann CellsR01NS045630 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI SIM, FRASER JAMES · 2003 to 2024
$5.9M
Transduction of Mechanical Stimuli in Myelination and Peripheral Nerve RepairR01NS110627 · NINDS · ALBANY MEDICAL COLLEGE · PI POITELON, YANNICK · 2020 to 2024
$2.1M
Role of a Fatty Acid Chaperone in Schwann Cell MyelinationR01NS134493 · NINDS · ALBANY MEDICAL COLLEGE · PI SOPHIE BELIN · 2024 to 2026
$1.5M
YAP/TAZ in Schwann Cells as Potential Therapeutic Targets in CMT1A and HNPP.F30NS125928 · NINDS · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI MOORE, SETH MICHAEL · 2022 to 2023
$66k
NINDS NIH HHS F30 NS125928NINDS NIH HHS NS045630NINDS NIH HHS NS110627NINDS NIH HHS NS125928NINDS NIH HHS NS134493NINDS NIH HHS R01 NS045630NINDS NIH HHS R01 NS110627NINDS NIH HHS R01 NS134493
6 · The paper itself

Abstract

Rapid nerve conduction in the peripheral nervous system (PNS) is facilitated by the multilamellar myelin sheath encasing many axons of peripheral nerves. Charcot-Marie-Tooth type 1A (CMT1A), and hereditary neuropathy with liability to pressure palsy (HNPP) are common demyelinating inherited peripheral neuropathies and are caused by mutations in the peripheral myelin protein 22 (PMP22) gene. Duplication of PMP22 leads to its overexpression and causes CMT1A, while its deletion results in PMP22 under expression and causes HNPP. Here, we investigated novel targets for modulating the protein level of PMP22 in HNPP. We found that genetic attenuation of the transcriptional coactivator Yap in Schwann cells reduces p-TAZ levels, increased TAZ activity, and increases PMP22 in peripheral nerves. Based on these findings, we ablated Yap alleles in Schwann cells of the Pmp22-haploinsufficient mouse model of HNPP and identified fewer tomacula on morphological assessment and improved nerve conduction in peripheral nerves. These findings suggest YAP modulation may be a new avenue for treatment of HNPP.

Indexed as

Adaptor Proteins, Signal TransducingArthrogryposisHereditary Sensory and Motor NeuropathyMyelin ProteinsSchwann CellsYAP-Signaling ProteinsAnimalsDisease Models, AnimalMiceMice, Inbred C57BLMice, TransgenicNeural ConductionTranscription FactorsAdaptor Proteins, Signal TransducingMyelin ProteinsPmp22 protein, mouseTranscription FactorsWwtr1 protein, mouseYap1 protein, mouseYAP-Signaling ProteinsHNPPPMP22Schwann cellTAZYAP

Identifiers

PMID38989661
PMCPMC11563883

What Socratic 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 Socratic graph.