Evidence map›Paper›PMID 42656528›Full record

ArticleFrontiers in molecular biosciences2026

Regulation of TMEM2-mediated hyaluronan degradation by CD44 and LYVE-1.

Yuki Tobisawa, Fumiakira Yano, Risa Tomioka-Inagawa, Fumitoshi Irie, Takuya Koie, Yu Yamaguchi

Abstract read
In one paragraph

Article in Frontiers in molecular biosciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

6 authors.

Yuki TobisawaDepartment of Urology, Gifu University Hospital, Gifu, Japan.
Fumiakira YanoDepartment of Urology, Gifu University Hospital, Gifu, Japan.
Risa Tomioka-InagawaDepartment of Urology, Gifu University Hospital, Gifu, Japan.
Fumitoshi IrieCenter for Neurologic Diseases, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, United States.
Takuya KoieDepartment of Urology, Gifu University Hospital, Gifu, Japan.
Yu YamaguchiCenter for Neurologic Diseases, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hyaluronan (HA) is a major glycosaminoglycan of the extracellular matrix that regulates cell migration, signaling, and tissue homeostasis. Its turnover is controlled by coordinated synthesis by HA synthases and degradation by hyaluronidases. Among these hyaluronidases, TMEM2, the only known transmembrane hyaluronidase, plays a unique role in HA degradation at the cell surface; however, the cellular conditions that support its activity remain incompletely understood. To address this, we developed a cell-based HA turnover assay to examine TMEM2-mediated degradation of endogenously synthesized HA, rather than exogenously added, fluorescently labeled HA used in previous studies. Using this system, we show that TMEM2 readily degrades high-molecular weight HA synthesized by co-expressed HAS3. This degradation occurs only when TMEM2 and HAS3 are co-expressed in the same cells (

Indexed as

CD44glycocalyxhyaluronanhyaluronidaseLYVE-1TMEM2

Identifiers

PMID42656528
PMCPMC13506898

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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.