Evidence map›Paper›PMID 39286493›Full record

ArticleiScience2024

A feedback loop between plakophilin 4 and YAP signaling regulates keratinocyte differentiation.

Lisa Müller, Tony Gutschner, Mechthild Hatzfeld

Abstract read
In one paragraph

Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024
    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

3 authors.

Lisa MüllerInstitute of Molecular Medicine, Section for Pathochemistry, Martin Luther University Halle-Wittenberg, Charles Tanford Protein Research Center, Kurt-Mothes-Str. 3A, 06120 Halle, Germany.
Tony GutschnerInstitute of Molecular Medicine, Section for RNA Biology and Pathogenesis, Martin Luther University Halle-Wittenberg, Charles Tanford Protein Research Center, Kurt-Mothes-Str. 3A, 06120 Halle, Germany.
Mechthild HatzfeldInstitute of Molecular Medicine, Section for Pathochemistry, Martin Luther University Halle-Wittenberg, Charles Tanford Protein Research Center, Kurt-Mothes-Str. 3A, 06120 Halle, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Hippo signaling pathway is an important regulator of organ growth and differentiation, and its deregulation contributes to the development of cancer. The activity of its downstream targets YAP/TAZ depends on adherens junctions. Plakophilin 4 (PKP4) is a cell-type specific adherens junction protein expressed in the proliferating cells of the epidermis. Here, we show that PKP4 diminishes proliferation as well as differentiation. Depletion of PKP4 increased proliferation but at the same time induced premature epidermal differentiation. PKP4 interacted with several Hippo pathway components, including the transcriptional co-activators YAP/TAZ, and promoted nuclear YAP localization and target gene expression. In differentiated keratinocytes, PKP4 recruited LATS and YAP to cell junctions where YAP is transcriptionally inactive. YAP depletion, on the other hand, reduced PKP4 levels and keratinocyte adhesion indicative of a feedback mechanism controlling adhesion, proliferation, and differentiation by balancing YAP functions.

Indexed as

Cell biologyMolecular biology

Identifiers

PMID39286493
PMCPMC11402648

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.