Evidence map›Paper›PMID 39532028›Full record

ReviewHuman immunology2024

Integrin mutations in blistering skin diseases and related genetically engineered mouse models.

Sanjana Dhulipalla, Whitney M Longmate

Abstract readReview
In one paragraph

Review in Human immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

2 authors.

Sanjana DhulipallaDepartment of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA.
Whitney M LongmateDepartment of Surgery Albany Medical College, Albany, NY 12208, USA; Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA. Electronic address: longmaw@amc.edu.

Funding

Roles of epidermal integrin α3β1 in age-dependent changes during cutaneous wound healingR21AR083049 · NIAMS · ALBANY MEDICAL COLLEGE · PI LONGMATE, WHITNEY MORGAN · 2024 to 2025
$391k
NIAMS NIH HHS R21 AR083049
6 · The paper itself

Abstract

As major receptors for cellular adhesion, integrins in the epidermis are critical to maintain skin integrity. Integrins α6β4 and α3β1 are among the most highly and widely expressed integrins in the skin. Perhaps not surprisingly, mutation in subunits associated with these integrins cause variations of a blistering skin disease called junctional epidermolysis bullosa (JEB), which is characterized by blisters that form between the epidermis and dermis of the skin. This review highlights how the differences in structural roles and functions for these epidermal integrins lead to distinct JEB phenotypes resulting from their absence. Additionally, much has been learned by using genetically engineered mouse models, which are featured throughout the review, as they closely resemble the disorders of human patients that harbor analogous mutations.

Indexed as

Disease Models, AnimalMutationAnimalsBlisterEpidermisEpidermolysis Bullosa, JunctionalHumansIntegrinsMiceMice, TransgenicPhenotypeSkinIntegrinsEpidermolysis bullosaIntegrinMouse modelsMutationSkin disease

Identifiers

PMID39532028
PMCPMC11637898

What OpenQuestion holds

Textmetadata
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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.