Evidence map›Paper›PMID 30089857›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2019

The direct binding of collagen XVII and collagen IV is disrupted by pemphigoid autoantibodies.

Mayumi Kamaguchi, Hiroaki Iwata, Wataru Nishie, Ellen Toyonaga, Hideyuki Ujiie, Ken Natsuga, Yoshimasa Kitagawa, Hiroshi Shimizu

Open access · bronzeAbstract readComparative Study
PubMed Publisher
In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. BP180/Collagen XVII: A Molecular View.International journal of molecular sciences · 2021
    Review
  6. Proteases in Pemphigoid Diseases.Frontiers in immunology · 2019
    Review
  7. 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

8 authors at 1 institution in 1 country.

Mayumi KamaguchiDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, 060-8638, Japan.
Hiroaki IwataDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, 060-8638, Japan. hiroaki.iwata@med.hokudai.ac.jp.
Wataru NishieDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, 060-8638, Japan.
Ellen ToyonagaDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, 060-8638, Japan.
Hideyuki UjiieDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, 060-8638, Japan.
Ken NatsugaDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, 060-8638, Japan.ORCID http://orcid.org/0000-0003-3865-6366
Yoshimasa KitagawaDepartment of Oral Diagnosis and Medicine, Hokkaido University Graduate School of Dental Medicine, Kita-ku, Sapporo, 060-8638, Japan.
Hiroshi ShimizuDepartment of Dermatology, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, 060-8638, Japan.
Hokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The basement membrane zone (BMZ) is framed by hemidesmosomes and extracellular matrix (ECM) including collagen IV (COL4). Hemidesmosomes are multiprotein complexes that include collagen XVII (COL17). BMZ proteins can be targeted in autoimmune subepidermal blistering diseases, e.g., pemphigoid targeting COL17. The blistering mechanisms in pemphigoid have not been fully elucidated, especially in mucous membrane pemphigoid (MMP), which mainly affects the mucosa. In this study, we showed that oral lesions in pemphigoid may be attributed to the inhibition of protein-protein interactions by autoantibodies. Using immunoprecipitation, we revealed that COL17 directly binds to COL4 in normal human keratinocytes and normal human oral keratinocytes. In particular, the C-terminus of COL17 is binding site to COL4 in oral keratinocytes. The precise COL4-binding region on COL17 was determined by protein-protein binding assay to be from amino acid Gly

Indexed as

AutoantibodiesAutoantigensCells, CulturedCollagen Type IVCollagen Type XVIIHumansKeratinocytesMouth MucosaNon-Fibrillar CollagensPemphigoid, Benign Mucous MembranePemphigoid, BullousAutoantibodiesAutoantigensCollagen Type IVCollagen Type XVIINon-Fibrillar Collagens

Identifiers

PMID30089857
OpenAlexW2887377479

What OpenQuestion holds

Textmetadata
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.