Evidence map›Paper›PMID 30923661›Full record

ArticleBiophysics and physicobiology2019

Functional significance of HCM mutants of tropomyosin, V95A and D175N, studied with

Shuya Ishii, Madoka Suzuki, Shin'ichi Ishiwata, Masataka Kawai

Open access · goldAbstract read
In one paragraph

Article in Biophysics and physicobiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Force Measurements From Myofibril to Filament.Frontiers in physiology · 2021
    Review
  6. 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

4 authors at 3 institutions in 2 countries.

Shuya IshiiDepartment of Physics, Faculty of Science and Engineering, Waseda University, Shinjuku-ku, Tokyo 169-8555, Japan.
Madoka SuzukiInstitute for Protein Research, Osaka University, Suita, Osaka 565-0871, Japan.
Shin'ichi IshiwataDepartment of Physics, Faculty of Science and Engineering, Waseda University, Shinjuku-ku, Tokyo 169-8555, Japan.
Masataka KawaiDepartment of Anatomy and Cell Biology, College of Medicine, University of Iowa, Iowa City, IA 52242, USA.
Waseda University · JPJapan Science and Technology Agency · JPUniversity of Iowa · US

Funding

Role of actin domains in force generation in myocardiumR01HL070041 · NHLBI · UNIVERSITY OF IOWA · PI KAWAI, MASATAKA · 2002 to 2011
$2.5M
NHLBI NIH HHS R01 HL070041
6 · The paper itself

Abstract

The majority of hypertrophic cardiomyopathy (HCM) is caused by mutations in sarcomere proteins. We examined tropomyosin (Tpm)'s HCM mutants in humans, V95A and D175N, with

Indexed as

Hypertrophic cardiomyopathyoptical tweezerssliding velocity and forceTIRFtropomyosin mutants

Identifiers

PMID30923661
PMCPMC6435021
OpenAlexW2914753850

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.