Evidence map›Paper›PMID 35447147›Full record

ArticleJournal of molecular and cellular cardiology2022

Obscurin regulates ankyrin macromolecular complex formation.

Janani Subramaniam, Gokay Yamankurt, Shane R Cunha

Open access · greenAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2022. 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
1.0field-weighted citation impact, top 24% 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. The varied functions of the giant muscle scaffold protein obscurin.Frontiers in cell and developmental biology · 2025
    Review
  3. Obscurin Maintains Myofiber Identity in Extraocular Muscles.Investigative ophthalmology & visual science · 2024
    Article
  4. Article
  5. Review
  6. Article
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 at 1 institution in 1 country.

Janani SubramaniamDepartment of Integrative Biology and Pharmacology, University of Texas Health Science Center at Houston, Houston, TX 77030, United States of America.
Gokay YamankurtDepartment of Integrative Biology and Pharmacology, University of Texas Health Science Center at Houston, Houston, TX 77030, United States of America.
Shane R CunhaDepartment of Integrative Biology and Pharmacology, University of Texas Health Science Center at Houston, Houston, TX 77030, United States of America. Electronic address: shane.r.cunha@uth.tmc.edu.
The University of Texas Health Science Center at Houston · US

Funding

American Heart Association-American Stroke Association 16GRNT30410011
6 · The paper itself

Abstract

Obscurin is a large scaffolding protein in striated muscle that maintains sarcolemmal integrity and aligns the sarcoplasmic reticulum with the underlying contractile machinery. Ankyrins are a family of adaptor proteins with some isoforms that interact with obscurin. Previous studies have examined obscurin interacting with individual ankyrins. In this study, we demonstrate that two different ankyrins interact with obscurin's carboxyl terminus via independent ankyrin-binding domains (ABDs). Using in-vitro binding assays, co-precipitation assays, and FLIM-FRET analysis, we show that obscurin interacts with small ankyrin 1.5 (sAnk1.5) and the muscle-specific ankyrin-G isoform (AnkG107). While there is no direct interaction between sAnk1.5 and AnkG107, obscurin connects the two ankyrins both in vitro and in cells. Moreover, AnkG107 recruits β-spectrin to this macromolecular protein complex and mutating obscurin's ABDs disrupts complex formation. To further characterize AnkG107 interaction with obscurin, we measure obscurin-binding to different AnkG107 isoforms expressed in the heart and find that the first obscurin-binding domain in AnkG107 principally mediates this interaction. We also find that AnkG107 does not bind to filamin-C and displays minimal binding to plectin-1 compared to obscurin. Finally, both sAnk1.5-GFP and AnkG107-CTD-RFP are targeted to the M-lines of ventricular cardiomyocytes and mutating their obscurin-binding domains disrupts the M-line localization of these ankyrin constructs. Altogether, these findings support a model in which obscurin can interact via independent binding domains with two different ankyrin protein complexes to target them to the sarcomeric M-line of ventricular cardiomyocytes.

Indexed as

AnkyrinsMuscle ProteinsProtein IsoformsProtein Serine-Threonine KinasesRho Guanine Nucleotide Exchange FactorsAnkyrinsMuscle ProteinsProtein IsoformsProtein Serine-Threonine KinasesRho Guanine Nucleotide Exchange FactorsAlternative splicingAnkG107AnkyrinObscurinsAnk1.5

Identifiers

PMID35447147
PMCPMC11057898
OpenAlexW4223963489

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.