Evidence map›Paper›PMID 24725425›Full record

ReviewInternational review of cell and molecular biology2014

New insights into the roles of Xin repeat-containing proteins in cardiac development, function, and disease.

Qinchuan Wang, Jenny Li-Chun Lin, Albert J Erives, Cheng-I Lin, Jim Jung-Ching Lin

Open access · greenAbstract readReview
In one paragraph

Review in International review of cell and molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
18.1field-weighted citation impact, top 1% 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

30 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  4. Colonization withbioRxiv : the preprint server for biology · 2025
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  8. Review
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  13. Cardiac Overexpression of XIN Prevents Dilated Cardiomyopathy Caused byFrontiers in cell and developmental biology · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Identifying modifier genes for hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology · 2020
    Article
  18. Article
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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

5 authors at 1 institution in 2 countries.

Qinchuan WangDepartment of Biology, University of Iowa, Iowa City, Iowa, USA.
Jenny Li-Chun LinDepartment of Biology, University of Iowa, Iowa City, Iowa, USA.
Albert J ErivesDepartment of Biology, University of Iowa, Iowa City, Iowa, USA.
Cheng-I LinInstitute of Physiology, National Defense Medical Center, Taipei, Taiwan, ROC.
Jim Jung-Ching LinDepartment of Biology, University of Iowa, Iowa City, Iowa, USA. Electronic address: jim-lin@uiowa.edu.
University of Iowa · US

Funding

Dissecting the transcriptional network governing differentiation of peridermR01DE023575 · NIDCR · UNIVERSITY OF WASHINGTON · PI CORNELL, ROBERT AARON, SCHUTTE, BRIAN C · 2013 to 2023
$4.3M
Xin proteins and cardiac rhythmsR01HL107383 · NHLBI · UNIVERSITY OF IOWA · PI LIN, JIM JUNG-CHING · 2011 to 2014
$1.5M
Novel Xin Protein in Cardiac Development and FunctionR01HL075015 · NHLBI · UNIVERSITY OF IOWA · PI LIN, JIM JUNG-CHING · 2004 to 2007
$1.3M
Dissecting the transcriptional network governing differentiation of peridermR56DE023575 · NIDCR · UNIVERSITY OF IOWA · PI CORNELL, ROBERT AARON · 2018 to 2018
$340k
SCOR IN PEDIATRIC CARDIOVASCULAR DISEASEP50HL042266 · NHLBI · UNIVERSITY OF IOWA · PI WEEKS, DANIEL L · 1990 to 1998
–
NHLBI NIH HHS HL075015NHLBI NIH HHS HL107383NHLBI NIH HHS HL42266NHLBI NIH HHS R01 HL075015NHLBI NIH HHS R01 HL107383NIDCR NIH HHS DE023575NIDCR NIH HHS R01 DE023575NIDCR NIH HHS R56 DE023575
6 · The paper itself

Abstract

Since the discovery of Xin repeat-containing proteins in 1996, the importance of Xin proteins in muscle development, function, regeneration, and disease has been continuously implicated. Most Xin proteins are localized to myotendinous junctions of the skeletal muscle and also to intercalated discs (ICDs) of the heart. The Xin gene is only found in vertebrates, which are characterized by a true chambered heart. This suggests that the evolutionary origin of the Xin gene may have played a key role in vertebrate origins. Diverse vertebrates including mammals possess two paralogous genes, Xinα (or Xirp1) and Xinβ (or Xirp2), and this review focuses on the role of their encoded proteins in cardiac muscles. Complete loss of mouse Xinβ (mXinβ) results in the failure of forming ICD, severe growth retardation, and early postnatal lethality. Deletion of mouse Xinα (mXinα) leads to late-onset cardiomyopathy with conduction defects. Molecular studies have identified three classes of mXinα-interacting proteins: catenins, actin regulators/modulators, and ion-channel subunits. Thus, mXinα acts as a scaffolding protein modulating the N-cadherin-mediated adhesion and ion-channel surface expression. Xin expression is significantly upregulated in early stages of stressed hearts, whereas Xin expression is downregulated in failing hearts from various human cardiomyopathies. Thus, mutations in these Xin loci may lead to diverse cardiomyopathies and heart failure.

Indexed as

Gene Expression RegulationActinsAnimalsbeta CateninCardiomyopathiesCortactinCytoskeletal ProteinsCytoskeletonDNA-Binding ProteinsDown-RegulationHeartHeart FailureHumansLIM Domain ProteinsMiceMutationActinsbeta CateninCMYA1 protein, mouseCortactinCytoskeletal ProteinsDNA-Binding ProteinsLIM Domain ProteinsNuclear ProteinsPotassium ChannelsXIRP2 protein, mouseCardiomyopathy with conduction defectCortactinDelayed K(+) rectifier current (I(k,slow1))Intercalated disc formationKChIP2Transient K(+) outward current (I(to,f))Xirpβ-Catenin

Identifiers

PMID24725425
PMCPMC4857591
OpenAlexW2400909037

What OpenQuestion holds

Textmetadata
LicenceTDM
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.