ArticleGenes & development1998
Knockout and knockin of the beta1 exon D define distinct roles for integrin splice variants in heart function and embryonic development.
Article in Genes & development, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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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.
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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.
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Who cites it
29 citing papers in PubMed, 96 citations in OpenAlex.
- Integrin-β1/FAK signaling is involved in electrical stimulation to prevent disuse muscular atrophy induced by tail suspension in mice.BMC musculoskeletal disorders · 2026Article
- Exercise training ameliorates myocardial dysfunction through fibronectin-mediated mechanotransduction in a swine model of ischemic heart disease.American journal of physiology. Heart and circulatory physiology · 2026Article
- Laminin Receptors in Peripheral Tissues: Functions Revealed by Analysis of Knockout Mice.The American journal of pathology · 2025Review
- Kindlin stabilizes the talin·integrin bond under mechanical load by generating an ideal bond.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Integrin α7 Mutations Are Associated With Adult-Onset Cardiac Dysfunction in Humans and Mice.Journal of the American Heart Association · 2022Article
- Integrin signaling: linking mechanical stimulation to skeletal muscle hypertrophy.American journal of physiology. Cell physiology · 2019Review
- Collagen XXV promotes myoblast fusion during myogenic differentiation and muscle formation.Scientific reports · 2019Article
- Whole exome sequencing identifies novel predisposing genes in neural tube defects.Molecular genetics & genomic medicine · 2019Article
- Conductive Silk-Polypyrrole Composite Scaffolds with Bioinspired Nanotopographic Cues for Cardiac Tissue Engineering.Journal of materials chemistry. B · 2018Article
- Identification and characterization of MYH9 locus for high efficient gene knock-in and stable expression in mouse embryonic stem cells.PloS one · 2018Article
- Exclusion of alternative exon 33 of CaProceedings of the National Academy of Sciences of the United States of America · 2017Article
- Mechanical Forces Reshape Differentiation Cues That Guide Cardiomyogenesis.Circulation research · 2016Review
- Integrins in development and cancer.Biophysical reviews · 2014Review
- Integrin inactivators: balancing cellular functions in vitro and in vivo.Nature reviews. Molecular cell biology · 2013Review
- Epithelial fusion during neural tube morphogenesis.Birth defects research. Part A, Clinical and molecular teratology · 2012Review
- β1D chain increases α7β1 integrin and laminin and protects against sarcolemmal damage in mdx mice.Human molecular genetics · 2012Article
- Emerging anticancer therapeutic targets and the cardiovascular system: is there cause for concern?Circulation research · 2010Review
- Integrins.Cell and tissue research · 2010Review
- Focal adhesion kinase signaling regulates the expression of caveolin 3 and beta1 integrin, genes essential for normal myoblast fusion.Molecular biology of the cell · 2009Article
- The impact of alternative splicing in vivo: mouse models show the way.RNA (New York, N.Y.) · 2007Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The beta1D integrin is a recently characterized isoform of the beta1 subunit that is specifically expressed in heart and skeletal muscle. In this study we have assessed the function of the beta1D integrin splice variant in mice by generating, for the first time, Cre-mediated exon-specific knockout and knockin strains for this splice variant. We show that removal of the exon for beta1D leads to a mildly disturbed heart phenotype, whereas replacement of beta1A by beta1D results in embryonic lethality with a plethora of developmental defects, in part caused by the abnormal migration of neuroepithelial cells. Our data demonstrate that the splice variants A and D are not functionally equivalent. We propose that beta1D is less efficient than beta1A in mediating the signaling that regulates cell motility and responses of the cells to mechanical stress.
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Registered trials
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.