ArticleGenesis (New York, N.Y. : 2000)2014
Temporal and tissue-specific disruption of LINC complexes in vivo.
Article in Genesis (New York, N.Y. : 2000), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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.
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.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Integration of nuclear mechanosensing with integrin-extracellular matrix adhesions.Nucleus (Austin, Tex.) · 2026Review
- NEMP1 organizes the meiotic telomere-LINC interface to control chromosome movement and telomere integrity.bioRxiv : the preprint server for biology · 2026Article
- Age-related decline in nuclear envelope LINC complex drives neuronal aging via axon initial segment dysfunction.EMBO reports · 2026Article
- Microtubule forces drive nuclear damage in LMNA cardiomyopathy.Nature cardiovascular research · 2025Article
- The LINC Complex Regulates Tendon Elastic Modulus, Collagen Crimp, and Lateral Expansion During Early Postnatal Development.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Osterix-driven LINC complex disruption in vivo diminishes osteogenesis at 8 weeks but not at 15 weeks.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024Article
- Prrx1-driven LINC complex disruption in vivo reduces osteoid deposition but not bone quality after voluntary wheel running.bioRxiv : the preprint server for biology · 2024Article
- Prrx1-driven LINC complex disruption in vivo reduces osteoid deposition but not bone quality after voluntary wheel running.PloS one · 2024Article
- Osterix-driven LINC complex disruptionbioRxiv : the preprint server for biology · 2023Article
- Orthodenticle homeobox 2 is transported to lysosomes by nuclear budding vesicles.Nature communications · 2023Article
- Nuclear lamin isoforms differentially contribute to LINC complex-dependent nucleocytoskeletal coupling and whole-cell mechanics.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Mislocalization of cone nuclei impairs cone function in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Fibroblasts lacking nuclear lamins do not have nuclear blebs or protrusions but nevertheless have frequent nuclear membrane ruptures.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Multiple Isoforms of Nesprin1 Are Integral Components of Ciliary Rootlets.Current biology : CB · 2017Article
- Nrl-Cre transgenic mouse mediates loxP recombination in developing rod photoreceptors.Genesis (New York, N.Y. : 2000) · 2016Article
- Validation of a Mouse Model to Disrupt LINC Complexes in a Cell-specific Manner.Journal of visualized experiments : JoVE · 2015Article
- A variant of Nesprin1 giant devoid of KASH domain underlies the molecular etiology of autosomal recessive cerebellar ataxia type I.Neurobiology of disease · 2015Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Migration and anchorage of nuclei within developing and adult tissues rely on Linkers of the Nucleoskeleton to the Cytoskeleton (LINC complexes). These macromolecular assemblies span the nuclear envelope and physically couple chromatin and nuclear lamina to cytoplasmic cytoskeletal networks. LINC complexes assemble within the perinuclear space through direct interactions between the respective evolutionary-conserved SUN and KASH domains of Sun proteins, which reside within the inner nuclear membrane, and Nesprins, which reside within the outer nuclear membrane. Here, we describe and validate a dominant-negative transgenic strategy allowing for the disruption of endogenous SUN/KASH interactions through the inducible expression of a recombinant KASH domain. Our approach, which is based on the Cre/Lox system, allows for the targeted disruption of LINC complexes in a wide array of mouse tissues or specific cell types thereof and bypasses the perinatal lethality and potential cell nonautonomous effects of current mouse models based on germline inactivation of genes encoding Sun proteins and Nesprins. For these reasons, this mouse model provides a useful tool to evaluate the physiological relevance of LINC complexes integrity during development and homeostasis in a wide array of mammalian tissues.
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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.