ArticleThe Journal of cell biology2006
Supervillin modulation of focal adhesions involving TRIP6/ZRP-1.
Article in The Journal of cell biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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.
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.
Who cites it
37 citing papers in PubMed, 63 citations in OpenAlex.
- G3BP1 reduction during cellular senescence promotes SVIL expression and selected senescence-associated phenotypes.Frontiers in cell and developmental biology · 2026Article
- Article
- Somatic Variants in SVIL in Cerebral Aneurysms.Neurology. Genetics · 2022Article
- Novel γ-sarcoglycan interactors in murine muscle membranes.Skeletal muscle · 2022Article
- TRIP6 promotes inflammatory damage via the activation of TRAF6 signaling in a murine model of DSS-induced colitis.Journal of inflammation (London, England) · 2022Article
- TRIP6 is required for tension at adherens junctions.Journal of cell science · 2021Article
- Loss of supervillin causes myopathy with myofibrillar disorganization and autophagic vacuoles.Brain : a journal of neurology · 2020Article
- TRIP6 enhances stemness property of breast cancer cells through activation of Wnt/β-catenin.Cancer cell international · 2020Article
- Supervillin promotes epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma in hypoxia via activation of the RhoA/ROCK-ERK/p38 pathway.Journal of experimental & clinical cancer research : CR · 2018Article
- Emerging roles for LPP in metastatic cancer progression.Journal of cell communication and signaling · 2018Review
- Generation and characterization of monoclonal antibodies that recognize human and murine supervillin protein isoforms.PloS one · 2018Article
- PP2A binds to the LIM domains of lipoma-preferred partner through its PR130/B″ subunit to regulate cell adhesion and migration.Journal of cell science · 2016Article
- Preparation and Affinity-Purification of Supervillin Isoform 4 (SV4) Specific Polyclonal Antibodies.The protein journal · 2016Article
- Gamma-sarcoglycan is required for the response of archvillin to mechanical stimulation in skeletal muscle.Human molecular genetics · 2015Article
- Trip6 promotes dendritic morphogenesis through dephosphorylated GRIP1-dependent myosin VI and F-actin organization.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Supervillin binds the Rac/Rho-GEF Trio and increases Trio-mediated Rac1 activation.Cytoskeleton (Hoboken, N.J.) · 2015Article
- An N-terminal, 830 residues intrinsically disordered region of the cytoskeleton-regulatory protein supervillin contains Myosin II- and F-actin-binding sites.Journal of biomolecular structure & dynamics · 2013Article
- Supervillin-mediated suppression of p53 protein enhances cell survival.The Journal of biological chemistry · 2013Article
- Role of the retinal vascular endothelial cell in ocular disease.Progress in retinal and eye research · 2013Review
- A possible mechanism behind autoimmune disorders discovered by genome-wide linkage and association analysis in celiac disease.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Cell-substrate contacts, called focal adhesions (FAs), are dynamic in rapidly moving cells. We show that supervillin (SV)--a peripheral membrane protein that binds myosin II and F-actin in such cells--negatively regulates stress fibers, FAs, and cell-substrate adhesion. The major FA regulatory sequence within SV (SV342-571) binds to the LIM domains of two proteins in the zyxin family, thyroid receptor-interacting protein 6 (TRIP6) and lipoma-preferred partner (LPP), but not to zyxin itself. SV and TRIP6 colocalize within large FAs, where TRIP6 may help recruit SV. RNAi-mediated decreases in either protein increase cell adhesion to fibronectin. TRIP6 partially rescues SV effects on stress fibers and FAs, apparently by mislocating SV away from FAs. Thus, SV interactions with TRIP6 at FAs promote loss of FA structure and function. SV and TRIP6 binding partners suggest several specific mechanisms through which the SV-TRIP6 interaction may regulate FA maturation and/or disassembly.
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What OpenQuestion holds
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.