ArticleMolecular and cellular biology2002
Fliih, a gelsolin-related cytoskeletal regulator essential for early mammalian embryonic development.
Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 87 citations in OpenAlex.
- Loss of the actin remodeling protein Flightless-1 impairs CD8 and regulatory T cell function.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Article
- Biallelic variants in FLII cause pediatric cardiomyopathy by disrupting cardiomyocyte cell adhesion and myofibril organization.JCI insight · 2023Article
- A human FLII gene variant alters sarcomeric actin thin filament length and predisposes to cardiomyopathy.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Increased Expression of Flightless I in Cutaneous Squamous Cell Carcinoma Affects Wnt/β-Catenin Signaling Pathway.International journal of molecular sciences · 2021Article
- Overexpression ofInternational journal of molecular sciences · 2021Article
- Attenuation of Flightless I Increases Human Pericyte Proliferation, Migration and Angiogenic Functions and Improves Healing in Murine Diabetic Wounds.International journal of molecular sciences · 2020Article
- Flightless anchors IQGAP1 and R-ras to mediate cell extension formation and matrix remodeling.Molecular biology of the cell · 2020Article
- In vitro analysis of the effect of Flightless I on murine tenocyte cellular functions.Journal of orthopaedic surgery and research · 2020Article
- Effect of Flightless I Expression on Epidermal Stem Cell Niche During Wound Repair.Advances in wound care · 2020Article
- The Activities of the Gelsolin Homology Domains of Flightless-I in Actin Dynamics.Frontiers in molecular biosciences · 2020Article
- Multifunctional Roles of the Actin-Binding Protein Flightless I in Inflammation, Cancer and Wound Healing.Frontiers in cell and developmental biology · 2020Review
- Flightless I exacerbation of inflammatory responses contributes to increased colonic damage in a mouse model of dextran sulphate sodium-induced ulcerative colitis.Scientific reports · 2019Article
- A Cell Density-Dependent Reporter in the Drosophila S2 Cells.Scientific reports · 2019Article
- Flightless I Alters the Inflammatory Response and Autoantibody Profile in an OVA-Induced Atopic Dermatitis Skin-Like Disease.Frontiers in immunology · 2018Article
- Cytoskeletal protein Flightless I inhibits apoptosis, enhances tumor cell invasion and promotes cutaneous squamous cell carcinoma progression.Oncotarget · 2015Article
- Attenuation of flightless I improves wound healing and enhances angiogenesis in a murine model of type 1 diabetes.Diabetologia · 2014Article
- Diet-induced over-expression of flightless-I protein and its relation to flightlessness in Mediterranean fruit fly, Ceratitis capitata.PloS one · 2013Article
- The influence of Flightless I on Toll-like-receptor-mediated inflammation in a murine model of diabetic wound healing.BioMed research international · 2013Article
- LRRFIP2 negatively regulates NLRP3 inflammasome activation in macrophages by promoting Flightless-I-mediated caspase-1 inhibition.Nature communications · 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
13 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Drosophila melanogaster flightless I gene is required for normal cellularization of the syncytial blastoderm. Highly conserved homologues of flightless I are present in Caenorhabditis elegans, mouse, and human. We have disrupted the mouse homologue Fliih by homologous recombination in embryonic stem cells. Heterozygous Fliih mutant mice develop normally, although the level of Fliih protein is reduced. Cultured homozygous Fliih mutant blastocysts hatch, attach, and form an outgrowing trophoblast cell layer, but egg cylinder formation fails and the embryos degenerate. Similarly, Fliih mutant embryos initiate implantation in vivo but then rapidly degenerate. We have constructed a transgenic mouse carrying the complete human FLII gene and shown that the FLII transgene is capable of rescuing the embryonic lethality of the homozygous targeted Fliih mutation. These results confirm the specific inactivation of the Fliih gene and establish that the human FLII gene and its gene product are functional in the mouse. The Fliih mouse mutant phenotype is much more severe than in the case of the related gelsolin family members gelsolin, villin, and CapG, where the homozygous mutant mice are viable and fertile but display alterations in cytoskeletal actin regulation.
Indexed as
Identifiers
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.