ArticlePloS one2014
Altered behavior in mice with deletion of the alpha2-antiplasmin gene.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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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
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.
- Alpha2-Antiplasmin: The Devil You Don't Know in Cerebrovascular and Cardiovascular Disease.Frontiers in cardiovascular medicine · 2020Pooled it
- Tail-rattling in rodents: more than a threat display.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2026Review
- α2-Antiplasmin as a Potential Therapeutic Target for Systemic Sclerosis.Life (Basel, Switzerland) · 2022Review
- The Fibrinolytic System: Mysteries and Opportunities.HemaSphere · 2021Review
- A growth-factor-activated lysosomal KNature · 2021Article
- α2-Antiplasmin as a potential regulator of the spatial memory process and age-related cognitive decline.Molecular brain · 2020Article
- α2AP is associated with the development of lupus nephritis through the regulation of plasmin inhibition and inflammatory responses.Immunity, inflammation and disease · 2020Article
- Alternatively activated macrophages are associated with the α2AP production that occurs with the development of dermal fibrosis : The role of alternatively activated macrophages on the development of fibrosis.Arthritis research & therapy · 2020Article
- The Role of Fibrinolytic Regulators in Vascular Dysfunction of Systemic Sclerosis.International journal of molecular sciences · 2019Review
- Reduced Neuroinflammation and Improved Functional Recovery after Traumatic Brain Injury by Prophylactic Diet Supplementation in Mice.Nutrients · 2019Article
- Mouse model of rare TOR1A variant found in sporadic focal dystonia impairs domains affected in DYT1 dystonia patients and animal models.Neurobiology of disease · 2016Article
- Proteolytic cleavage of proBDNF into mature BDNF in the basolateral amygdala is necessary for defeat-induced social avoidance.Learning & memory (Cold Spring Harbor, N.Y.) · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe α2-antiplasmin (α2AP) protein is known to be a principal physiological inhibitor of plasmin, and is expressed in various part of the brain, including the hippocampus, cortex, hypothalamus and cerebellum, thus suggesting a potential role for α2AP in brain functions. However, the involvement of α2AP in brain functions is currently unclear.
objectivesThe goal of this study was to investigate the effects of the deletion of the α2AP gene on the behavior of mice.
methodsThe motor function was examined by the wire hang test and rotarod test. To evaluate the cognitive function, a repeated rotarod test, Y-maze test, Morris water maze test, passive or shuttle avoidance test and fear conditioning test were performed. An open field test, dark/light transition test or tail suspension test was performed to determine the involvement of α2AP in anxiety or depression-like behavior. RESULTS AND
conclusionsThe α2AP knockout (α2AP-/-) mice exhibited impaired motor function compared with α2AP+/+ mice. The α2AP-/- mice also exhibited impairments in motor learning, working memory, spatial memory and fear conditioning memory. Furthermore, the deletion of α2AP induced anxiety-like behavior, and caused an anti-depression-like effect in tail suspension. Therefore, our findings suggest that α2AP is a crucial mediator of motor function, cognitive function, anxiety-like behavior and depression-like behavior, providing new insights into the role of α2AP in the brain functions.
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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.