ArticleThe Journal of comparative neurology2010
Role of the cytoplasmic domain of the L1 cell adhesion molecule in brain development.
Article in The Journal of comparative neurology, 2010. 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.
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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
17 citing papers in PubMed, 25 citations in OpenAlex.
- The Life of a Trailing Spouse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Mutations in MAGEL2 and L1CAM Are Associated With Congenital Hypopituitarism and Arthrogryposis.The Journal of clinical endocrinology and metabolism · 2019Article
- α1ACT Is Essential for Survival and Early Cerebellar Programming in a Critical Neonatal Window.Neuron · 2019Article
- A Fragment of Adhesion Molecule L1 Binds to Nuclear Receptors to Regulate Synaptic Plasticity and Motor Coordination.Molecular neurobiology · 2018Article
- A serine protease KLK8 emerges as a regulator of regulators in memory: Microtubule protein dependent neuronal morphology and PKA-CREB signaling.Scientific reports · 2018Article
- Conditional deletion of L1CAM in human neurons impairs both axonal and dendritic arborization and action potential generation.The Journal of experimental medicine · 2016Article
- The role of Arp2/3 in growth cone actin dynamics and guidance is substrate dependent.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- LGR5 is a proneural factor and is regulated by OLIG2 in glioma stem-like cells.Cellular and molecular neurobiology · 2013Article
- Bergmann glia function in granule cell migration during cerebellum development.Molecular neurobiology · 2013Review
- L1CAM and its cell-surface mutants: new mechanisms and effects relevant to the physiology and pathology of neural cells.Journal of neurochemistry · 2013Article
- Transsynaptic coordination of synaptic growth, function, and stability by the L1-type CAM Neuroglian.PLoS biology · 2013Article
- TAG1 regulates the endocytic trafficking and signaling of the semaphorin3A receptor complex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- EphB regulates L1 phosphorylation during retinocollicular mapping.Molecular and cellular neurosciences · 2012Article
- Endocytosis and endosomes at the crossroads of regulating trafficking of axon outgrowth-modifying receptors.Traffic (Copenhagen, Denmark) · 2011Review
- Dscam mutation leads to hydrocephalus and decreased motor function.Protein & cell · 2011Article
- Polarized targeting of L1-CAM regulates axonal and dendritic bundling in vitro.The European journal of neuroscience · 2010Article
- Olfactory ensheathing glia express aquaporin 1.The Journal of comparative neurology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Mutations in the human L1CAM gene cause X-linked hydrocephalus and MASA (Mental retardation, Aphasia, Shuffling gait, Adducted thumbs) syndrome. In vitro studies have shown that the L1 cytoplasmic domain (L1CD) is involved in L1 trafficking, neurite branching, signaling, and interactions with the cytoskeleton. L1cam knockout (L1(KO)) mice have hydrocephalus, a small cerebellum, hyperfasciculation of corticothalamic tracts, and abnormal peripheral nerves. To explore the function of the L1CD, we made three new mice lines in which different parts of the L1CD have been altered. In all mutant lines L1 protein is expressed and transported into the axon. Interestingly, these new L1CD mutant lines display normal brain morphology. However, the expression of L1 protein in the adult is dramatically reduced in the two L1CD mutant lines that lack the ankyrin-binding region and they show defects in motor function. Therefore, the L1CD is not responsible for the major defects observed in L1(KO) mice, yet it is required for continued L1 protein expression and motor function in the adult.
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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.