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The correlation between the tumor size and the amount of CHL1 secretion could be examined in this study, and showed a significant positive correlation in a tumor size-dependent manner.
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investigated temporal discounting in CHL1-deficient (KO) mice and their wild-type littermates. Although no discounting differences were found under baseline conditions, CHL1-KO mice showed increased impulsive choice following chronic unpredictable stress (fewer % larger-later choices, and reduced area under the discounting curve). Impulsive choice alterations were reversed by the 5-HT2C agonist Ro 60-0175.
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The results of the present study indicate that CHL1 triggers PTCH1-, SMO-, RhoA- and ROCK-dependent signal transduction pathways to promote neuronal survival after cessation of the major morphogenetic events during mouse cerebellar development.
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These results provide strong support for a 'two-hit' (genes x environment) effect on latent inhibition in CHL1-deficient mice, and identify CHL1-deficient mice as a model of schizophrenia-like learning and attention impairments.
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Findings indicate that disrupted-in-schizophrenia 1 (DISC1) and close homolog of L1 may engage in physical and functional interaction in neural development, supporting the notion that DISC1 regulates neurite outgrowth with a receptor belonging to the neural cell adhesion molecules.
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results demonstrate that CHL1 regulates signal transduction pathways through constitutively active 5-HT2c receptor isoforms, thereby altering 5-HT2c receptor functions and implicating CHL1 as a new modulator of the serotonergic system.
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This study provided novel evidence for the functional importance of CHL1 in the post-natal maturation and maintenance of inhibitory circuits and synaptic plasticity in the mouse hippocampus.
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homophilic CHL1 transinteractions regulate early differentiation of NSCs. heterophilic transinteractions of CHL1 with vitronectin, integrins, and plasminogen activators regulate neuritogenesis and neural cell migration later in cerebellar morphogenesis.
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CHL1 is a novel intrinsic factor that is involved in carotid body function and in the ventilatory response to acute hypoxia.
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CHL1 endocytosis are required for CHL1-dependent neurite outgrowth.
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CHL1 might play an important role in hypoxia damage regulation.
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BACE1(-/-) axon guidance defects are likely the result of abrogated BACE1 processing of CHL1 and BACE1 deficiency produces a CHL1 loss-of-function phenotype
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L1 and CHL1 are cleaved by BACE1 under physiological conditions
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This study provided evidence that the CHL1 affect the repair of the blood-spinal cord barrier repair in soinal cord injury.
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Results describe the negative modulation of the proliferation and neuronal differentiation of neural progenitor cells by CHL1/ERK1/2 MAPK signaling.
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The results of this study implicated a novel mechanism in which L1 and CHL1 interact with individual EphA receptors and cooperate to guide subpopulations of thalamic axons to distinct neocortical areas essential for thalamocortical connectivity.
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a novel role for CHL1
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Elevated CHL1 expression by reactive astrocytes requires activation of PI3K/PKCdelta-dependent pathways; reduction of PI3K/PKCdelta activity represents a therapeutic target to downregulate CHL1 expression, benefitting axonal regeneration after SCI.
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data show that the permanent absence of CHL1 results in misguided axonal projections and aberrant axonal connectivity and alters the exploratory behavior in novel environments, suggesting deficits in information processing in CHL1-deficient mice.
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a role of the protein in the lesioned central nervous system
