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The protein encoded by CHL1 is a member of the L1 gene family of neural cell adhesion molecules.
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Results indicate that close homolog of L1 protein (CHL1) is downregulated by hypermethylation and that this epigenetic alteration is an independent prognostic factor in breast cancer (BC).
CHL1 expression patient-derived lymphoblasts correlated with clinical outcome in depressive disorder patients.
our findings suggest that miR-590-5p acts as an oncogene by targeting the CHL1 gene and promotes cervical cancer proliferation
There was no statistical association between polymorphisms of the CHL1 gene and idiopathic scoliosis in a Chinese population.
Our data collectively indicate that miR (show MLXIP ELISA Kits)-182 in PTC (show F9 ELISA Kits) promotes cell proliferation and invasion through direct suppression of CHL1 (show DDX11 ELISA Kits), supporting the potential utility of miR (show MLXIP ELISA Kits)-182 inhibition as a novel therapeutic strategy against PTC (show F9 ELISA Kits).
The rs2272522 polymorphism (in the CHL1 gene) was found to exhibit a highly significant association with schizophrenia in the Qatari population.
In 1 of 113 Colombian children with refractory epilepsy, MLPA showed a subtelomeric duplication of exon 3 of CHL1, also present in 2 relatives.
CHL1 has a role in human breast tumorigenesis and progression
The miRNA miR (show MLXIP ELISA Kits)-151-3p had 6.7-fold higher basal expression in paroxetine-sensitive LCLs. This corresponds with lower expression of CHL1 (show DDX11 ELISA Kits), a target of miR (show MLXIP ELISA Kits)-151-3p
BACE1(-/-) axon guidance defects are likely the result of abrogated BACE1 processing of CHL1 and BACE1 deficiency produces a CHL1 loss-of-function phenotype
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 (show TROVE2 ELISA Kits)-0175.
The results of the present study indicate that CHL1 triggers PTCH1 (show PTCH1 ELISA Kits)-, SMO-, RhoA (show RHOA ELISA Kits)- and ROCK-dependent signal transduction pathways to promote neuronal survival after cessation of the major morphogenetic events during mouse cerebellar development.
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.
Findings indicate that disrupted-in-schizophrenia 1 (DISC1 (show DISC1 ELISA Kits)) and close homolog of L1 may engage in physical and functional interaction in neural development, supporting the notion that DISC1 (show DISC1 ELISA Kits) regulates neurite outgrowth with a receptor belonging to the neural cell adhesion molecules.
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.
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.
homophilic CHL1 transinteractions regulate early differentiation of NSCs. heterophilic transinteractions of CHL1 with vitronectin (show VTN ELISA Kits), integrins, and plasminogen (show PLG ELISA Kits) activators regulate neuritogenesis and neural cell migration later in cerebellar morphogenesis.
CHL1 is a novel intrinsic factor (show GIF ELISA Kits) that is involved in carotid body function and in the ventilatory response to acute hypoxia.
CHL1 endocytosis are required for CHL1-dependent neurite outgrowth.
CHL1 might play an important role in hypoxia damage regulation.
The protein encoded by this gene is a member of the L1 gene family of neural cell adhesion molecules. It is a neural recognition molecule that may be involved in signal transduction pathways. The deletion of one copy of this gene may be responsible for mental defects in patients with 3p- syndrome. This protein may also play a role in the growth of certain cancers. Alternate splicing results in both coding and non-coding variants.
L1 cell adhesion molecule 2
, cell adhesion molecule with homology to L1CAM (close homolog of L1)
, cell adhesion molecule with homology to L1CAM (close homologue of L1)
, close homolog of L1
, neural cell adhesion molecule L1-like protein
, chl1-like protein
, cell adhesion molecule L1-like