anti-Cell Adhesion Molecule with Homology To L1CAM (Close Homolog of L1) (CHL1) Antikörper

Human Cell Adhesion Molecule with Homology To L1CAM (Close Homolog of L1) (CHL1) Interaktionspartner

1. Results identified a new tumor suppressor, CHL1, located at 3p26 which was frequently deleted in esophageal squamous cells carcinoma (ESCC). Reduced expression of CHL1 correlated with poor differentiation, increased invasion, lymph-node metastasis, advanced tumor stage, and decreased overall survival. Further data support CHL1 as an important tumor suppressor with both anti-proliferation and anti-metastasis abilities.

2. Expression level of miR-21-5p increased in both colon adenocarcinoma (COAD) tissues and cells. The result of in vivo experiments showed that down-regulation of miR-21-5p decreased the volume and weight of tumor, while knockdown of CHLI stimulated tumor growth. The overexpression of miR-21-5p can promote propagation and invasiveness of (COAD) cells through inhibiting the expression of CHL1.

3. CHL1 was found to have greater than 15-fold higher expression in fragments per kilobase million in HCC compared with benign Hurthle cell tumors. This was confirmed by qRT-PCR. Moreover, the immunoreactivity score of the CHL1 protein was significantly higher in HCC compared with benign Hurthle cell nodules.

4. 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).

5. CHL1 expression patient-derived lymphoblasts correlated with clinical outcome in depressive disorder patients.

6. our findings suggest that miR-590-5p acts as an oncogene by targeting the CHL1 gene and promotes cervical cancer proliferation

7. There was no statistical association between polymorphisms of the CHL1 gene and idiopathic scoliosis in a Chinese population.

8. Our data collectively indicate that miR-182 in PTC promotes cell proliferation and invasion through direct suppression of CHL1, supporting the potential utility of miR-182 inhibition as a novel therapeutic strategy against PTC.

9. The rs2272522 polymorphism (in the CHL1 gene) was found to exhibit a highly significant association with schizophrenia in the Qatari population.

10. In 1 of 113 Colombian children with refractory epilepsy, MLPA showed a subtelomeric duplication of exon 3 of CHL1, also present in 2 relatives.

11. CHL1 has a role in human breast tumorigenesis and progression

12. The miRNA miR-151-3p had 6.7-fold higher basal expression in paroxetine-sensitive LCLs. This corresponds with lower expression of CHL1, a target of miR-151-3p

13. BACE1(-/-) axon guidance defects are likely the result of abrogated BACE1 processing of CHL1 and BACE1 deficiency produces a CHL1 loss-of-function phenotype

14. miR-10a expression is upregulated in cervical cancer tissues, and miR-10a promotes cell growth, migration and invasion by targeting CHL1 in human cervical cancer cells.

15. Overall, our study found a significant association of IL-17RC gene polymorphisms with AIS in a Chinese Han population, indicating IL-17RC gene may be as a susceptibility gene for AIS.

16. CHL1 is involved in the development of different human cancers.

17. Genome-wide transcriptional profiling of in vitro phenotyped LCLs identified CHL1 and additional genes implicated in synaptogenesis and brain circuitry as putative SSRI response biomarkers.

18. An association between a missense polymorphism in the close homologue of L1 (CHL1, CALL) gene and schizophrenia.

19. L1 could drive progression by enhancing cell migration and tumor growth in ovarian carcinoma.

20. MAP kinase pathway regulates L1-CAM-mediated nerve growth by modulating ankyrin binding.

Mouse (Murine) Cell Adhesion Molecule with Homology To L1CAM (Close Homolog of L1) (CHL1) Interaktionspartner

1. here we identify a number of novel roles for CHL1 in establishment of the midbrain dopamine pathways, functions that are reinforced by evidence in other neuronal networks, yet roles that are also unique to this discrete population of neurons. Supported by spatial and temporal expression within the VM, and validated in CHL1 deficient mice.

2. 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.

3. 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.

4. 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.

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. CHL1 is a novel intrinsic factor that is involved in carotid body function and in the ventilatory response to acute hypoxia.

11. CHL1 endocytosis are required for CHL1-dependent neurite outgrowth.

12. CHL1 might play an important role in hypoxia damage regulation.

13. BACE1(-/-) axon guidance defects are likely the result of abrogated BACE1 processing of CHL1 and BACE1 deficiency produces a CHL1 loss-of-function phenotype

14. L1 and CHL1 are cleaved by BACE1 under physiological conditions

15. This study provided evidence that the CHL1 affect the repair of the blood-spinal cord barrier repair in soinal cord injury.

16. Results describe the negative modulation of the proliferation and neuronal differentiation of neural progenitor cells by CHL1/ERK1/2 MAPK signaling.

17. 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.

18. a novel role for CHL1

19. 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.

20. 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.