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- Table of Contents
Facts about Neural cell adhesion molecule L1-like protein.
Plays a role in neuronal placement of pyramidal neurons and in regulation of both the amount of interneurons and the efficacy of GABAergic synapses. May play a role in regulating cell migration in nerve regeneration and cortical development.
Human | |
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Gene Name: | CHL1 |
Uniprot: | O00533 |
Entrez: | 10752 |
Belongs to: |
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immunoglobulin superfamily |
CALL; CALLClose homolog of L1; cell adhesion molecule with homology to L1CAM (close homolog of L1); cell adhesion molecule with homology to L1CAM (close homologue of L1); CHL1; CHL-1; FLJ44930; L1CAM-2; L1CAM2L1 cell adhesion molecule 2; MGC132578; neural cell adhesion molecule L1-like protein
Mass (kDA):
135.071 kDA
Human | |
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Location: | 3p26.3 |
Sequence: | 3; NC_000003.12 (196588..409417) |
Expressed in the fetal and adult brain as well as in Schwann cell culture. Also detected in adult peripheral tissues.
Cell membrane; Single-pass type I membrane protein. Soluble forms produced by cleavage/shedding also exist.; [Processed neural cell adhesion molecule L1-like protein]: Secreted, extracellular space, extracellular matrix.
Scientists have the option to submit their results to Boster and receive credit for any work done with CHL1 marker. This can be useful for samples or applications specific to a species. These product credits can be applied for by all scientists worldwide, not just Boster scientists. Submitting results for species or applications has many benefits. These benefits are detailed in the following paragraphs. These are the top reasons to use CHL1 as a marker.
In mouse models, overexpression of CHL1 inhibits DDP and PTX-mediated repression of tumor growth and promotes apoptosis. CHL1 knockdown caused neurite retraction, and elevated levels of activated Caspase-3. These combined results suggest that CHL1 may be an important tumor suppressor in the treatment for glioma/glioblastoma.
Numerous studies have shown a significant increase in CHL1 expression in various types human cancers. For example, a recent study published in Acta Biochim Pol showed that CHL1 mRNA levels are higher in non-metastatic colorectal cancers than in the metastatic subtype of colorectal cancer. Additionally, microRNA expression signatures were found to be significantly higher than in other types cancers such as gliomas or melanoma.
CHL1 is a tumor-suppressor. However, it's not known if CHL1 plays an oncogene or cancer-causing role. CHL1 belongs to the L1 group of cell adhesion proteins. However, CHL1 may play multiple roles in the progression and growth of cancer. CHL1 deregulation may promote metastasis, invasive growth, and metastasis in esophageal Squamous Cell Carcinoma.
CHL1 expression decreased in A549 cells. CHL1 expression was reduced in A549 cells, which led to increased cell survival and decreased apoptosis. CHL1 overexpression however increased NSCLC chemosensitivity. CHL1 might be an important target to increase chemosensitivity for lung cancer. CHL1 can only be partially regulated.
CHL1 was found to be important in CRC chemotherapy resistance in vitro. In addition, overexpression of CHL1 increased the sensitivity of resistant cells, whereas knockdown of CHL1 led to the opposite effect. It is therefore important that we understand the role of CHL1 in CRC chemotherapy resistance.
Autocrine signaling occurs through the CHL1 protein's extracellular domain. It promotes cell mobility and decreases cell adhesion. It promotes Purkinje-cell survival and migration. It is essential for normal fertility and developmental processes. CHL1 mutations can result in cell proliferation defects which are not lineage-dependent. Furthermore, CHL1 has been linked to abnormalities of the thalamocortical circuitry in some Asian populations.
A melanoma cell adhesion gene called CHL1 controls the fate of mesenchymal stromal cells, which make up the bulk of the melanoma. This gene is also involved in the maintenance of hematopoietic stem and progenitor cells. The gene can be overexpressed or mutated, with results that are different from one another.
CHL1 encodes transmembraneCAM. This gene can undergo heterophilic as well as homophilic interactions. It is a member of the L1 family of immunoglobulins, which includes NrCAM, L1, and CHL1. L1CAM has been linked to melanoma. It is involved in synaptic plasticity as well as neuronal migration.
CHL1 is a cytoplasmic protein that has anti-proliferation and anti-metastasis functions. CHL1 overexpression in breast cancer cells can lead to tumor progression and initiation. CHL1 acts as tumor suppressor and inhibits cell proliferation, migration and invasion. CHL1 is essential in normal development and fertility. An abnormal expression of this gene may be related to several diseases, such as schizophrenia and thalamocorticalcircuitry.
Multiple studies have shown an increase in chemosensitivity of NSCLC cell lines when CHL1 is overexpressed. A549 cells were treated with SC66, which is a CHL1 inhibitor. This resulted in enhanced chemosensitivity. CHL1 depletion led to increased resistance to chemoradiation. Overexpression of CHL1 promoted apoptosis, decreased cell survival, and increased clone formation. Although the mechanism by which CHL1 inhibits tumor cell growth is still unclear, CHL1 could be an option for lung cancer chemotherapies.
CHL1 is an important marker for cancer. It is also expressed in certain types of cells that are resistant to chemotherapy. CHL1 has also been linked to NSCLC's chemoresistance, which is a major cause of cancer recurrence. However, further research is needed to understand its role in this disease. CHL1 could also affect the response of colorectal tumor cells to chemoradiation.
CHL1 knockdown decreases colony growth in A549 cell lines. Colony development was suppressed when CHL1 was silenced using siRNAs. The optical density of cells at 546 nm was determined using U251, SHG44 and U87 MG cells. A549 cells showed significantly lower colony formation after knockdown than those with negative control siRNA.
In neuroblastoma, nearly half of patients had CHL1 or NrCAM. Overexpression of these genes was associated with tumor invasiveness in vitro and metastatic dissemination in adult patients. CHL1 was also associated with a better outcome in pediatric neuroblastoma. These findings suggest CHL1 may promote cell death in certain types tumors, such as neuroblastoma.
CHL1 can be found in rodents in their carotid body. It is a key oxygen detector. CHL1/ mice show an increase in glomus cells and tyrosinehydroxylase, a marker for glomus. CHL1-/ mice also have higher levels of plasma catecholamines and arterial blood pressure during hypoxia.
A new study by UCLA researchers says that electroencephalograms may be used to predict whether a patient will be cured by a certain psychopharmacological treatment. The study was led by Dr. Andrew Leuchter from the Semel Institute. It can be done in ten minutes and can predict a patient’s likelihood of remission within one week. Patients don't need to wait weeks to know if the medication will work. Knowing whether the medication will work could eliminate the need to wait weeks.
The biomarker was created by Dr. Mark Rasenick at the University of Illinois. He is also a distinguished professor of physiology at Steven Targum. It could soon be used for determining if a patient's health is suitable to take SSRIs. These results are promising and could lead to a simple genetic test doctors can use to recommend a specific antidepressant to patients.
Researchers analyzed brain responses to antidepressants. They found that depression severity is associated with brain levels regulated by the ABCB1 protein. P-glycoprotein was also associated with brain drug penetration. The researchers used a transgenic mouse model to determine the effects of P-glycoprotein on the brain's penetration of antidepressants.
Researchers have also tested the potential effectiveness of pharmacogenomic tests to predict which medications are most effective for a patient's depression. Some studies have shown a 95% accuracy rate. In addition, a number of patients tested for biomarkers have a low-severity mood disorder. Ultimately, biomarkers will not be able to determine whether a patient will be cured or not.
PMID: 9799093 by Wei M.-H., et al. In silico-initiated cloning and molecular characterization of a novel human member of the L1 gene family of neural cell adhesion molecules.