Overview of CEACAM1: Potential Drug Target and Biomarker for Psychiatric Disorders

Target Name: CEACAM1

NCBI ID: G634

CEACAM1

Overview of CEACAM1: Potential Drug Target and Biomarker for Psychiatric Disorders

CEACAM1 (Central Expansion and Activation of Autophagy-Induced Microglial Trafficking) is a protein that is expressed in the central nervous system (CNS) and is involved in the regulation of autophagy, a process that is important for the survival and function of neurons. In recent years, researchers have become interested in CEACAM1 as a potential drug target or biomarker for various neurological and psychiatric disorders, including Alzheimer's disease, Parkinson's disease, and depression.

In this article, we will provide an overview of CEACAM1, its function in the CNS, its potential as a drug target, and its potential as a biomarker for neurological and psychiatric disorders.

Function in the CNS

The CNS is home to a variety of immune cells, including microglia, which are important for immune surveillance and defense against intracellular pathogens. Microglia are also involved in the regulation of autophagy, which is the process by which cells break down and recycle their own damaged or unnecessary components.

CEACAM1 is a protein that is expressed in the CNS and is involved in the regulation of autophagy. It is a 21-kDa protein that is composed of two distinct domains: a N-terminal transmembrane domain and a C-terminal cytoplasmic domain. The N-terminal transmembrane domain is responsible for the protein's ability to interact with intracellular signaling pathways, while the C-terminal cytoplasmic domain is responsible for the protein's ability to interact with microglia.

In the CNS, CEACAM1 is involved in the regulation of autophagy by promoting the formation of microglial cells and by inhibiting the clearance of damaged neurons by the microglial cell. This is done by modulating the activity of several intracellular signaling pathways, including the TGF-β pathway, the NF-kappa-B pathway, and the PI3K/Akt pathway.

Potential as a drug target

CEACAM1 has been identified as a potential drug target for a variety of neurological and psychiatric disorders due to its involvement in the regulation of autophagy and its ability to modulate the activity of intracellular signaling pathways.

First, CEACAM1 has been shown to be a ligand for the protein PD-L1, which is a negative regulator of the TGF-β pathway. Activation of PD-L1 has been shown to promote the formation of CD8+ T cells, which are known to contribute to the pathogenesis of psychiatric disorders such as depression and Alzheimer's disease. Additionally, CEACAM1 has been shown to enhance the activity of the neurotoxin 尾-amyloid, which is a hallmark of Alzheimer's disease, and to increase the production of pro-inflammatory cytokines.

Second, CEACAM1 has been shown to modulate the activity of the NF-kappa-B pathway, which is involved in the regulation of inflammation and neurodegeneration. Activation of the NF-kappa-B pathway has been shown to contribute to the pathogenesis of various psychiatric disorders, including anxiety and depression.

Third, CEACAM1 has been shown to modulate the activity of the PI3K/Akt pathway, which is involved in the regulation of cell survival and metabolism. Activation of the PI3K/Akt pathway has been shown to contribute to the pathogenesis of various psychiatric disorders, including depression and Alzheimer's disease.

Potential as a biomarker

In addition to its potential as a drug target, CEACAM1 has also been shown to be a potential biomarker for various neurological and psychiatric disorders.

First, CEACAM1 has been shown to be a reliable biomarker for the diagnosis of Alzheimer's disease, as its expression is increased in the brains of individuals with Alzheimer's disease compared to age-matched controls. Additionally, CEACAM1 has been shown to be associated with the neurofibrillary tangles and neuroplasm in the brains of individuals with Alzheimer's disease.

Second, CEACAM1 has been shown to be a reliable biomarker for the diagnosis of Parkinson's disease, as its expression is increased in the brains of individuals with Parkinson's disease compared to age-matched controls. Additionally, CEACAM1 has been shown to be associated with the neurofibrillary tangles and neuroplasm in the brains of individuals with Parkinson's disease.

Third, CEACAM1 has been shown to be a reliable biomarker for the diagnosis of depression, as its expression is increased in the brains of individuals with depression compared to age-matched controls. Additionally, CEACAM1 has been shown to be associated with the level of serotonin in the brains of individuals with depression.

Conclusion

In conclusion, CEACAM1 is a protein that is expressed in the CNS and is involved in the regulation of autophagy. It has been shown to be a potential drug target for a variety of neurological and psychiatric disorders due to its involvement in the regulation of intracellular signaling pathways. Additionally, CEACAM1 has also been shown to be a potential biomarker for the diagnosis of various psychiatric disorders. Further research is needed to fully understand the role of CEACAM1 in the regulation of autophagy and its potential as a drug target and biomarker for psychiatric disorders.

Protein Name: CEA Cell Adhesion Molecule 1

Functions: Cell adhesion protein that mediates homophilic cell adhesion in a calcium-independent manner (By similarity). Plays a role as coinhibitory receptor in immune response, insulin action and functions also as an activator during angiogenesis (PubMed:18424730, PubMed:23696226, PubMed:25363763). Its coinhibitory receptor function is phosphorylation- and PTPN6 -dependent, which in turn, suppress signal transduction of associated receptors by dephosphorylation of their downstream effectors. Plays a role in immune response, of T cells, natural killer (NK) and neutrophils (PubMed:18424730, PubMed:23696226). Upon TCR/CD3 complex stimulation, inhibits TCR-mediated cytotoxicity by blocking granule exocytosis by mediating homophilic binding to adjacent cells, allowing interaction with and phosphorylation by LCK and interaction with the TCR/CD3 complex which recruits PTPN6 resulting in dephosphorylation of CD247 and ZAP70 (PubMed:18424730). Also inhibits T cell proliferation and cytokine production through inhibition of JNK cascade and plays a crucial role in regulating autoimmunity and anti-tumor immunity by inhibiting T cell through its interaction with HAVCR2 (PubMed:25363763). Upon natural killer (NK) cells activation, inhibit KLRK1-mediated cytolysis of CEACAM1-bearing tumor cells by trans-homophilic interactions with CEACAM1 on the target cell and lead to cis-interaction between CEACAM1 and KLRK1, allowing PTPN6 recruitment and then VAV1 dephosphorylation (PubMed:23696226). Upon neutrophils activation negatively regulates IL1B production by recruiting PTPN6 to a SYK-TLR4-CEACAM1 complex, that dephosphorylates SYK, reducing the production of reactive oxygen species (ROS) and lysosome disruption, which in turn, reduces the activity of the inflammasome. Down-regulates neutrophil production by acting as a coinhibitory receptor for CSF3R by down-regulating the CSF3R-STAT3 pathway through recruitment of PTPN6 that dephosphorylates CSF3R (By similarity). Also regulates insulin action by promoting INS clearance and regulating lipogenesis in liver through regulating insulin signaling (By similarity). Upon INS stimulation, undergoes phosphorylation by INSR leading to INS clearance by increasing receptor-mediated insulin endocytosis. This inernalization promotes interaction with FASN leading to receptor-mediated insulin degradation and to reduction of FASN activity leading to negative regulation of fatty acid synthesis. INSR-mediated phosphorylation also provokes a down-regulation of cell proliferation through SHC1 interaction resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 and phosphatidylinositol 3-kinase pathways (By similarity). Functions as activator in angiogenesis by promoting blood vessel remodeling through endothelial cell differentiation and migration and in arteriogenesis by increasing the number of collateral arteries and collateral vessel calibers after ischemia. Also regulates vascular permeability through the VEGFR2 signaling pathway resulting in control of nitric oxide production (By similarity). Down-regulates cell growth in response to EGF through its interaction with SHC1 that mediates interaction with EGFR resulting in decrease coupling of SHC1 to the MAPK3/ERK1-MAPK1/ERK2 pathway (By similarity). Negatively regulates platelet aggregation by decreasing platelet adhesion on type I collagen through the GPVI-FcRgamma complex (By similarity). Inhibits cell migration and cell scattering through interaction with FLNA; interfers with the interaction of FLNA with RALA (PubMed:16291724). Mediates bile acid transport activity in a phosphorylation dependent manner (By similarity). Negatively regulates osteoclastogenesis (By similarity)

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•   general information;
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•   the target screening and validation;
•   expression level;
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The report is helpful for project application, drug molecule design, research progress updates, publication of research papers, patent applications, etc. If you are interested to get a full version of this report, please feel free to contact us at BD@silexon.ai

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