Catalog | Product Name | Gene Name | Species | Morphology | Price |
---|---|---|---|---|---|
ACC-RI0061 | Human CHRNA3/CHRNB4 Stable Cell Line-CHO | CHRNB4 | Human | Epithelial-like | INQUIRY |
The neuronal acetylcholine receptor subunit beta-4 is a protein that is encoded by the CHRNB4 gene in humans.
Existing studies have shown that the nicotinic acetylcholine receptor (NACHR) is a member of the ligand-gated ion channel superfamily, which mediates rapid synaptic signal transmission. Among them, NACHR is considered to be a (heterologous) pentamer composed of homologous subunits.
In 1992, Tarroni et al. used the rat β-4 subunit probe to screen a human neuroblastoma cDNA library and cloned part of the β-4 subunit cDNA. Later, they used Northern blot and RT-PCR to find that the human β-4 subunit is expressed in the form of 3.1 kb mRNA in neuroblastoma and small cell lung cancer cell lines. In 1996, researchers isolated a complete β-4 clone from a neuroblastoma cell line cDNA library. The clone predicted that the encoded 498 amino acid protein is 84% similar to the rat β-4 protein. In subsequent studies, some scientists also cloned a complete beta-4 cDNA from neuroblastoma cell line mRNA. It was also found that the human β-4 subunit expressed a 2.4 kb mRNA in the neuroblastoma cell line.
Existing research results show that nicotinic acetylcholine receptors are the key mediator of the effect of nicotine on the central nervous system. The neuronal subtypes of NACHR include various homomeric or heteromeric combinations of 12 different nicotinic subunits: α2 to α10 and β2 to β4. The gene cluster on chromosome 15 where the CHRNA5-CHRNA3-CHRNB4 is located encodes α5, α3 and β4 subunits. Studies have shown that this gene cluster is closely related to nicotine addiction. There is consistent evidence that there are variations in the nicotinic receptor clusters (CHRNA5, CHRNA3, CHRNB4) on chromosome 15 in patients with nicotine dependence. Analysis in people of European descent has detected a phenotype associated with nicotine addiction and a missense single nucleotide polymorphism (SNP) in a gene that changes a conservative amino acid in the gene from aspartic acid to asparagine). In addition, nicotine and alcohol dependence are usually comorbid diseases, which suggests that there may be common pathways leading to the risks of these two diseases. Since the nicotinic receptor cluster is closely related to nicotine addiction, it may also be involved in the regulation of alcohol dependence.
Figure 1. The Genetic Locus CHRNA5 CHRNA3 CHRNB4 the Subunits of a Nicotinic Acetylcholine Receptor (nAChR). (Glenda Lassi, et al.; 2016)
The results of the study indicate that the expression of CHRNB4 is limited to the medial habenula, olfactory bulb and a few other regions. Although most of the research areas of CHRNA5-CHRNA3-CHRNB4 are concentrated in CHRNA5 and CHRNA3, the existing results indicate that CHRNB4 has a correlation in nicotine addiction. For example, in a study of CHRNB4-deficient mice, it was found that homozygous deletion mice showed reduced anxiety in elevated plus mazes and light and dark boxes, but increased anxiety during social isolation. Further research found that the lack of CHRNB4 does not damage spatial learning or situational fear conditioning, which indicates that the receptor is not involved in cognitive function. However, these mice have undergone tremendous changes in the physiological and behavioral changes of nicotine, which are characterized by reduced seizures and hypokinesia responses to nicotine. Related behaviors also reduce withdrawal and reduction of nicotine induced analgesia. Heterozygous mice showed normal enhancement of intercranial self-stimulation after nicotine withdrawal. These mice showed a normal nicotine-promoting effect on situational fear conditioning. In addition, the study also found that the SNP in CHRNB4 is related to the increased risk of schizophrenia and the regulation of α5 expression.
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