scholarly journals The Oncogenic Functions of Nicotinic Acetylcholine Receptors

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Yue Zhao
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Mammalian Cells ◽  
Acetylcholine Receptors ◽  
Association Studies ◽  
Nicotine Addiction ◽  
Signal Pathways ◽  
Genome Wide Association Studies ◽  
Nicotinic Acetylcholine ◽  
Lung Cancers ◽  
Numerous Cell

Nicotinic acetylcholine receptors (nAChRs) are ion channels that are expressed in the cell membrane of all mammalian cells, including cancer cells. Recent findings suggest that nAChRs not only mediate nicotine addiction in the brain but also contribute to the development and progression of cancers directly induced by nicotine and its derived carcinogenic nitrosamines whereas deregulation of the nAChRs is observed in many cancers, and genome-wide association studies (GWAS) indicate that SNPs nAChRs associate with risks of lung cancers and nicotine addiction. Emerging evidences suggest nAChRs are posited at the central regulatory loops of numerous cell growth and prosurvival signal pathways and also mediate the synthesis and release of stimulatory and inhibitory neurotransmitters induced by their agonists. Thus nAChRs mediated cell signaling plays an important role in stimulating the growth and angiogenic and neurogenic factors and mediating oncogenic signal transduction during cancer development in a cell type specific manner. In this review, we provide an integrated view of nAChRs signaling in cancer, heightening on the oncogenic properties of nAChRs that may be targeted for cancer treatment.

scholarly journals Nicotinic acetylcholine receptors and nicotine addiction: A brief introduction

2020 ◽  
Vol 177 ◽  
pp. 108256 ◽  
Author(s):  
Ruthie E. Wittenberg ◽  
Shannon L. Wolfman ◽  
Mariella De Biasi ◽  
John A. Dani
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Acetylcholine Receptors ◽  
Nicotine Addiction ◽  
Nicotinic Acetylcholine

scholarly journals Counting Bungarotoxin Binding Sites of Nicotinic Acetylcholine Receptors in Mammalian Cells with High Signal/Noise Ratios

2010 ◽  
Vol 99 (10) ◽  
pp. L81-L83 ◽  
Author(s):  
Paul D. Simonson ◽  
Hannah A. DeBerg ◽  
Pinghua Ge ◽  
John K. Alexander ◽  
Okunola Jeyifous ◽  
...  
Keyword(s):  
Nicotinic Acetylcholine Receptors ◽  
Binding Sites ◽  
Mammalian Cells ◽  
Acetylcholine Receptors ◽  
High Signal ◽  
Nicotinic Acetylcholine ◽  
Signal Noise

scholarly journals Single-Molecule Imaging of AMPA and Nicotinic Acetylcholine Receptors in Mammalian Cells

2009 ◽  
Vol 96 (3) ◽  
pp. 29a
Author(s):  
Paul D. Simonson ◽  
John Alexander ◽  
Okunola Jeyifous ◽  
William N. Green ◽  
Paul R. Selvin
Keyword(s):  
Single Molecule ◽  
Nicotinic Acetylcholine Receptors ◽  
Mammalian Cells ◽  
Acetylcholine Receptors ◽  
Single Molecule Imaging ◽  
Nicotinic Acetylcholine

scholarly journals The α5 Nicotinic Acetylcholine Receptor Subunit Differentially Modulates α4β2* and α3β4* Receptors

2020 ◽  
Vol 12 ◽  
Author(s):  
Petra Scholze ◽  
Sigismund Huck
Keyword(s):  
Gene Cluster ◽  
Nicotinic Acetylcholine Receptors ◽  
Association Studies ◽  
Cellular Level ◽  
Chronic Obstructive ◽  
Genome Wide Association Studies ◽  
Nachr Subunit ◽  
Nicotinic Acetylcholine ◽  
Genetically Engineered Mice ◽  
Wide Range

Nicotine, the principal reinforcing compound in tobacco, acts in the brain by activating neuronal nicotinic acetylcholine receptors (nAChRs). This review summarizes our current knowledge regarding how the α5 accessory nAChR subunit, encoded by the CHRNA5 gene, differentially modulates α4β2* and α3β4* receptors at the cellular level. Genome-wide association studies have linked a gene cluster in chromosomal region 15q25 to increased susceptibility to nicotine addiction, lung cancer, chronic obstructive pulmonary disease, and peripheral arterial disease. Interestingly, this gene cluster contains a non-synonymous single-nucleotide polymorphism (SNP) in the human CHRNA5 gene, causing an aspartic acid (D) to asparagine (N) substitution at amino acid position 398 in the α5 nAChR subunit. Although other SNPs have been associated with tobacco smoking behavior, efforts have focused predominantly on the D398 and N398 variants in the α5 subunit. In recent years, significant progress has been made toward understanding the role that the α5 nAChR subunit—and the role of the D398 and N398 variants—plays on nAChR function at the cellular level. These insights stem primarily from a wide range of experimental models, including receptors expressed heterologously in Xenopus oocytes, various cell lines, and neurons derived from human induced pluripotent stem cells (iPSCs), as well as endogenous receptors in genetically engineered mice and—more recently—rats. Despite providing a wealth of available data, however, these studies have yielded conflicting results, and our understanding of the modulatory role that the α5 subunit plays remains incomplete. Here, we review these reports and the various techniques used for expression and analysis in order to examine how the α5 subunit modulates key functions in α4β2* and α3β4* receptors, including receptor trafficking, sensitivity, efficacy, and desensitization. In addition, we highlight the strikingly different role that the α5 subunit plays in Ca2+ signaling between α4β2* and α3β4* receptors, and we discuss whether the N398 α5 subunit variant can partially replace the D398 variant.

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