Basic and modern concepts on cholinergic receptor: A review

Tiwari, Prashant; Dwivedi, Shubhangi; Singh, Mahendra Prasad; Mishra, Raj Kumar; Chandy, Anish

doi:10.1016/s2222-1808(13)60094-8

Cited by 56 publications

(28 citation statements)

References 48 publications

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“…During the development of the melanocytes and melanoma cells, ␣-MSH is produced and activates MC1R (G s protein couple receptor) thus increasing adenylyl cyclase activity. ACh functions as a ligand agonist of mAChR and nicotinic acetylcholine receptor (nAChR) (30). When activated, mAChR M2 and M4 subtypes coupled with G i proteins inhibit adenylyl cyclase activity, leading to a decrease in cAMP level in cells (31).…”

Section: Ach Reduces Melanin Productionmentioning

confidence: 99%

Microphthalmia-associated transcription factor up-regulates acetylcholinesterase expression during melanogenesis of murine melanoma cells

Fung

et al. 2018

Journal of Biological Chemistry

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Acetylcholinesterase (AChE) hydrolyzes the neurotransmitter acetylcholine in neurons. However, AChE has been proposed to also have nonneuronal functions in different cell types. Here, we report that AChE is expressed in melanocytes and melanoma cells, and that the tetrameric (G4) form is the major AChE isoform in these cells. During melanogenesis of B16F10 murine melanoma cells, AChE levels decreased markedly. The differentiation of melanoma cells led to (i) an increase in melanin and tyrosinase, (ii) a change in intracellular cAMP levels, and (iii) a decrease in microphthalmia-associated transcription factor (MITF). We hypothesized that the regulation of AChE during melanogenesis is mediated by two transcription factors: cAMP-response element-binding protein (CREB) and MITF. In melanoma cells, exogenous cAMP suppressed AChE expression and the promoter activity of the gene. This suppression was mediated by a cAMP-response element (CRE) located on the promoter, as mutation of CRE relieved the suppression. In melanoma, MITF overexpression induced transcription, and mutation of an E-box site in human promoter blocked this induction. An AChE inhibitor greatly enhanced acetylcholine-mediated responses of melanogenic gene expression levels ; however, this enhancement was not observed in the presence of agonists of the muscarinic acetylcholine receptor. These results indicate that transcription is regulated by cAMP-dependent signaling during melanogenesis of B16F10 cells, and the effect of this enzyme on melanin production suggests that it has a potential role in skin pigmentation.

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Section: Ach Reduces Melanin Productionmentioning

confidence: 99%

Microphthalmia-associated transcription factor up-regulates acetylcholinesterase expression during melanogenesis of murine melanoma cells

Fung

et al. 2018

Journal of Biological Chemistry

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“…Peripherally, cholinergic neurons control the sympathetic and parasympathetic branches of the autonomous nervous system on the ganglionic level. Additionally, parasympathetic terminals release Ach and thereby mediate the ‘rest and digest’ functionality in the autonomous nervous system ( Tiwari et al, 2013 ). In the central nervous system (CNS), Ach acts as a neurotransmitter and neuromodulator upon release from key groups of cholinergic projection and interneurons in both brain as well as spinal cord, details of which are discussed below.…”

Section: Introductionmentioning

confidence: 99%

Molecular, Cellular and Circuit Basis of Cholinergic Modulation of Pain

2018

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“…AChE activity. Acetylcholine is an organic chemical and neurotransmitter, a chemical message released by nerve cells to send signals to neuron cells (Tiwari, Dwivedi, Singh, Mishra, & Chandy, 2013). AChE is an enzyme that actives the degradation of acetylcholine, and AChE activity may serve as a useful tool for diagnosis of AD symptoms including cognitive, memory and behavior impairment (Bonner & Peskind, 2002).…”

Section: Determination Of Neuroprotective Effect Of Peptides/hydrolysmentioning

confidence: 99%

Mechanisms of Neuroprotective Effects of Peptides Derived from Natural Materials and Their Production and Assessment

Lee

2019

Comp Rev Food Sci Food Safe

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In this review, we provide an overview of the main mechanisms by which peptides derived from natural materials exhibit neuroprotective effects. We also review methods for the production of these peptides and various methods for determining their neuroprotective effects in vitro and in vivo. Neuroprotective peptides are closely associated with protection against apoptosis, with proteins related to the cell death/survival signaling pathway, with acetylcholine activity and with inhibition of oxidative stress and inflammation. Neuroprotective peptides derived from natural materials typically have a molecular weight below 1 kDa; they are most often derived using the extraction enzymes papain and alcalase. The neuroprotective peptides identified in the literature are mainly composed of hydrophobic amino acids with low molecular weight, with Asp and Glu at the N‐terminal position. These observations may guide the development of novel peptides with potential neuroprotective effects.

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Basic and modern concepts on cholinergic receptor: A review

Cited by 56 publications

References 48 publications

Microphthalmia-associated transcription factor up-regulates acetylcholinesterase expression during melanogenesis of murine melanoma cells

Microphthalmia-associated transcription factor up-regulates acetylcholinesterase expression during melanogenesis of murine melanoma cells

Molecular, Cellular and Circuit Basis of Cholinergic Modulation of Pain

Mechanisms of Neuroprotective Effects of Peptides Derived from Natural Materials and Their Production and Assessment

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