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Relevant bibliographies by topics / MCHR1

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Academic literature on the topic 'MCHR1'

Author: Grafiati

Published: 4 June 2021

Last updated: 31 January 2023

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Journal articles on the topic "MCHR1"

1

Chee, Melissa J. S., Pavlos Pissios, Deepthi Prasad, and Eleftheria Maratos-Flier. "Expression of Melanin-Concentrating Hormone Receptor 2 Protects Against Diet-Induced Obesity in Male Mice." Endocrinology 155, no. 1 (January 1, 2014): 81–88. http://dx.doi.org/10.1210/en.2013-1738.

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Melanin-concentrating hormone (MCH) is an orexigenic neuropeptide that is a ligand for two subtypes of MCH receptors, MCHR1 and MCHR2. MCHR1 is universally expressed in mammals ranging from rodents to humans, but the expression of MCHR2 is substantially restricted. In mammals, MCHR2 has been defined in primates as well as other species such as cats and dogs but is not seen in rodents. Although the role of MCHR1 in mediating the actions of MCH on energy balance is clearly defined using mouse models, the role of MCHR2 is harder to characterize because of its limited expression. To determine any potential role of MCHR2 in energy balance, we generated a transgenic MCHR1R2 mouse model, where human MCHR2 is coexpressed in MCHR1-expressing neurons. As shown previously, control wild-type mice expressing only native MCHR1 developed diet-induced obesity when fed a high-fat diet. In contrast, MCHR1R2 mice had lower food intake, leading to their resistance to diet-induced obesity. Furthermore, we showed that MCH action is altered in MCHR1R2 mice. MCH treatment in wild-type mice inhibited the activation of the immediate-early gene c-fos, and coexpression of MCHR2 reduced the inhibitory actions of MCHR1 on this pathway. In conclusion, we developed an experimental animal model that can provide insight into the action of MCHR2 in the central nervous system and suggest that some actions of MCHR2 oppose the endogenous actions of MCHR1.

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Åstrand, Annika, Mohammad Bohlooly-Y, Sara Larsdotter, Margit Mahlapuu, Harriet Andersén, Jan Tornell, Claes Ohlsson, Mike Snaith, and David G. A. Morgan. "Mice lacking melanin-concentrating hormone receptor 1 demonstrate increased heart rate associated with altered autonomic activity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 4 (October 2004): R749—R758. http://dx.doi.org/10.1152/ajpregu.00134.2004.

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Melanin-concentrating hormone (MCH) plays an important role in energy balance. The current studies were carried out on a new line of mice lacking the rodent MCH receptor (MCHR1−/− mice). These mice confirmed the previously reported lean phenotype characterized by increased energy expenditure and modestly increased caloric intake. Because MCH is expressed in the lateral hypothalamic area, which also has an important role in the regulation of the autonomic nervous system, heart rate and blood pressure were measured by a telemetric method to investigate whether the increased energy expenditure in these mice might be due to altered autonomic nervous system activity. Male MCHR1−/− mice demonstrated a significantly increased heart rate [24-h period: wild type 495 ± 4 vs. MCHR1−/− 561 ± 8 beats/min ( P < 0.001); dark phase: wild type 506 ± 8 vs. MCHR1−/− 582 ± 9 beats/min ( P < 0.001); light phase: wild type 484 ± 13 vs. MCHR1−/− 539 ± 9 beats/min ( P < 0.005)] with no significant difference in mean arterial pressure [wild type 110 ± 0.3 vs. MCHR1−/− 113 ± 0.4 mmHg ( P > 0.05)]. Locomotor activity and core body temperature were higher in the MCHR1−/− mice during the dark phase only and thus temporally dissociated from heart rate differences. On fasting, wild-type animals rapidly downregulated body temperature and heart rate. MCHR1−/− mice displayed a distinct delay in the onset of this downregulation. To investigate the mechanism underlying these differences, autonomic blockade experiments were carried out. Administration of the adrenergic antagonist metoprolol completely reversed the tachycardia seen in MCHR1−/− mice, suggesting an increased sympathetic tone.

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Francke, Felix, Richard J. Ward, Laura Jenkins, Elaine Kellett, Dietmar Richter, Graeme Milligan, and Dietmar Bächner. "Interaction of Neurochondrin with the Melanin-concentrating Hormone Receptor 1 Interferes with G Protein-coupled Signal Transduction but Not Agonist-mediated Internalization." Journal of Biological Chemistry 281, no. 43 (August 31, 2006): 32496–507. http://dx.doi.org/10.1074/jbc.m602889200.

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Screening of a human brain cDNA library using the C-terminal tail of the melanin-concentrating hormone receptor 1 (MCHR1) as bait in a yeast two-hybrid assay resulted in the identification of the neurite-outgrowth related factor, neurochondrin. This interaction was verified in overlay, pulldown, and co-immunoprecipitation assays. Deletion mapping confined the binding to the C terminus of neurochondrin and to the proximal C terminus of MCHR1, a region known to be involved in G protein binding and signal transduction. This region of the MCHR1 is also able to interact with the actin- and intermediate filament-binding protein, periplakin. Interactions of MCHR1 with neurochondrin and periplakin were competitive, indicating that these two proteins bind to overlapping regions of MCHR1. Although neurochondrin did not interfere with melanin-concentrating hormone-mediated internalization of the receptor, it did inhibit G protein-coupled signal transduction via both Gαi/o and Gαq/11 family G proteins as measured by each of melanin-concentrating hormone-induced G protein-activated inwardly rectifying K+ channel activity of voltage-clamped amphibian oocytes, by calcium mobilization in transfected mammalian cells, and by reduction in the capacity of melanin-concentrating hormone to promote binding of [35S]guanosine 5′-3-O-(thio)triphosphate to both Gαo1 and Gα11. Immunohistochemistry revealed co-expression of neurochondrin and MCHR1 within the rodent brain, suggesting that neurochondrin may be involved in the regulation of MCHR1 signaling and play a role in modulating melanin-concentrating hormone-mediated functions in vivo.

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Lim, Gyutae, Ka Young You, Jeong Hyun Lee, Moon Kook Jeon, Byung Ho Lee, Jae Yong Ryu, and Kwang-Seok Oh. "Identification and New Indication of Melanin-Concentrating Hormone Receptor 1 (MCHR1) Antagonist Derived from Machine Learning and Transcriptome-Based Drug Repositioning Approaches." International Journal of Molecular Sciences 23, no. 7 (March 30, 2022): 3807. http://dx.doi.org/10.3390/ijms23073807.

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Melanin-concentrating hormone receptor 1 (MCHR1) has been a target for appetite suppressants, which are helpful in treating obesity. However, it is challenging to develop an MCHR1 antagonist because its binding site is similar to that of the human Ether-à-go-go-Related Gene (hERG) channel, whose inhibition may cause cardiotoxicity. Most drugs developed as MCHR1 antagonists have failed in clinical development due to cardiotoxicity caused by hERG inhibition. Machine learning-based prediction models can overcome these difficulties and provide new opportunities for drug discovery. In this study, we identified KRX-104130 with potent MCHR1 antagonistic activity and no cardiotoxicity through virtual screening using two MCHR1 binding affinity prediction models and an hERG-induced cardiotoxicity prediction model. In addition, we explored other possibilities for expanding the new indications for KRX-104130 using a transcriptome-based drug repositioning approach. KRX-104130 increased the expression of low-density lipoprotein receptor (LDLR), which induced cholesterol reduction in the gene expression analysis. This was confirmed by comparison with gene expression in a nonalcoholic steatohepatitis (NASH) patient group. In a NASH mouse model, the administration of KRX-104130 showed a protective effect by reducing hepatic lipid accumulation, liver injury, and histopathological changes, indicating a promising prospect for the therapeutic effect of NASH as a new indication for MCHR1 antagonists.

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Bohlooly-Y, Mohammad, Margit Mahlapuu, Harriet Andersén, Annika Åstrand, Stephan Hjorth, Lennart Svensson, Jan Törnell, Michael R. Snaith, David G. Morgan, and Claes Ohlsson. "Osteoporosis in MCHR1-deficient mice." Biochemical and Biophysical Research Communications 318, no. 4 (June 2004): 964–69. http://dx.doi.org/10.1016/j.bbrc.2004.04.122.

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Pałasz, Artur, Aneta Piwowarczyk-Nowak, Aleksandra Suszka-Świtek, Katarzyna Bogus, Łukasz Filipczyk, Alessandra Della Vecchia, Kinga Mordecka-Chamera, et al. "Escitalopram as a modulator of proopiomelanocortin, kisspeptin, Kiss1R and MCHR1 gene expressions in the male rat brain." Molecular Biology Reports 47, no. 10 (September 10, 2020): 8273–78. http://dx.doi.org/10.1007/s11033-020-05806-8.

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Abstract Neuropeptides are important, multifunctional regulatory factors of the nervous system, being considered as a novel, atypical sites of antidepressants action. It has already been proven that some of them, such as selective serotonin reuptake inhibitors (SSRI), are able to affect peptidergic pathways in various brain regions. Despite these reports, there is so far no reports regarding the effect of treatment with SSRIs on brain proopiomelanocortin (POMC), kisspeptin, Kiss1R and MCHR1 gene expression. In the current study we examined POMC, kisspeptin, Kiss1R and MCHR1 mRNA expression in the selected brain structures (hypothalamus, hippocampus, amygdala, striatum, cerebellum and brainstem) of rats chronically treated with a 10 mg/kg dose of escitalopram using quantitative Real-Time PCR. Long-term treatment with escitalopram led to the upregulation of MCHR1 expression in the rat amygdala. Kisspeptin mRNA level was also increased in the amygdala, but Kiss1R mRNA expressions were elevated in the hippocampus, hypothalamus and cerebellum. POMC mRNA expressions were in turn decreased in the hippocampus, amygdala, cerebellum and brainstem. These results may support the hypothesis that these neuropeptides may be involved in the site-dependent actions of SSRI antidepressants. This is the first report of the effects of escitalopram on POMC, kisspeptin, Kiss1R and MCHR1 in animal brain. Our findings shed a new light on the pharmacology of SSRIs and may contribute to a better understanding of the alternative, neuropeptide-dependent modes of antidepressant action.

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Vetlugin, Eduard A., Eugenii R. Bychkov, Maxim E. Abrosimov, Alexandr R. Moskalyev, Anna G. Pshenichnaya, Sarng S. Pyurveev, Victor A. Lebedev, Andrei A. Lebedev, and Petr D. Shabanov. "Anxiolytic and antidepressant effects of melanin-concentrating hormone 1 receptor antagonist SNAP 94847." Pediatrician (St. Petersburg) 13, no. 1 (May 31, 2022): 25–34. http://dx.doi.org/10.17816/ped13125-34.

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Background: Melatonin Concentrating Hormone (MCH) is a neuropeptide involved in the regulation of eating behavior, energy balance, mood, and the sleep/wake cycle. Aim: To study the effect of SNAP 94847, a selective melanin-concentrating hormone receptor type 1 (MCHR1) antagonist, on exploratory and emotional behavior in rats. Materials and methods: 38 male Wistar rats were used in the work. The selective MCHR1 antagonist SNAP 94847 was administered intranasally. The behavior of the animals was assessed in the tests: open field, elevated plus maze, Porsolt forced swimming, resident-intruder. Results: After intranasal administration SNAP 94847 there were an increase in the number of sniffs, the time of locomotion, and the number of squares crossed in open field test. In elevated plus maze test, after the administration of SNAP 94847, a decrease in the time spent by the animals in the closed arms of the maze was observed. In Porsolt forced swim test, the immobilization time decreased and the passive swimming time increased in experimental group. Conclusion: In animal tests, the antidepressant and anxiolytic effects of the selective MCHR1 antagonist SNAP 94847 have been shown.

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Andersen, Denise, Thomas Storz, Pingli Liu, Xin Wang, Leping Li, Pingchen Fan, Xiaoqi Chen, et al. "Stereoselective Synthesis of a MCHr1 Antagonist." Journal of Organic Chemistry 72, no. 25 (December 2007): 9648–55. http://dx.doi.org/10.1021/jo701894v.

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9

Wermter, Anne-Kathrin, Kathrin Reichwald, Thomas Büch, Frank Geller, Cornelia Platzer, Klaus Huse, Claudia Hess, et al. "Mutation analysis of the MCHR1 gene in human obesity." European Journal of Endocrinology 152, no. 6 (June 2005): 851–62. http://dx.doi.org/10.1530/eje.1.01917.

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Objective: The importance of the melanin-concentrating hormone (MCH) system for regulation of energy homeostasis and body weight has been demonstrated in rodents. We analysed the human MCH receptor 1 gene (MCHR1) with respect to human obesity. Design: This consisted of genomic screening of 13.4 kb encompassing the MCHR1 in extremely obese German children and adolescents and association analyses for two coding single nucleotide polymorphisms (SNPs). To confirm initial positive association results, additional association studies and transmission disequilibrium tests in further German, Danish, French and American samples were conducted. Selected SNPs were investigated using functional in vitro studies and reporter gene assays. Methods: Single-stranded conformation polymorphism analysis, re-sequencing, PCR-restriction fragment length polymorphism analyses, tetra-primer amplification refractory mutation systems, matrix-assisted laser desorption/ionization time of flight mass spectrometry and reporter gene assays were carried out as well as measuring inositol phosphate formation, inhibition of cAMP formation and activation of p42/44 MAP kinase. Results: We identified 11 infrequent variations and two SNPs in the MCHR1 coding sequence and 18 SNPs (eight novel) in the flanking sequence. Association and transmission disequilibrium with obesity were detected for several SNPs in independent study groups of German obese children and adolescents and controls. In two German samples, encompassing 4056 and 295 individuals, trends towards association with obesity were detected. Findings in a second epidemiological German sample and in Danish, French and American samples were negative. Functional in vitro studies as well as reporter gene assays revealed no significant results. Conclusion: Our initial association of MCHR1 alleles/haplotype detected might be related to juvenile-onset obesity, conditional on a particular genetic and/or environmental background. Alternatively, we could not exclude the possibility that the initially detected association represented a false positive finding.

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Berbari, Nicolas F., Andrew D. Johnson, Jacqueline S. Lewis, Candice C. Askwith, and Kirk Mykytyn. "Identification of Ciliary Localization Sequences within the Third Intracellular Loop of G Protein-coupled Receptors." Molecular Biology of the Cell 19, no. 4 (April 2008): 1540–47. http://dx.doi.org/10.1091/mbc.e07-09-0942.

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Primary cilia are sensory organelles present on most mammalian cells. The functions of cilia are defined by the signaling proteins localized to the ciliary membrane. Certain G protein–coupled receptors (GPCRs), including somatostatin receptor 3 (Sstr3) and serotonin receptor 6 (Htr6), localize to cilia. As Sstr3 and Htr6 are the only somatostatin and serotonin receptor subtypes that localize to cilia, we hypothesized they contain ciliary localization sequences. To test this hypothesis we expressed chimeric receptors containing fragments of Sstr3 and Htr6 in the nonciliary receptors Sstr5 and Htr7, respectively, in ciliated cells. We found the third intracellular loop of Sstr3 or Htr6 is sufficient for ciliary localization. Comparison of these loops revealed a loose consensus sequence. To determine whether this consensus sequence predicts ciliary localization of other GPCRs, we compared it with the third intracellular loop of all human GPCRs. We identified the consensus sequence in melanin-concentrating hormone receptor 1 (Mchr1) and confirmed Mchr1 localizes to primary cilia in vitro and in vivo. Thus, we have identified a putative GPCR ciliary localization sequence and used this sequence to identify a novel ciliary GPCR. As Mchr1 mediates feeding behavior and metabolism, our results implicate ciliary signaling in the regulation of body weight.

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Dissertations / Theses on the topic "MCHR1"

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Schaller, David Andreas [Verfasser]. "Synergistic Target Combinations Against Obesity: Focus on MCHR1/H3R Modulation / David Andreas Schaller." Berlin : Freie Universität Berlin, 2020. http://d-nb.info/1215099746/34.

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Appl, Thomas. "Neurochemical and functional characterisation of the melanin concentrating hormone system in the rat brain." Phd thesis, [S.l.] : [s.n.], 2007. http://opus.kobv.de/ubp/volltexte/2007/1460.

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Thody, Anthony J., Martin J. Hoogduijn, Janis Ancans, Siân E. Estdale, and I. Suzuki. "Melanin-concentrating hormone and its receptor are expressed and functional in human skin." 2009. http://hdl.handle.net/10454/2739.

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No
In this study, we have demonstrated the presence of melanin-concentrating hormone (MCH) and melanin-concentrating hormone receptor (MCHR1) transcripts in human skin. Sequence analysis confirmed that the transcripts of both genes were identical to those previously found in human brain. In culture, endothelial cells showed pro-MCH expression whereas no signal was found in keratinocytes, melanocytes, and fibroblasts. MCHR1 expression was restricted to melanocytes and melanoma cells. Stimulation of cultured human melanocytes with MCH reduced the ¿-MSH-induced increase in cAMP production. Furthermore, the melanogenic actions of ¿-MSH were inhibited by MCH. We propose that the MCH/MCHR1 signalling system is present in human skin and may have a role with the melanocortins in regulating the melanocyte.

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Kamba, Tisianna K. "Assessing neuronal ciliary localization of Melanin Concentrating Hormone Receptor 1 in vivo." Thesis, 2021. http://dx.doi.org/10.7912/C2/78.

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Indiana University-Purdue University Indianapolis (IUPUI)
Obesity is a growing pandemic that claims close to three hundred thousand lives per year in the United States alone. Despite strong interest and investment in potential treatments, obesity remains a complex and challenging disorder. In the study of obesity, mouse models have been excellent tools that help in understanding the function of different genes that contribute to this disease of energy homeostasis. However, it was surprising when disfunction in primary cilia was found to be linked to syndromic obesity. To understand the role of primary cilia in obesity, a growing subset of GPCRs have been identified to selectively localize to the organelle. Several of which have known roles in energy homeostasis. In some examples, ciliary GPCRs appear to dynamically localize to the organelle; such is the case of GPR161 and smoothened in the hedgehog signaling pathway. Thus, we were interested to see if other GPCRs dynamically localize to the primary cilia as part of their regulation of energy homeostasis. For example, the GPCR MCHR1 selectively localizes to the cilia and is involved in energy homeostasis. Although much is known about the expression of the receptor in the brain, how its ciliary subcellular localization impacts its roles in energy homeostasis is unknown. Observing neuronal cilia in vivo remains a difficult task as some of the available tools such as tagged alleles rely on overexpression of ciliary protein which may impact function. Additionally, most of the work is done in vitro, leaving much to be discovered about neuronal cilia in vivo. In this thesis, we show that using a newly constructed reporter allele mCherryMCHR1, we can see ciliary expression of MCHR1 in the brain of developing and adult mice; more specifically in the ARC and PVN. Subsequently, using a novel Artificial intelligence analysis approach, we measured the length and composition of MCHR1 positive cilia under physiological conditions associated with MCHR1 function. Although in this work we are reporting no changes in dynamic localization of MCHR1 in the hypothalamus specifically, we are not excluding the potential for changes in other regions of the brain or under other conditions; and we are suggesting that pharmacological approaches may help highlight potential ciliary GPCR dynamic localization.

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Plamondon, Pascale. "Identification and characterization of a novel two-partner secretion system in Moraxella catarrhalis composed of MCHA1, MCHA2, and MCHB." 2008. http://proquest.umi.com/pqdweb?did=1546808251&sid=8&Fmt=2&clientId=39334&RQT=309&VName=PQD.

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Thesis (Ph.D.)--State University of New York at Buffalo, 2008.
Title from PDF title page (viewed on Dec. 4, 2008) Available through UMI ProQuest Digital Dissertations. Thesis adviser: Campagnari, Anthony A. Includes bibliographical references.

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Books on the topic "MCHR1"

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Read, C. MCHR 6 Horses. Macmillan ELT, 2014.

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Ormerod, M. MCHR 4 Elephants. Macmillan Children Readers, 2013.

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Ormerod, M. MCHR 2 Carnival. Macmillan Children Readers, 2013.

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Ormerod, M. MCHR 2 Monkeys. Macmillan Children Readers, 2013.

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Read, C. MCHR 4 Riverboat Bill. Macmillan Children Readers, 2004.

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Read, C. MCHR 2 Pat's Picture. Macmillan Children Readers, 2004.

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MCHR 4 Riverboat Bill. Macmillan ELT, 2013.

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Read, C. MCHR 2 Pat's Picture. Macmillan ELT, 2014.

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Ormerod, M. MCHR 3 Endangered Animals. Macmillan Children Readers, 2013.

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Shipton, Paul. MCHR 6 The Deep. Macmillan Children Readers, 2012.

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Book chapters on the topic "MCHR1"

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Hamamoto, Akie, Yuki Kobayashi, and Yumiko Saito. "Melanin-Concentrating Hormone Receptor 1 (MCHR1)." In Encyclopedia of Signaling Molecules, 3075–82. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101710.

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Hamamoto, Akie, Yuki Kobayashi, and Yumiko Saito. "Melanin-Concentrating Hormone Receptor 1 (MCHR1)." In Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101710-1.

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Singh, Nivedita, M. Balasubramaniam, and Jitendra Singh. "Speech Recognition for Medical Conversations Health Record (MCHR)." In Proceedings of Emerging Trends and Technologies on Intelligent Systems, 191–201. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-3097-2_16.

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"MCHR1." In Encyclopedia of Signaling Molecules, 3020. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102213.

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Philippe, Cécile, and Markus Mitterhauser. "The Potential Role of the MCHR1 in Diagnostic Imaging: Facts and Trends." In Melanin. InTech, 2017. http://dx.doi.org/10.5772/67185.

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"MCH1R." In Encyclopedia of Signaling Molecules, 3020. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_102212.

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Oh, Kean T., and Kent Small. "North Carolina Macular Dystrophy/Mcdr1." In Genetic Diseases of the Eye, 421–25. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780195326147.003.0027.

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"Marriage by Cohabitation with Habit and Repute: Review And Requiem?" In Continuity, Influences and Integration in Scottish Legal History, edited by Hector L. MacQueen, 191–215. Edinburgh University Press, 2021. http://dx.doi.org/10.3366/edinburgh/9781474488761.003.0010.

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The doctrine of marriage by cohabitation with habit and repute (MCHR) was long established in Scots law before its abolition by statute in 2006 but was not always well understood. There was disagreement about its origins, whether traced to an Act of the Scots Parliament passed in 1503, or to the medieval Canon law. There was controversy too about the role of the doctrine in modern Scots law: was it merely a method of proof, or was it in some sense also part of the constitution of marriage? This chapter seeks, first, to explain the background to the Act of 1503 (actually 1504) and to demonstrate the relationship of that Act to the preceding medieval Canon law; and secondly, to argue that MCHR was always no more than a method of proof.

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Conference papers on the topic "MCHR1"

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Li, Haifeng, Xiaoxia Yang, and Yiqiang Ouyang. "MCHRC: Min-Conflict Heuristic Based Web Services Chain Reconfiguration Approach." In 2009 International Conference on Computational Intelligence and Software Engineering. IEEE, 2009. http://dx.doi.org/10.1109/cise.2009.5365664.

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Nowakowski, Kevin E., Jithma P. Abeykoon, Mary J. Stenson, Michael M. Timm, Curtis A. Hanson, Daniel L. Van Dyke, Anne J. Novak, Xiaosheng Wu, and Thomas E. Witzig. "Abstract 650: MCIR1: A patient-derived ibrutinib-resistant mantle cell lymphoma line for the study of ibrutinib resistance and drug discovery." In Proceedings: AACR Annual Meeting 2020; April 27-28, 2020 and June 22-24, 2020; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-650.

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