Localization of the Genes Encoding the Melanocortin-2 (Adrenocorticotropic Hormone) and Melanocortin-3 Receptors to Chromosomes 18p11.2 and 20q13.2-q13.3 by Fluorescence in Situ Hybridization

Gantz, Ira; Tashiro, Takao; Barcroft, Christine L.; Konda, Yoshitaka; Shimoto, Yoshimasa; Miwa, Hiroto; Glover, Thomas W.; Munzert, Gerd; Yamada, Tadataka

doi:10.1006/geno.1993.1448

Cited by 80 publications

(64 citation statements)

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“…2 ± 6 The human melanocortin 3 receptor (MC3R) is a single exon gene encoding a protein of 360 amino acids (1083 nucleotides, Genbank L06155) that has been mapped to this region (20q13.2-q13.3) using¯uores-cence in situ hybridization (FISH). 7 MC3R belongs to a family of G-protein coupled melanocortin receptors, ®ve of which have been cloned. 8 ± 13 MC1R is expressed in skin (melanocytes) and pituitary, MC2R in adrenal cortex, and MC5R in several different organs including endocrine glands and adipose tissue.…”

Section: Introductionmentioning

confidence: 99%

Melanocortin 3 receptor (MC3R) gene variants in extremely obese women

Joo

Furlong³

et al. 2000

Int J Obes

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OBJECTIVE: Following several reports of linkage of obesity related phenotypes to human chromosome 20q we sought to determine whether variations of the melanocortin 3 receptor (MC3R) gene are associated with obesity. DESIGN: We screened the MC3R gene coding region and approximately 2 kb of 5 H and 3 H¯a nking sequences for DNA variants in unrelated extremely obese women and average weight controls using polymerase chain reaction (PCR) single strand conformation polymorphism (SSCP) analysis and DNA sequencing. SUBJECTS: 124 unrelated extremely obese women (body mass index, (BMI) ! 40 kgam 2 ) and 85 average weight controls (BMI`27 kgam 2 ). MEASUREMENTS: Radiation hybrid (RH) mapping was performed to localize the MC3R gene. 5 H and 3 H¯a nking sequences of MC3R gene were cloned. PCR-SSCP and DNA sequencing were used to detect mutations in the MC3R gene coding region and¯anking sequences. RESULTS: RH mapping localized the MC3R gene to 20q13, between markers D20S100 and D20S149. 1083 bp 5 H and 653 bp 3 H¯a nking region of the MC3R gene were cloned. A missense mutation ( 241, codon 81 ATTaGTT, Ile 3 Val) was found in the MC3R coding region. Four more variants were detected in the 5 H¯a nking sequence: À201(C 3 G), À239 (A 3 G), À762(A 3 T) and À769(T 3 C). Compared with controls, no signi®cant allele frequency differences were found. Racial differences were found for the 241, À201, À239 and À762 polymorphisms. CONCLUSIONS: Several sequence variants were found in the MC3R gene coding region and in 5 H¯a nking sequences. However, none of the variants were associated with obesity phenotypes. The linkage of extreme human obesity on 20q13 is likely caused by genes other than MC3R.

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Section: Introductionmentioning

confidence: 99%

Melanocortin 3 receptor (MC3R) gene variants in extremely obese women

Joo

Furlong³

et al. 2000

Int J Obes

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“…To date, five melanocortin receptor (MC-R) subtypes have been identified [3,[7][8][9][12][13][14][15][24][25][26]30]. Three of these, MC3-R, MC4-R and MC~-R are expressed in the nervous system.…”

Section: Introductionmentioning

confidence: 99%

Melanocortin receptors mediate α-MSH-induced stimulation of neurite outgrowth in neuro 2A cells

Adan

Kraan

Doornbos

et al. 1996

Molecular Brain Research

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Melanocortins (MC), neuropeptides derived from pro-opiomelanocortin, have been implicated in enhancing neurite outgrowth via an as yet unknown mechanism. Recently, five MC receptors have been identified, three of which, the MC3-R, the MC4-R and the MCs-R, are expressed in the nervous system. In this study, a-MSH and the melanocortin analog [D-PheT]ACTH (4-10) were able to stimulate neurite outgrowth in the neuroblastoma cell line Neuro 2A. ACTH (4-10), -/2-MSH and ORG2766 were inactive. In addition, the MCa-R antagonist [D-Arg8]ACTH (4-10), inhibited the a-MSH effect, indicating that the MCa-R mediated stimulation of neurite outgrowth by o~-MSH. Indeed, the presence of MCa-R mRNA in Neuro 2A cells was demonstrated by a RNase protection assay. Heterologous expression of the MCs-R in Neuro 2A cells lead to the recruitment of a responsiveness to -/2-MSH, but did not increase the effect of a-MSH on neurite outgrowth. This finding indicated that the function of MC4-R can also be exerted by another MC receptor, suggesting that the coupling to G,, which they have in common, plays an essential role in the neurite outgrowth promoting effect. This was further substantiated by the fact that forskolin treatment per se induced neurite outgrowth in a similar fashion. These data imply that the neurotrophic properties of a-MSH are likely to result from G~-coupled MC receptor activity in neuronal cells.

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“…In addition, it has been shown that the anti-inflammatory action of ␣-MSH is due to its ability to block proinflammatory signaling such as activation of nuclear factor B (NF B) (13,14). ␣-MSH exerts its cellular effects by binding to five different G protein-coupled receptors called melanocortin receptors (MC 1 R MC 5 R) (15)(16)(17)(18). Ligand binding to MCRs activates adenyl cyclase, which leads to the production of cAMP and subsequent activation of protein kinase A (PKA) (15,19,20).…”

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confidence: 99%

α-Melanocyte-stimulating Hormone Inhibits Lipopolysaccharide-induced Tumor Necrosis Factor-α Production in Leukocytes by Modulating Protein Kinase A, p38 Kinase, and Nuclear Factor κB Signaling Pathways

Yoon

Goh

Chun

et al. 2003

Journal of Biological Chemistry

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The neuropeptide ␣-melanocyte-stimulating hormone (␣-MSH) inhibits inflammation by down-regulating the expression of proinflammatory cytokines such as tumor necrosis factor-␣ (TNF-␣) in leukocytes via stimulation of ␣-MSH cell surface receptors. However, the signaling mechanism of ␣-MSH action has not yet been clearly elucidated. Here, we have investigated signaling pathways by which ␣-MSH inhibits lipopolysaccharide (LPS)-induced TNF-␣ production in leukocytes such as THP-1 cells. We focused on the possible roles of protein kinase A (PKA), p38 kinase, and nuclear factor B (NF B) signaling. In THP-1 cells, LPS is known to activate p38 kinase, which in turn activates NF B to induce TNF-␣ production. We found that pretreatment of cells with ␣-MSH blocked LPS-induced p38 kinase and NF B activation as well as TNF-␣ production. This response was proportional to ␣-MSH receptor expression levels, and addition of an ␣-MSH receptor antagonist abolished the inhibitory effects. In addition, ␣-MSH treatment activated PKA, and PKA inhibition abrogated the inhibitory effects of ␣-MSH on p38 kinase activation, NF B activation, and TNF-␣ production. Taken together, our results indicate that stimulation of PKA by ␣-MSH causes inhibition of LPS-induced activation of p38 kinase and NF B to block TNF-␣ production.

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Localization of the Genes Encoding the Melanocortin-2 (Adrenocorticotropic Hormone) and Melanocortin-3 Receptors to Chromosomes 18p11.2 and 20q13.2-q13.3 by Fluorescence in Situ Hybridization

Cited by 80 publications

References 0 publications

Melanocortin 3 receptor (MC3R) gene variants in extremely obese women

Melanocortin 3 receptor (MC3R) gene variants in extremely obese women

Melanocortin receptors mediate α-MSH-induced stimulation of neurite outgrowth in neuro 2A cells

α-Melanocyte-stimulating Hormone Inhibits Lipopolysaccharide-induced Tumor Necrosis Factor-α Production in Leukocytes by Modulating Protein Kinase A, p38 Kinase, and Nuclear Factor κB Signaling Pathways

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