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As, Chen; Jm, Metzger; Me, Trumbauer; Guan, Xiao; H, Yu; Eg, Frazier; Dj, Marsh; Mj, Forrest; Gopal-Truter, Shobhna; Fisher, Jill K.; Re, Camacho; Am, Strack; Tn, Mellin; De, MacIntyre; Hy, Chen; Lh, Van der Ploeg

doi:10.1023/a:1008983615045

Cited by 229 publications

(65 citation statements)

References 34 publications

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“…We evaluated ambulatory activity and fine movements of individually housed mice with a cage rack Photobeam Activity System (San Diego Instruments) as described (22).…”

Section: Methodsmentioning

confidence: 99%

“…We analyzed whole body composition by dual energy x-ray absorptiometry (DEXA; QDR 4500, Hologic, Waltham, MA), using the QDR 4500 SMALL ANIMAL STUDIES software version 9.0 as described (22).…”

Section: Methodsmentioning

confidence: 99%

“…We measured plasma leptin, insulin, total T4, and corticosterone levels as described (22). Plasma glucose and triglyceride levels were measured by enzyme-colorimetric assays (Sigma and Roche Diagnostics, respectively).…”

Section: Methodsmentioning

confidence: 99%

“…We measured metabolic rate by indirect calorimetry with a 16-chamber open-circuit Oxymax system (Columbus Instruments, Columbus, OH) as described (22).…”

Section: Methodsmentioning

confidence: 99%

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Melanin-concentrating hormone 1 receptor-deficient mice are lean, hyperactive, and hyperphagic and have altered metabolism

Marsh

Weingarth²,

Novi³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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537

371

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Melanin-concentrating hormone (MCH) is a cyclic 19-aa hypothalamic neuropeptide derived from a larger prohormone precursor of MCH (Pmch), which also encodes neuropeptide EI (NEI) and neuropeptide GE (NGE). Pmch-deficient (PmchM elanin-concentrating hormone (MCH) is expressed in the central nervous system predominantly in neurons in the lateral hypothalamus and zona incerta, which project broadly throughout the brain (1, 2). MCH mRNA levels are increased in response to fasting and are elevated in leptin-deficient ob͞ob mice relative to control mice (3), suggesting that leptin negatively regulates MCH. Rodent pharmacology further supports a role for MCH in the control of energy homeostasis, as centrally administered MCH stimulates food intake in rats (3, 4).In addition to MCH, prohormone precursor of MCH (Pmch) also encodes neuropeptide EI (NEI) and neuropeptide GE (NGE) (5) and may potentially give rise to an alternative splice variant termed MCH-gene-overprinted-polypeptide (MGOP; ref. 6), as well as encode a portion of the recently identified antisense-RNA-overlapping-MCH (AROM; ref. 7). Two recently described mouse genetic models further implicate MCH in the regulation of energy homeostasis. Pmch Ϫ/Ϫ mice are lean, hypophagic, and have an increased metabolic rate (8). In contrast, transgenic mice overexpressing Pmch develop mild obesity, are hyperphagic, and become insulin-resistant (9). As both these models represent genetic manipulations of Pmch, one must consider the possibility that in addition to alterations in MCH, changes in the levels of NEI and NGE, as well as potentially MGOP and AROM, may also contribute to the phenotypes of these models.The MCH 1 receptor (MCH1R) was initially identified as an orphan G protein-coupled receptor that bound MCH with high affinity (10). Subsequently, a second high-affinity MCH receptor (MCH2R) with moderate amino acid identity to MCH1R was identified in humans (11-15). Both receptors are highly selective for MCH and are not activated by NEI, neuropeptide GE, or MCH-gene-overprinted-polypeptide (13, 16, 17); however, in vivo validation for these receptors is still lacking. We generated Mch1r Ϫ/Ϫ mice to evaluate the physiological function of MCH1R, and to determine whether it is involved in mediating the effects of MCH on energy homeostasis. Additionally, we hoped to gain insight into what aspects of the Pmch Ϫ/Ϫ and Pmch overexpressing phenotypes are likely attributed to MCH. Materials and MethodsAnimal Care and Maintenance. All animal protocols used in these studies were approved by the Merck Research Laboratories Institutional Animal Care and Use Committee in Rahway, NJ. We housed mice in microisolator cages (Lab Products, Maywood, NJ) in a barrier facility with an air shower entrance or in a specific pathogen-free facility. Mice were maintained on either regular chow [Teklad (Madison, WI) 7012: 14.8% kcal from fat; Harlan Teklad], a moderate-fat diet (D12266B: 32% kcal from fat; Research Diets, New Brunswick, NJ), or a high-fat diet (Teklad 97070: 60% kcal from fat)...

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“…We evaluated ambulatory activity and fine movements of individually housed mice with a cage rack Photobeam Activity System (San Diego Instruments) as described (22).…”

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…We measured metabolic rate by indirect calorimetry with a 16-chamber open-circuit Oxymax system (Columbus Instruments, Columbus, OH) as described (22).…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Melanin-concentrating hormone 1 receptor-deficient mice are lean, hyperactive, and hyperphagic and have altered metabolism

Marsh

Weingarth²,

Novi³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

537

371

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show abstract

“…Measurements of oxygen consumption indicate that obese A y mice have a lower resting metabolic rate when tested between 2 and 12 mo of age (19), but not when tested at 6 wk of age. Finally, the metabolic rate of adult Mc4r-null, that were significantly heavier than control mice, was less than either lean controls or diet-induced obese controls when normalized to total body weight (20).…”

mentioning

confidence: 88%

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors

Marie

Miura²,

Marsh³

et al. 2000

Proc. Natl. Acad. Sci. U.S.A.

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338

209

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Core body temperature of Mc4r-null mice was normal, and they responded normally to cold exposure. Young nonobese Mc4r-null females were unable to induce uncoupling protein 1 (UCP1) in brown adipose tissue in response to peripheral leptin administration, whereas UCP1 mRNA was increased by 60% in the WT females. These results indicate that Mc4r deficiency enhances caloric efficiency, similar to that seen in the agouti obesity syndrome and in melanocortin-3 receptor-null mice.

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Cyclotides as grafting frameworks for protein engineering and drug design applications

2013

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Cyclotides are a family of naturally occurring backbone-cyclized macrocyclic mini-proteins from plants that have a knotted trio of intramolecular disulfide bonds. Their structural features imbue cyclotides with extraordinary stability against degradation at elevated temperatures or in the presence of proteolytic enzymes. The plasticity of their intracysteine loop sequences is exemplified by the more than 250 natural cyclotides sequenced to date, and this tolerance to sequence variation, along with their diverse bioactivities, underpins the suitability of the cyclic cystine knot motif as a valuable drug design scaffold and research tool for protein engineering studies. Here, we review the recent literature on applications of cyclotides for the stabilization of peptide epitopes and related protein engineering studies. Possible future directions in this field are also described.

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Cited by 229 publications

References 34 publications

Melanin-concentrating hormone 1 receptor-deficient mice are lean, hyperactive, and hyperphagic and have altered metabolism

Melanin-concentrating hormone 1 receptor-deficient mice are lean, hyperactive, and hyperphagic and have altered metabolism

A metabolic defect promotes obesity in mice lacking melanocortin-4 receptors

Cyclotides as grafting frameworks for protein engineering and drug design applications

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