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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Neuromedin U

NMU, neuromedin U
may induce uterine smooth muscle contraction and selective vasoconstriction [RGD, Feb 2006] (from NCBI)
Top mentioned proteins: ACID, HAD, Neuropeptide, FM3, CAN
Papers on NMU
Central administration of the anorexigenic peptide neuromedin U decreases alcohol intake and attenuates alcohol-induced reward in rodents.
New
Jerlhag et al., Göteborg, Sweden. In Addict Biol, Feb 2016
In contrast to the common view of the function of gut-brain peptides, such as neuromedin U (NMU), to regulate food intake and appetite, a novel role in reinforcement mediation has been implied.
Enhancement of NAD+-dependent SIRT1 deacetylase activity by methylselenocysteine resets the circadian clock in carcinogen-treated mammary epithelial cells.
New
Zarbl et al., United States. In Oncotarget, Jan 2016
We previously reported that dietary methylselenocysteine (MSC) inhibits N-methyl-N-nitrosourea (NMU)-induced mammary tumorigenesis by resetting circadian gene expression disrupted by the carcinogen at the early stage of tumorigenesis.
Identification of a Degrading Enzyme in Human Serum that Hydrolyzes a C-terminal Core Sequence of Neuromedin U.
New
Hayashi et al., Hachiōji, Japan. In Biopolymers, Dec 2015
UNASSIGNED: Neuromedin U (NMU), an anorexigenic peptide, has attracted attention as a candidate for development of drugs against obesity.
Trypanosoma cruzi extracts elicits protective immune response against chemically-induced colon and mammary cancers.
New
Osinaga et al., Montevideo, Uruguay. In Int J Cancer, Dec 2015
We investigated whether immunity to T. cruzi antigens could induce anti-tumor activity, using two rat models which reproduce human carcinogenesis: colon cancer induced by 1,2-dimethylhydrazine (DMH), and mammary cancer induced by N-nitroso-N-methylurea (NMU).
Neuromedin U: a multifunctional neuropeptide with pleiotropic roles.
Review
New
O'Driscoll et al., Dublin, Ireland. In Clin Chem, Mar 2015
BACKGROUND: Neuromedin U (NmU) belongs to the neuromedin family, comprising a series of neuropeptides involved in the gut-brain axis and including neuromedins B and C (bombesin-like), K (neurokinin B), L (neurokinin A or neurotensin), N, S, and U. CONTENT: Although initially isolated from porcine spinal cord on the basis of their ability to induce uterine smooth muscle contraction, these peptides have now been found to be expressed in several different tissues and have been ascribed numerous functions, from appetite regulation and energy balance control to muscle contraction and tumor progression.
Suppression of insulin production and secretion by a decretin hormone.
New
Impact
Kim et al., Stanford, United States. In Cell Metab, Mar 2015
Targeted knockdown of CG9918, a Drosophila ortholog of Neuromedin U receptors (NMURs), in insulin-producing cells phenocopied limostatin deficiency and attenuated insulin suppression by purified Lst, suggesting CG9918 encodes an Lst receptor.
Optimizing production of Fc-amidated peptides by Chinese hamster ovary cells.
Eipper et al., Farmington, United States. In Bmc Biotechnol, 2014
PAM substrates generated by expressing peptidylglycine substrates (glucagon-like peptide 1-Gly, peptide YY-Gly and neuromedin U-Gly) fused to the C-terminus of immunoglobulin Fc in CHO cell lines producing targeted PAM.
Adaptive capacity to bacterial diet modulates aging in C. elegans.
Impact
Curran et al., Los Angeles, United States. In Cell Metab, 2014
Mechanistically, the alh-6 mutation triggers diet-induced mitochondrial defects and increased generation of ROS, likely due to accumulation of its substrate 1-pyrroline-5-carboxylate. We also identify that neuromedin U receptor signaling is essential for diet-induced mitochondrial changes and premature aging.
New insights into the physiology of bone regulation: the role of neurohormones.
Review
Matucha et al., Praha, Czech Republic. In Physiol Res, 2013
In addition to reviewing neurohormones with anabolic effects, this article also reviews neurohormones with unambiguously catabolic effects on the skeleton, such as neuropeptide Y and neuromedin U.
Age-related decline in melatonin and its MT1 receptor are associated with decreased sensitivity to melatonin and enhanced mammary tumor growth.
Review
Blask et al., New Orleans, United States. In Curr Aging Sci, 2013
Analysis of the rate of growth in transplanted, tissue-isolated, mammary tumors induced by N-nitroso-n-methyl-urea (NMU) showed a significant increase in the senescent rats, but not in the young or adult rats Additionally, diminished response to the inhibitory action on tumor growth of exogenous MLT was noted in senescent rats such that tumor growth was suppressed by only 33% compared to 48% and 66% in adult and young rats, respectively.
Differential cardiorespiratory and sympathetic reflex responses to microinjection of neuromedin U in rat rostral ventrolateral medulla.
GeneRIF
Pilowsky et al., Sydney, Australia. In J Pharmacol Exp Ther, 2012
Functional evidence is presented describing a complex differential modulatory activity of NMU on cardiovascular and reflex responses that are integrated in the rostral ventrolateral medulla.
[Neuro-skeletal biology and its importance for clinical osteology].
Review
Zofková, Praha, Czech Republic. In Cesk Fysiol, 2011
This article reviews the neuro-hormonal factors with osteoanabolic (central isoform of serotonin, melatonin, cannabinoids, beta 1 adrenergic system, oxytocin, ACTH and TSH) or osteocatabolic effects (neuropeptide Y, neuromedin U, beta2 adrenergic system).
Orphan GPCRs and methods for identifying their ligands.
Review
Kangawa et al., Suita, Japan. In Methods Enzymol, 2011
We subsequently identified ghrelin, neuromedin U, and neuromedin S as endogenous ligands of various orphan GPCRs and have proposed various mechanisms through which these peptides regulate physiological functions through their cognate GPCRs.
Effects of peripherally administered neuromedin U on energy and glucose homeostasis.
GeneRIF
Marsh et al., Rahway, United States. In Endocrinology, 2011
investigation of neuromedin U effects on factors associated with obesity/diabetes: NMU reduced food consumption/body weight; NMU increased body temperature/metabolic rate; NMU improved glucose tolerance; these effects seem to be mediated by NMUR1
Inactivation of the von Hippel-Lindau tumour suppressor gene induces Neuromedin U expression in renal cancer cells.
GeneRIF
Maxwell et al., London, United Kingdom. In Mol Cancer, 2010
Inactivation of the von Hippel-Lindau tumour suppressor gene induces Neuromedin U expression in renal cancer cells.
Emerging pharmacology and physiology of neuromedin U and the structurally related peptide neuromedin S.
Review
GeneRIF
Davenport et al., Cambridge, United Kingdom. In Br J Pharmacol, 2009
[review] Taken together with its vascular actions, NMU may be a functional link between energy balance and the cardiovascular system and may provide a future target for therapies directed against the disorders that comprise metabolic syndrome.
Appetite-modifying actions of pro-neuromedin U-derived peptides.
GeneRIF
Luckman et al., Manchester, United Kingdom. In Am J Physiol Endocrinol Metab, 2009
proNMU(104-136) is a novel modulator of energy balance and may contribute to the phenotype exhibited by NMU knockout mice.
Bone remodeling, energy metabolism, and the molecular clock.
Review
Impact
Rosen, West Scarborough, United States. In Cell Metab, 2008
Two of the studies add to our knowledge of the complex hypothalamic modulation of bone turnover mediated by NMU and NPY via the sympathetic nervous system, while the other two focus on the peripheral neural target, the osteoblast, and its regulation by neuropeptides and osteocalcin.
Central control of bone remodeling by neuromedin U.
Impact
GeneRIF
Takeda et al., Tokyo, Japan. In Nat Med, 2007
Central control of bone remodeling by Nmu is reported.
Neuromedin U has a novel anorexigenic effect independent of the leptin signaling pathway.
Impact
GeneRIF
Kojima et al., Kurume, Japan. In Nat Med, 2004
NMU plays an important role in the regulation of feeding behavior and energy metabolism independent of the leptin signaling pathway.
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