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  • 1
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    Multinodal regulation of the arcuate/paraventricular nucleus circuit by leptin [Neuroscience] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-01-05
    Description: Melanocortin-4 receptor (MC4R) is critical for energy homeostasis, and the paraventricular nucleus of the hypothalamus (PVN) is a key site of MC4R action. Most studies suggest that leptin regulates PVN neurons indirectly, by binding to receptors in the arcuate nucleus or ventromedial hypothalamus and regulating release of products like α-melanocyte-stimulating hormone (α-MSH), neuropeptide Y (NPY), glutamate, and GABA from first-order neurons onto the MC4R PVN cells. Here, we investigate mechanisms underlying regulation of activity of these neurons under various metabolic states by using hypothalamic slices from a transgenic MC4R-GFP mouse to record directly from MC4R neurons. First, we show that in vivo leptin levels regulate the tonic firing rate of second-order MC4R PVN neurons, with fasting increasing firing frequency in a leptin-dependent manner. We also show that, although leptin inhibits these neurons directly at the postsynaptic membrane, α-MSH and NPY potently stimulate and inhibit the cells, respectively. Thus, in contrast with the conventional model of leptin action, the primary control of MC4R PVN neurons is unlikely to be mediated by leptin action on arcuate NPY/agouti-related protein and proopiomelanocortin neurons. We also show that the activity of MC4R PVN neurons is controlled by the constitutive activity of the MC4R and that expression of the receptor mRNA and α-MSH sensitivity are both stimulated by leptin. Thus, leptin acts multinodally on arcuate nucleus/PVN circuits to regulate energy homeostasis, with prominent mechanisms involving direct control of both membrane conductances and gene expression in the MC4R PVN neuron.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Independent and additive effects of central POMC and leptin pathways on murine obesity (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: The lethal yellow (AY/a) mouse has a defect in proopiomelanocortin (POMC) signaling in the brain that leads to obesity, and is resistant to the anorexigenic effects of the hormone leptin. It has been proposed that the weight-reducing effects of leptin are thus transmitted primarily by way of POMC neurons. However, the central effects of defective POMC signaling, and the absence of leptin, on weight gain in double-mutant lethal yellow (AY/a) leptin-deficient (lepob/lepob) mice were shown to be independent and additive. Furthermore, deletion of the leptin gene restored leptin sensitivity to AY/a mice. This result implies that in the AY/a mouse, obesity is independent of leptin action, and resistance to leptin results from desensitization of leptin signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boston, B A -- Blaydon, K M -- Varnerin, J -- Cone, R D -- DK/AR517330/DK/NIDDK NIH HHS/ -- DK02404/DK/NIDDK NIH HHS/ -- HD33703/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1641-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pediatrics, Oregon Health Sciences University, Portland, OR 97201, USA. Laboratories, Rahway, NJ 07065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9374468" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Agouti Signaling Protein ; Alleles ; Animals ; Arcuate Nucleus of Hypothalamus/*metabolism ; Blood Glucose/analysis ; Corticosterone/blood ; Crosses, Genetic ; Eating/drug effects ; Energy Metabolism ; Female ; Homeostasis ; Insulin/blood ; *Intercellular Signaling Peptides and Proteins ; Leptin ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Neurons/metabolism ; Obesity/genetics/*metabolism ; Pro-Opiomelanocortin/*metabolism ; Proteins/genetics/*metabolism/pharmacology ; Signal Transduction ; Weight Gain
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    G-protein-independent coupling of MC4R to Kir7.1 in hypothalamic neurons (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-01-21
    Description: The regulated release of anorexigenic alpha-melanocyte stimulating hormone (alpha-MSH) and orexigenic Agouti-related protein (AgRP) from discrete hypothalamic arcuate neurons onto common target sites in the central nervous system has a fundamental role in the regulation of energy homeostasis. Both peptides bind with high affinity to the melanocortin-4 receptor (MC4R); existing data show that alpha-MSH is an agonist that couples the receptor to the Galphas signalling pathway, while AgRP binds competitively to block alpha-MSH binding and blocks the constitutive activity mediated by the ligand-mimetic amino-terminal domain of the receptor. Here we show that, in mice, regulation of firing activity of neurons from the paraventricular nucleus of the hypothalamus (PVN) by alpha-MSH and AgRP can be mediated independently of Galphas signalling by ligand-induced coupling of MC4R to closure of inwardly rectifying potassium channel, Kir7.1. Furthermore, AgRP is a biased agonist that hyperpolarizes neurons by binding to MC4R and opening Kir7.1, independently of its inhibition of alpha-MSH binding. Consequently, Kir7.1 signalling appears to be central to melanocortin-mediated regulation of energy homeostasis within the PVN. Coupling of MC4R to Kir7.1 may explain unusual aspects of the control of energy homeostasis by melanocortin signalling, including the gene dosage effect of MC4R and the sustained effects of AgRP on food intake.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383680/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4383680/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ghamari-Langroudi, Masoud -- Digby, Gregory J -- Sebag, Julien A -- Millhauser, Glenn L -- Palomino, Rafael -- Matthews, Robert -- Gillyard, Taneisha -- Panaro, Brandon L -- Tough, Iain R -- Cox, Helen M -- Denton, Jerod S -- Cone, Roger D -- 5R01 DK082884-03/DK/NIDDK NIH HHS/ -- DK020593/DK/NIDDK NIH HHS/ -- F31 DK102343/DK/NIDDK NIH HHS/ -- P30 DK020593/DK/NIDDK NIH HHS/ -- R01 DK064265/DK/NIDDK NIH HHS/ -- R01 DK070332/DK/NIDDK NIH HHS/ -- R01DK064265/DK/NIDDK NIH HHS/ -- R01DK070332/DK/NIDDK NIH HHS/ -- R25 GM059994/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Apr 2;520(7545):94-8. doi: 10.1038/nature14051. Epub 2015 Jan 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology &Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA. ; Department of Chemistry &Biochemistry, University of California, Santa Cruz, California 95064, USA. ; 1] Department of Molecular Physiology &Biophysics, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA [2] Department of Pharmacology, Meharry Medical College, Nashville, Tennessee 37208, USA. ; King's College London, Wolfson Centre for Age-Related Diseases, Guy's Campus, London SE1 1UL, UK. ; 1] Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA [2] Department of Pharmacology, Vanderbilt University Medical Center, Nashville, Tennessee 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25600267" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Agouti-Related Protein/metabolism ; Animals ; Eating/genetics ; Energy Metabolism ; Female ; *GTP-Binding Protein alpha Subunits, Gs ; HEK293 Cells ; Homeostasis/genetics ; Humans ; Ligands ; Male ; Melanocortins/metabolism ; Mice ; Neurons/*metabolism ; Paraventricular Hypothalamic Nucleus/*cytology ; Potassium Channels, Inwardly Rectifying/*metabolism ; Receptor, Melanocortin, Type 4/genetics/*metabolism ; Signal Transduction/genetics ; alpha-MSH/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Neuroscience: a cellular basis for the munchies (2015)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2015-02-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Patel, Sachin -- Cone, Roger D -- England -- Nature. 2015 Mar 5;519(7541):38-40. doi: 10.1038/nature14206. Epub 2015 Feb 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vanderbilt University Medical Center, Department of Molecular Physiology and Biophysics, Nashville, Tennessee 37232-0615, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25707800" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cannabinoids/*pharmacology ; Eating/*drug effects/*physiology ; Hypothalamus/*cytology ; Male ; Neurons/*drug effects/*metabolism ; Pro-Opiomelanocortin/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 5
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    Developmental control of the melanocortin-4 receptor by MRAP2 proteins in zebrafish (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-23
    Description: The melanocortin-4 receptor (MC4R) is essential for control of energy homeostasis in vertebrates. MC4R interacts with melanocortin receptor accessory protein 2 (MRAP2) in vitro, but its functions in vivo are unknown. We found that MRAP2a, a larval form, stimulates growth of zebrafish by specifically blocking the action of MC4R. In cell culture, this protein binds MC4R and reduces the ability of the receptor to bind its ligand, alpha-melanocyte-stimulating hormone (alpha-MSH). A paralog, MRAP2b, expressed later in development, also binds MC4R but increases ligand sensitivity. Thus, MRAP2 proteins allow for developmental control of MC4R activity, with MRAP2a blocking its function and stimulating growth during larval development, whereas MRAP2b enhances responsiveness to alpha-MSH once the zebrafish begins feeding, thus increasing the capacity for regulated feeding and growth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255277/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4255277/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sebag, Julien A -- Zhang, Chao -- Hinkle, Patricia M -- Bradshaw, Amanda M -- Cone, Roger D -- DK020593/DK/NIDDK NIH HHS/ -- DK070332/DK/NIDDK NIH HHS/ -- DK075721/DK/NIDDK NIH HHS/ -- DK19974/DK/NIDDK NIH HHS/ -- F23DK091055/DK/NIDDK NIH HHS/ -- R01 DK070332/DK/NIDDK NIH HHS/ -- R01 DK075721/DK/NIDDK NIH HHS/ -- T32 DK007563/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2013 Jul 19;341(6143):278-81. doi: 10.1126/science.1232995.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23869017" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Embryo, Nonmammalian/metabolism ; Energy Metabolism ; HEK293 Cells ; Humans ; Receptor Activity-Modifying Proteins/genetics/*metabolism ; Receptor, Melanocortin, Type 4/*metabolism ; Zebrafish/*embryology/metabolism ; Zebrafish Proteins/genetics/*metabolism ; alpha-MSH/metabolism/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Activation of central melanocortin pathways by fenfluramine (2002)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2002-07-27
    Description: D-fenfluramine (d-FEN) was once widely prescribed and was among the most effective weight loss drugs, but was withdrawn from clinical use because of reports of cardiac complications in a subset of patients. Discerning the neurobiology underlying the anorexic action of d-FEN may facilitate the development of new drugs to prevent and treat obesity. Through a combination of functional neuroanatomy, feeding, and electrophysiology studies in rodents, we show that d-FEN-induced anorexia requires activation of central nervous system melanocortin pathways. These results provide a mechanistic explanation of d-FEN's anorexic actions and indicate that drugs targeting these downstream melanocortin pathways may prove to be effective and more selective anti-obesity treatments.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heisler, Lora K -- Cowley, Michael A -- Tecott, Laurence H -- Fan, Wei -- Low, Malcolm J -- Smart, James L -- Rubinstein, Marcelo -- Tatro, Jeffrey B -- Marcus, Jacob N -- Holstege, Henne -- Lee, Charlotte E -- Cone, Roger D -- Elmquist, Joel K -- F31HG00201/HG/NHGRI NIH HHS/ -- P01DK056116/DK/NIDDK NIH HHS/ -- P01DK55819/DK/NIDDK NIH HHS/ -- R01MH061583/MH/NIMH NIH HHS/ -- R01MH44694/MH/NIMH NIH HHS/ -- R01MH61624/MH/NIMH NIH HHS/ -- R03TW01233/TW/FIC NIH HHS/ -- New York, N.Y. -- Science. 2002 Jul 26;297(5581):609-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12142539" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetite Depressants/*pharmacology ; Arcuate Nucleus of Hypothalamus/*drug effects/metabolism ; Feeding Behavior/*drug effects ; Fenfluramine/*pharmacology ; Male ; Melanocyte-Stimulating Hormones/pharmacology ; Mice ; Mice, Obese ; Mice, Transgenic ; Neurons/drug effects/metabolism ; Paraventricular Hypothalamic Nucleus/drug effects/metabolism ; Patch-Clamp Techniques ; Pro-Opiomelanocortin/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor, Melanocortin, Type 3 ; Receptor, Melanocortin, Type 4 ; Receptor, Serotonin, 5-HT2C ; Receptors, Corticotropin/metabolism ; Receptors, Serotonin/metabolism ; Serotonin/metabolism ; Serotonin Agents/pharmacology ; alpha-MSH/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    The cloning of a family of genes that encode the melanocortin receptors (1992)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1992-08-28
    Description: Melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH) regulate pigmentation and adrenal cortical function, respectively. These peptides also have a variety of biological activities in other areas, including the brain, the pituitary, and the immune system. A complete understanding of the biological activities of these hormones requires the isolation and characterization of their corresponding receptors. The murine and human MSH receptors (MSH-Rs) and a human ACTH receptor (ACTH-R) were cloned. These receptors define a subfamily of receptors coupled to guanine nucleotide-binding proteins that may include the cannabinoid receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mountjoy, K G -- Robbins, L S -- Mortrud, M T -- Cone, R D -- R01 DK43859-02/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1992 Aug 28;257(5074):1248-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute for Advanced Biomedical Research, Oregon Health Sciences University, Portland 97201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1325670" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/metabolism ; Amino Acid Sequence ; Animals ; Blotting, Northern ; Cloning, Molecular ; Dose-Response Relationship, Drug ; GTP-Binding Proteins/metabolism ; Humans ; Melanocyte-Stimulating Hormones/physiology ; Melanocytes/metabolism ; Mice ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA, Messenger/biosynthesis ; Receptors, Corticotropin ; Receptors, Pituitary Hormone/biosynthesis/*genetics ; Sequence Homology, Nucleic Acid
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Tissue-specific and ectopic expression of genes introduced into transgenic mice by retroviruses (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-12
    Description: Recombinant retroviruses containing the complete genomic human beta globin gene (under the control of its own promoter) and the bacterial neomycin phosphotransferase gene (under the control of the normal or enhancerless viral promoter) were used to derive transgenic mouse strains by infection of preimplantation embryos. Expression of the beta globin gene in hematopoietic tissues was observed in all transgenic strains. In addition, one strain showed ectopic expression of beta globin in the same tissues that also expressed high levels of RNA from the viral promoter. It is likely that expression from the long terminal repeat (LTR), in contrast to expression from the internal promoter, is dependent on the site of integration. Thus, retroviral vectors can be used for tissue-specific expression of foreign genes in transgenic mice, as well as for the identification of loci that allow developmental activation of a provirus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soriano, P -- Cone, R D -- Mulligan, R C -- Jaenisch, R -- HD-19105/HD/NICHD NIH HHS/ -- P01-CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1986 Dec 12;234(4782):1409-13.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3024318" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; Globins/genetics ; Humans ; Kanamycin Kinase ; Mice/genetics ; Phosphotransferases/genetics ; Promoter Regions, Genetic ; RNA, Viral/immunology ; Repetitive Sequences, Nucleic Acid ; Retroviridae/*genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Tissue-specific expression of functionally rearranged lambda 1 Ig gene through a retrovirus vector (1987)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1987-05-22
    Description: To explore the potential use of retrovirus vectors for the transfer of genomic DNA sequences into mammalian cells, recombinant retroviral genomes were constructed that encode a functionally rearranged murine lambda 1 immunoglobulin gene. Several of these genomes could be transmitted intact to recipient cells by viral infection, although successful transmission depended both on the orientation of the lambda 1 sequences and on their specific placement within vector sequences. The lambda 1 gene transduced by viral infection was expressed in a cell lineage-specific manner, albeit at lower levels than endogenous lambda 1 gene expression in cells from the B-lymphocyte lineage. Vectors yielding integrated proviruses that lacked viral transcriptional enhancer sequences were used to show that neither viral transcription nor the viral transcriptional sequences themselves had any effect on the tissue specificity of lambda 1 gene expression or the absolute amount of lambda 1 transcription. Vector transcription did, however, dramatically decrease the amount of lambda 1 protein that could be detected in tranduced cells. These results suggest that retrovirus vectors may be useful reagents not only for the expression of complementary DNA sequences but also for studies of tissue-specific transcription in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cone, R D -- Reilly, E B -- Eisen, H N -- Mulligan, R C -- CA26712/CA/NCI NIH HHS/ -- CA38497/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1987 May 22;236(4804):954-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3107128" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; B-Lymphocytes/immunology ; Cells, Cultured ; Enhancer Elements, Genetic ; *Genes ; *Genes, Viral ; Genetic Vectors ; Immunoglobulin lambda-Chains/*genetics ; Retroviridae/*genetics ; *Transcription, Genetic
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Electronic Resource
    Electronic Resource
    Physiology Does gut hormone PYY 3–36 decrease food intake in rodents? (reply) (2004)
    [s.l.] : Nature Publishing Group
    Nature 430 (2004), S. 0 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Batterham et al. reply The results of Tschöp et al. on the lack of effect of peripheral administration of PYY3–36 on food intake in rodents are at odds with both the published literature (our Table 1) and with earlier data generated by ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/nature02666
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