Search Results - (Author, Cooperation:R. D. Palmiter)
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1Latest Papers from Table of Contents or Articles in PressM. A. Penzo ; V. Robert ; J. Tucciarone ; D. De Bundel ; M. Wang ; L. Van Aelst ; M. Darvas ; L. F. Parada ; R. D. Palmiter ; M. He ; Z. J. Huang ; B. Li
Nature Publishing Group (NPG)
Published 2015Staff ViewPublication Date: 2015-01-21Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Central Amygdaloid Nucleus/cytology/*physiology ; Conditioning (Psychology)/physiology ; Fear/*physiology/psychology ; Female ; Male ; Memory/physiology ; Mice ; Neural Pathways/cytology/*physiology ; Neuronal Plasticity ; Neurons/metabolism ; Receptor, trkB/metabolism ; Somatostatin/metabolism ; Thalamus/cytology/*physiology ; Time FactorsPublished by: -
2Latest Papers from Table of Contents or Articles in PressStaff View
Publication Date: 2012-03-16Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Agouti-Related Protein/metabolism ; Animals ; Appetite/drug effects/*physiology ; Body Weight/drug effects ; Feeding Behavior/drug effects/physiology ; Female ; Glutamic Acid/metabolism ; Hypothalamus/*cytology/drug effects/*physiology ; Male ; Mice ; Mice, Inbred C57BL ; Neurons/drug effects/*physiology ; Ondansetron/pharmacology ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Serotonergic Neurons/drug effects/metabolism ; Solitary Nucleus/cytology ; Starvation/drug therapy/physiopathology/prevention & control ; Weight Gain/drug effects/physiology ; gamma-Aminobutyric Acid/metabolismPublished by: -
3Latest Papers from Table of Contents or Articles in PressM. E. Carter ; M. E. Soden ; L. S. Zweifel ; R. D. Palmiter
Nature Publishing Group (NPG)
Published 2013Staff ViewPublication Date: 2013-10-15Publisher: Nature Publishing Group (NPG)Print ISSN: 0028-0836Electronic ISSN: 1476-4687Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsKeywords: Amygdala/anatomy & histology/cytology/drug effects/physiology ; Animals ; Appetite/drug effects/*genetics/*physiology ; Calcitonin Gene-Related Peptide/metabolism ; Eating/drug effects/genetics/physiology ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Neural Pathways/drug effects/*physiology ; Neurons/drug effects ; Optogenetics ; Pons/anatomy & histology/cytology/drug effects/physiology ; Proto-Oncogene Proteins c-fos/metabolism ; Satiety Response/drug effects/*physiology ; Starvation/drug therapyPublished by: -
4Latest Papers from Table of Contents or Articles in PressS. C. Johnson ; M. E. Yanos ; E. B. Kayser ; A. Quintana ; M. Sangesland ; A. Castanza ; L. Uhde ; J. Hui ; V. Z. Wall ; A. Gagnidze ; K. Oh ; B. M. Wasko ; F. J. Ramos ; R. D. Palmiter ; P. S. Rabinovitch ; P. G. Morgan ; M. M. Sedensky ; M. Kaeberlein
American Association for the Advancement of Science (AAAS)
Published 2013Staff ViewPublication Date: 2013-11-16Publisher: American Association for the Advancement of Science (AAAS)Print ISSN: 0036-8075Electronic ISSN: 1095-9203Topics: BiologyChemistry and PharmacologyComputer ScienceMedicineNatural Sciences in GeneralPhysicsKeywords: Animals ; Brain/drug effects/enzymology/pathology ; Disease Models, Animal ; Electron Transport Complex I/genetics/metabolism ; Glycolysis/drug effects ; Leigh Disease/*drug therapy/genetics/pathology ; Mice ; Mice, Knockout ; Mice, Mutant Strains ; Mitochondria/drug effects/enzymology ; Mitochondrial Diseases/*drug therapy/genetics/pathology ; *Molecular Targeted Therapy ; Multiprotein Complexes/*antagonists & inhibitors ; Neuroprotective Agents/*therapeutic use ; Sirolimus/*therapeutic use ; TOR Serine-Threonine Kinases/*antagonists & inhibitorsPublished by: -
5Articles: DFG German National LicensesAdams, J. M. ; Harris, A. W. ; Pinkert, C. A. ; Corcoran, L. M. ; Alexander, W. S. ; Cory, S. ; Palmiter, R. D. ; Brinster, R. L.
[s.l.] : Nature Publishing Group
Published 1985Staff ViewISSN: 1476-4687Source: Nature Archives 1869 - 2009Topics: BiologyChemistry and PharmacologyMedicineNatural Sciences in GeneralPhysicsNotes: [Auszug] Transgenic mice bearing the cellular myc oncogene coupled to the immunoglobulin μ or κ enhancer frequently develop a fatal lymphoma within a few months of birth. Since the tumours represent both immature and mature B lymphocytes, constitutive c-myc expression appears to be highly ...Type of Medium: Electronic ResourceURL: -
6Articles: DFG German National LicensesStaff View
ISSN: 1432-0428Keywords: Insulin ; islet amyloid polypeptide ; pancreas ; secretionSource: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary To determine whether chronic overproduction of islet amyloid polypeptide alters beta-cell function, we studied a line of transgenic mice which overexpress islet amyloid polypeptide in their beta-cells. At 3 months of age, these transgenic mice had greater pancreatic content of both islet amyloid polypeptide and insulin. Further, basal and glucose-stimulated secretion of both islet amyloid polypeptide and insulin were also elevated in the perfused pancreas of the transgenic animals. These findings demonstrate that chronic overproduction and secretion of islet amyloid polypeptide are associated with increased insulin storage and enhanced secretion of insulin in vitro. This increase in insulin storage and secretion may be due to a direct effect of islet amyloid polypeptide on the beta-cell or a betacell adaptation to islet amyloid polypeptide-induced insulin resistance.Type of Medium: Electronic ResourceURL: -
7Articles: DFG German National LicensesStaff View
ISSN: 1432-0428Keywords: Key words Insulin, islet amyloid polypeptide, pancreas, secretion.Source: Springer Online Journal Archives 1860-2000Topics: MedicineNotes: Summary To determine whether chronic overproduction of islet amyloid polypeptide alters beta-cell function, we studied a line of transgenic mice which overexpress islet amyloid polypeptide in their beta-cells. At 3 months of age, these transgenic mice had greater pancreatic content of both islet amyloid polypeptide and insulin. Further, basal and glucose-stimulated secretion of both islet amyloid polypeptide and insulin were also elevated in the perfused pancreas of the transgenic animals. These findings demonstrate that chronic overproduction and secretion of islet amyloid polypeptide are associated with increased insulin storage and enhanced secretion of insulin in vitro. This increase in insulin storage and secretion may be due to a direct effect of islet amyloid polypeptide on the beta-cell or a beta-cell adaptation to islet amyloid polypeptide-induced insulin resistance. [Diabetologia (1994) 37: 725–728]Type of Medium: Electronic ResourceURL: -
8Articles: DFG German National LicensesStaff View
ISSN: 1432-1203Source: Springer Online Journal Archives 1860-2000Topics: BiologyMedicineNotes: Summary We have assigned the structural gene (Mt-1) coding for the murine metal-binding protein metallothionein I (MT-1) to mouse chromosome 8 by using a cloned DNA probe for mouse Mt-1 in combination with a panel of Chinese hamstermouse somatic cell hybrid clones segregating mouse chromosomes. Analysis of hybrid cell extracts for the presence of mouse Mt-1 or MT-1 mRNA revealed concordant segregation of Mt-1 with mouse glutathione reductase, an enzyme marker for mouse chromosome 8, but discordant segregation with enzyme markers for 14 other mouse chromosomes. Karyotype analyses of seven informative hybrid clones confirmed the assignment of mouse Mt-1 to chromosome 8. Menkes' disease in man and the mottled mutation (Mo) in the mouse, which provides an animal model of Menkes' disease, are both X-linked degenerative neurologic disorders involving abnormal copper metabolism and increased levels of intracellular metallothionein protein. Fibroblasts from Mo male mice have increased amounts of MT-1 mRNA, suggesting that both Mo and Menkes' disease may be due to a metallothionein gene mutation. However, our assignment of Mt-1 to mouse chromosome 8, rather than the X chromosome, demonstrates that a mutation in mouse Mt-1 or a closely linked regulatory gene is not the primary defect in Mo, and implies that a metallothionein gene mutation is not the genetic defect in human Menkes' disease.Type of Medium: Electronic ResourceURL: