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Berlin Brandenburg

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  • 1
    In: Nature Neuroscience, 2010, Vol.14(1), p.54
    Description: Binding of target-derived neurotrophins to Trk receptors at nerve terminals are required to stimulate neuronal survival, differentiation, innervation and synaptic plasticity. The distance between the soma and nerve terminal is tremendous, making efficient anterograde Trk transport critical for their synaptic translocation and signaling. The mechanism responsible for this trafficking remains poorly understood. Here we show that the sorting receptor sortilin interacts with TrkA, -B, and -C and enables their anterograde axonal transport, thereby enhancing neurotrophin signaling. Cultured DRG neurons lacking sortilin exhibit blunted MAPK signaling and reduced neurite outgrowth upon stimulation with NGF. Moreover, deficiency for sortilin considerably aggravates TrkA, -B- and -C phenotypes present in p75NTR knockouts, and results in increased embryonic lethality and sympathetic neuropathy in mice heterozygous for TrkA. Our findings demonstrate a novel and unexpected role for sortilin as an anterograde trafficking receptor for Trk and a positive modulator of neurotrophin-induced neuronal survival
    Keywords: Receptors ; Sensory Systems ; Neurodegeneration ; Anatomy & Physiology;
    ISSN: 1097-6256
    E-ISSN: 15461726
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  • 2
  • 3
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 13 March 2007, Vol.104(11), pp.4443-8
    Description: In the developing muscle, a pool of myogenic progenitor cells is formed and maintained. These resident progenitors provide a source of cells for muscle growth in development and generate satellite cells in the perinatal period. By the use of conditional mutagenesis in mice, we demonstrate here that the major mediator of Notch signaling, the transcription factor RBP-J, is essential to maintain this pool of progenitor cells in an undifferentiated state. In the absence of RBP-J, these cells undergo uncontrolled myogenic differentiation, leading to a depletion of the progenitor pool. This results in a lack of muscle growth in development and severe muscle hypotrophy. In addition, satellite cells are not formed late in fetal development in conditional RBP-J mutant mice. We conclude that RBP-J is required in the developing muscle to set aside proliferating progenitors and satellite cells.
    Keywords: Gene Expression Regulation ; Immunoglobulin J Recombination Signal Sequence-Binding Protein -- Physiology ; Muscles -- Metabolism ; Satellite Cells, Skeletal Muscle -- Cytology ; Stem Cells -- Cytology
    ISSN: 0027-8424
    E-ISSN: 10916490
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  • 4
    In: Cell, May 18, 2001, Vol.105(4), p.533(14)
    Description: Research has been conducted on the beta-catenin, an important molecule in Wnt/wingless signaling which controls steps in embryogenesis. The role of beta-catenin in skin development has been investigated via the conditional mutation of the epidermis and hair follicle gene and the results indicate that beta-catenin mutation has blocked placode formation which generates hair follicles.
    Keywords: Cytological Research -- Analysis ; Morphogenesis -- Physiological Aspects ; Stem Cells -- Physiological Aspects ; Hair Follicles -- Genetic Aspects ; Gene Mutation -- Physiological Aspects ; Epidermis -- Genetic Aspects
    ISSN: 0092-8674
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  • 5
    Language: English
    In: The Journal of cell biology, 22 May 2006, Vol.173(4), pp.559-70
    Description: Titin, the largest protein known to date, has been linked to sarcomere assembly and function through its elastic adaptor and signaling domains. Titin's M-line region contains a unique kinase domain that has been proposed to regulate sarcomere assembly via its substrate titin cap (T-cap). In this study, we use a titin M line-deficient mouse to show that the initial assembly of the sarcomere does not depend on titin's M-line region or the phosphorylation of T-cap by the titin kinase. Rather, titin's M-line region is required to form a continuous titin filament and to provide mechanical stability of the embryonic sarcomere. Even without titin integrating into the M band, sarcomeres show proper spacing and alignment of Z discs and M bands but fail to grow laterally and ultimately disassemble. The comparison of disassembly in the developing and mature knockout sarcomere suggests diverse functions for titin's M line in embryonic development and the adult heart that not only involve the differential expression of titin isoforms but also of titin-binding proteins.
    Keywords: Genes, Lethal -- Genetics ; Heart Defects, Congenital -- Genetics ; Muscle Proteins -- Genetics ; Myocardium -- Metabolism ; Myocytes, Cardiac -- Metabolism ; Protein Kinases -- Genetics ; Sarcomeres -- Metabolism
    ISSN: 0021-9525
    E-ISSN: 15408140
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  • 6
    Language: English
    In: Brain Research, 1996, Vol.733(1), pp.73-82
    Description: Cytochrome P45011BI (11(3-hydroxylase) was detected in the brain of male rats by in situ hybridization methods. Normal Sprague-Dawley rats were compared to the transgenic strain TGR(mRen2)27, characterized by the expression of the murine Ren-2 d renin gene and the development of severe hypertension. Specific riboprobes were generated by in vitro transcription of a 152 base-pair long cDNA template. 35S-labeled riboprobes were hybridized to cryostat sections from adrenal glands and from two different levels of the brain using standard protocols and varying washing conditions. After exposure of the radiolabeled sections to X-ray film, the signals were quantified and compared. Following autoradiography and counterstaining, cytochrome P45011B1 mRNA was clearly localized in the zona fasciculata/reticularis of the adrenal cortex and in distinct layers of the cerebral cortex. High signal densities were obtained in the layers 11-1V of the neocortex and in the layer 11 of the piriform cortex, although the concentrations of cytochrome P45011B1 mRNA were remarkably lower in the central nervous system as compared to adrenal glands. As revealed by the semi-quantitative analysis, there was a slight increase in adrenal 11β-hydroxylase mRNA in the transgenic rats, whereas the brain seems to express nearly the same amount of this enzyme in both strains. The cytochrome P4501IB1 mRNA expression in distinct cells, probably nerve cells, and especially in regions with high densities of glucocorticoid receptors points to a possible function of brain derived corticosterone in receptor activation.
    Keywords: Cytochrome P4501ib1 ; Cerebral Cortex ; In Situ Hybridization ; Neurosteroid ; Transgenic Rat ; Hypertension
    ISSN: 0006-8993
    E-ISSN: 18726240
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  • 7
    Language: English
    In: Proceedings of the National Academy of Sciences of the United States of America, 25 June 2002, Vol.99(13), pp.8880-5
    Description: The ErbB2 (Her2) proto-oncogene encodes a receptor tyrosine kinase, which is frequently amplified and overexpressed in human tumors. ErbB2 provides the target for a novel and effective antibody-based therapy (Trastuzumab/Herceptin) used for the treatment of mammary carcinomas. However, cardiomyopathies develop in a proportion of patients treated with Trastuzumab, and the incidence of such complications is increased by combination with standard chemotherapy. Gene ablation studies have previously demonstrated that the ErbB2 receptor, together with its coreceptor ErbB4 and the ligand Neuregulin-1, are essential for normal development of the heart ventricle. We use here Cre-loxP technology to mutate ErbB2 specifically in ventricular cardiomyocytes. Conditional mutant mice develop a severe dilated cardiomyopathy, with signs of cardiac dysfunction generally appearing by the second postnatal month. We infer that signaling from the ErbB2 receptor, which is enriched in T-tubules in cardiomyocytes, is crucial for adult heart function. Conditional ErbB2 mutant mice provide a model of dilated cardiomyopathy. In particular, they will allow a rigorous assessment of the role of ErbB2 in the heart and provide insight into the molecular mechanisms that underlie the adverse effects of anti-ErbB2 antibodies.
    Keywords: Mutation ; Cardiomyopathy, Dilated -- Genetics ; Myocardium -- Metabolism ; Receptor, Erbb-2 -- Physiology
    ISSN: 0027-8424
    E-ISSN: 10916490
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  • 8
    In: Nature, 2006, Vol.445(7124), p.206
    Description: Touch and mechanical pain are first detected at our largest sensory surface, the skin. The cell bodies of sensory neurons that detect such stimuli are located in the dorsal root ganglia, and subtypes of these neurons are specialized to detect specific modalities of mechanical stimuli. Molecules have been identified that are necessary for mechanosensation in invertebrates but so far not in mammals. In Caenorhabditis elegans, mec-2 is one of several genes identified in a screen for touch insensitivity and encodes an integral membrane protein with a stomatin homology domain. Here we show that about 35% of skin mechanoreceptors do not respond to mechanical stimuli in mice with a mutation in stomatin-like protein 3 (SLP3, also called Stoml3), a mammalian mec-2 homologue that is expressed in sensory neurons. In addition, mechanosensitive ion channels found in many sensory neurons do not function without SLP3. Tactile-driven behaviours are also impaired in SLP3 mutant mice, including touch-evoked pain caused by neuropathic injury. SLP3 is therefore indispensable for the function of a subset of cutaneous mechanoreceptors, and our data support the idea that this protein is an essential subunit of a mammalian mechanotransducer. [PUBLICATION ]
    Keywords: Neurons ; Proteins ; Stimuli ; Touch ; Mechanoreceptors ; Mice ; Pain ; Mammals ; General and Nonclassified (MD) ; General and Nonclassified (EC) ; General and Nonclassified (Ed) ; General and Nonclassified (Ep) ; Surveying, Theory, and Analysis (CE) ; Design Principles, Theory, and Analysis (Mt) ; Computing Milieux (General) (Ci) ; Electronics and Communications Milieux (General) (Ea) ; Solid State Milieux (General) (So) ; Article;
    ISSN: 0028-0836
    E-ISSN: 14764687
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  • 9
    Language: English
    In: Cell, 2001, Vol.105(4), pp.533-545
    Description: β-Catenin is an essential molecule in Wnt/wingless signaling, which controls decisive steps in embryogenesis. To study the role of β-catenin in skin development, we introduced a conditional mutation of the gene in the epidermis and hair follicles using Cre/loxP technology. When β-catenin is mutated during embryogenesis, formation of placodes that generate hair follicles is blocked. We show that β-catenin is required genetically downstream of tabby / downless and upstream of bmp and shh in placode formation. If β-catenin is deleted after hair follicles have formed, hair is completely lost after the first hair cycle. Further analysis demonstrates that β-catenin is essential for fate decisions of skin stem cells: in the absence of β-catenin, stem cells fail to differentiate into follicular keratinocytes, but instead adopt an epidermal fate.
    Keywords: Biology;
    ISSN: 0092-8674
    E-ISSN: 10974172
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  • 10
    Language: English
    In: The Journal of cell biology, 11 October 2004, Vol.167(1), pp.149-60
    Description: Plakophilins are proteins of the armadillo family that function in embryonic development and in the adult, and when mutated can cause disease. We have ablated the plakophilin 2 gene in mice. The resulting mutant mice exhibit lethal alterations in heart morphogenesis and stability at mid-gestation (E10.5-E11), characterized by reduced trabeculation, disarrayed cytoskeleton, ruptures of cardiac walls, and blood leakage into the pericardiac cavity. In the absence of plakophilin 2, the cytoskeletal linker protein desmoplakin dissociates from the plaques of the adhering junctions that connect the cardiomyocytes and forms granular aggregates in the cytoplasm. By contrast, embryonic epithelia show normal junctions. Thus, we conclude that plakophilin 2 is important for the assembly of junctional proteins and represents an essential morphogenic factor and architectural component of the heart.
    Keywords: Gene Expression Regulation, Developmental ; Heart -- Embryology ; Proteins -- Genetics
    ISSN: 0021-9525
    E-ISSN: 15408140
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