Transgenic activation of Ras in neurons promotes hypertrophy and protects from lesion-induced degeneration

Journal of Cell Biology

Volumn 151, Issue 7, 2000, Pages 1537-1548

  Heumann, Rolf ^a   Goemans, Christoph ^a   Bartsch, Daniela ^a   Lingenhöhl, Kurt ^c   Waldmeier, Peter C ^c   Hengerer, Bastian ^c   Allegrini, Peter R ^c   Schellander, Karl ^f   Wagner, Erwin F ^d   Arendt, Thomas ^e   Kamdem, Rigobert H ^e   Obst Pernberg, Kirstin ^b   Narz, Frank ^a   Wahle, Petra ^b   Berns, Hartmut ^a  

^a RUHR UNIVERSITY BOCHUM   (Germany)

^b Developmental Neurobiology   (Germany)

^c NOVARTIS PHARMA AG   (Switzerland)

^d RESEARCH INSTITUTE OF MOLECULAR PATHOLOGY   (Austria)

^e Paul Flechsig Instititute for Brain Research   (Germany)

^f UNIVERSITY OF BONN   (Germany)

Author keywords

Mouse; Neuron; Protection; Ras; Transgenic

Indexed keywords

1,2,3,6 TETRAHYDRO 1 METHYL 4 PHENYLPYRIDINE; CHOLINE ACETYLTRANSFERASE; COMPLEMENTARY DNA; GLUTATHIONE TRANSFERASE; MESSENGER RNA; NEUROPEPTIDE Y; OXIDOPAMINE; PHOSPHATIDYLINOSITOL KINASE; RAS PROTEIN; TYROSINE 3 MONOOXYGENASE;

ANIMAL CELL; ANIMAL MODEL; ARTICLE; BRAIN; BRAIN PROTECTION; CONTROLLED STUDY; DEGENERATIVE DISEASE; ENZYME PHOSPHORYLATION; IN SITU HYBRIDIZATION; MOUSE; NERVE CELL CULTURE; NEUROLOGIC DISEASE; NONHUMAN; PRIORITY JOURNAL; SIGNAL TRANSDUCTION; TRANSGENIC MOUSE;

1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE; 1-METHYL-4-PHENYLPYRIDINIUM; 1-PHOSPHATIDYLINOSITOL 3-KINASE; ANIMALS; AXOTOMY; BRAIN; CELL COUNT; CELL SIZE; CELLS, CULTURED; CHOLINE O-ACETYLTRANSFERASE; ENZYME ACTIVATION; HYPERTROPHY; MICE; MICE, TRANSGENIC; MITOGEN-ACTIVATED PROTEIN KINASES; MOTOR NEURONS; MUTATION; NEURODEGENERATIVE DISEASES; NEUROPEPTIDE Y; NEUROPROTECTIVE AGENTS; OXIDOPAMINE; PHOSPHORYLATION; PROTEIN-SERINE-THREONINE KINASES; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; PROTO-ONCOGENE PROTEINS C-BCL-2; PROTO-ONCOGENE PROTEINS P21(RAS); RNA, MESSENGER; SIGNAL TRANSDUCTION; SUBSTANTIA NIGRA; TYROSINE 3-MONOOXYGENASE;

EID: 0034739850     PISSN: 00219525     EISSN: None     Source Type: Journal    
DOI: 10.1083/jcb.151.7.1537     Document Type: Article

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