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Hannes Vogel

Researcher at Stanford University

Publications -  279
Citations -  29967

Hannes Vogel is an academic researcher from Stanford University. The author has contributed to research in topics: Glioma & Gene. The author has an hindex of 83, co-authored 270 publications receiving 25688 citations. Previous affiliations of Hannes Vogel include Lucile Packard Children's Hospital & Baylor College of Medicine.

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p63 is a p53 homologue required for limb and epidermal morphogenesis.

TL;DR: P63 is essential for several aspects of ectodermal differentiation during embryogenesis, including hair follicles, teeth and mammary glands, which are absent in p63-deficient mice.
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Purification and Characterization of Progenitor and Mature Human Astrocytes Reveals Transcriptional and Functional Differences with Mouse.

TL;DR: The development of an immunopanning method to acutely purify astrocytes from fetal, juvenile, and adult human brains and to maintain these cells in serum-free cultures is reported, finding that human astroCytes have abilities similar to those of murine astroicytes in promoting neuronal survival, inducing functional synapse formation, and engulfing synaptosomes.
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Neuronal Activity Promotes Oligodendrogenesis and Adaptive Myelination in the Mammalian Brain

TL;DR: In vivo optogenetic techniques in awake, behaving mice are used to provide direct evidence that neuronal activity regulates changes in myelin-forming cells within an active circuit, suggesting that adaptive changes inMyelin-form cells represent a type of behaviorally relevant neural plasticity.
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Neurodegeneration, myocardial injury, and perinatal death in mitochondrial superoxide dismutase-deficient mice.

TL;DR: Observations indicate that SOD2 deficiency causes increased susceptibility to oxidative mitochondrial injury in central nervous system neurons, cardiac myocytes, and other metabolically active tissues after postnatal exposure to ambient oxygen concentrations.
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Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin

TL;DR: It is shown that inhibition of Drosophila Pink1 function results in energy depletion, shortened lifespan, and degeneration of select indirect flight muscles and dopaminergic neurons, and the level of Parkin protein is significantly reduced in dPink1 RNA interference animals.