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Barbara L. Hempstead
Researcher at Cornell University
Publications - 164
Citations - 29368
Barbara L. Hempstead is an academic researcher from Cornell University. The author has contributed to research in topics: Neurotrophin & Trk receptor. The author has an hindex of 76, co-authored 162 publications receiving 27193 citations. Previous affiliations of Barbara L. Hempstead include Indiana University & National Institutes of Health.
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Journal ArticleDOI
Microglia Promote Learning-Dependent Synapse Formation through Brain-Derived Neurotrophic Factor
Christopher N. Parkhurst,Guang Yang,Ipe Ninan,Jeffrey N. Savas,John R. Yates,Juan J. Lafaille,Barbara L. Hempstead,Dan R. Littman,Wen-Biao Gan +8 more
TL;DR: It is found that microglia could be specifically depleted from the brain upon diphtheria toxin administration and removal of brain-derived neurotrophic factor (BDNF) frommicroglia largely recapitulated the effects of microglian depletion.
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Regulation of cell survival by secreted proneurotrophins.
TL;DR: It is shown that the proforms of nerve growth factor (NGF) and the pro forms of brain derived neurotrophic factor (BDNF) are secreted and cleaved extracellularly by the serine protease plasmin and by selective matrix metalloproteinases (MMPs).
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The trk proto-oncogene product: a signal transducing receptor for nerve growth factor
TL;DR: Affinity cross-linking and equilibrium binding experiments with 125I-labeled NGF indicate that p140prototrk binds NGF specifically in cultured cells with a dissociation constant of 10(-9) molar.
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Genetic variant BDNF (Val66Met) polymorphism alters anxiety-related behavior
Zhe-Yu Chen,Deqiang Jing,Kevin G. Bath,Alessandro Ieraci,Tanvir Khan,Chia-Jen Siao,Daniel G. Herrera,Miklós Tóth,Chingwen Yang,Bruce S. McEwen,Barbara L. Hempstead,Francis S. Lee +11 more
TL;DR: A variant BDNF mouse (BDNFMet/Met) is generated that reproduces the phenotypic hallmarks in humans with the variant allele and may play a key role in genetic predispositions to anxiety and depressive disorders.
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High-affinity NGF binding requires coexpression of the trk proto-oncogene and the low-affinity NGF receptor.
TL;DR: Reconstitution experiments reveal a new growth factor receptor-mediated mechanism of cellular differentiation involving trk and the low-affinity NGF receptor and the tyrosine kinase trk gene product.