About: Steven W. Levison

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher

Attributes	Values
rdf:type	Item
description	researcher (en) 연구원 (ko) গবেষক (bn) 研究者 (ja) ഗവേഷകൻ (ml) araştırmacı (tr) дослідник (uk) эрдэмтэн (mn) वैज्ञानिक (hi) 研究者 (zh) հետազոտող (hy) hulumtues (sq) onderzoeker (nl)
rdfs:label	Steven W. Levison (en) Steven W. Levison (es) Steven W. Levison (nl) Steven W. Levison (sl) Steven W. Levison (ast)
skos:prefLabel	Steven W. Levison (en) Steven W. Levison (es) Steven W. Levison (nl) Steven W. Levison (sl) Steven W. Levison (ast)
name	Steven W. Levison (en) Steven W. Levison (es) Steven W. Levison (nl) Steven W. Levison (sl) Steven W. Levison (ast)
Scopus author ID	wds:Q46521372-CB6695D4-4D86-487E-9966-74CE6554AD29
Scopus author ID	7004323964
given name	wds:Q46521372-BCA1B6F3-2FF4-4584-A827-FE4543343676
given name	Steven
instance of	wds:Q46521372-08770310-12F3-4EAE-872A-E714457E7B22
instance of	Homo sapiens
skos:altLabel	Steven Levison (en)
occupation	wds:Q46521372-E903F1B4-3DA5-4749-BCEC-3EB76DCEE9E5
employer	wds:Q46521372-19FC7F98-DEE2-44C9-B2A0-3E1561AEDDB3
sex or gender	wds:Q46521372-4149AAB9-821C-4E52-B233-DEDC525AA6FB
ISNI	wds:Q46521372-46C1AB97-3C64-4815-A53C-F99C61DE15FB
VIAF ID	wds:Q46521372-13451B9B-3588-454C-A94B-213C4CF2B9A9
Library of Congress authority ID	wds:Q46521372-C8F8357E-C751-407E-9976-61695B9124BB
IdRef ID	wds:Q46521372-016581BE-2880-41ED-A3C6-D4868290C934
National Library of Israel J9U ID	wds:Q46521372-AC4B4279-803E-4538-8CC9-B0CEC2F63274
VIAF ID	http://viaf.org/viaf/62650701
Library of Congress authority ID	http://id.loc.gov/authorities/names/no2005068385
IdRef ID	http://www.idref.fr/10153647X/id
occupation	researcher
employer	New Jersey Medical School
sex or gender	male
ISNI	0000000044487317
VIAF ID	62650701
Library of Congress authority ID	no2005068385
IdRef ID	10153647X
National Library of Israel J9U ID	987007355256905171
ORCID iD	wds:Q46521372-45963BC5-A3D1-4E6F-9D82-1CE3CA90D8DD
ORCID iD	https://orcid.org/0000-0002-1264-7309
ORCID iD	0000-0002-1264-7309
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q46521372
is author of	Activation of the mammalian target of rapamycin (mTOR) is essential for oligodendrocyte differentiation Neonatal hypoxic/ischemic brain injury induces production of calretinin-expressing interneurons in the striatum Insulin-Like Growth Factor Receptor Signaling is Necessary for Epidermal Growth Factor Mediated Proliferation of SVZ Neural Precursors in vitro Following Neonatal Hypoxia-Ischemia Sustained neocortical neurogenesis after neonatal hypoxic/ischemic injury. Ciliary neurotrophic factor stimulates astroglial hypertrophy in vivo and in vitro. Astrocytic ceruloplasmin expression, which is induced by IL-1beta and by traumatic brain injury, increases in the absence of the IL-1 type 1 receptor Interleukin-1 and the interleukin-1 type 1 receptor are essential for the progressive neurodegeneration that ensues subsequent to a mild hypoxic/ischemic injury. Differential expression of protein tyrosine kinase genes during microglial activation Diabetic retinopathy: more than meets the eye. Neuroinflammation and both cytotoxic and vasogenic edema are reduced in interleukin-1 type 1 receptor-deficient mice conferring neuroprotection Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) signaling and cell death in the immature central nervous system after hypoxia-ischemia and inflammation. Pro-regenerative properties of cytokine-activated astrocytes. Cycling cells in the adult rat neocortex preferentially generate oligodendroglia. Perinatal hypoxia/ischemia damages and depletes progenitors from the mouse subventricular zone. IL-6-type cytokines enhance epidermal growth factor-stimulated astrocyte proliferation Comparison and quantitation of Ia antigen expression on cultured macroglia and ameboid microglia from Lewis rat cerebral cortex: analyses and implications Transforming growth factor beta1 prevents IL-1beta-induced microglial activation, whereas TNFalpha- and IL-6-stimulated activation are not antagonized Interleukin-1: a master regulator of neuroinflammation Minocycline reduces proinflammatory cytokine expression, microglial activation, and caspase-3 activation in a rodent model of diabetic retinopathy The Ins2Akita mouse as a model of early retinal complications in diabetes Neural stem/progenitor cells participate in the regenerative response to perinatal hypoxia/ischemia. CNTF-activated astrocytes release a soluble trophic activity for oligodendrocyte progenitors Enhanced neurogenesis following stroke. The role of inflammation in perinatal brain injury Ciliary neurotrophic factor and interleukin-6 differentially activate microglia Ciliary neurotrophic factor induces expression of the IGF type I receptor and FGF receptor 1 mRNAs in adult rat brain oligodendrocytes. Insulin and IGF receptor signalling in neural-stem-cell homeostasis. Expression of the anaphylatoxin C5a receptor in the oligodendrocyte lineage. PDGF-responsive progenitors persist in the subventricular zone across the lifespan Pitfalls in the quest of neuroprotectants for the perinatal brain Delayed IGF-1 administration rescues oligodendrocyte progenitors from glutamate-induced cell death and hypoxic-ischemic brain damage. Ionizing Radiation Perturbs Cell Cycle Progression of Neural Precursors in the Subventricular Zone Without Affecting Their Long-Term Self-Renewal Leukemia inhibitory factor is essential for subventricular zone neural stem cell and progenitor homeostasis as revealed by a novel flow cytometric analysis. Brain injury expands the numbers of neural stem cells and progenitors in the SVZ by enhancing their responsiveness to EGF Molecular features of neural stem cells enable their enrichment using pharmacological inhibitors of survival-promoting kinases Death effector activation in the subventricular zone subsequent to perinatal hypoxia/ischemia Astrogliosis is delayed in type 1 interleukin-1 receptor-null mice following a penetrating brain injury Neural stem cells in the subventricular zone are a source of astrocytes and oligodendrocytes, but not microglia The FLT3 tyrosine kinase receptor inhibits neural stem/progenitor cell proliferation and collaborates with NGF to promote neuronal survival. IGF-II promotes stemness of neural restricted precursors. Astrocytes produce CNTF during the remyelination phase of viral-induced spinal cord demyelination to stimulate FGF-2 production.

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