Signals Involved in Reactive Gliosis - Tae Oh

Abstract

Funding Agency

Agency: National Institute of Health (NIH)
Institute: National Institute of Neurological Disorders and Stroke (NINDS)
Type: Research Project (R01)
Project #: 5R01NS034534-02
Application #: 2273797
Study Section: Special Emphasis Panel (ZRG1-NEUA (01))

Project Start: 1995-08-15
Project End: 1999-07-31
Budget Start: 1996-08-01
Budget End: 1997-07-31
Support Year: 2
Fiscal Year: 1996
Total Cost
Indirect Cost

Institution

Name: University of Maryland Baltimore
Department: Anatomy/Cell Biology
Type: Schools of Medicine
DUNS #: 003255213

City: Baltimore
State: MD
Country: United States
Zip Code: 21201

Related projects


NIH 1998 R01 NS	Signals Involved in Reactive Gliosis Oh, Tae H. / University of Maryland Baltimore
NIH 1998 R01 NS	Signals Involved in Reactive Gliosis Oh, Tae H. / University of Maryland Baltimore
NIH 1997 R01 NS	Signals Involved in Reactive Gliosis Oh, Tae H. / University of Maryland Baltimore
NIH 1997 R01 NS	Signals Involved in Reactive Gliosis Oh, Tae H. / University of Maryland Baltimore
NIH 1996 R01 NS	Signals Involved in Reactive Gliosis Oh, Tae H. / University of Maryland Baltimore
NIH 1995 R01 NS	Signals Involved in Reactive Gliosis Oh, Tae H. / University of Maryland Baltimore

Publications

Lee, Y B; Du, S; Rhim, H et al. (2000) Rapid increase in immunoreactivity to GFAP in astrocytes in vitro induced by acidic pH is mediated by calcium influx and calpain I. Brain Res 864:220-9

Du, S; Rubin, A; Klepper, S et al. (1999) Calcium influx and activation of calpain I mediate acute reactive gliosis in injured spinal cord. Exp Neurol 157:96-105

Kim, Y C; Kim, S R; Markelonis, G J et al. (1998) Ginsenosides Rb1 and Rg3 protect cultured rat cortical cells from glutamate-induced neurodegeneration. J Neurosci Res 53:426-32

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