NF-κB is activated and promotes cell death in focal cerebral ischemia

被引：582

作者：

Schneider, A

Martin-Villalba, A

Weih, F

Vogel, J

Wirth, T

Schwaninger, M

机构：

[1] Heidelberg Univ, Dept Neurol, D-69120 Heidelberg, Germany

[2] BASF LYNX Biosci AG, Dept Neurosci, D-69120 Heidelberg, Germany

[3] Forschungszentrum Karlsruhe, Inst Genet, D-76021 Karlsruhe, Germany

[4] Dept Physiol, D-69120 Heidelberg, Germany

[5] Inst Radiobiol & Cell Res, D-97078 Wurzburg, Germany

来源：

NATURE MEDICINE | 1999年 / 5卷 / 05期

关键词：

D O I：

10.1038/8432

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The transcription factor NF-kappa B is a regulator of cell death or survival. To investigate the role of NF-kappa B in neuronal cell death, we studied its activation in a rodent model of stroke. In the ischemic hemisphere, NF-kappa B was activated, as determined by increased expression of an NF-kappa B-driven reporter transgene, nuclear translocation of NF-kappa B in neurons and enhanced DNA binding of NF-kappa B subunits RelA and p50. In p50 knockout mice, ischemic damage was significantly reduced. This indicates a cell death-promoting role of NF-kappa B in focal ischemia. NF-kappa B may provide a new pharmacological target in neurologic disease.

引用

页码：554 / 559

页数：6

共 47 条

[1] Amyloid β-peptide stimulates nitric oxide production in astrocytes through an NFκB-dependent mechanism [J].