Post-translational modification of endothelial nitric oxide synthase (eNOS) by heat shock protein 90 (Hsp90): Effects on newborn pulmonary vascular tone

被引：0

作者：

Aschner, JL

Basehore, MJ

Lecras, TD

机构：

[1] Wake Forest Univ, Bowman Gray Sch Med, Winston Salem, NC USA

[2] Univ Colorado, Sch Med, Denver, CO USA

来源：

CIRCULATION | 2001年 / 104卷 / 17期

关键词：

D O I：

暂无

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

991

引用

页码：206 / 206

页数：1

共 50 条

[1] Heat shock protein 90 (Hsp90): Nitric oxide synthase (NOS) interactions modulate vascular tone in newborn pig lungs
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[2] Decreased association of heat shock protein 90 (hsp90) impairs endothelial nitric oxide synthase (eNOS) in fetal lambs with persistent pulmonary hypertension of newborn (PPHN)
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[6] Heat shock protein 90 (Hsp90):endothelial nitric oxide synthase (eNOS) interactions influence pulmonary vascular reactivity by altering the balance between nitric oxide (NO) and superoxide (O2-) generation
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[7] Inhibition of heat shock protein 90 (hsp90) in proliferating endothelial cells uncouples endothelial nitric oxide synthase activity
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[8] Endothelial nitric oxide synthase (eNOS) degradation is regulated by HSP90 not by phosphorylation
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[9] Heat shock protein 90 modulates endothelial nitric oxide synthase activity and vascular reactivity in the newborn piglet pulmonary circulation
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[10] Heatshock protein 90 (Hsp90) regulates endothelial nitric oxide synthase (eNOS) generation of nitric oxide (NO) and superoxide anion (O2•).
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