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短暂性脑缺血后新皮质中酪氨酸磷酸化的变化。

Changes in tyrosine phosphorylation in neocortex following transient cerebral ischaemia.

作者信息

Hu B R, Wieloch T

机构信息

Experimental Brain Research, Lund Hospital, Lund University, Sweden.

出版信息

Neuroreport. 1993 Feb;4(2):219-22. doi: 10.1097/00001756-199302000-00027.

DOI:10.1097/00001756-199302000-00027
PMID:7680914
Abstract

Growth factor receptors activate protein tyrosine kinases, which are important for cell growth and survival. The protein tyrosine kinase (PTK) activity and the levels of phosphotyrosine (Ptyr) containing proteins were studied in the rat neocortex exposed to 15 min of transient cerebral ischaemia. The levels of the Ptyr containing proteins increase during recovery in the synaptosomal fraction, while the changes in the light membrane fraction are less marked. Protein tyrosine phosphorylation in the cytosol decreases. The differential changes in the levels of phosphotyrosine proteins in the particulate and cytosolic fractions suggest that the signal cascade from membrane bound receptors through tyrosine phosphorylation in the cytosol may be interrupted following ischaemia. This may be of importance for the development of neuronal damage.

摘要

生长因子受体激活蛋白酪氨酸激酶,这对细胞生长和存活至关重要。研究了暴露于15分钟短暂性脑缺血的大鼠新皮质中的蛋白酪氨酸激酶(PTK)活性以及含磷酸酪氨酸(Ptyr)蛋白的水平。含Ptyr蛋白的水平在突触体部分恢复过程中升高,而轻膜部分的变化则不太明显。胞质溶胶中的蛋白质酪氨酸磷酸化减少。颗粒部分和胞质部分中磷酸酪氨酸蛋白水平的差异变化表明,缺血后从膜结合受体通过胞质溶胶中酪氨酸磷酸化的信号级联可能被中断。这可能对神经元损伤的发展具有重要意义。

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