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首页> 外文期刊>Cell biology international. >Human glutamylcysteine synthetase protects HEK293 cells against UV-induced cell death through inhibition of c-Jun NH2-terminal kinase.
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Human glutamylcysteine synthetase protects HEK293 cells against UV-induced cell death through inhibition of c-Jun NH2-terminal kinase.

机译：人谷氨酰半胱氨酸合成酶通过抑制c-Jun NH2末端激酶来保护HEK293细胞免受紫外线诱导的细胞死亡。

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摘要

Human glutamylcysteine ligase catalytic subunit (GCLC) is the rate-limiting enzyme for glutathione synthesis. The heavy subunit possesses all the catalytic activities. UV irradiation (UV-C, 30 J/m(2)) induced apoptosis in HEK293 cells, but the morphological changes were inhibited significantly by expression of GCLC. MTS assay and flow cytometry results also indicated that GCLC and JNK1(APF) expression enhanced cellular resistance to UV irradiation. Western blotting showed that irradiation strongly activated the c-Jun NH(2)-terminal kinases (JNKs) and caspase-3 as well as p38 in HEK293 cells. Interestingly, existing data show that GCLC blocks JNK1 phosphorylation but does not affect p38 phosphorylation. Therefore, overexpression of GCLC protected HEK293 cells against UV irradiation-induced cell death by inhibiting the phosphorylation and activation of JNK1, concomitantly with the inhibition of caspase-3 activation and p21(WAF1)-luciferase activity downstream of JNK.
机译：人谷氨酰半胱氨酸连接酶催化亚基（GCLC）是谷胱甘肽合成的限速酶。重亚基具有所有催化活性。紫外线（UV-C，30 J / m（2））诱导HEK293细胞凋亡，但GCLC的表达显着抑制了形态变化。 MTS分析和流式细胞仪结果还表明，GCLC和JNK1（APF）表达增强了细胞对紫外线照射的抵抗力。西方印迹表明，辐射强烈激活了HEK293细胞中的c-Jun NH（2）末端激酶（JNKs）和caspase-3以及p38。有趣的是，现有数据显示GCLC可以阻断JNK1磷酸化，但不会影响p38磷酸化。因此，GCLC的过表达通过抑制JNK1的磷酸化和激活，同时抑制JNK下游的caspase-3激活和p21（WAF1）-荧光素酶活性，从而保护HEK293细胞免受UV辐射诱导的细胞死亡。

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