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肿瘤坏死因子α选择性地使人类免疫缺陷病毒感染的细胞对热和辐射敏感。

Tumor necrosis factor alpha selectively sensitizes human immunodeficiency virus-infected cells to heat and radiation.

作者信息

Wong G H, McHugh T, Weber R, Goeddel D V

机构信息

Department of Molecular Biology, Genentech, Inc., South San Francisco, CA 94080.

出版信息

Proc Natl Acad Sci U S A. 1991 May 15;88(10):4372-6. doi: 10.1073/pnas.88.10.4372.

Abstract

We report here that infection of the human T-cell line HUT-78 with human immunodeficiency virus (HIV) increases its sensitivity to heat and radiation toxicity. A possible explanation for this result may be the reduced expression of manganous superoxide dismutase (MnSOD) in HIV-infected cells compared to uninfected cells. Tumor necrosis factor alpha (TNF-alpha) further sensitizes HIV-infected cells but not uninfected cells to heat and radiation. This is consistent with the ability of TNF-alpha to induce the expression of MnSOD in uninfected but not in HIV-infected cells. HIV-infected HUT-78 cell lines engineered to overexpress MnSOD are more resistant to heat and radiation than HIV-infected cells that do not overexpress MnSOD. However, treatment with TNF-alpha still sensitizes these cells to heat and radiation.

摘要

我们在此报告,人类免疫缺陷病毒(HIV)感染人类T细胞系HUT - 78会增加其对热和辐射毒性的敏感性。该结果的一个可能解释是,与未感染细胞相比,HIV感染细胞中锰超氧化物歧化酶(MnSOD)的表达降低。肿瘤坏死因子α(TNF-α)会进一步使HIV感染细胞而非未感染细胞对热和辐射敏感。这与TNF-α在未感染而非HIV感染细胞中诱导MnSOD表达的能力一致。经过基因工程改造以过表达MnSOD的HIV感染HUT - 78细胞系比未过表达MnSOD的HIV感染细胞对热和辐射更具抗性。然而,用TNF-α处理仍会使这些细胞对热和辐射敏感。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/347b/51661/89bb6c1fdcd2/pnas01060-0323-a.jpg

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