The scid defect results in much slower repair of DNA double-strand breaks but not high levels of residual breaks.
The scid defect results in much slower repair of DNA double-strand breaks but not high levels of residual breaks.
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scid 缺陷会导致 DNA 双链断裂的修复速度慢得多，但不会导致高水平的残留断裂。
DOI：
10.2307/3579619
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发表时间：
1997
影响因子：
3.4
通讯作者：
P. Hahn
中科院分区：
文献类型：
--
作者：
B. Nevaldine;J. Longo;P. Hahn
严重联合免疫缺陷（scid）小鼠不能产生成熟的B和T细胞，对电离辐射敏感。它们在DNA依赖性蛋白激酶的460 kDa催化亚基中含有突变，该亚基参与V（D）J重新连接和DNA双链断裂（DSB）修复。在scid细胞和亲本C.B-17细胞中，在3、7.5和10戈伊三种不同剂量的X射线照射后，定量DSB再连接的动力学。DNA双链断裂的修复采用脉冲场凝胶电泳、Southern杂交和荧光图像分析。在X射线照射后，使细胞在37 ℃下修复长达1小时或长达24小时。两种细胞系之间最深刻的差异是scid细胞中DSB修复的缓慢成分的速率大大降低。C.B-17细胞在1小时内修复了大部分损伤，而scid细胞在相同剂量后需要4至6小时才能达到类似水平。剂量高达10戈伊后24 h，在两种细胞系中均未检测到残留或不可修复的DSB。scid细胞接受两个剂量的1.5戈伊，间隔时间增加，没有能力修复剂量之间的亚致死损伤，而C.B-17细胞接受两个剂量的3.75戈伊，间隔时间增加，确实显示出增加的存活水平。这些结果表明，scid细胞可以修复辐射诱导的DNA双链断裂，虽然速度降低，但它们缺乏修复亚致死损伤的能力。
Severe combined immune deficiency (scid) mice fail to produce mature B and T cells and are sensitive to ionizing radiation. They contain a mutation in the 460-kDa catalytic subunit of the DNA-dependent protein kinase that is involved in both V(D)J rejoining and DNA double-strand break (DSB) repair. The kinetics of DSB rejoining was quantified in both scid cells and the parental C.B-17 cells after three different doses of X irradiation: 3, 7.5 and 10 Gy. Repair of DNA DSBs was determined using pulsed-field gel electrophoresis, Southern hybridization and phosphor image analysis. After X irradiation, the cells were allowed to repair at 37 degrees C for up to 1 h or up to 24 h. The most profound difference between the two cell lines was the greatly reduced rate of the slow component of DSB repair in scid cells. C.B-17 cells repaired most of the damage within 1 h, whereas scid cells required 4 to 6 h to reach a similar level after the same dose. No residual or unrepairable DSBs were detected in either cell line 24 h after doses as high as 10 Gy. The scid cells subjected to two doses of 1.5 Gy separated by increasing amounts of time showed no ability to repair sublethal damage between doses, whereas C.B-17 cells receiving two doses of 3.75 Gy separated by increasing periods did show increased levels of survival. These results indicate that scid cells can repair radiation-induced DNA DSBs, although at a reduced rate, but they lack the ability to undergo repair of sublethal damage.
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通过过早染色体凝结测量 scid 细胞中染色体畸变的诱导和修复。
影响因子：
3.4
作者：
Evans,JW;Liu,XF;Kirchgessner,CU;Brown,JM
通讯作者：
Brown,JM
DOI：
10.1016/s0021-9258(18)67534-9
发表时间：
1986-08
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
T. Mimori;J. Hardin
通讯作者：
T. Mimori;J. Hardin
一种定量 DNA 双链断裂修复的测定方法，适用于少量未标记的细胞。
DOI：
--
发表时间：
1997
期刊：
Radiation research.
影响因子：
--
作者：
Longo,JA;Nevaldine,B;Longo,SL;Winfield,JA;Hahn,PJ
通讯作者：
Hahn,PJ
scid 基因编码介导 Ig 基因重排重新连接事件的反式作用因子。
影响因子：
10.5
作者：
Hendrickson,EA;Schatz,DG;Weaver,DT
通讯作者：
Weaver,DT
scid/scid 小鼠中辐射诱导的染色体损伤的缺陷修复。
DOI：
10.1159/000133196
发表时间：
1992
期刊：
Cytogenetics and cell genetics
影响因子：
--
作者：
Disney,JE;Barth,AL;Shultz,LD
通讯作者：
Shultz,LD