增强SV40病毒的功能作为一个体质高突变向元素,具有潜在的致癌活性
bioRxiv : the preprint server for biology
|January 23, 2024
概括
激活诱导的cytidine deaminase (AID) 可以通过准对SV40增强器的体质突变 (SHM) 来切断Simian virus 40 (SV40) 大瘤抗原 (LT). 这种机制可能会导致与SV40相关的人类癌症.
科学领域:
- 病毒学 病毒学
- 在瘤学瘤学.
- 分子生物学分子生物学
背景情况:
- 类似病毒40 (SV40) 与人体癌症如间皮瘤和淋巴瘤有关,但其致癌机制尚不清楚.
- 默克尔细胞多瘤病毒 (MCPyV) 是SV40的亲属,通过通过APOBEC酶突变表达截断的大型瘤抗原 (LT),导致默克尔细胞癌.
- 激活诱导的cytidine deaminase (AID) 是一个APOBEC家族成员,对于通过体型突变 (SHM) 实现抗体多样化至关重要,并与淋巴发育有关.
结论:
- SV40增强器将SHM导向LT的能力是LT截断的一个潜在机制.
- 这种由AID驱动的LT切断可能有助于在各种人体组织中发展SV40相关的癌症.
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