biological consequence
Recently Published Documents


TOTAL DOCUMENTS

21
(FIVE YEARS 1)

H-INDEX

11
(FIVE YEARS 0)

2021 ◽  
Vol 66 (1) ◽  
Author(s):  
Ilya Zakharov ◽  
Elena Shaikevich

Maternal transmission ensures the joint transmission and simultaneous presence in populations of individuals with certain variants of the bacterial symbiont and host mitochondrial DNA. Such “quasi-linkage” of cytoplasmic genomes among insects and other arthropods is widespread. The symbiont acts as a “driver” of mitochondria and the obvious biological consequence is the spread of the “linked” mitochondrial haplotype in the population, which itself does not have increased selective value to the organism. Examples of such indirect selective mitochondrial sweep in insects are discussed, as well as biological consequences of this phenomenon and mechanisms of increasing the frequency of symbiont-infected individuals in the population.


2015 ◽  
Vol 11 (12) ◽  
pp. e1004572 ◽  
Author(s):  
Zev N. Kronenberg ◽  
Edward J. Osborne ◽  
Kelsey R. Cone ◽  
Brett J. Kennedy ◽  
Eric T. Domyan ◽  
...  

2015 ◽  
Vol 87 (21) ◽  
pp. 10693-10697 ◽  
Author(s):  
Tyron Turnbull ◽  
Michael Douglass ◽  
David Paterson ◽  
Eva Bezak ◽  
Benjamin Thierry ◽  
...  

2013 ◽  
Vol 28 (suppl 4) ◽  
pp. iv1-iv7 ◽  
Author(s):  
K. Kanasaki ◽  
M. Kitada ◽  
M. Kanasaki ◽  
D. Koya

2012 ◽  
Vol 93 (7) ◽  
pp. 1563-1572 ◽  
Author(s):  
Xin Wang ◽  
Mei Qi ◽  
Xiuping Yu ◽  
Yan Yuan ◽  
Weiming Zhao

Human papillomavirus type 58 (HPV-58) is a very common HPV type in eastern Asia. Little is known about its biology and tumorigenesis. In this study, HPV-58 E2 protein (58E2) was found to interact with E7 protein (58E7), and the hinge domain of 58E2 was shown to be responsible for binding to the 58E7 protein. Interestingly, the E2–E7 interaction appears to be HPV type-specific, as we found that the HPV-16 E2 could not bind to the 58E7 protein, and neither did 58E2 interact with HPV-16 E7. The biological consequence(s) of the E2–E7 interaction in HPV-58, especially in viral tumorigenesis, was investigated. Results showed that, through interacting with 58E7, 58E2 prevented E7-induced retinoblastoma protein (pRb) degradation and prolonged the half-life of pRb in cells. Additionally, 58E2 abrogated 58E7-induced cell proliferation. These observations collectively suggest that direct interaction with 58E7 is another mechanism for 58E2 to inhibit 58E7-associated carcinogenesis in addition to regulating expression of the 58E7 gene.


Sign in / Sign up

Export Citation Format

Share Document