Publication & Citation Trends
Publications
0 total
Differentiation dependent HPV genome amplification is delayed rather than abolished in the absence of E1^E4. OA
Cited by 0
Semantic Scholar
16E1^E4 expression drives nuclear accumulation of wild type but not mutant 16E1 and enhances E1/E2-mediated HPV16 ori-dependent replication. OA
Cited by 0
Semantic Scholar
16E1^E4 expression sustains JNK activation and cytoplasmic sequestration. OA
Cited by 0
Semantic Scholar
Loss of full length E1^E4 does not affect NIKS cell growth or the early stages of either the HPV16 or HPV18 life cycle. OA
Cited by 0
Semantic Scholar
16 E1^E4 contributes to p38 MAPK and ERK1/2 activity during the HPV16 life cycle. OA
Cited by 0
Semantic Scholar
The G2 arrest function of HPV16 E1^E4 contributes to viral genome amplification and L1 expression. OA
Cited by 0
Semantic Scholar
E1^E4 expression is required for the maintenance of activated pJNK in the cytoplasm during the late stages of the HPV16 life cycle. OA
Cited by 0
Semantic Scholar
Primer and Probe. OA
Cited by 1
Semantic Scholar
Research Topics
Cancer-related Molecular Pathways
(31)
Cervical Cancer and HPV Research
(28)
Molecular Biology Techniques and Applications
(28)
Mathematical Biology Tumor Growth
(13)
Genomics and Chromatin Dynamics
(12)
Affiliations
Tokyo University of Science
University of Cambridge
The Francis Crick Institute
The Cancer Institute Hospital
Genesis Research Institute