scholarly journals The role of NH4Cl and cysteine proteases in Human Papillomavirus type 16 infection

2009 ◽  
Vol 6 (1) ◽  
pp. 109 ◽  
Author(s):  
Sarah A Dabydeen ◽  
Patricio I Meneses
Keyword(s):  
Human Papillomavirus ◽  
Cysteine Proteases ◽  
Human Papillomavirus Type 16

scholarly journals E1∧E4 Protein of Human Papillomavirus Type 16 Associates with Mitochondria

2004 ◽  
Vol 78 (13) ◽  
pp. 7199-7207 ◽  
Author(s):  
Kenneth Raj ◽  
Samuel Berguerand ◽  
Shirley Southern ◽  
John Doorbar ◽  
Peter Beard
Keyword(s):  
Human Papillomavirus ◽  
Terminal Portion ◽  
Hpv Dna ◽  
Human Papillomavirus Type 16 ◽  
Dead Box ◽  
Virion Production ◽  
Severe Reduction ◽  
Initial Binding ◽  
Binding To Mitochondria

ABSTRACT The human papillomavirus (HPV) E1∧E4 protein is the most abundantly expressed viral protein in HPV-infected epithelia. It possesses diverse activities, including the ability to bind to the cytokeratin network and to DEAD-box proteins, and in some cases induces the collapse of the former. E1∧E4 is also able to prevent the progression of cells into mitosis by arresting them in the G2 phase of the cell cycle. In spite of these intriguing properties, the role of this protein in the life cycle of the virus is not clear. Here we report that after binding to and collapsing the cytokeratin network, the HPV type 16 E1∧E4 protein binds to mitochondria. When cytokeratin is not present in the cell, E1∧E4 appears associated with mitochondria soon after its synthesis. The leucine cluster within the N-terminal portion of the E1∧E4 protein is pivotal in mediating this association. After the initial binding to mitochondria, the E1∧E4 protein induces the detachment of mitochondria from microtubules, causing the organelles to form a single large cluster adjacent to the nucleus. This is followed by a severe reduction in the mitochondrial membrane potential and an induction of apoptosis. HPV DNA replication and virion production occur in terminally differentiating cells which are keratin-rich, rigid squamae that exfoliate after completion of the differentiation process. Perturbation of the cytokeratin network and the eventual induction of apoptotic properties are processes that could render these unyielding cells more fragile and ease the exit of newly synthesized HPVs for subsequent rounds of infection.

The interaction between steroid hormones, human papillomavirus type 16, E6 oncogene expression, and cervical cancer

2003 ◽  
Vol 13 (6) ◽  
pp. 834-842 ◽  
Author(s):  
M. Moodley ◽  
S. Sewart ◽  
C. S. Herrington ◽  
R. Chetty ◽  
R. Pegoraro ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Steroid Hormones ◽  
Housekeeping Gene ◽  
Hpv 16 ◽  
Tissue Samples ◽  
Hpv Dna ◽  
Human Papillomavirus Type 16 ◽  
Transforming Proteins

Various risk factors have been implicated in the causation of cervical cancer including human papillomavirus (HPV), the early genes (E6 and E7) of which encode the main transforming proteins. Studies have suggested that steroid hormones may enhance the expression of these genes leading to loss of p53 gene-mediated cell apoptosis. A total of 120 cervical tissue samples were obtained from patients with proven cervical cancer. Patients who used depo-medroxyprogesterone acetate steroid contraception were recruited as part of the steroid arm. Only HPV DNA type 16 samples were used for the study. Controls included three cell lines (CaSki, SiHa, & C33A) and glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was used as an internal housekeeping gene. Of 120 patients, there were 111 patients with HPV type 16 identified. Of this number, RNA was present in 63 samples. There were 30 women (30/63) who used steroid contraception. In relation to patients who used contraception, HPV 16 E6 gene expression was present in 79% (n = 23) and 88% (n = 30) of steroid users compared to nonusers, respectively. In total there were 25 patients (40%) with expression of the HPV 16 E6*I gene and 30 patients with expression of the E6*II gene. There were 57% of steroid users (n = 17) who had expression of the E6*I/E6*II gene, compared to 52% (n = 17) of nonusers (P = 0.800). From a molecular level, this study does not confirm the role of injectable progesterones in cervical carcinogenesis.

scholarly journals Role of Calpain in the Formation of Human Papillomavirus Type 16 E1^E4 Amyloid Fibers and Reorganization of the Keratin Network

2011 ◽  
Vol 85 (19) ◽  
pp. 9984-9997 ◽  
Author(s):  
J. Khan ◽  
C. E. Davy ◽  
P. B. McIntosh ◽  
D. J. Jackson ◽  
S. Hinz ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Amyloid Fibers ◽  
Human Papillomavirus Type 16

Role of Human Papillomavirus Type 16 in Squamous Cell Carcinoma of Upper Aerodigestive Tracts in Colombian Patients

2011 ◽  
Vol 7 (3) ◽  
pp. 222-232 ◽  
Author(s):  
Lida Ines Manci ◽  
Edwin Carrascal ◽  
Oscar Mario Tama ◽  
Felipe Garcia ◽  
Salvatore Vaccarella ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Human Papillomavirus ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Human Papillomavirus Type 16

scholarly journals The role of human papillomavirus type 16 E6/E7 oncoproteins in cervical epithelial-mesenchymal transition and carcinogenesis

2011 ◽  
Vol 3 (3) ◽  
pp. 667-671 ◽  
Author(s):  
YA-MIN CHENG ◽  
CHENG-YANG CHOU ◽  
YI-CHIANG HSU ◽  
MING-JENN CHEN ◽  
LIH-YUH C. WING
Keyword(s):  
Human Papillomavirus ◽  
Epithelial Mesenchymal Transition ◽  
Mesenchymal Transition ◽  
Human Papillomavirus Type 16

scholarly journals Human Papillomavirus Type 16 E6-Induced Degradation of E6TP1 Correlates with Its Ability To Immortalize Human Mammary Epithelial Cells

2001 ◽  
Vol 75 (9) ◽  
pp. 4459-4466 ◽  
Author(s):  
Qingshen Gao ◽  
Latika Singh ◽  
Ajay Kumar ◽  
Seetha Srinivasan ◽  
David E. Wazer ◽  
...  
Keyword(s):  
Human Papillomavirus ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Cellular Transformation ◽  
Mammary Epithelial ◽  
Human Mammary Epithelial Cells ◽  
Human Papillomavirus Type 16 ◽  
Human Mammary Epithelial ◽  
E6 Protein

ABSTRACT Recent analyses have identified a number of binding partners for E6, including E6AP, ERC55, paxillin, hDlg, p300, interferon regulatory factor 3, hMCM7, Bak, and E6TP1. Notably, association with E6 targets p53, E6TP1, myc, hMCM7, and Bak for degradation. However, the relative importance of the various E6 targets in cellular transformation remains unclear. E6 alone can dominantly immortalize normal human mammary epithelial cells (MECs), permitting an assessment of the importance of various E6 targets in cellular transformation. Studies in this system indicate that E6-induced degradation of p53 and E6 binding to ERC55 or hDlg do not correlate with efficient immortalization. Here, we have examined the role of E6TP1, a Rap GTPase-activating protein, in E6-induced immortalization of MECs. We tested a large set of human papillomavirus type 16 E6 mutants for their ability to bind and target E6TP1 for degradation in vitro and in vivo. We observed a strict correlation between the ability of E6 protein to target E6TP1 for degradation and its ability to immortalize MECs. Recent studies have identified telomerase as a target of E6 protein. Previous analyses of E6 mutants have revealed this trait to closely correlate with MEC immortalization. We examined our entire panel of E6 mutants for rapid induction of telomerase activity and found in general a strong correlation with immortalizing ability. The tight correlation between E6TP1 degradation and MEC immortalization strongly supports a critical role of functional inactivation of E6TP1 in E6-induced cellular immortalization.

Sign in / Sign up

Export Citation Format

Share Document