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Alterations in Critical Cellular Pathways During Lytic Epstein-Barr Virus Infection
Başlık:
Alterations in Critical Cellular Pathways During Lytic Epstein-Barr Virus Infection
Yazar:
Jeffus, Dana A., author.
ISBN:
9780438092518
Yazar Ek Girişi:
Fiziksel Tanımlama:
1 electronic resource (110 pages)
Genel Not:
Source: Masters Abstracts International, Volume: 57-06M(E).
Advisors: Amy L. Adamson Committee members: Karen Katula; Paul Steimle.
Özet:
Epstein-Barr Virus (EBV) is a human herpesvirus that infects approximately 90% of the global human population. Infection with EBV is associated with several diseases, such as Burkitt's Lymphoma, nasopharyngeal carcinoma, and gastric carcinoma. In both latent and lytic states, EBV produces gene products that interfere with normal host cell signaling mechanisms. Promoter regions within the EBV genome contain binding sites for a variety of cellular transcription factors. EBV also lacks the machinery necessary for synthesis of viral proteins, and therefore must exploit major cell signaling pathways for cap-dependent translation. The PI3K--Akt--mTOR and MAPK pathways stimulate downstream targets to promote biogenesis. EBV interaction with proteins in these pathways can result in uncontrolled cell growth, proliferation, and apoptosis resistance, potentially leading to carcinogenesis. Previous research shows that under rapamycin-induced inhibition of mTORC1, a major component of PI3K--Akt--mTOR pathway, EBV lytic protein production varies in a cell-type specific manner, suggesting that EBV utilizes these pathways differently among B cells and epithelial cells. For this study, I investigated the molecular targets of EBV within these pathways to gain further insight into the mechanisms involved in synthesis of EBV lytic gene products. The results show that EBV activates variable levels of proteins within the PI3K--Akt--mTOR and MAPK pathways in different cell types during lytic replication, the MAPK pathways are used as a major alternative pathway when mTORC1 is inhibited, and inhibition of the mTOR and MAPK pathways utilized by EBV does not attenuate viral replication.
Notlar:
School code: 0154
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Yer Numarası | Demirbaş Numarası | Shelf Location | Lokasyon / Statüsü / İade Tarihi |
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