Publications by authors named "Alexander M Pham"

Unlabelled: Merkel cell polyomavirus (MCPyV) is a double-stranded tumor virus that is the main causative agent of Merkel cell carcinoma (MCC). The MCPyV large T antigen (LT), an essential viral DNA replication protein, maintains viral persistence by interacting with host Skp1-Cullin 1-F-box (SCF) E3 ubiquitin ligase complexes, which subsequently induces LT's proteasomal degradation, restricting MCPyV DNA replication. SCF E3 ubiquitin ligases require their substrates to be phosphorylated to bind them, utilizing phosphorylated serine residues as docking sites.

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Senescent cells accumulate in the host during the aging process and are associated with age-related pathogeneses, including cancer. Although persistent senescence seems to contribute to many aspects of cellular pathways and homeostasis, the role of senescence in virus-induced human cancer is not well understood. Merkel cell carcinoma (MCC) is an aggressive skin cancer induced by a life-long human infection of Merkel cell polyomavirus (MCPyV).

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Merkel cell carcinoma (MCC) is a rare but aggressive form of skin cancer predominantly caused by the human Merkel cell polyomavirus (MCPyV). Treatment for MCC includes excision and radiotherapy of local disease, and chemotherapy or immunotherapy for metastatic disease. The schweinfurthin family of natural compounds previously displayed potent and selective growth inhibitory activity against the NCI-60 panel of human-derived cancer cell lines.

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Article Synopsis
  • MCPyV large tumor (LT) antigen is a crucial DNA binding protein that promotes viral gene transcription and replication while also regulating its own degradation through interactions with E3 ligases.
  • * Researchers utilized a web server to identify ubiquitination sites on the LT, pinpointing lysine 585 as a key site responsible for its degradation and stability in relation to viral oncogenesis.
  • * Deleting lysine 585 from truncated LT proteins stabilized their expression in tumors, but altering this site also affected the virus's ability to replicate, highlighting its dual role in protein turnover and genome replication.*
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