How do cells infected with HPV that become cancerous are able to be basically immortal? Take a look at the attached diagram and make sure to refer to molecules that are normally involved in the G1/S checkpoint and how the virus evades this checkpoint, which allows infected cells to divide indefinitely. Prevention of p53 and BAK-mediated apoptosis Blockade of IRF3 function E7 rescues E6 from INK4A inhibition INK4A counteracts E6 functions E6 activities Cooperative functions Essential functions for immortalization Activation of telomerase Proliferation Progression E6 prevents apoptosis caused by a high expression of E7 INK4A becomes functionally inactive E7 activities Cooperative functions Essential functions for immortalization Release of phosphorylated RB results in upregulation of INK4A Activation of SRC kinases Induction of chromosomal instabillity by inhibition of p53-mediated DNA repair E2F release, bypass of cyclin-D- CDK4 regulation Stimulation of S-phase genes cyclins A and E Functional inactivation of WAF1+ KIP1 Proliferation Progression Synergistic effect in cell immortalization Centriole amplification, induction of aneuploidy
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Normally, cells have a checkpoint called the G1/S checkpoint, which ensures that the cell is ready to divide and replicate its DNA. This checkpoint is regulated by various molecules, including INK4A, RB, cyclin-D, CDK4, and WAF1+ KIP1. Show moreā¦
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We know that the human papilloma virus (HPV) is the major cause of cervical cancer. HPV expresses several proteins, but two of the has been linked to cancer: E6 binds p53, while E7 binds to Rb. Why would HPV infection potentially lead to cancer? For reference, the figures below describe the normal functions of p53 and the Rb. Select one: a. E6 prevents apoptosis while E7 frees E2F allowing S-phase genes involved in DNA replication to be transcribed. b. E7 prevents apoptosis while E6 directly stimulates S-phase genes involved in DNA transcription. c. E6 prevents activation of telomerase while E7 phosphorylates E2F allowing S-phase genes involved in DNA replication to be transcribed. d. E6 induces p53-mediated DNA repair while E7 activates telomerase and immortalizes the cells.
Adi S.
Human papilloma virus (HPV) is the major cause of cervical cancer. HPV expresses two interesting proteins (E6 and E7) that play different roles in transforming cells to become cancerous. E6 promotes p53 degradation, while E7 binds to Rb and disrupts the Rb-E2F interaction. Why would HPV infection potentially lead to cancer? For reference, the figures below describe the normal functions of p53 and the Rb-E2F complex.
Shyam P.
Question 15 Human papillomavirus (HPV) is a viral infection that is transmitted mainly through skin-to-skin contact. Following transmission, HPV enters host cells and integrates into the host genome, eventually causing the cells to synthesize the viral protein E6. In turn, E6 inactivates the host protein p53, a tumor suppressor that arrests the cell cycle or induces apoptosis (programmed cell death) when DNA damage is detected. Which of the following claims is best supported by the information above? I. HPV increases the synthesis of tumor suppressor proteins in infected cells. II. HPV results into inactivation of tumor suppressor protein. III. HPV causes infected cells to exit the cell cycle. IV. HPV causes uncontrolled cell division in infected cells.
Md.Daniyal A.
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