Cultured cells were treated with a compound in early Gap 1 (G₁) phase resulting to arrest before entering S phase. It was identified that similar checkpoint acts during G₁ phase to ensure that sufficient growth has occurred before the cells enter S phase. Which of the following was the most plausible mechanism of arrest? (A) Inhibition of Rb activity (B) Overproduction of E2F (C) Inhibition of DNA polymerase (D) Inhibition of G₁ cyclin transcription

You plan to synthesize a peptide to be used as a vaccine to treat melanoma, a particularly aggressive form of skin cancer. Normally, gp100, a protein on the surface of melanocytes, activates cell growth when it is bound by its ligand. Activation of the growth pathway depends on the presence of threonine in the ligand. The effective peptide vaccine will mimic the natural ligand, but won’t cause cell growth and division. Below is the sequence of the natural ligand:   LDMKTAG   In order to ensure your newly designed peptide vaccine does not cause cell growth upon binding, you must substitute the Threonine residue at position 5. What amino acid would you replace it with, bearing in mind that the peptide should still be similar enough to bind to the gp100 protein in the surface of melanocytes. Explain your choice. Your vaccine will be administered as a topical cream, and you require your peptide to have an overall neutral charge in order to be functional. At what pH should you formulate…

Human cells are highly resistant to transformation. Experiments have shown that 5 regulatory circuits (pathways) have to be altered before human cells can grow as tumor cells in immunocompromised mice. State each of these circuits. Explain how the alteration of the protein of that particular circuit leads to uncontrolled growth.        the mitogenic signaling pathway controlled by Ras. the cell cycle checkpoint controlled by pRb. the alarm pathway controlled by p53. the telomere maintenance pathway controlled by hTERT. the signaling pathways are controlled by protein phosphatase 2A, which modulates the activity of the mTOR, Myc, β-catenin, and PKB/ Akt signaling proteins.

When the gene encoding a certain cellular kinase is deleted, the resulting mutant cells arrest in the cell cycle and do not divide. These mutants can be rescued when a gene encoding an N-terminal GFP fusion of the protein is expressed, but not when a gene encoding a C-terminal GFP fusion is expressed. Which fusion protein is appropriate to use in studying cellular localization and activity? Explain why.