11. Cancer cells survive rapamycin treatment in the presence of serumwhera sbece

Question

11. Cancer cells survive rapamycin treatment in the presence of serumwhera sbece and presence of serum are. undergo apoptosis. The reason for the different effects of rapamycin in the absence and presence of serum are A. In the presence of serum there are growth factors that suppress apoptosis. . F ßtatspresentins rum activatessig alsthat are suppress arrest by rapa male ingtoG1 cloe C. In the absence of serum/TGF-p, inhibition of mTOR with rapamycin does not arrest cells in G1 and the cels proceed into S-phase where inhibition of mTOR activates an apoptotic program. D. In the absence of serum, cancer cells exit the cell ycle into a state of quiescence (GO) where suppression of mTOR activates an apoptotic program. 12. Catacholamines (tyrosine derivatives) have Ko's in the low micro-Molar range, whereas peptide hormones such as insulin generally have Ko's in the low nano-Molar range. The reason for different Ko's is due mostly to: A. There are more catecholamine receptors per cell and you therefore need more hormone to saturate all the receptors. B. There are relatively many fewer insulin receptors per cell and therefore you need less hormone to saturate he receptor C. Both A and B. D. Insulin is much larger than a catacholamine and can make more chemical contacts with the receptor that prevent dissociation. 13. Why is START in the yeast cell cycle likely different from the mammalian Restriction point? A. START is relatively late in G1. B. START responds primarily to nutrients. C. START does not respond to growth factors. D. All of the above. 14. Why is the lack of Rb in cancer cells similar to defects in TGF- signaling? A. Because TGF-B signals inhibit cyclin E-CDK2, which phosphorylates and inhibits Rb B. Because TGF-B signals inhibit cyclin D-CDK4, which phosphorylates and inhibits Rb C. Because TGF-B signals liberates E2F family transcription factors from Rb D. Because E2F stimulates the expression of both TGF-B and Rb. 15. At what point is complete growth factor independence achieved during G1 cell cycle progression? A. When cyclin D levels go down. B. When cyclin E levels go up. C. When Skp2 is expressed and can ubiquinate p27 and target it for degredation. D. When cyclin E-CDK2 hyperphosphorylates Rb E. When TGF-B signaling is suppressed by mTORC1

Explanation / Answer

11) C option is right because in the absence of serum TGF beta rapamycine inhibits mTOR kinase pathways which activates program cell death.

12) d option is right because of value is depends on the dissociation of the ligand binding . More the chemical bonding more the affinity that's why insulin being large make more chemical contact with receptor

13) D, all of above

14) b option is right , TGF beta inhibits D-CDK4 which phosphorylates and inhibits RB.

15)

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