19. How do white blood cells internalize bacteria? B) Phagocytosis D) Receptor-m

Question

19. How do white blood cells internalize bacteria? B) Phagocytosis D) Receptor-mediated endocytosis E) Any type of endocytosis 20. Synthetic known as A) agonists B) receptor upregulators C) specific proteoglycans. D) syndecans. E) antagonists. 21. Kinases and phosphatases are essential in cells because they A) help turn proteins "on and off through changes in phosphorylation status. B) are enzymes that destroy damaged proteins C) sense short poly-A tails in mRNAs as a signal to degrade them D) destroy second messengers, thereby turning off a signal transduction pathway E) all of the above 22. You have recently identfied a molecule that you believe to be a signal transduction pathway's ligand As a result, you expect it to interact All you know about this ligand is that chemically it is hydrophilic. with its receptor A) at the outer cell surface. B) within the cytoplasm of the cell C) within the nucleus of the cell DI) on the oytoplasmic side of the plasma membrane. E) all of the above 23. technique that could be used to demonstrate that Glut1 and Glut3 are overexpressed in cancer cells as compared to normal cells is A) DNA sequencing B) Mass spectrometry C) Western blotting D) Thin layer chromatography E) Electron microscopy 24. Allosteric enzyme inhibitors are a) Likely to compete with the substrate for the active site b) Can c) Bind to site distinct from the active site d) Cannot be competed out by excess substrate e) Both choices C and D be competed out by excess substrate

Explanation / Answer

18 - (B) pyagocytosis

21- (1) kinases does phosharylation

phoshatases does dephospharylation

phoshprylation - add phosphate (turn protien on)

dephospharylation reamove phosohate (turn protien off)

24 - (E ) allosteric enzyme inhibitor

- binds to site other than active (allosteric site) - non compatative inhibitor

excess of substrate -- no effect

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