Suppose that Protein J which is a hypothetical protein kinase receptor was determined to be related to the progression of cancer through its activation. It was also determined that the protein exists in the active and inactive forms. The said active form is highly similar to the Protein K's conformation. Ligands A, B, and C, which are lead inhibitor compounds, were optimized to inhibit Protein J. The affinities of the ligands are shown in the table. Kp values Active Protein J Inactive Protein J Protein K Ligand A 10 mM 20 nM 5 mM Ligand B 20 nM 10 mM 15 nM Ligand C 20 nM 15 nM 15 nM Question: Describe the relative binding affinities of Ligand A to Protein K and to the active and inactive forms of Protein J. Determine which will Ligand A bind with the highest, medium, and lowest affinity.

What are conformational changes and why are they important ? Then describe two examples of conformational changes and their impacts during cellular signaling.

Steroid hormones are required by the body at puberty and into adolescence to regulate growth and cell division at more rapid pace than in later life.  This regulation occurs via their interaction with cellular receptors and the signaling cascades/pathways that follow.  Describe for me the difference between the two major classes of steroids, anabolic and catabolic steroids.  What might you expect the result of signaling cascades to be in cells receiving either anabolic or catabolic “signals”? (B) At some point in late adolescence, steroid production decreases by almost 100 fold, as we transition into “adulthood”.  Why might we wish to stop these signals from constantly being in our blood stream, (like, Say, between 17-24 years of age)?  What result might these steroids have on cancer cells where abhorrent signaling is already causing an increased rate of cell division/growth? Could steroid use result in Cancer?

Binding EGF to the EGF receptor causes phosphorylation of tyrosines on the cytoplasmic tail of the receptor. Which of the following best describes the mechanism by which this phosphorylation activates downstream signaling complexes? Select one    A. Causes degradation of receptor by proteasome pathway   B. Causes EGF receptor to be internalized so it can interact directly with downstream signaling molecules   C. Tyrosine phosphorylation alters 3D structure of downstream signaling proteins causing them to change from an inactive to active conformation   D. Causes release of EGF from receptor   E. Alters the localization of downstream signaling partners in the cytoplasm

For the protein Calmodulin-1: 1) this protein have any secondary, tertiary and/or quaternary structures present? 2)  Are there any molecular additions to this protein that are not amino acids?For both questions, can you explain if so, where specifically?  The protein Calmodulin-1 is stated to have the molecular function of signaling receptor binding which is interrelated with the biological function of calcium-mediated signaling.   Can you explain this relationship?

ras GDP ras ras P.P P.P GTP raf Inactive Active raf Inside of cell Refer to the figure above. A portion of a signal transduction pathway is shown in the figure. The molecule raf is a protein kinase. This molecule becomes activated when a GTP-ras complex binds to it. Which equation describes how activated raf transmits the signal in this pathway? O ATP. --> CAMP +PPi O CAMP --> AMP Inactive enzyme + ATP --> active phosphorylated enzyme + ADP O Inactive phosphorylated enzyme + ADP --> inactive enzyme + ATP Inactive enzyme + ADP --> active phosphorylated enzyme + ATP Assessment Navigator Submit Questionmark Ondemand licensed to University of Dundee PPIP

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The seed of the castor bean (Ricinus communis) contains large amounts of ricin, a deadly poison for animals, including humans. One of the two subunits of this toxin is a lectin that binds terminal N-acetylgalactosamine residues on glycoproteins on the surface of eukaryotic cells, allowing the other subunit to enter the cell and kill it by preventing proteins from being made. Select the possible antidotes that could prevent or reverse ricin-mediated entry of the toxin. a high concentration of N-acetylgalactosamine an oligosaccharide with the same structure as that recognized by ricin a compound that prevents synthesis of extracellular glycoproteins a compound that activates enzymes that break down glycogen into glucose an enzyme that degrades lipopolysaccharides

Cyclin-dependent kinases are a type of "microchip" protein that require multiple inputs (i.e., structural alterations) to be activated-- and thus are active only under specific conditions (as shown in the diagram below). How does limiting activity to when all conditions have been met help the cell function properly? INPUTS has this phosphate been removed? been added? has this is cyclin present? phosphate

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