The figure below shows how normal signaling works with a Ras protein acting down

Question

The figure below shows how normal signaling works with a Ras protein acting downstream of an RTK. You examine a cell line with a constitutively active Ras protein that is always signaling.

a) What type of mutations could cause Ras to be constitutively active?

b) Which of the following conditions will turn off signaling in this cell line with the constitutively active Ras?

addition of a drug that prevents protein X from activating Ras

addition of a drug that increases the affinity of protein Y and Ras

addition of a drug that blocks protein Y from interacting with its target

addition of a drug that increases the activity of protein Y

NORMAL SIGNALING REQUIRES Ras AND TWO PROTEINSX AND Y signal molecule active Ras protein CYTOSOL GTP active signaling protein Y active receptor tyrosine kinase actiwe signaling protein X SIGNALING

Explanation / Answer

The receptor tyrosine kinases (RTKs) are the second major type of cell-surface receptors that we discuss in detail in this chapter (see Figure 20-3d, right). The ligands for RTKs are soluble or membrane-bound peptide/protein hormones including nerve growth factor (NGF), platelet-derived growth factor (PDGF), fibroblast growth factor (FGF), epidermal growth factor (EGF), and insulin. Binding of a ligand to this type of receptor stimulates the receptor’s intrinsic protein-tyrosine kinase activity, which subsequently stimulates a signal-transduction cascade leading to changes in cellular physiology and/or patterns of gene expression (see Figure 20-6). RTK signaling pathways have a wide spectrum of functions including regulation of cell proliferation and differentiation, promotion of cell survival (Section 23.8), and modulation of cellular metabolism.

Some RTKs have been identified in studies on human cancers associated with mutant forms of growth-factor receptors, which send a proliferative signal to cells even in the absence of growth factor. One such mutant receptor, encoded at the neu locus, contributes to the uncontrolled proliferation of certain human breast cancers (Section 24.3). Other RTKs have been uncovered during analysis of developmental mutations that lead to blocks in differentiation of certain cell types in C. elegans, Drosophila, and the mouse.

In this section we discuss activation of RTKs and how they transmit a hormone signal to Ras, the GTPase switch protein that functions in transducing signals from many different RTKs. The second part of RTK-Ras signaling pathways, the transduction of signals downstream from Ras to a common cascade of serine/threonine kinases, is covered in the next section.

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