RTKs and Adaptor Proteins Quiz
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RTKs and Adaptor Proteins Quiz

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Questions and Answers

What role do GAP proteins play in relation to GTPase activity?

  • They accelerate the hydrolysis of GTP to GDP. (correct)
  • They activate GTP-bound proteins.
  • They inhibit the binding of ligands to RTKs.
  • They convert GDP to GTP.

    • What could happen if there is a lack of RAS-GTPase activity in the presence of a growth factor?

  • The signaling pathway would be completely inactivated.
  • MEK activation would decrease significantly.
  • There would be increased GDP-RAS levels.
  • RAS signaling would become permanently active. (correct)

    • What is a dominant-negative effect as related to RTK mutations?

  • Increased signaling due to mutations.
  • Inhibition of ligand binding due to a mutation. (correct)
  • Enhanced phosphorylation sites on RTKs.
  • Complete activation of all RTKs.

    • How does the activation of a RAS-GEF affect RAS signaling?

    <p>It leads to increased levels of RAS-GTP.</p> Signup and view all the answers

    What effect does RAS-GAP activation have on RAS activity?

    <p>It decreases RAS activity by converting it to RAS-GDP.</p> Signup and view all the answers

    What initiates the RTK signaling pathways?

    <p>The binding of ligands and receptor dimerization</p> Signup and view all the answers

    Which of the following best describes the role of adaptor proteins?

    <p>They link proteins without having any enzymatic activity</p> Signup and view all the answers

    What distinguishes Group 1 adaptor proteins from Group 2?

    <p>Group 1 has membrane localization domains, while Group 2 does not</p> Signup and view all the answers

    What is the primary function of activated RAS in RTK signaling?

    <p>To trigger the MAPK cascade</p> Signup and view all the answers

    How does nitric oxide (NO) affect smooth muscle in blood vessels?

    <p>It relaxes smooth muscle cells causing vasodilation</p> Signup and view all the answers

    What role does cGMP play in vascular relaxation?

    <p>It decreases calcium levels in smooth muscle cells</p> Signup and view all the answers

    What enzyme is primarily responsible for the synthesis of nitric oxide from L-arginine?

    <p>Nitric oxide synthase</p> Signup and view all the answers

    What is the effect of phosphodiesterases on cyclic nucleotides?

    <p>They convert cyclic nucleotides into their monophosphate forms</p> Signup and view all the answers

    What is the effect of GTPase activity on RAS in the absence of a signal?

    <p>It causes the background activity of RAS to increase.</p> Signup and view all the answers

    In which scenario would RAS signaling be most likely to become saturating?

    <p>When all RAS molecules are saturated with GTP.</p> Signup and view all the answers

    What is likely to happen when a mutant receptor tyrosine kinase (RTK) is sequestered at the cell surface?

    <p>Endogenous signaling may be suppressed.</p> Signup and view all the answers

    What occurs as a result of RAS-GEF activation in the context of RAS signaling?

    <p>It promotes increased RAS-GTP levels.</p> Signup and view all the answers

    What is the primary consequence of RAS-GAP activation?

    <p>Decreased MEK activation.</p> Signup and view all the answers

    What is the primary structural characteristic of Group 1 adaptor proteins?

    <p>They have multiple tyrosine phosphorylation sites.</p> Signup and view all the answers

    Which protein is specifically mentioned as binding to both RTKs and non-receptor tyrosine kinases?

    <p>GRB2</p> Signup and view all the answers

    How does nitric oxide (NO) influence vascular smooth muscle cells?

    <p>It leads to muscle cell relaxation.</p> Signup and view all the answers

    What downstream effect is initiated by activated RAS?

    <p>Initiation of the MAPK cascade.</p> Signup and view all the answers

    What role does PKG play in smooth muscle cell relaxation?

    <p>Activates myosin phosphatase.</p> Signup and view all the answers

    What happens to blood vessels during vasodilation?

    <p>Blood flow is enhanced.</p> Signup and view all the answers

    What is the effect of decreased vascular resistance in relation to arterial blood pressure?

    <p>It leads to a decrease in arterial blood pressure.</p> Signup and view all the answers

    What type of proteins do adaptor proteins primarily link?

    <p>Signaling proteins.</p> Signup and view all the answers

    Study Notes

    RTKs and Adaptor Proteins

    • RTKs are activated by ligand binding, leading to dimerization and trans-phosphorylation.
    • Phosphorylated tyrosine residues on RTKs recruit downstream signaling molecules, either directly or through adaptor proteins.
    • Adaptor proteins lack enzymatic activity and function as linkers between proteins.
    • Two groups of adaptor proteins exist, categorized by structure and function:
      • Docking proteins have multiple tyrosine phosphorylation sites, binding downstream signaling proteins.
      • SH3/SH2 domain proteins lack phosphorylation sites and membrane localization structures.
    • GRB2 is an example of an SH3/SH2 domain adapter protein, binding to:
      • RTKs
      • Non-receptor tyrosine kinases (e.g., FAK)
      • SOS1, a guanine-nucleotide exchange factor (GEF) for RAS.

    L-Arginine and NO Generation in Vasodilation

    • L-arginine serves as a substrate for nitric oxide (NO) production catalyzed by endothelial nitric oxide synthase (eNOS).
    • NO acts as a vasodilator, relaxing smooth muscle cells in arteries, increasing blood flow and reducing blood pressure.
    • NO binds to soluble guanylyl cyclase, triggering cGMP production.
    • cGMP activates protein kinase G (PKG), leading to relaxation of smooth muscle cells through calcium release from intracellular stores.

    GTPase Activity and Ras Signaling

    • Ras and other small GTPases possess intrinsic GTPase activity, responsible for hydrolyzing GTP to GDP.
    • GAP proteins accelerate this GTPase activity, returning Ras to the inactive GDP-bound state.
    • A lack of GAP activity can lead to sustained Ras signaling, potentially causing an overactivation of downstream pathways.

    Effects of RTK Mutations

    • Mutations that prevent ligand binding render the RTK inactive, halting downstream signaling.
    • Mutations affecting the kinase domain or tyrosine phosphorylation sites similarly inactivate the RTK.
    • Dominant-negative mutations can sequester ligands, suppressing endogenous signaling.

    RAS-GEF and RAS-GAP Impact on RAS Activity

    • RAS-GEF activation promotes Ras activation (positive feedback), increasing the level of RAS-GTP and downstream MEK activity.
    • RAS-GAP activation promotes Ras inactivation (negative feedback), converting RAS-GTP to inactive RAS-GDP and reducing MEK activity.

    RTKs and Adaptor Proteins

    • RTK Signaling Pathways: Start with ligand binding and receptor dimerization, leading to trans-phosphorylation. Phosphorylated tyrosine residues recruit and activate downstream signaling molecules.
    • Adaptor Proteins: Do not possess enzymatic activity but link proteins. Classified into two groups:
      • Docking Proteins: Contain multiple tyrosine phosphorylation sites, bind downstream signaling proteins, and often have membrane localization domains. (Examples: GAB, IRS).
      • SH2/SH3 Domain Proteins: Lack membrane localization structures and phosphorylation sites. (Example: GRB2).

    L-Arginine and NO Generation in Vasodilation

    • NO Generation: L-arginine is a substrate for nitric oxide (NO) generation catalyzed by endothelial nitric oxide synthase (eNOS).
    • NO Effects: NO relaxes smooth muscle cells in arteries, leading to vasodilation and increased blood supply. This decreases arterial blood pressure and heart rate.
    • Molecular Mechanism: NO binds soluble guanylyl cyclase, stimulating cGMP production, which activates PKG (cGMP-dependent protein kinase). PKG activates myosin phosphatase, enabling calcium release from intracellular stores in smooth muscle cells, resulting in relaxation.

    GTPase Activity and Ras Signaling

    • GTPase Activity: Intrinsic to Ras and other small GTPases, as well as G-proteins. GAP proteins accelerate GTP hydrolysis to GDP.
    • RAS Signaling: In the absence of a signal, lack of GTPase activation can cause background activity and a shift towards GTP-bound RAS. In presence of a growth factor signaling through an RTK, lack of GTPase activity sustains RAS signaling until saturation.

    Effects of RTK Mutations

    • Inactive RTK (Ligand Binding Issue): Mutation prevents ligand binding. No effect on signaling pathway.
    • Inactive RTK (Kinase Domain Issue): Mutation removes kinase domain and tyrosine phosphorylation sites. May suppress endogenous signaling due to ligand buffering by the mutant at the cell surface (dominant-negative effect).

    RAS-GEF and RAS-GAP Impact on RAS Activity

    • RAS-GEF Activation: Activates RAS (positive feedback), increasing RAS-GTP levels, which in turn, activates MEK downstream.
    • RAS-GAP Activation: Decreases RAS activity (negative feedback) by converting RAS-GTP to GDP, leading to decreased MEK activation downstream.

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    General Pathways PDF

    Description

    Test your knowledge on Receptor Tyrosine Kinases (RTKs) and the role of adaptor proteins in cellular signaling. This quiz covers the activation of RTKs, the function of adaptor proteins, and specific examples such as GRB2. Challenge yourself to understand the intricate details of cellular communication and signal transduction pathways.

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