Concept explainers
DRAW IT Draw the following apoptotic pathway, which operates in human immune cells. A death signal is received when a molecule called Fas binds its cell-surface receptor. The binding of many Fas molecules to receptors causes receptor clustering. The intracellular regions of the receptors, when together, bind proteins called adaptor proteins. These in turn bind to inactive molecules of caspase-8, which become activated and then activate caspase-3. Once activated, caspase-3 initiates apoptosis.
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- Help constructing a concept map? Example provided below. Many studies have indicated that autophagy and apoptosis play an important role in the pathogenesis of spinal cord injury. In recent years, research on autophagy-related signal transduction pathways has demonstrated that the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway is closely associated with the initiation of autophagy. However, the mechanism of the pathological relationship between this signaling pathway and apoptosis in spinal cord injury is unclear. In this study, we used an in vitro model of spinal cord injury to observe the mechanism of the PI3K/Akt/mTOR signaling pathway and the apoptosis of neurons via the mitochondrial pathway. Mitochondrial pathway apoptosis-related proteins were detected by western blot. Akt and mTOR phosphorylation levels peaked 4 h after mechanical damage and then decreased. Following administration of the PI3K-specific…arrow_forwardwhich of hthe following would result in a persisting proliferation response to growth factor receptor activation after the ligand is no longer binding to its rceptor kinase? 1. Both a mutation that blocks the GTPas activity of Ras and a mutation that blocks the exchange of GDP with GTP would cause the response to persist. 2. a mutation that blocks the GTPas activity of Ras 3. neither a mutation that blocks the GTPas activity of Ras nor a mutation that blocks the exchange of GDP with GTP would cause the response to persist 4. a mutatiaon that blocks the exchange of GDP with GTParrow_forwardIllustrate a complete cell signaling cascade from signal to response. Each protein in the pathways must be shown. You can choose either a GPCR or an RTK mediated pathway.arrow_forward
- 47. Order the sequence of Canonical signaling via Frizzled receptors. i) β-catenin can now promote proliferation and stem cell state ii) Frizzled receptor signals for dishevelled and axin binding to itself iii) LRP assisted with Wnt binding to frizzled receptor iv) Preventing the activation of GSK-β which signals for phosphorylation A. iii ->ii-> iv-> i B. iv-> iii -> ii-> i C. i-> ii-> iv-> iii D. iii-> iv-> ii-> iarrow_forwardEGF signals by binding to cell surface EGF receptors. Which of these observations, if true, would BEST explain EGF’s mechanism of action? A. EGF is hydrophilic and can easily diffuse through the cell membrane B. EGF is hydrophobic and can easily diffuse through the cell membrane C. EGF is hydrophilic and cannot diffuse through the cell membrane D. EGF is hydrophobic and cannot diffuse through the cell membranearrow_forwardYou isolated two mutant cells (Cell A and Cell B) which have a problem in the signal transduction pathway. Both cells show activated response to one of RTK mediated signaling without ligand, suggesting the signaling pathway has been constitutively activated by mutations. You introduced mutant Ras that blocks Ras activation step in both cells. When the mutant Ras was expressed in cell A, the signaling pathway was no longer activated. On the other hand, when the mutant Ras was expressed in cell B, the signaling pathway was still active. From these results; Q1) Which protein of the signaling pathway in Cell A might have the mutation? How does that mutation affect the function of that protein? Why do you think so? Q2) Which protein of the signaling pathway in Cell B might have the mutation? How does that mutation affect the function of that protein? Why do you think so?arrow_forward
- 1. List one example of AMPLIFICATION OF SIGNAL during the cell’s response to Hedgehog. Makesure to write out full steps and not just the name of a protein. Do not choose the example from2h or 2i if you chose amplification of signal as your answer to those questions.arrow_forward5. Explain the signaling steps that take place after the EGF receptor is dimerized, up to the poiunt when Ras gets activated. Draw a schematic to make it easier for your classmates to understand.6. Explain why the RTK signaling pathway includes the extra complication of having a protein (Ras) that switches between GTP- and GDP-bound states. PLEASE ANDWER BOTHarrow_forwardFigure 9.8 HER2 is a receptor tyrosine kinase. In 30 percent of human breast cancers, HER2 is permanently activated, resulting in unregulated cell division. Lapatinib, a drug used to treat breast cancer, inhibits HER2 receptor tyrosine kinase autophosphorylation (the process by which the receptor adds phosphates onto itself), thus reducing tumor growth by 50 percent. Besides autophosphorylation, which of the following steps would be inhibited by Lapatinib? Signaling molecule binding, dimerization, and the downstream cellular response. Dimerization, and the downstream cellular response. The downstream cellular response. Phosphatase activity, dimerization, and the downsteam cellular response.arrow_forward
- Biology 2eBiologyISBN:9781947172517Author:Matthew Douglas, Jung Choi, Mary Ann ClarkPublisher:OpenStaxBiology: The Dynamic Science (MindTap Course List)BiologyISBN:9781305389892Author:Peter J. Russell, Paul E. Hertz, Beverly McMillanPublisher:Cengage Learning