Interaction of certain growth factors with their receptors leads to following sequence of events given below. Protein X becomes activated when it binds to which of the following? Binding of growth factor ligand Autophosphorylation of tyrosine residues Interaction with SOS proteins Activation of X protein Activation of Raf kinase Activation of MAP kinase O 35 36 Answers AE A GTP B ATP C Ubiquitin D UTP E Ca2+ O
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- Put the following steps for the outline of the growth factor signaling pathway in order: Map Kinase Kinase is Phosphorylated Proteins involved in gene transcription are activated Growth factor binds to its receptor in the cytoplasmic membrane Receptor recruits adaptor protein and GEF Autophosphorylation of tyrosine residues on the receptor Structural change of the receptor activates Tyrosine Kinase Map Kinase Kinase Kinase is phosphorylated Ras, a small GTPase, is activated by the exchange of GTP for GDP Map Kinase is Phosphorylated Map Kinase enters the nucleuswhich 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 GTPCell lines divide normally in a defined medium containing growth factors, but fail to divide in the absence AGF (a growth factor). However, a mutant cell line continues to divide even in the absence of AGF. Elevated levels of Rb phosphorylation and the effects of receptor and Mek inhibitors suggest a mutation activating an oncogene. Inhibitors of Mek inhibit cell division of the mutant cell line, but inhibitors to the ADGF receptor, a receptor tyrosine kinase (RTK) with homology to EGFR, do not. Outline the RTK pathway leading to the phosphorylation of Rb to form p-Rb.
- Cancers are often caused by overactive growth factor receptor signaling (remember growth factor receptors are enzyme-linked receptor pathways). If you were able to use gene therapy to overexpress a particular protein in a cancer cell, which of the following might be useful to overexpress in order to combatt cancer? a GAP that acts on Ras a phosphatase that acts on GPCR a protein that enhances the activity of Akt a ubiqtuin ligase that acts on the MAPK phophataseDescribe the action of the following molecular playersin signal transduction pathways: growth factors, growthfactor receptors, kinase cascades, and transcriptionfactorsThe output of RTK pathways is often the activation of MAP Kinase. Explain how MAPK can lead to activation of a specific subset of proteins, leading to distinct effects in different cell types in response to the same growth signal.
- Below are two cell signalling pathways that work together to regulate cell growth, proliferation and ultimately the size of organs in O.Extremus. In other closely related organisms, dysfunction of these pathways has been associated with tumor growth. mTOR pathway: 1. Growth factors bind and stimulate the receptors. 2. Receptors can activate the phosphatidylinositol 3 kinase (PI3K) – Akt signaling pathway. 3. The activated Akt, a serine threonine kinase, inhibits theTSC1–TSC2 complex, allowing Rheb to activate mTORC1. 4. In parallel, amino acids activate the mTORC1 pathway through a mechanism requiring the Rag– Ragulator complex. Hippo pathway: 1. The binding of the ligand activates the receptors which activate Mst and Lats. 2. YAP activity is modulated by phosphorylation of Mst and Lats. YAP upregulates miR-29, which in turn downregulates PTEN, an inhibitor of PI(3)K and Akt. So, the two pathways crosstalk and coordinate cell number and growth. a) What purpose does this forward…An SH2-containing protein contains a mutation that changes its binding pocket such that tyrosine and phosphotyrosine bind with equal affinity. As a result, MEK activity: does not change with receptor dimerization and transautophosphorylation decreases due to changes in Raf activation increases with ligand binding-induced dimerization decreases due to allosteric inhibition of SH2-domain bindingCyclic adenosine monophosphate (CAMP) is a molecule that can act as anallosteric activator of kinase enzymes inside of the cytoplasm. Describehow CAMP molecules affect kinase enzymes?
- Protein phosphorylation is commonly involved with all of thefollowing except(A) activation of receptor tyrosine kinases.(B) activation of protein kinase molecules.(C) activation of G protein-coupled receptors.(D) regulation of transcription by signaling molecules.1. What cellular event happens in response to the binding of a growth factor to its respective receptor on the membrane of the growth factor’s target cell? Describe what happens to a tyrosine kinase receptor once it binds the growth factor signal. 2. Describe the three domains of a receptor tyrosine kinase. Explain the structure of the transmembrane domain and the amino acid composition and arrangement of this part of the receptor PLEASE ANSWER BOTHThe G protein coupled receptor (GPCR) pathway elicits diverse intracellular responses in different cells. The basic steps of GPCR signaling are outlined in this diagram. Which of the following statements correctly describes the process of GPCR signaling? The GPCR activation is reversible after the signal of the ligand diminishes. The membrane-embedded enzyme uses GTP as a secondary messenger to initiate gene expression. The ligand attaches to both the GPCR and the membrane-embedded enzyme to activate the GPCR pathway. The ligand-bound GPCR sends a GTP molecule to an enzyme in the membrane and switches it into an active state.