es that stimulate Il will get to the response step or not. Keep in mind the purpose of this pathway is to cause skin cell division Growth Factor (GF-signal) Activation of GF Receptor (RTK-receptor) To cause Cell proliferation/cell division (Response) Plasma membrane Grb2 (Ras GEF) (adapter) Raf MAPKKK Mek MAPKK Activation of t proliferation Erk МАРК You have a skin cell in a dish and have added Neural Growth Factor (NGF) to the cell media (the liquid the cell needs to live).
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- TLRs activate NFkB, AP-1, and IRF transcription factors to induce the expression of inflammatory cytokines and type I interferons. A key feature of TLR signaling is the ability to induce inflammatory cytokine gene expression extremely rapidly following TLR stimulation. This is accomplished by signaling pathways using several mechanisms to activate transcription factors that are already present in the cell prior to TLR stimulation, but are kept in an inactive state. These signaling pathways use all of the following mechanisms EXCEPT: Induced ubiquitination leading to protein degradation Induced ubiquitination inducing protein–protein interactions Induced phosphorylation leading to nuclear translocation Induced phosphorylation leading to kinase activation Induced phosphorylation preventing protein degradationPut 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 nucleusA mutant B cell line is examined by confocal microscopy after incubation with a microbial pathogen recognized by the BCR on these B cells. The B cells have been stained with antibodies to visualize the localization of polymerized actin and microtubules. As a control, wild-type B cells are examined. The results are shown in the figure below, with the numbers indicating the proportion of cells examined that show each pattern of staining. To identify the specific signaling defect in these mutant B cells, a reasonable biochemical assay would be to: Determine if BCR stimulation of mutant B cells produces enhanced binding of the B cell to the microbe Determine whether the mutant B cells have reduced levels of the enzyme Protein kinase C-q Determine whether the mutant B cells are overexpressing the enzyme Vav Determine whether BCR stimulation of mutant B cells promotes exchange of GDP for GTP on cdc42 Determine whether BCR stimulation of mutant B cells produces increased levels of DAG
- Binding of TGF-β to its receptors can elicit a variety of responses in different cell types. For example, TGF-β induces plasminogen activator inhibitor 1 in epithelial cells and specific immunoglobulins in B cells. In both cell types, Smad3 is activated. Given the conservation of the signaling pathway, what accounts for the diversity of the response to TGF-β in various cell types?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…Biologic agents can block cell migration to sites of inflammation and reduce immune responses. Natalizumab is a humanized monoclonal antibody directed at the a4-integrin protein, a subunit of VLA-4, the binding partner of VCAM-1 expressed on endothelium in the central nervous system, and of a4b-integrin, the binding partner of MadCAM-1 expressed on endothelium in the gut. While natalizumab has had great success in alleviating the symptoms of autoimmune diseases such as multiple sclerosis and Crohn’s disease, a small number of patients have acquired life threatening infections of the neurotrophic virus, JC. Why are patients on natalizumab particularly susceptible to a virus infection of the central nervous system?
- An epithelial cell line expressed a fluorescence-based cAMP biosensor in all cells, but only expressed a GPCR in ~30% of those cells. When you treated the cells with the GPCR ligand, fluorescence from the cAMP sensor immediately turned on in most cells (not just those expressing the GPCR). In one sentence suggest a simple explanation for why cAMP increased in non-GPCR-expressing cells.Tumor necrosis factor alpha (TNF-α) is an important cytokine used by immune cells to initiate and coordinate inflammatory responses. Inflammation is a key response to cell damage or infection, but can, in some diseases, spiral out of control and become more of a problem than the original cause (COVID-19 lung damage is a relevant example...). TNF-α receptors exist on many cell types. Let’s study the interaction between TNF-α (T) and its receptor (R), to form an activated complex C: T + R ↔ C A macrophage is measured to have ~105 TNF-α receptors on its surface. If the macrophage is immersed in a high concentration of TNF-α molecules (i.e. L0 ≅ L), how will the number of activated receptors change over time? Plot this trend for the case L0 =10 nM, kf=106 M-1 min-1, kr=0.1 min-1. There is constant ligand concentration and an initial condition of C0 = 0. We are given the constants needed to model the number of activated receptors over time and can use the following equation:Describe three different responses of a cell-surfacereceptor on binding a signaling molecule and undergoing aconformational change.
- Non-canonical Hedgehog signaling results in actin cytoskeleton rearrangements, leading to cellmovement and changes in cell shape. Describe how changes to the actin cytoskeleton lead to cellmovement and changes in cell shape.You do not need to draw out the signaling pathway again (#1b). Your answer should focus onthe changes to the actin cytoskeleton. Drawings will be helpful!Aberrant signaling through the EGF receptor signal transduction pathway drives many forms of breast cancer, while misregulation of PI3K drives many prostate cancers. PI3K is one of MANY downstream effectors of EGF receptor signaling, and there are several known activating mutations of PI3K. Would a small molecule that targets PI3K be an effective treatment for a breast cancer that is driven by aberrant signaling through the EGF receptor? Briefly explain your choice. (THIS CAN BE DONE IN LESS THAN TWO SENTENCES, AND MINIMALLY IN ABOUT EIGHT WORDS.)You are given a project to characterize the effect of mutation on two newly discovered G protein coupled-receptors, GPCR-UCI and GPCR-UC2, both of which bind to the same ligand. For the cell signalling assay, you have the UMR-106 cell line that expresses both GPCR-UC1, CPCR- UC2, the corresponding G proteins, and adenyl-cyclase. A basal adenylyl cyclase activity, and thus, a baseline cAMP concentration, is detected in the cell line. (i) You found that, upon binding to the ligand, the mutation in GPCR-UC1 results in increased CAMP level but the mutation in GPCR-UC2 results in a low cAMP concentration. Based on these results, identify the subclass of G protein isoforms that the GPCRs activate. Explain your answer. (ii) If the mutation affects the G protein from GDP release, how would this affect the CAMP production after ligand binding? Explain your answer.