Possible associated G proteins Gs Gq G₁/Go Possible marker genes: - Solute carrier family 17 Glutamate decarboxylase Possible ionotropic targets: - Dopamine B hydroxylase Choline acetyltransferase Cayl channels Ca 2 channels GIRK channels - Tryptophan hydroxylase 2 Tyrosine hydroxylase Histidine decarboxylase M-type K channels HCN channels BK and SK channels
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- 7. Fill in the table below, outlining different aspects of glutamate singlaing in the mammalian brain. A legend of possible entries is provided below the table, specifically for the columns "marker genes", “associated G proteins" and "ionotropic targets" Marker gene Ionotropic receptors Possible associated G proteins Gs Gą G₁/Go Possible marker genes: Choline acetyltransferase Solute carrier family 17 Glutamate decarboxylase Dopamine ß hydroxylase Possible ionotropic targets: Cayl channels Cav2 channels GIRK channels M-type K¹ channels BK channels SK channels Metabotropic Associated receptors G protein mGluR 1,5 mGluR 2-4,6-7- Pre- or post- Ionotropic Neuronal effects synaptic action? target(s) Tryptophan hydroxylase 2 Tyrosine hydroxylase Histidine decarboxylase79 55. One week after a cadaveric kidney allograft, a 45-year-old man develops a fever. He has a 24-hour urine output of 100 mL and a serum creatinine concentration of 3.5 these cells, IL-2 receptor is a useful marker of which of the following cellular processes? mg/dL. A renal biopsy specimen shows an infiltrate of CD3+ T lymphocytes that are positive for interleukin-2 (IL-2) receptor (CD25) on immunocytochemical testing. For A) Activation B) Differentiation C) Ontogenic development OD) Senescence1 of 16 Data from an experiment is shown in the figure below. In the experiment, murine cells were treated with a specific a ligand that activates receptor R. In some cases, the cells were exposed to one of two drugs (X or Y) as well as the ligand or were left untreated (UT). After 30 minutes of treatment, the cells were lysed with a detergent-based buffer to release the soluble membrane, cyosolic and nuclear proteins. Samples from each cell extract were run (in duplicate) by SDS-PAGE (SDS-polyacrylamide gel electrophoresis) in order to separate the proteins by molecular mass (size). The separated proteins were then transferred to a nitrocellulose membrane which was then probed with different antibodies in a western blotting procedure to detect specific phosphorylated proteins or total proteins. If present in the cell extract, these proteins appear as a dark band in the relevant western blot image within the figure. Drug X Drug Y UT Ligand Ligand Ligand Western blotting antibodies…
- 5) Briefly explain why the formation of a tumour can pose a risk to a person's homeostasis. 6) The functioning of the "Ras/MAPK" signal transduction pathway is absolutely essential in order for cells to grow, divide, and migrate. One important protein that is part of this pathway is BRAF. This protein is a kind of enzyme called a "kinase" – an enzyme that transfers a phosphate group onto another protein. In some melanomas, a mutated form of BRAF called BRAF Val600AGlu drives the progression of the cancer. The drug "vemurafenib" slows the progression of the cancer by slowing the production of the mutant BRAF protein. (National Cancer Institute. 2019. Types of Cancer Treatment. Retrieved from: https://www.cancer.gov/about-cancer/treatment/types/ Is this an example of a traditional cancer therapy or a targeted therapy? Briefly explain your reasoning in the space provided, using information provided in the text to support your answer. Type of therapy (traditional or targeted)?: Brief…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?a.What would happen if IKKbeta did not phosphorylate IkappaB? b.Why is it so hard to make cytokine therapies? c.Why would you use the MyD88 independent pathway versus the MyD88 dependent pathway?
- 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 nucleusTab. 9. Main immunohistochemical markers Name Pancytokeratin (CK) Vimentin Photomicrographs of marker expression Task Mark on the picture: 1 - areas of pancytokeratin expression; 2- areas of absence of pancytokeratin expression. Vimentin expression in the colon wall What cells express pancytokeratin? Specify the differentiation of these cells. Specify the localization of marker expression: Expression of pancytokeratin in epidermal a) membrane tissue b) cytoplasmic c) nuclear Mark on the picture: 1 - areas of vimentin expression; 2- areas of absence of vimentin expression. What cells express vimentin? Specify the differentiation of these cells. Specify the localization of marker expression: a) membrane b) cytoplasmic c) nuclear Use of markersDescribe in detail the effect of loss or mutation of LAT & Blk of the following molecules/proteins/genes/domains in immune signaling. Be sure to include the normal function and the function effected by the mutation. Include all relevant players and their roles. You may use diagrams if needed.
- 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…Hormone H regulates these effects via its receptors which are found at both the cell surface (csRH) and within the cell (içRH). The signalling pathways that become activated in the presence of hormone H are depicted and described below. hormone H. H H extracellular fluid inactive GTP inactive RAS Lyn cell-surface receptor for H (csR») icR GDP RAS-GTP hexose metabolism cell survival H icR G, phase (resting) Raf HK GSK-3P MEK M G2 icR - hexose kinase ERK promoter HRE CDK1 Cyclin A nucleus cyclin A Fos A promoter Created in BioRender.com bio Signalling via the cell surface receptor Hormone H mediates its cell cycle stimulatory and pro-survival effects by binding to and activating the cell surface hormone H receptor (csRH). The activated CSRH activates Lyn, which activates RAS and ultimately the Raf/MEK/ERK kinase cascade. Active ERK: o phosphorylates and inactivates GSK-3B. Inhibition of GSK-3ß promotes cell survival. inhibits p27, preventing it from inhibiting cell cycle progression.…i) For serotonin receptor associated with the G protein class of subtype Gs, list the various ways how cell signalling can be terminated at stage 0 and 2 shown in Figure 1. 1 Reception ExtracellularA Hama Membra ely Malecle 2 Transduction 3 Response At Select by putting an arrow at the end of the correct choice(s). 2 a) - ) Cytoplase