i want the solution of this assingment please. 1- Typical N-terminal signal sequence ( include description, function, and how they work) 2- list address codes for different parts of the cell 3- Stop transfer sequence ( description, function, how they work)
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i want the solution of this assingment please.
1- Typical N-terminal signal sequence ( include description, function, and how they work)
2- list address codes for different parts of the cell
3- Stop transfer sequence ( description, function, how they work)
Step by step
Solved in 3 steps with 1 images
- Why do signals indicating damage to cells result in increase in the expression of p21Cip1? I need new answerA temperature-sensitive mutant yeast strain stops dividing when shifted from 25°C to 37°C. These cells are analyzed at different temperatures by a machine that measures the amount of DNA they contain, and the following graphs are obtained. number of cells number of cells [ Select] [Select] [Select] 25°C [Select] مل Cells in G1 phase should have [Select] Which of the following would explain the behavior of your mutant? Mark yes or no for each of the following choices. 2 amount of DNA/cell (arbitrary units) 37°C 1 2 amount of DNA/cell (arbitrary units) unit(s) amount of DNA. ✓ Inability to initiate DNA replication Defect in chromosome condensation ✓Defect in centrosome duplication ✓Defect in cytokinesisBCL2 binds to and inactivates BAX and other pro-apoptotic proteins, thereby inhibiting apoptosis. Venetoclax has been approved for marketing in patients with chronic lymphocytic leukemia (CLL) Venetoclax is a highly selective BCL2 inhibitor that disrupts the interaction of this protein with BH3 domain proteins thereby permitting apoptosis. Proapoptotic Proapoptotic proteins protein binds to BCL2 BCL2 Venetoclax Venetoclax displaces proapoptotic proteins BCL2 Venetoclax Proapoptotic proteins No venetoclax binding BCL2 Glys01Val mutation Which of the following can you conclude from this information? Select all that apply Bcl2- mutations that prevent Ventoclax binding promote cell survival Venetoclax binding to Bcl2 promotes cell survival . Venetoclax binding to Bcl2 promotes cell death Proapoptotic protein binding to Bcl2 promotes cell survival
- Figure 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.how do i expand this into 1000 words The methodology employed to identify differentially expressed genes (DEGs) in breast cancer using RNA-Seq data involves several systematic steps integrating data retrieval, analysis, normalization, DEG identification, and functional annotation. Initially, raw RNA-Seq data is retrieved from the NCBI GEO database, specifically from dataset GSE216238 (Nakshatri, 2023), which encompasses samples from both breast cancer and normal tissue. Subsequently, the raw data was imported into Excel for initial analysis, leveraging its widespread availability and user-friendly interface. Gene expression data for breast cancer analysis was obtained from the Gene Expression Omnibus (GEO) database. The GEO homepage (https://www.ncbi.nlm.nih.gov/geo/) was accessed, and the "Query & Browse" tab was selected. Advanced Search: Under "Search GEO DataSets," an advanced search was conducted (https://www.ncbi.nlm.nih.gov/gds/advanced). Keywords "breast" and "cancer" were…Question:- Describe the path a cell surface receptor will take when being synthesized (starting at the beginning of translation) to its expression on the plasma membrane; indicate the orientation of the receptor and any other processing that is undergoes. Describe the different possible fates of a receptor once it is internalized by receptor-mediated endocytosis.
- NO answer needs more than 2 sentences, some require just a couple words. 7. GTP-y-s is an analog of GTP that cannot be hydrolyzed. How would you expect a Co-IP experiment between G-alpha and G-beta proteins to differ in the presence of GTP-y-a and GDP? 8. 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. 9. Taxol is a drug that inhibits microtubule dynamics and is often used for cancer chemotherapy because it preferentially affects dividing cells. What microtubule-based structure is likely disrupted by Taxol so that it specifically affects proliferating cells? 10. Patients with Marfan’s syndrome have a mutation in the fibrillin gene and are at risk of…GTP binding proteins are molecular switches. How do GTP binding proteins work? Provide two examples of GTP binding proteins that function in intracellular protein transport. Make a drawing that illustrates the function of each of these proteins in their respective roles. Predict the direct outcome of a mutation that: Inhibits GTPase activity Inhibits interaction with the GEFCan I get help please with this question? Two mutations have occurred to proteins within the glucagon signaling pathway: A) The glucagon receptor has a mutation. This mutation causes this GPCR to always have a conformation that will induce nucleotide exchange for any associated heterotrimeric G proteins, even without glucagon binding to the receptor. B) The alpha subunit of the heterotrimeric G protein has a mutation. This mutation causes the Gαarginine finger to always be in a position to properly order the catalytic residues within the Gαsubunit to promote catalysis. Question: What will the combined effect of both mutations be on the signaling pathway and what is the mechanistic reason for this effect?
- Answer both to get a like or don't attempt.Thanks Question 9 Listen Transphosphorylation, the bidirectional recpiprocal phosphorylation of growth factor dimers, results in the phosphorylation of an array of tyrosine residues present in cytoplasmic portions of the growth factor receptor outside the kinase domain. Question 9 options: TRUE FALSE Question 10 Listen For the EGF receptor: Question 10 options: Spontaneous receptor dimerization precedes receptor binding. The EGF ligand serves as a bridge to dimerize receptors. Are overexpressed in many human cancers making them hyper-responsive to low levels of ligand. A and C are both correct. B and C are both correct.1117 increase in the number of passive glucose transporter on the muscle cell surface thus increases the uptake of glucose into the cell and decreases blood glucose level. Indicate whether the following conditions/practice will likely lead to diabetes (mark Yes or No). [Select] a mutation in a V-SNARE in islet cells that blocks all secretion Q Search ******* 40 ****** 99+ app.honorlock.com is CThe activity provides you with a version of the NGF pathway, an example of a RTK. All of the proteins involved can be in ON/OFF states. Using this cell signaling pathway you will be asked a variety of questions to determine how the molecules are regulated, but also how a cell would respond if this cell signaling party steps were interrupted or activated. Neural Growth Factir (NGF) Ras- Ras- GDP GTP Trk-A Ras-GEF braf braf МЕК МЕК ERK ERK ERK ERK STAT STAT Spiouty DNA Nucleus Cytosol