Modification H3Ac H3K9(me2) Rat with enrichment for this modification (normal or hypertensive) ACE1 expression in rat with modification (Higher or lower) Activation of ACE1 leads to the constriction of blood vessels and the retention of salt and water, increased blood volume leading to hypertension. In comparing normal to hypertensive rats, it was determined that there was a difference in the histone modifications in certain tissues
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- Proteins found in the blood respond to blood vessel damage by clumping together forming a clot that physically blocks the hole in the vessel and prevents further blood loss. If clotting proteins were active all the time, they would create clots throughout your circulatory system. Which of the following would be the most efficient way for the body to regulate the expression of the proteins involved in clotting? A. Tightly package the genes for clotting proteins so that RNA polymerase cannot access them unless they are needed. B. Produce and store the clotting protein in an inactive form. When the protein is needed, use another protein to activate the clotting protein. C. Constantly make the clotting proteins, but then break them down instantly after translation if they are not needed. D. Use a repressor protein to keep clotting genes turned off until they are needed.APC is a tumor suppressor and acts in the Wnt signaling pathway to prevent the TCF complex from turning on Wnt-responsive genes. Mice that lack the gene encoding TCF4 do not have the ability to maintain the pool of proliferating gut stem cells needed to renew the gut lining. What do you predict will happen in mice that lack the APC gene?Many organisms have a class of genes called ' heat shock proteins.' These genes are expressed at high levels when cells are exposed to high temperatures. once they are transcribed and translated, they help stabilize other proteins in the cell to protect them form the high temperature. What kind of response to the enviornment is the elevated expression of heat-shock proteins? - mutational response - direct response - gene-mediated response
- Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions If you wanted to measure the kinase activity of VEGFR-2, what are some of the conventional methods/assays you would use?Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions How would you determine robustness of the assay and validate the assay?Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions How would you apply a TR-FRET assay to measure the in vitro kinase activity of VEGFR-2? Describe in steps the assay design and potential readout outcome.
- Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions What is the advantage of measuring autophosphorylation of the receptor rather than phosphorylation of the substrate?Vascular endothelial growth factor receptor 2 (VEGFR-2) is an endothelial cell-specific receptor that has inherent tyrosine kinase activity. The binding of the Vascular endothelial growth factor (VEGF) ligand to its receptor plays an important role in angiogenesis, a process by which new capillaries are formed. Enhanced angiogenesis is associated with a number of diseases including cancer. Your goal is to develop a homogeneous in vitro TR-FRET kinase assay for VEGFR-2 (purified protein) in an attempt to identify small molecules that inhibit kinase activity and in turn modulate angiogenesis. Based on this background, please answer the following questions While setting up your experiment, you accidentally discovered autophophorylation of receptor. What observation/results led you to believe that there was autophosphorylation of the receptor?Once an activated signaling pathway has elicited the proper changes in target gene expression, the pathway must be inactivated. Otherwise, pathological consequences may result, as exemplified by persistent growth factor initiated signaling in many cancers. Many signaling pathways possess intrinsic negative feedback by which a downstream event in a pathway turns off an upstream event. Describe the negative feedback that down-regulates signals induced by (a) erythropoietin and (b) TGF-β.
- Erythritol is a natural sugar abundant in fruits and fermentingfoods. Pathogenic bacterial strains that catabolize erythritolcontain four closely spaced genes, all involved in erythritolmetabolism. One of the four genes (eryD) encodes a productthat represses the expression of the other three genes. Erythritolcatabolism is stimulated by erythritol. Present a regulatorymodel to account for the regulation of erythritol catabolism insuch bacterial strains. Does this system appear to be underinducibleor repressible control?The BMP-Nodal gradient so vital to amphibian and fish development may be critically important in other vertebrates (including humans) as well. Moreover, can any field of pluripotent cells (such as human embryonic stem cells)respond to gradients of BMP and Nodal signals?Corticosteroids are powerful anti-inflammatory drugs that alter the transcription of many genes. Corticosteroids are anti-inflammatory drugs that are used to treat individuals with allergies, asthma, autoimmune diseases, or organ transplants. These compounds have a wide range of effects on leukocytes and on inflammatory cytokine production. One common use for corticosteroids is as an inhaled treatment for individuals with asthma. Interestingly, inhaled corticosteroids provide significant benefit to asthma patients with high numbers of eosinophils in their airways, but not to those patients with high numbers of neutrophils, but normal numbers of eosinophils. One reason for this finding may be that: Corticosteroids don’t inhibit IL-13 production in the airways Corticosteroids don’t inhibit release of IL-33 by airway epithelial cells Corticosteroids induce apoptosis of Treg cells Corticosteroids induce apoptosis of eosinophils Corticosteroids don’t work well as combination therapy with…