Match the following. Write correct answer in the form of 1a, 5b, etc. in the space provided. 1. Gene Replacement A. No active gene is present 2. Gene Knockout B. Only mutant gene is active 3. Gene Addition C. Both normal and mutant genes are active
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Match the following. Write correct answer in the form of 1a, 5b, etc. in the space provided.
|
1. Gene Replacement |
A. No active gene is present |
|
2. Gene Knockout |
B. Only mutant gene is active |
|
3. Gene Addition |
C. Both normal and mutant genes are active |
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- a. What is your epigenome (i.e. epigenetics)? b. Does lifestyle affect your epigenome? Explain c. Does your epigenome change with age? Explain d. What is epigenetic therapy? Is it working? Explain Edit View Insert Format Tools Table 12pt v Paragraph v BIUA 2v T? Addre DELLa. What is your epigenome (i.e. epigenetics)? b. Does lifestyle affect your epigenome? Explain -c. Does your epigenome change with age? Explain d. What is epigenetic therapy? Is it working? Explain Edit View Insert Format Tools Table 12pt v Paragraph v в I Address DELL F7 F8 F9 F10 F1 F4 F5 F6 # % & 3 4 6. 7 8 9 Y ...A. Somatic cells are aslo called B. In irder to clone a gene, a gene is inserted into a:
- Write TRUE or FALSE. If false, write the word/s that make(s) the statement incorrect. 1.Metabolic pathways can be switched on or off by hormones only. 2.In epigenetics, the chemical tag ethyl group can result in the inhibition of gene expression.Below is the genotyping results using PCR and gel electrophoresis for a DNA-binding regulatory transcription factor called TF111. Write down the genotypes for normal wild type, skin tumor B, and skin tumor C. DNA Wild type Skin tumor Skin tumor ladder control Cell type B Cell type C 1,000bp 900bp wild type TF111 allele 700bp 500bp 300bp 200bp 40bp mutant TF111 allele Primer dimer www Genotype for Wild type control: Genotype for skin tumor cell type B: Genotype for skin tumor cell type C:Research cancer mutation. Provide the link to the research article that gives you your information. One good resource to use is PubMed. Then answer the following questions, in 3 paragraphs, 3-5 sentences each. 1. What kind of disease/cancer does this mutation cause? 2.What happens during transcription to cause this mutation? 3. Is this trait passed on to progeny? Can the progeny be a carrier or simply affected?
- Discuss about temperature-sensitive mutationsPinpointing a disease gene requires a combination of approaches. Mutations in the XIAP gene are known to cause a serious condition called X-linked lymphoproliferative disease (XLPD). In the case of XLPD, in which the blood contains too many lymphocytes (white blood cells of the immune system), crowding out the oxygen-carrying red blood cells and damaging the liver. When compairing the XIAP amino acid sequence of one affected patient to other human and animal standard RefSeq, the patient has an amino acid substitution at position 203, from cystenine (C) to tyrosing (Y). This evolutionary conservation suggests Group of answer choices that the standard RefSeq does not provide enough information to determine a possible cause of XIAP function. mutations in the XIAP gene and XLPD are not associated. that the mutation in the affected patient has no impact on XIAP function. that the mutation in the affected patient might alter XIAP function.. The website CBioPortal (http://www.cbioportal.org)is an exceptionally useful program for visualizing thecancer genes and genomes of tumors from thousandsof patients with different kinds of cancer that havebeen analyzed by whole genome sequencing and insome cases, by RNA-Seq.Go the the CBioPortal site and click All underSelect Cancer Study and in Enter Gene Set typePTEN, then hit Submit. On the page that is returnedyou will see how the coding region of the PTEN geneis altered in tumors investigated in the various studies.Hitting the tab Mutations will let you see the detailsof these mutations relative to the PTEN protein, whilethe tab Expression lets you see how the gene’s expression (in terms of cDNA reads) is altered in individual tumor samples.a. Is PTEN an oncogene or a tumor suppressor gene?What kinds of evidence lead you to this conclusion?b. What kinds of cancer are most likely to involvealterations of PTEN?c. How would you identify patients whose tumorcells are particularly…
- You have two patients. Both patients have very low levels of P53 protein. Patient #1 also has very low levels of MDM2 protein; patient #2 has very high levels of MDM2. For each patient briefly describe (briefly justify your answers); Which of the two genes are mutated?P53 or MDM2? Is this an oncogenic or tumor suppressor mutation? Would treatment of the patient with Nutlins be appropriate?a. When gene probes, fi ngerprinting, and sequencing make it possible for you to know about genetic diseases in you or one of your children, would you wish to use this technology to fi nd out? b. What if it were used as a screen for employment or insurance? c. Most of us would agree to growth hormone therapy for a child with dwarfi sm, but how do we deal with parents who want to give growth hormones to their 8-year-old son so that he will be “better at sports”?ABOUT Phenylketonuria Explain Potential technical issues and limitations of PCR technology are mentioned Correct information about tissue that can be used to test for a genetic disease and justification of tissue selection Detailed information about the position (exact base pair number) of the new mutation relative to the sequence of the PAH gene. Numbering is based on the start of transcription of the PAH gene. PLEASE ANSWER ALLLL PLEASEE