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- One of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and use the information and link-outs from the page to answer the following question. GIVE YOUR ANSWER AS A NUMBER ONLY, NO UNITS: What is the size in amino acid residues of the CACNA1S transcript named CACNA1S-202? Answer: The size of the CACNA1S transcript named CACNA1S-202 is how many amino acid residues.One of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and ensure that you click to reveal the transcript table. Then use the information in the table to answer the following question. PLEASE GIVE YOUR ANSWER AS A NUMBER ONLY, NO UNITS What is the size in base pairs of the CACNA1S transcript named CACNA1S-202? Answer: The size of the CACNA1S transcript named CACNA1S-202 isOne of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and use the information and link-outs from the page to answer the following questions ANSWER ONLY IN UPPERCASE LETTERS, NO UNITS: Using the left-hand menu to view the sequence for CACNA1S, what are the last three nucleic acid bases of exon 1?
- One of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and use the information and link-outs from the page to answer the following question. What is the NCBI accession number (including the version) of the RefSeq Match for the first transcript (CACNA1S-201)?What is the underlying genetic defect that causes xeroderma pigmentosum?How can the symptoms of this disease be explained by the genetic defect?What is the simplest explanation for why patients have been identified with only one copy of the phosphofructokinase-1 gene (heterozygous), but no patients have been identified that lack both copies of the phosphofructokinase-1 gene (homozygous)? Patients lacking both copies of the phosphofructokinase-1 genes will be found once DNA sequencing technology can sequence whole genomes. Phosphofructokinase-1 is needed for nitrogen metabolism and there are no enzymes to replace this function, so cells die from ammonia toxicity. Phosphofructokinase-1 is a required enzyme for carbohydrate metabolism in all living cells, complete loss of this enzyme would be lethal. There are 6 phosphofructokinase-1 paralogous genes in humans and it is impossible to lack both type 1 copies when there are also types 4, 5, and 6.
- Leber Congenital Amaurosis (LCA) causes progressive vision loss due to defects in the gene that encodes RPE65 isomerase. Affected individuals are homozygous recessive for mutant alleles of the RPE65 gene. You are trying to determine the molecular nature of the mutations in three individuals with LCA. For ease of analysis, you may assume that each individual is homozygous for the same mutant allele (though the three individuals have different mutations than each other). You use the polymerase chain reaction to amplify DNA from each patient and you determine the sequence of the DNA and compare it to unaffected individuals. You identify the following differences. Note that the non-template strand of DNA is given and the changes are highlighted using red boldface. You can assume that the sequences are in the first reading frame (eg. the first three nucleotides of each sequence is a codon). The coding region of the gene is 1602 bp and the position of the sequences shown below is…Describe how polymorphisms is found at 13910-C/T and 22018-G/A in the regulatory area of the lactase gene (LCT). And elaborate the mechanism for two polymorphisms causing mutation from 13910-C/T and 22018-G/A to 13910-C/C or 22018-G/G variants in lactase intolerance disorder. also, how LCT gene is corelated to lactase intolerance disorder?What are the possible genotypes of the PTC locus?
- Gene A, which encodes alcohol dehydrogenase, is labeled with a red fluorophore in a FISH experiment with one chromosome of a homologous pair, with results shown below. Gene B is labeled in green and encodes Notch2NL, a gene which may help to explain brain size differences between humans and chimpanzees, and which with increased dosage, may lead to a condition referred to as macrocephaly (enlarged head circumference sometimes associated with learning disabilities). What can you infer about these two genes given the results seen below?How does the HAEIII enzyme discriminate between the C-G polymorphism in the TAS2R38 gene?Like Hurler syndrome, Fabry disease involves an abnormal accumulationof substances within lysosomes. However, the lysosomesof individuals with Fabry disease show an abnormal accumulationof lipids. The defective enzyme is α-galactosidase A, which is alysosomal enzyme that functions in lipid metabolism. The enzymaticdefect causes cell damage, especially to the kidneys, heart,and eyes. The gene that encodes α-galactosidase A is found on theX chromosome. Let’s suppose a phenotypically unaffected coupleproduces two sons with Fabry disease and one phenotypicallyunaffected daughter. What is the probability that the daughter willhave an affected son?
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