The Use Of Anticancer Drugs ( Cytochrome P450s )?

My gene is located at chromosome 9 on the long (q) arm at position 34, 9q34.

D1S80 locus is placed on the short arm of the chromosome 1. This locus does not code for the arrangement for protein, yet it codes for a series of tandem repeats of 16 bp in human. Distinctive number of this allele has different number of repeats. These quantities of repeats are exceptional to every human. Primer

Part C: Assume that the genes from the previous example are located along the chromosome

The mammalian cytochrome P450 CYP belongs to superfamily and mainly encodes enzymes involved in the metabolism of pharmaceuticals, foreign chemicals and pollutants [1]. Several mutations were observed in CYP genes which are responsible for inborn errors of metabolism leading to multiple diseases. It was observed from previous studies, gene nomenclature was simpler before arrival of complete genome. This is due to the fact that detailed information about gene position on the chromosome did not affect the gene names. Therefore, in the past names were assigned only on the basis of sequence similarity and evolutionary divergence [4, 5]. But now genes occur in clusters, with several related genes, and many pseudogenes. Also, genes in subfamilies are found to be clustered with genes of other subfamilies [6]. Pseudogenes are found to be manily involved

The results of the experiment’s chi-squared data revealed a critical p-value thus rejecting the null hypothesis. The p value was concluded to be a result of genetic linkages on the chromosome causing the traits to be unable

The first possible gene is ras1 or raspberry gene. This gene is located on the X chromosome and at 9E1-9E2 on the cytogenetic map. The location on the recombination map is unknown. The ras1 gene is a possible choice due to the dark red and orange color combination that it expresses. (Nash et al. 1994) Another gene is the Pur1 or the purplish ruby gene. This gene is located at 3-39.5 on the recombination map. The Pur1 gene could be responsible for the mutant’s eye coloration due to the red and brown pigments that are present. (Aparisi and Najera 1990) The pr1 or purple gene is another possible explanation for the mutant’s eye color. This gene is located at 38B3-38B3 on the cytogenetic map. It’s location on the recombination map is 2-54.5. The purple gene has a high probability of being responsible for the mutant’s eye color due to the light reddish color combined with a touch of orange and the similar texture that it possesses. (Kim et al. 1996) Another possible gene is ry1 or rosy. This gene is located on the 3R chromosome. Its location on the recombination map is 3-52.0. The rosy gene can be located at 87D9-87D9 on the cytogenetic map. Rosy gene is another possibility because it possess a red shade with more orange and brown pigments that could compensate for the lighting when viewing the mutant specimen through the stereoscope. (Zhou and Riddiford

The most probable is autosomal dominant inheritance with variable expressivity, contiguous gene duplication at 11p15, and genomic imprinting resulting from a defective or absent copy of the maternally derived gene.

Cytochrome P450 1A1 (CYP1A1) metabolizes various suspected pro carcinogens, particularly polycyclic aromatic hydrocarbons (PAHs), and is a phase I detoxification enzyme which are usually coupled to glutathione or other groups, generating water-soluble compounds, also the difference in activity of these

The liver’s complex biochemical process of detoxification is a two phase process, converting the byproducts of metabolism and toxins to render them into safer substance. Phase one, an enzymatic process, involves approximately 100 enzymes in the cytochrome P450 system. In Phase one, the chemical reaction known as biotransformation changes the toxin in to a less toxic, water-soluble substance to allow it to be safely excreted through the kidneys or colon. Enzymes do this through oxidation, the loss of electrons, or reduction, the gain of elections. Most of the time, the enzymatic reactions in Phase one decrease the toxicity of the substance, however, a more toxic intermediate substance may be produced, this is known as bioactivation.

Peil et al. (2003) studied this phenomenon in detail. For dominant markers, five different polymorphic configurations are possible in a single cross when female and male progeny are considered separately and they found four of them. For 43 AFLP markers, complete co-segregation between the AFLP fragment and male sex was observed. Twenty-three sex-linked AFLP markers showed other segregation patterns. There was also recombination between sex-linked AFLP markers. Peil et al. (2003) found a recombination rate of 25% between sex and the completely linked AFLP marker loci AGA*GAA510 and AGA*AAT330 on X as well as on Y.

Researchers screened over 3,000 genes and selected 19 random genomic regions for their comparisons, which was much more than previously cited studies. The regions that were chosen for comparison were attached to a core SNP in the coding region of a gene. This was further qualified using only fully known genomic sequence up to 160 kb in either direction of the core SNP and having a frequency of at least 35% in all ethnic groups sampled. The choice of high-frequency SNPs was explained by known factors that affect the rate. Mainly, that they tend to be found in all populations, when LD are around rare alleles the are expected to extend further because these alleles are younger and have had less recombination, and when around common alleles they tend to be more closely associated with diseases. The researchers examined 251,310 bp and found a total of 272 high-frequency SNP’s of which they chose the 19 that they examined and analyzed for this

Recently other mutations have been picked up in GISTs. These compromise of SDH, RAS-P and different loci of kit mutation on Exon 9,11,13,14 and 17.

Common changes in the human genome are the rearrangement between repeated sequences during meiosis may result in gametes with different copy numbers of specific regions of the genome in different members of a family. These CNVs can make members of a family unique in that even sibling can have large differences in copy numbers in their genomes. As an example whole genome sequencing of six individual domesticated cows were done and compared find that there was 1265 unique CNVs between them. Within the duplicated region there was 413 complete genes that changed copy number between the individual cows and thus could contribute to the variation in gene function. These CNVs can occur in many areas throughout the genome where repeats exist but are usually found in regions of the genome where duplication occurred as a tandem array. These regions are prone to misalignment during the recombination phase of meiosis resulting in the production of two gametes with one having an extra copy of the duplicated segment while the other has one less. CNVs have also been documented to have an effect on phenotype; with one example being in dogs where the duplication of a block of DNA contains 4 specific genes plays a role in the development of a hair ridge characteristic

The karyotype showed 46, XY, del(18)(q23) and the FISH result is .ish del(18)(q23q23)(VIJrRM2050-), both representing the deletion of the region 23 from the q arm of chromosome 18. The microarray displays an outstanding result: .arr 18q22.3q23(72,363,115-78,012,800)x1 which identifies more precisely in which the abnormal genes lie than the karyotype or FISH.

Biosynthesis of 20-HETE from arachidonic acid by the cytochrome P450 4A (CYP450 4A) isoforms is a key component of vascular homeostasis, especially in renal circulation.