1. The main aim of the Human Genome Project was to determine the DNA Sequence of every human gene.
2. Variation in skin colour is an example of polygenic inheritance
This Human Karyotype is unusual because it has an extra chromosome at chromosome 21.
Klinefelters syndrome is shown in the second figure
Explanation:
1. The Human Genome Project's main goal was to sequence all the 30,000 genes and 3 million base pairs in their makeup for the early detection of diseases, gene therapy and molecular level studies.
2. Human skin colour is determined by the pigment melanin. The Dominant allele is responsible for dark colours as it produces more melanin. The melanocortin 1 receptor (MC1R) gene and Tyrosinase enzyme codes for the human skin colour. Polygenic inheritance are the traits which are controlled by one or more genes.
<u>figures:</u>
<u>The extra chro</u>mosome at the 21st chromosome pairs is called trisomy 21 or Down's Syndrome. It is due to the abnormal cell division/meiosis resulting in an extra X chromosome. This leads to thechanges the in physical development of the individual.
Klinefelter's Syndrome: There are 47 chromosomes and 2 or more X chromosomes in this syndrome of males. The resulting male suffering from Klinefelter would be sterile and have poorly developed testicles.
"Waste" -- in the form of urine and feces -- how the body removes the parts of food we ingest that is not used for nutrition and also is a way to rid the body of toxins. The kidneys filter the blood, removing "waste" products such as excess vitamins or drugs (this is why your urine can have a bright color if you take high doses of vitamin c) and liquid waste is held in the bladder before being released. Food travels through the gut to be digested -- broken down into usable bits and waste. After breaking down in the stomach, the material travels through the small and large intestines. The small intestine is lined with villi -- tiny protrusions that add surface area so nutrients can be absorbed into the bloodstream. In the large intestine and colon, water is pulled from the mass so it becomes more solid. Eventually the solidified waste passed through the rectum and out the anus as feces. The build-up of waste in the body can itself be toxic -- if the kidneys do not function properly to clean the waste out, the buildup can be fatal. When the body goes into emergency mode to eliminate a toxic substance -- such as e. Coli in the case of food poisoning -- the intestines don't both absorbing water and the result is the liquid fecal matter being quickly passed through and ejected as diarrhea.
Protein-protein interactions within the CARMA1-BCL10-MALT1 complex:
- The T-cell receptor and B-cell receptor-dependent NF-B induction and lymphocyte activation are mediated by the CBM complex, which is made up of the proteins CARMA1, BCL10, and MALT1.
- Each of the proto-oncoproteins CARMA1, BCL10, and MALT1 is a somatic gain-of-function mutation or chromosomal translocation, and dysregulation of CBM signaling is a characteristic of numerous lymphoid malignancies, including Activated B-cell Diffuse Large B-cell Lymphoma.
- Moreover, a number of immunological dysregulation diseases have been linked to both gain- and loss-of-function germline mutations in CBM complex proteins.
- Over the past ten years, careful examination of the interactions of CBM components has yielded a wealth of detailed structural knowledge.
- Here, we discuss important discoveries about the molecular nature of these protein-protein interactions that have helped the research develop a detailed understanding of how these proteins come together to form high-order filamentous CBM complexes.
- Approaches to therapeutic suppression of the CBM complex have thus far centered on obstructing MALT1 protease activity in order to treat lymphoid malignancy and/or autoimmunity.
- The structural effects of MALT1 protease inhibitors on significant protein-protein interactions are also reviewed in detail.
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