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Allan-Herndon-Dudley Syndrome

1501 Words7 Pages

Thyroid hormone is an essential hormone which requires plasma membrane transport protein to travel into the cells to help the brain function properly throughout the life. Thyroid hormone deficiency leads to hyporeflexia, lethargy, brain damage and etc. depending on onset and duration of time period. Thyroid hormones perform various different roles in life from age to age as people grow from infant to elderly. The mice were mostly used to understand the aspect of thyroid physiology and the thyroid hormone due to similar posture to human brain. Knock out (KO) and knock in (KI) conditioned mice were used since 1990s however, hypothyroid and hyperthyroid mice were used prior to KO and KI. Thyroid hormone’s active form was found to be T3 binding to the nuclear receptor. Monocarboxylate transporter 8 (MCT8) was stated to be the particular transporter for T3. MCT8 is located in pituitary gland, thyroid gland, liver, brain and kidneys. Allan-Herndon-Dudley Syndrome (AHDS) is result of mutation in MCT8. This experiment was performed on two different types …show more content…

The visual detection of antibodies has been used by fluorescent dye, enzyme etc. however, in this experiment the detection tool was DAB. Lastly, the reaction of antibody-antigen was seen by light microscope and images were captured (shown in results section). The primary antibody for this experiment was monocarboxylate transporter 8 polyclonal, chose according to their characteristics. Since, advantages and disadvantages occur when choosing a monoclonal or polyclonal primary antibody. Polyclonal antibody was used due to its characteristic. It is derived from various B-cell lineages within the body, compare to monoclonal antibody which is derived from a single cell lineage. These antibodies have been obtained from the immunoglobulin molecules which react with specific

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