Sandbox Reserved 1779
From Proteopedia
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== Grave's Disease == | == Grave's Disease == | ||
Grave’s disease is an autoimmune disease that is a result of hyperthyroidism. Hyperthyroidism indicates that the body is producing too much Thyroid Stimulating Hormone (TSH). The binding of TSH to TSHR results in the receptor remaining in its active conformation. This is important as the thyroid gland controls metabolism in the body and overstimulation can lead to many side effects. This is including but not limited to: eye and skin problems, weight loss, fatigue, muscle weakness, trouble tolerating heat/ profuse sweating, enlarged thyroid glands (goiter). This disease effects 1 in 100 Americans and especially women or people older than 30 years of age. [https://www.niddk.nih.gov/health-information/endocrine-diseases/graves-disease Grave's Disease] | Grave’s disease is an autoimmune disease that is a result of hyperthyroidism. Hyperthyroidism indicates that the body is producing too much Thyroid Stimulating Hormone (TSH). The binding of TSH to TSHR results in the receptor remaining in its active conformation. This is important as the thyroid gland controls metabolism in the body and overstimulation can lead to many side effects. This is including but not limited to: eye and skin problems, weight loss, fatigue, muscle weakness, trouble tolerating heat/ profuse sweating, enlarged thyroid glands (goiter). This disease effects 1 in 100 Americans and especially women or people older than 30 years of age. [https://www.niddk.nih.gov/health-information/endocrine-diseases/graves-disease Grave's Disease] | ||
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== Hypothyroidism == | == Hypothyroidism == | ||
Hypothyroidism is the converse of Grave’s Disease as there is not enough TSH produced in the body with this disease. The most common cause of Hypothyroidism is Hashimoto’s disease. Without enough TSH to bind TSHR, the pathway remains inactive and thus metabolic processes are inhibited in this pathway. This results in many symptoms including, but not limited to fatigue, cold sensitivity, weight gain, irregular/heavy menstrual cycle, thinning of hair, and depression. This disease effects women and those older than the age of 60. This disease can also occur in infancy. [https://www.mayoclinic.org/diseases-conditions/hypothyroidism/symptoms-causes/syc-20350284#:~:text=Hypothyroidism%20happens%20when%20the%20thyroid,symptoms%20in%20its%20early%20stages Hypothyroidism] | Hypothyroidism is the converse of Grave’s Disease as there is not enough TSH produced in the body with this disease. The most common cause of Hypothyroidism is Hashimoto’s disease. Without enough TSH to bind TSHR, the pathway remains inactive and thus metabolic processes are inhibited in this pathway. This results in many symptoms including, but not limited to fatigue, cold sensitivity, weight gain, irregular/heavy menstrual cycle, thinning of hair, and depression. This disease effects women and those older than the age of 60. This disease can also occur in infancy. [https://www.mayoclinic.org/diseases-conditions/hypothyroidism/symptoms-causes/syc-20350284#:~:text=Hypothyroidism%20happens%20when%20the%20thyroid,symptoms%20in%20its%20early%20stages Hypothyroidism] | ||
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== Leucine Rich Region == | == Leucine Rich Region == | ||
The Leucine Rich region is part of the <scene name='95/952708/Tshr_chainr_ecd/1'>extracellular domain (ECD)</scene> of TSHR. The highlighted region contains 10-11 Leucine repeats within the structure. The specific residues from TSHR interacting with TSH are <scene name='95/952707/Lrr/2'>Lys209 and Lys 58</scene>. These interact with Asp111 and Glu118 in the seatbelt region of TSH forming a salt bridge and initiating the conformational change in the receptor<ref name="Duan et al.">PMID: 35940204</ref>. This interaction is specific to TSH and TSHR. When other agonists or antagonists bind to the receptor, the interaction is a result of different residues interacting. The Leucine residues likely play a role in how the ECD folds and which residues are located on the exterior protein. As Leucine is hydrophobic, it would be forced into the interior of the protein during folding exposing other residues that are more hydrophobic to the surface. | The Leucine Rich region is part of the <scene name='95/952708/Tshr_chainr_ecd/1'>extracellular domain (ECD)</scene> of TSHR. The highlighted region contains 10-11 Leucine repeats within the structure. The specific residues from TSHR interacting with TSH are <scene name='95/952707/Lrr/2'>Lys209 and Lys 58</scene>. These interact with Asp111 and Glu118 in the seatbelt region of TSH forming a salt bridge and initiating the conformational change in the receptor<ref name="Duan et al.">PMID: 35940204</ref>. This interaction is specific to TSH and TSHR. When other agonists or antagonists bind to the receptor, the interaction is a result of different residues interacting. The Leucine residues likely play a role in how the ECD folds and which residues are located on the exterior protein. As Leucine is hydrophobic, it would be forced into the interior of the protein during folding exposing other residues that are more hydrophobic to the surface. | ||
| - | == Thyroid Stimulating Hormone Antibody == | ||
| - | This is a sample scene created with SAT to <scene name="/12/3456/Sample/1">color</scene> by Group, and another to make <scene name="/12/3456/Sample/2">a transparent representation</scene> of the protein. You can make your own scenes on SAT starting from scratch or loading and editing one of these sample scenes. | ||
| - | === Wow === | ||
</StructureSection> | </StructureSection> | ||
== References == | == References == | ||
<references/> | <references/> | ||
Revision as of 19:20, 27 March 2023
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| This Sandbox is Reserved from February 27 through August 31, 2023 for use in the course CH462 Biochemistry II taught by R. Jeremy Johnson at the Butler University, Indianapolis, USA. This reservation includes Sandbox Reserved 1765 through Sandbox Reserved 1795. |
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References
- ↑ Duan J, Xu P, Luan X, Ji Y, He X, Song N, Yuan Q, Jin Y, Cheng X, Jiang H, Zheng J, Zhang S, Jiang Y, Xu HE. Hormone- and antibody-mediated activation of the thyrotropin receptor. Nature. 2022 Aug 8. pii: 10.1038/s41586-022-05173-3. doi:, 10.1038/s41586-022-05173-3. PMID:35940204 doi:http://dx.doi.org/10.1038/s41586-022-05173-3
