Sandbox Reserved 1779: Difference between revisions

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=== 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 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 TSH. The binding of <scene name='95/952708/Tsh_7t9i/1'>TSH</scene> to <scene name='95/952709/Initial_scene_with_edited_7utz/2'>TSHR</scene> 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]

=== Hypothyroidism ===

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===TSH Agonist===

[[Image:NAG.png|200 px|left|thumb|Figure 4]]

Thyroid-stimulating hormone <scene name='95/952708/Tsh_7t9i/1'>(TSH)</scene>, as previously mentioned, is a hormone that stimulates the thyroid gland to produce proteins that are vital for many metabolic pathways in the body's tissue. TSH activates the TSHR protein by binding to the concave surface of the LRRD and hinge region to keep TSHR in its active state by clashing with the membrane <ref name="Duan"> DOI:10.1038/s41586-022-05173-3</ref>. (Figure 3). This clash is caused by glycosylations of an N52 residue on the alpha subunit of TSH ~~(GREEN LINK)~~. These modifications to the N residue are N-acetyl glucosamine modifications (Figure 4). They stick out from the alpha subunit of TSH to clash with the cell membrane and keep TSH in the active state.

Thyroid-stimulating hormone <scene name='95/952708/Tsh_7t9i/1'>(TSH)</scene>, as previously mentioned, is a hormone that stimulates the thyroid gland to produce proteins that are vital for many metabolic pathways in the body's tissue. TSH activates the TSHR protein by binding to the concave surface of the LRRD and hinge region to keep TSHR in its active state by clashing with the membrane <ref name="Duan"> DOI:10.1038/s41586-022-05173-3</ref>. (Figure 3). This clash is caused by glycosylations of an N52 residue on the <scene name='95/952707/Tsh_7t9i/1'>alpha subunit of TSH</scene>. These modifications to the N residue are N-acetyl glucosamine modifications (Figure 4). They stick out from the alpha subunit of TSH to clash with the cell membrane and keep TSH in the active state.

Sandbox Reserved 1779: Difference between revisions

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@@ Line 7: / Line 7: @@
 === 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 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 TSH. The binding of <scene name='95/952708/Tsh_7t9i/1'>TSH</scene> to <scene name='95/952709/Initial_scene_with_edited_7utz/2'>TSHR</scene> 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]
 === Hypothyroidism ===
@@ Line 40: / Line 40: @@
 ===TSH Agonist===
 [[Image:NAG.png|200 px|left|thumb|Figure 4]]
-Thyroid-stimulating hormone <scene name='95/952708/Tsh_7t9i/1'>(TSH)</scene>, as previously mentioned, is a hormone that stimulates the thyroid gland to produce proteins that are vital for many metabolic pathways in the body's tissue. TSH activates the TSHR protein by binding to the concave surface of the LRRD and hinge region to keep TSHR in its active state by clashing with the membrane <ref name="Duan"> DOI:10.1038/s41586-022-05173-3</ref>. (Figure 3). This clash is caused by glycosylations of an N52 residue on the alpha subunit of TSH (GREEN LINK). These modifications to the N residue are N-acetyl glucosamine modifications (Figure 4). They stick out from the alpha subunit of TSH to clash with the cell membrane and keep TSH in the active state.
+Thyroid-stimulating hormone <scene name='95/952708/Tsh_7t9i/1'>(TSH)</scene>, as previously mentioned, is a hormone that stimulates the thyroid gland to produce proteins that are vital for many metabolic pathways in the body's tissue. TSH activates the TSHR protein by binding to the concave surface of the LRRD and hinge region to keep TSHR in its active state by clashing with the membrane <ref name="Duan"> DOI:10.1038/s41586-022-05173-3</ref>. (Figure 3). This clash is caused by glycosylations of an N52 residue on the <scene name='95/952707/Tsh_7t9i/1'>alpha subunit of TSH</scene>. These modifications to the N residue are N-acetyl glucosamine modifications (Figure 4). They stick out from the alpha subunit of TSH to clash with the cell membrane and keep TSH in the active state.