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Cat.No.: F2455
| Dilution |
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|
| Application |
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| WB, IHC, IF, FCM |
| Reactivity |
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| Mouse, Rat, Human |
| Source |
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| Rabbit Monoclonal Antibody |
| Storage Buffer |
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| PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3 |
| Storage (from the date of receipt) |
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| -20°C (avoid freeze-thaw cycles), 2 years |
| Predicted MW Observed MW |
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| 305 kDa 294-300 kDa |
| *Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. |
| Positive Control | Rat thyroid tissue; Human thyroid tissue; Mouse thyroid tissue; ICR thyroid tissue; Human thyroid gland papillary carcinoma tissue; Human thyroid gland follicular carcinoma tissue; Human thyroid carcinoma epithelial cells |
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| Negative Control |
| Specificity |
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| Thyroglobulin Antibody [K18H12] detects endogenous levels of total Thyroglobulin protein. |
| Clone |
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| K18H12 |
| Synonym(s) |
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| Thyroglobulin; Tg; TG |
| Background |
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| Thyroglobulin (Tg) is a large glycoprotein that acts as the precursor for thyroid hormones T3 and T4. It is primarily synthesized and secreted by thyroid follicular cells into the colloid lumen, where it undergoes iodination. Tg is a dimer composed of three main regions: region I contains 10-11 type-1 repeats; region II features three type-2 repeats forming arrowhead-like motifs stabilized by inter-domain disulfide bonds; and region III includes type-3 repeats, all leading up to a C-terminal ChEL domain near the dimer core. Key hormonogenic tyrosines, such as sites B and D, are strategically positioned for iodination, and conserved cysteine motifs like CWCV in type-1 domains help maintain structural integrity. Tg serves as the scaffold for thyroid peroxidase-mediated iodination and the coupling of iodotyrosines to produce T3/T4 precursors. These precursors are endocytosed and proteolyzed in lysosomes, releasing thyroid hormones into circulation. Tg intrinsically regulates thyroid hormone biosynthesis by suppressing the transcription of essential genes, including Tg itself, TPO, NIS (Slc5a5), and DUOX2, through apical interactions. This negative feedback mechanism counteracts TSH stimulation, helping to maintain follicular heterogeneity and optimize hormone output. The cycle of Tg accumulation and resorption is crucial for this regulation. Disruptions, such as Tg mutations leading to ER stress and impaired secretion, are linked to diseases like congenital hypothyroidism. |
| References |
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