Key Specifications Table
|Species Reactivity||Key Applications||Host||Format||Antibody Type|
|Ca, H, R, Sh, Fe||IH(P)||Rb||Serum||Polyclonal Antibody|
|Description||Anti-Thyroid Stimulating Hormone Antibody|
|Presentation||Liquid rabbit antiserum containing 0.1% sodium azide.|
|Safety Information according to GHS|
|Storage and Shipping Information|
|Storage Conditions||Lyophilized: 20°C for up to 18 months. Reconstituted: -20° C for up to 12 months. Do not thaw and refreeze reconstituted material.|
|Material Size||500 µL|
Anti-Thyroid Stimulating Hormone Antibody SDS
|Reference overview||Application||Pub Med ID|
|Insm1 controls development of pituitary endocrine cells and requires a SNAG domain for function and for recruitment of histone-modifying factors.|
Welcker, JE; Hernandez-Miranda, LR; Paul, FE; Jia, S; Ivanov, A; Selbach, M; Birchmeier, C
Development (Cambridge, England) 140 4947-58 2013
The Insm1 gene encodes a zinc finger factor expressed in many endocrine organs. We show here that Insm1 is required for differentiation of all endocrine cells in the pituitary. Thus, in Insm1 mutant mice, hormones characteristic of the different pituitary cell types (thyroid-stimulating hormone, follicle-stimulating hormone, melanocyte-stimulating hormone, adrenocorticotrope hormone, growth hormone and prolactin) are absent or produced at markedly reduced levels. This differentiation deficit is accompanied by upregulated expression of components of the Notch signaling pathway, and by prolonged expression of progenitor markers, such as Sox2. Furthermore, skeletal muscle-specific genes are ectopically expressed in endocrine cells, indicating that Insm1 participates in the repression of an inappropriate gene expression program. Because Insm1 is also essential for differentiation of endocrine cells in the pancreas, intestine and adrenal gland, it is emerging as a transcription factor that acts in a pan-endocrine manner. The Insm1 factor contains a SNAG domain at its N-terminus, and we show here that the SNAG domain recruits histone-modifying factors (Kdm1a, Hdac1/2 and Rcor1-3) and other proteins implicated in transcriptional regulation (Hmg20a/b and Gse1). Deletion of sequences encoding the SNAG domain in mice disrupted differentiation of pituitary endocrine cells, and resulted in an upregulated expression of components of the Notch signaling pathway and ectopic expression of skeletal muscle-specific genes. Our work demonstrates that Insm1 acts in the epigenetic and transcriptional network that controls differentiation of endocrine cells in the anterior pituitary gland, and that it requires the SNAG domain to exert this function in vivo.
|Expression of P2Y receptors in the rat anterior pituitary.|
Yu, Q; Guo, W; Song, X; Liu, X; Xiang, Z; He, C; Burnstock, G
Purinergic signalling 7 207-19 2011
In this study, the distribution patterns of P2Y(1), P2Y(2) P2Y(4), P2Y(6), P2Y(12), and P2Y(13) receptors in the anterior pituitary cells of rat were studied with double-labeling immunofluorescence and Western blot. The results showed that P2Y receptors were widely expressed in the anterior pituitary. P2Y(1) and P2Y(4) receptors were found to be expressed in the majority of gonadotrophs and thyrotrophs, P2Y(2) receptors were expressed in a small subpopulation of lactotrophs and almost all the folliculo-stellate cells, that were also stained with S100 protein immunoreactivity. P2Y(6) receptors were expressed in macrophages. P2Y(13) receptors were expressed in a small subpopulation of cells in the rat anterior pituitary, the identity of which needs to be clarified. P2Y(1) and P2Y(4) receptors are co-expressed in some gonadotrophs and thyrotrophs. Corticotrophs and somatotrophs were found not to express P2Y receptors in this study. FSH and TSH were shown to coexist in the same endocrine cells in rat anterior pituitary. The present data suggests that purines and/or pyrimidines could be involved in regulating the functions of gonadotrophs and thyrotrophs via P2Y(1) and P2Y(4) receptors, some lactotrophs via P2Y(2) receptors, and folliculo-stellate cells via P2Y(2) receptors in the rat anterior pituitary.Full Text Article
|Rat thyroid hyperplasia induced by gestational and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin.|
N Nishimura, J Yonemoto, Y Miyabara, M Sato, C Tohyama, N Nishimura, J Yonemoto, Y Miyabara, M Sato, C Tohyama
Endocrinology 144 2075-83 2003
Effects of gestational and lactational exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on thyroid function of offspring were investigated in the rat. Pregnant Holtzman rats, TCDD-sensitive strain, were given a single oral dose of 200 ng or 800 ng TCDD/kg on gestational day 15. Parameters related to the thyroid functions were examined on postnatal days (PNDs) 21 and 49. Serum T(4) levels in offspring decreased significantly on PND21 in the two TCDD-exposed groups but increased on PND 49 only in the high-dose group. A dose of 800 ng TCDD/kg exerted a more than 2-fold increase in serum TSH level in male offspring on PNDs 21 and 49. A significant induction of uridine diphosphate-glucuronosyltransferase-1 gene by TCDD was observed on PND 21 but returned to basal levels on PND 49. Gene expression of cytochrome P4501A1 was markedly induced in the liver treated with TCDD. Even a single oral perinatal exposure to 800 ng TCDD/kg resulted in hyperplasia of the thyroid gland of offspring on PND 49. Proliferating cell nuclear antigen immunocytochemistry also supported this finding. Thus, gestational and lactational exposure to TCDD was found to disrupt thyroid hormone homeostasis, which results in a sustained excessive secretion of TSH, followed by the hyperplasia of thyroid follicular cells.
|Immunohistochemical localization of thyroid stimulating hormone induced by a low oral dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin in female Sprague-Dawley rats.|
Noriko Nishimura, Yuichi Miyabara, Mikio Sato, Junzo Yonemoto, Chiharu Tohyama
Toxicology 171 73-82 2002
We have investigated how a low dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) affects thyroid hormone regulation, especially in relation to the localization of thyroid stimulating hormone (TSH) in the pituitary and that of thyroxin (T4) of the thyroid in the rat. Female Sprague-Dawley rats were given a single oral administration of TCDD ranging from 1.0 to 4.0 microg/kg body weight (bw), and then tissue specimens were removed on day 7 post-administration. Thyroid hormone concentrations were measured in serum, and the expression of the TCDD-responsive genes, UDP-glucuronosyltransferase-1 (UGT1) and cytochrome P4501A1 (CYP1A1) were examined in the liver. TCDD administration resulted in an increase in both immunostaining intensity and the number of TSH-positive cells in the anterior pituitary. T4 was found to localize only in the follicular lumen of the thyroid in vehicle-treated control rats, while TCDD administration caused a foamy change in the colloid of some follicles, an indication of accelerating the biosynthesis of T4 in the thyroid. By morphometrical analysis, the ratio of parenchymal/lumenal area of the thyroid was found to increase in response to TCDD. TCDD treatment as low as 2.0 microg TCDD/kg bw induced a significant decrease in both serum total T4 (TT4) and free T4 (FT4) concentrations in the rats, with a significant increase in serum TSH levels in the 4.0 microg TCDD/kg bw rats. Serum total triiodothyronine (TT3) level was unchanged in all groups. The UGT1 gene was significantly induced at a TCDD dose as low as 1.0 microg/kg bw in a dose-dependent manner. TCDD concentrations in the serum, liver and adipose tissues were detected in a dose-related fashion. The present immunohistochemical results clearly support the earlier biochemical findings on the perturbation of the thyroid-pituitary axis by TCDD and suggest that UGT1 is an immediate target of a low TCDD exposure that triggers the perturbation.
|Immunohistochemical study of the postnatal development of pituitary thyrotrophs in the rat, with special reference to cluster formation.|
Yashiro, T, et al.
Cell Tissue Res., 216: 39-46 (1981) 1981
The postnatal development of rat pituitary thyrotrophs was investigated immunohistochemically on days 1, 3, 5, 10, 15 and 25. Fetal thyrotrophs are strongly immunoreactive. In the postnatal period, however, weakly immunoreactive thyrotrophs increase in number to constitute clusters on days 3--5. The numbers and dimensions of the clusters reach a maximum on day 10. Thereafter the clusters break down to give rise to single, scattered neogenic thyrotrophs. Thyrotrophs in clusters on day 10 were investigated by electron microscopy in adjacent sections. They can be characterized as an immature type of basophil, according to the classification of Yoshimura et al. (1977): 1) Type I basophils, which are irregularly shaped with elongate processes, and characterized by rows of secretory granules about 100 nm in diameter. 2) Type I/II basophils, i.e., forms intermediate between Types I and II, containing less numerous secretory granules about 100--150 nm in diameter. Type II basophils which correspond to the classical thyrotrophs are not fully developed on day 10. Thus, most thyrotrophs develop from the clusters in the neonatal period. Such neogenic thyrotrophs retain the immature characteristics of Type I and I/II cells and may develop into Type II cells during subsequent maturation.
|Localization of thyrotropin (TSH) in the dog pituitary gland.|
el-Etreby, M F and el-Bab, M R
Cell Tissue Res., 186: 399-412 (1978) 1978
Using the immunoperoxidase technique and antisera to the specific beta (beta) subunits of bovine and rat TSH, selective immunocytochemical staining was localized in a specific cell population in the pars distalis of the dog pituitary gland. These TSH cells were found to be positive to aldehyde fuchsin, alcian blue, periodic acid-Schiff (PAS) and aniline blue. With the performic acid-alcian blue (pH 0.2) -PAS-orange G procedure these cells stained blue-purple, demonstrating FSH/LH cells (blue or turquoise), ACTH/MSH cells (red-purple) and PRL cells (orange-red). The TSH cells were further differentiated from other functional cell types of the pars distalis on the basis of their typical cytological features, intraglandular distribution and by immunocytochemical double staining. In the pars distalis of adult male dogs the TSH cells were mostly shown to be smaller in size and less numerous than in bitches in the anestrous phase of the sexual cycle. Moreover, cytological alterations in the immunoreactive thyrotrophs in the pituitary of male and female dogs generally paralleled the spontaneous changes in thyroid function associated with thyroid atrophy and/or pituitary insufficiency, and thyroid hyperplasia or goiter. In conclusion, because of their specificity and high potency, the antisera to the beta-subunits of bovine and rat TSH represent an effective tool for the selective immunocytochemical localization of TSH in the dog pituitary. This allows the study of the morphology and function of TSH cells under different physiological, pathological and experimental conditions.