產(chǎn)品編號(hào) | bs-3618R |
英文名稱 | Rabbit Anti-HSD11B2 antibody |
中文名稱 | 羥基類固醇脫氫酶11β2抗體 |
別 名 | Corticosteroid 11 beta dehydrogenase isozyme 2; 11 beta HSD2; 11 beta hydroxysteroid dehydrogenase type 2; 11 DH2; AME; AME1; HSD11K; HSD2; Hydroxysteroid 11 beta dehydrogenase 2; Hydroxysteroid 11 beta dehydrogenase isoenzyme 2; NAD dependent 11 beta hydroxysteroid dehydrogenase; SDR9C3; Short chain dehydrogenase/reductase family 9C, member 3. |
Specific References (5) | bs-3618R has been referenced in 5 publications.
[IF=6.291] Xue-Ting Shi. et al. Gestational cadmium exposure impairs placental angiogenesis via activating GC/GR signaling. Ecotox Environ Safe. 2021 Nov;224:112632 IHC ; Human.
[IF=4.225] Haojing Liuet al. Glucocorticoid Exposure Induces Preeclampsia via DampeningLipoxin A4, an Endogenous Anti-Inflammatory and Proresolving Mediator. Front Pharmacol
. 2020 Jul 28;11:1131. WB ; rat.
[IF=3.636] Nakanishi Tomoya. et al. Cortisol induces follicle regression, while FSH prevents cortisol-induced follicle regression in pigs. Mol Hum Reprod. 2021 May;: WB,IF ; Pig.
[IF=2.7] Ding, Ying-xue, et al. "Regulation of glucocorticoid-related genes and receptors/regulatory enzyme expression in intrauterine growth restriction filial rats." Life Sciences (2016). WB ; Rat.
[IF=2.589] Wang et al. Preeclampsia induced by cadmium in rats is related to abnormal local glucocorticoid synthesis in placenta. (2014) Reprod.Biol.Endocrino. 12:77 IHC-P ; Rat.
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研究領(lǐng)域 | 腫瘤 免疫學(xué) 信號(hào)轉(zhuǎn)導(dǎo) 細(xì)胞凋亡 轉(zhuǎn)錄調(diào)節(jié)因子 激酶和磷酸酶 |
抗體來(lái)源 | Rabbit |
克隆類型 | Polyclonal |
交叉反應(yīng) | Human,Mouse,Rat,Horse (predicted: Dog) |
產(chǎn)品應(yīng)用 | WB=1:200-1000,ICC/IF=1:100
not yet tested in other applications. optimal dilutions/concentrations should be determined by the end user. |
理論分子量 | 45kDa |
細(xì)胞定位 | 細(xì)胞漿 |
性 狀 | Liquid |
濃 度 | 1mg/ml |
免 疫 原 | Recombinant human HSD11B2 protein |
亞 型 | IgG |
純化方法 | affinity purified by Protein A |
緩 沖 液 | 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol. |
保存條件 | Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles. |
注意事項(xiàng) | This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications. |
PubMed | PubMed |
產(chǎn)品介紹 |
There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. The type I isozyme has both 11-beta-dehydrogenase (cortisol to cortisone) and 11-oxoreductase (cortisone to cortisol) activities. The type II isozyme, encoded by this gene, has only 11-beta-dehydrogenase activity. In aldosterone-selective epithelial tissues such as the kidney, the type II isozyme catalyzes the glucocorticoid cortisol to the inactive metabolite cortisone, thus preventing illicit activation of the mineralocorticoid receptor. In tissues that do not express the mineralocorticoid receptor, such as the placenta and testis, it protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development. Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension. [provided by RefSeq, Feb 2010] Function: Catalyzes the conversion of cortisol to the inactive metabolite cortisone. Modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids. Subunit: Interacts with ligand-free cytoplasmic NR3C2. Subcellular Location: Microsome. Endoplasmic reticulum. Tissue Specificity: Found in placenta, kidney, pancreas, prostate, ovary, small intestine and colon. Similarity: Belongs to the short-chain dehydrogenases/reductases (SDR) family. SWISS: P80365 Gene ID: 3291 Database links: Entrez Gene: 3291 Human Entrez Gene: 15484 Mouse Omim: 218030 Human SwissProt: P80365 Human SwissProt: P51661 Mouse SwissProt: P51976 Rabbit SwissProt: P50168 Sheep Unigene: 1376 Human Unigene: 5079 Mouse Unigene: 10186 Rat [DISEASE] Defects in HSD11B2 are the cause of apparent mineralocorticoid excess (AME) [MIM:218030]. An autosomal recessive form of low-renin hypertension. It is usually diagnosed within the first years of life and is characterized by polyuria and polydipsia, failure to thrive, hypernatremia, severe hypertension with low renin and aldosterone levels, profound hypokalemia with metabolic alkalosis, and most often nephrocalcinosis. |
產(chǎn)品圖片 |
Sample:
Kidney (Mouse) Lysate at 40 ug
Primary: Anti-HSD11B2 (bs-3618R) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 45 kD
Observed band size: 48 kD
Sample:
Lane 1: Mouse Liver tissue lysates
Lane 2: Rat Stomach tissue lysates
Primary: Anti- HSD11B2 (bs-3618R) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 45 kDa
Observed band size: 45 kDa
Sample:
Lane 1: Mouse Stomach tissue lysates
Lane 2: Rat Stomach tissue lysates
Primary: Anti-HSD11B2 (bs-3618R) at 1/1000 dilution
Secondary: IRDye800CW Goat Anti-Rabbit IgG at 1/20000 dilution
Predicted band size: 45 kDa
Observed band size: 45 kDa
A431 cell; 4% Paraformaldehyde-fixed; Triton X-100 at room temperature for 20 min; Blocking buffer (normal goat serum, C-0005) at 37°C for 20 min; Antibody incubation with (HSD11B2) polyclonal Antibody, Unconjugated (bs-3618R) 1:100, 90 minutes at 37°C; followed by a conjugated Goat Anti-Rabbit IgG antibody at 37°C for 90 minutes, DAPI (blue, C02-04002) was used to stain the cell nuclei.
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