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Mouse Anti-HSD11B2 Recombinant Antibody (CBFYH-1994) (CBMAB-H3005-FY)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
CBFYH-1994
Antibody Isotype
IgG2a
Application
WB, IHC

Basic Information

Immunogen
E. coli-derived recombinant human 11 beta-HSD2, Met105-Arg405
Specificity
Human
Antibody Isotype
IgG2a
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Lyophilized
Buffer
PBS
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.

Target

Full Name
Hydroxysteroid 11-Beta Dehydrogenase 2
Introduction
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.
Entrez Gene ID
3291
UniProt ID
P80365
Alternative Names
Hydroxysteroid 11-Beta Dehydrogenase 2; Short Chain Dehydrogenase/Reductase Family 9C Member 3; NAD-Dependent 11-Beta-Hydroxysteroid Dehydrogenase; 11-Beta-Hydroxysteroid Dehydrogenase Type II; 11-Beta-Hydroxysteroid Dehydrogenase Type 2; 11-Beta-HSD Type II; 11-HSD Type II; 11-Beta-HSD2; 11-DH2; HSD11K; SDR9C3
Function
Catalyzes the conversion of biologically active 11beta-hydroxyglucocorticoids (11beta-hydroxysteroid) such as cortisol, to inactive 11-ketoglucocorticoids (11-oxosteroid) such as cortisone, in the presence of NAD+ (PubMed:7859916, PubMed:8538347, PubMed:10497248, PubMed:22796344, PubMed:27927697, PubMed:30902677, PubMed:33387577, PubMed:12788846, PubMed:17314322).

Functions as a dehydrogenase (oxidase), thereby decreasing the concentration of active glucocorticoids, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids (PubMed:7859916, PubMed:10497248, PubMed:33387577, PubMed:12788846, PubMed:17314322).

Plays an important role in maintaining glucocorticoids balance during preimplantation and protects the fetus from excessive maternal corticosterone exposure (By similarity).

Catalyzes the oxidation of 11beta-hydroxytestosterone (11beta,17beta-dihydroxyandrost-4-ene-3-one) to 11-ketotestosterone (17beta-hydroxyandrost-4-ene-3,11-dione), a major bioactive androgen (PubMed:22796344, PubMed:27927697).

Catalyzes the conversion of 11beta-hydroxyandrostenedione (11beta-hydroxyandrost-4-ene-3,17-dione) to 11-ketoandrostenedione (androst-4-ene-3,11,17-trione), which can be further metabolized to 11-ketotestosterone (PubMed:27927697).

Converts 7-beta-25-dihydroxycholesterol to 7-oxo-25-hydroxycholesterol in vitro (PubMed:30902677).

7-beta-25-dihydroxycholesterol (not 7-oxo-25-hydroxycholesterol) acts as ligand for the G-protein-coupled receptor (GPCR) Epstein-Barr virus-induced gene 2 (EBI2) and may thereby regulate immune cell migration (PubMed:30902677).

May protect ovulating oocytes and fertilizing spermatozoa from the adverse effects of cortisol (By similarity).
Biological Process
Cortisol metabolic process Source: UniProtKB
Female pregnancy Source: Ensembl
Regulation of blood volume by renal aldosterone Source: Ensembl
Response to food Source: Ensembl
Response to glucocorticoid Source: Ensembl
Response to hypoxia Source: Ensembl
Response to insulin Source: Ensembl
Response to xenobiotic stimulus Source: Ensembl
Cellular Location
Microsome; Endoplasmic reticulum
Involvement in disease
Apparent mineralocorticoid excess (AME):
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.
More Infomation

Tavares Pereira, M., Schuler, G., Aslan, S., Payan-Carreira, R., Reichler, I. M., Reynaud, K., & Kowalewski, M. P. (2023). Utero-placental expression and functional implications of HSD11B1 and HSD11B2 in canine pregnancy. Biology of Reproduction, 108(4), 645-658.

Wei, X., Yuan, Y., & Yang, Q. (2022). Long noncoding RNA PVT1 accelerates the growth of placental trophoblasts in preeclampsia through the microRNA‐24‐3p/HSD11B2 axis. Molecular Reproduction and Development, 89(7), 271-280.

Theodoridi, A., Dinarello, A., Badenetti, L., Pavlidis, M., Dalla Valle, L., & Tsalafouta, A. (2021). Knockout of the hsd11b2 gene extends the cortisol stress response in both zebrafish larvae and adults. International Journal of Molecular Sciences, 22(22), 12525.

De Santis, D., Castagna, A., Danese, E., Udali, S., Martinelli, N., Morandini, F., ... & Pizzolo, F. (2021). Detection of urinary exosomal HSD11B2 mRNA expression: A useful novel tool for the diagnostic approach of dysfunctional 11β-HSD2-Related hypertension. Frontiers in Endocrinology, 12, 681974.

Qi, L., Zhang, Y., Song, F., & Ding, Y. (2020). Chinese herbal medicine promote tissue differentiation in colorectal cancer by activating HSD11B2. Archives of biochemistry and biophysics, 695, 108644.

Zheng, H. T., Fu, T., Zhang, H. Y., Yang, Z. S., Zheng, Z. H., & Yang, Z. M. (2020). Progesterone-regulated Hsd11b2 as a barrier to balance mouse uterine corticosterone. Journal of Endocrinology, 244(1), 177-187.

Fan, P., Lu, Y. T., Yang, K. Q., Zhang, D., Liu, X. Y., Tian, T., ... & Zhou, X. L. (2020). Apparent mineralocorticoid excess caused by novel compound heterozygous mutations in HSD11B2 and characterized by early-onset hypertension and hypokalemia. Endocrine, 70, 607-615.

Sai, S., Esteves, C., Kelly, V., Sakaguchi, K., McAndrew, R., Chudleigh, S., ... & Chapman, K. E. (2020). Reciprocal regulation of HSD11B1 and HSD11B2 predicts glucocorticoid sensitivity in childhood acute lymphoblastic leukemia. The Journal of pediatrics, 220, 249-253.

Capron, L. E., Ramchandani, P. G., & Glover, V. (2018). Maternal prenatal stress and placental gene expression of NR3C1 and HSD11B2: The effects of maternal ethnicity. Psychoneuroendocrinology, 87, 166-172.

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For research use only. Not intended for any clinical use.

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