Anti-17 beta-Estradiol monoclonal antibody (DMABT-49063MH)

Mouse anti-Human 17 beta-Estradiol monoclonal antibody for ELISA

Specifications


Host Species
Mouse
Antibody Isotype
IgG1
Clone
5T53
Species Reactivity
Human, Broad
Immunogen
17-beta-estradiol conjugated to Bovine Serum Albumin at position 6.
Conjugate
Unconjugated

Applications


Application Notes
ELISA: 1/50 - 1/500
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
17?-Estradiol; E2; ethynyl Estradiol; Oestradiol; Estradiol

Citations


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References


Ameliorative Effects of Quercetin and Metformin and Their Combination Against Experimental Endometriosis in Rats

REPRODUCTIVE SCIENCES

Authors: Jamali, Navid; Zal, Fatemeh; Mostafavi-Pour, Zohreh; Samare-Najaf, Mohammad; Poordast, Tahereh; Dehghanian, Amirreza

Endometriosis, as the leading cause of infertility, is attributed to oxidative stress, inflammation, and autophagy dysregulation. This study was conducted to evaluate the effect of quercetin and metformin, alone or in combination, on the ectopic and eutopic endometrial tissues in a rat model of endometriosis. We divided 60 female rats into 6 groups, including SH, Endo, Endo + Oil, Endo + Q, Endo + M, and Endo + Q + M. The last five groups underwent a surgery, so that we could induce endometriosis, and after 4 weeks, daily treatment began, lasting for a month. Subsequently, the size and histoarchitecture of the endometrial implants, serum levels of 17 beta-estradiol, progesterone and tumor necrosis factor (TNF)-alpha, and markers of oxidative stress and autophagy were assessed utilizing ELISA and gene expression analysis. Our results shed light to the fact that serum TNF-alpha and 17 beta-estradiol levels significantly increased in endometriosis rats. Moreover, NADPH: quinone oxidoreductase (NQO1) enzyme activity and gene expression levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and autophagy markers significantly decreased; meanwhile, mammalian target of rapamycin (mTOR) gene expression increased in the ectopic endometrial tissues, as compared with eutopic ones. Surprisingly, our results demonstrated that the treatment in which we applied the combination of quercetin and metformin significantly reversed these changes and had a pronounced effect on the endometrial implant size and gene expression levels of mTOR and autophagy markers in ectopic endometrium. The findings of the present study suggest that quercetin, metformin, and their combination were of potential therapeutic effects on the rat model of endometriosis.

Reciprocality Between Estrogen Biology and Calcium Signaling in the Cardiovascular System

FRONTIERS IN ENDOCRINOLOGY

Authors: Tran, Quang-Kim

17 beta-Estradiol (E-2) is the main estrogenic hormone in the body and exerts many cardiovascular protective effects. Via three receptors known to date, including estrogen receptors alpha (ER alpha) and beta (ER beta) and the G protein-coupled estrogen receptor 1 (GPER, aka GPR30), E(2)regulates numerous calcium-dependent activities in cardiovascular tissues. Nevertheless, effects of E(2)and its receptors on components of the calcium signaling machinery (CSM), the underlying mechanisms, and the linked functional impact are only beginning to be elucidated. A picture is emerging of the reciprocality between estrogen biology and Ca(2+)signaling. Therein, E(2)and GPER, via both E-2-dependent and E-2-independent actions, moderate Ca2+-dependent activities; in turn, ER alpha and GPER are regulated by Ca(2+)at the receptor level and downstream signaling via a feedforward loop. This article reviews current understanding of the effects of E(2)and its receptors on the cardiovascular CSM andvice versawith a focus on mechanisms and combined functional impact. An overview of the main CSM components in cardiovascular tissues will be first provided, followed by a brief review of estrogen receptors and their Ca2+-dependent regulation. The effects of estrogenic agonists to stimulate acute Ca(2+)signals will then be reviewed. Subsequently, E-2-dependent and E-2-independent effects of GPER on components of the Ca(2+)signals triggered by other stimuli will be discussed. Finally, a case study will illustrate how the many mechanisms are coordinated to moderate Ca2+-dependent activities in the cardiovascular system.

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