Estradiol [HRP] (DAGA-025B-HRP)

Estradiol HRP Conjugated, Synthetic antigen for ELISA

Nature
Synthetic
Tag/Conjugate
HRP
Alternative Names
Estradiol
Application Notes
Matched pair antibody available for 17a-Estradiol(3) [HRP]: Estradiol antibody (Catalog # HMABPY028)
Procedure
None
Format
Liquid
Concentration
Batch dependent - please inquire should you have specific requirements.
Size
1mg
Buffer
0.01M pH7.4 PBS
Preservative
None
Storage
Shipped at 4°C. Upon delivery aliquot and store at -20°C. Avoid freeze / thaw cycles.
Keywords
Estradiol

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Estradiol [AP] (DAG2986)
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References


NDV-D90 inhibits 17 beta-estradiol-mediated resistance to apoptosis by differentially modulating classic and nonclassic estrogen receptors in breast cancer cells

JOURNAL OF CELLULAR BIOCHEMISTRY

Authors: Shan, Peng; Tang, Bo; Xie, Shanshan; Zhang, Zengling; Fan, Jiehou; Wei, Zheng; Song, Chun

Newcastle disease virus (NDV) is endowed with the oncolytic ability to kill tumor cells, while rarely causing side effects in normal cells. Both estrogen receptor alpha (ER alpha) and the G protein estrogen receptor (GPER) modulate multiple biological activities in response to estrogen, including apoptosis in breast cancer (BC) cells. Here, we investigated whether NDV-D90, a novel strain isolated from natural sources in China, promoted apoptosis by modulating the expression of ER alpha or the GPER in BC cells exposed to 17 beta-estradiol (E2). We found that NDV-D90 significantly killed the tumor cell lines MCF-7 and BT549 in a time- and dose-dependent manner. We also found that NDV-D90 exerted its effects on the two cell lines mainly by inducing apoptosis but not necrosis. NDV-D90 induced apoptosis via the intrinsic and extrinsic signaling pathways in MCF-7 cells (ER-positive cells) during E2 exposure not only by disrupting the E2/ER alpha axis and enhancing GPER expression but also by modulating the expression of several apoptosis-related proteins through ER alpha-and GPER-independent processes. NDV-D90 promoted apoptosis via the intrinsic signaling pathway in BT549 cells (ER-negative cells), possibly by impairing E2-mediated GPER expression. Furthermore, NDV-D90 exerted its antitumor effects in vivo by inducing apoptosis. Overall, these results demonstrated that NDV-D90 promotes apoptosis by differentially modulating the expression of ER alpha and the GPER in ER-positive and negative BC cells exposed to estrogen, respectively, and can be utilized as an effective approach to treating BC.

Early-life exposure to bisphenol A and reproductive-related outcomes in rodent models: a systematic review and meta-analysis

AGING-US

Authors: Ren, Xiaohan; Zhang, Tongtong; Chen, Xinglin; Wei, Xiyi; Tian, Ye; Li, Guangyao; Zhang, Xu; Zhang, Wei; You, Zebing; Wang, Shangqian; Qin, Chao

We performed this meta-analysis to elucidate the associations between early-life BPA exposure and reproductive-related outcome indicators. The standardized mean differences (SMDs) and its 95% confidence intervals (CIs) were measured by fixed-effects or random-effects models. The results revealed that BPA exposure at extremely-high dose (>50mg/kg/day) was significantly associated with negative reproductive-related outcomes (Prostate weight: SMD: -4.21; 95% Cl: -5.97, -2.44; Testis weight: SMD: -1.92; 95% Cl: -2.61, 1.23; Epididymis weight: SMD: -2.16; 95% Cl: -3.47, -0.86; Daily sperm production; SMD: -1.90; 95% Cl: -3.27, 0.53; Epididymal sperm count; SMD: -3.42; 95% Cl: -3.87, -2.97). Meanwhile, regardless of the dose, early-life BPA exposure could result in an adverse effect on sperm parameters of F1 generation male rodents at any period. Also, we found the non-monotonic dose response curves of BPA in specific tissues or organs, which may challenge the traditional mindset of "safe dose". This study demonstrated that bisphenol A exposure was relevant to adverse reproductive-related outcomes at specially appointed dose and period of life. Yet the assumption that no adverse effects can occur below the "safe" dose is suspected.

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