mProX™ Human ESR1 Stable Cell Line

Product Information

Target Protein

ESR1

Target Family

Estrogen Receptor

Target Protein Species

Human

Host Cell Type

SUM-44; CHO-K1; HEK293

Target Classification

Nuclear Receptor

Target Research Area

Cancer Research; Reproductive Research

Related Diseases

Estrogen Resistance; Breast Cancer

Gene ID

2099

UniProt ID

P03372

Product Properties

Biosafety Level

Level 1

Activity

Yes

Quantity

10⁶ cells per vial

Applications

NR3A1, or estrogen receptor alpha, is one of the two primary forms of estrogen receptors. The human gene ESR1 (EStrogen Receptor 1) encodes ERα. To varied degrees, ERα contributes to the physiological development and operation of several organ systems, including as the reproductive, central nervous, skeletal, and cardiovascular systems. As a result, ERα is widely expressed in many different parts of the body, such as the pituitary gland, uterus, ovary, male reproductive organs, bone, heart, hypothalamus, liver, lung, kidney, spleen, and adipose tissue. Animal models devoid of functioning ERα genes, like the ERα knockout mouse (ERKO), cause disturbances in the development and function of certain tissues, offering an initial comprehension of ERα function at particular target organs. The customized ESR1 stable cell line can be used in antibody discovery and development, potential drug candidate screening and signaling pathway researches.

Protocols

Please visit our protocols page.

Customer Reviews

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FAQ

chat Thomas (Verified Customer)

Does the ESR1 cell line have a tag? Where is the tag? Mar 08 2023

chat Sherry Smith (Creative Biolabs Scientific Support)

We can customize tags to suit your needs. Mar 08 2023

chat Karen (Verified Customer)

What's the significance of ESR1 mutation? Dec 25 2022

chat Sherry Smith (Creative Biolabs Scientific Support)

The ESR1 mutation is a common resistance mutation. Resistance mutations are ways that cancer develops after being treated with certain cancer therapies. Dec 25 2022

Published Data

Fig.1 Immunoblot for ERα in MCF-7 and SUM-44 cells.

WHSC1L1 knockdown decreased ERα protein levels in SUM-44 cells, which express much more ERα than MCF-7 cells do (the ESR1 gene is not amplified nor point-mutated in SUM-44 cells).

Ref: Irish, Jonathan C., et al. "Amplification of WHSC1L1 regulates expression and estrogen-independent activation of ERα in SUM-44 breast cancer cells and is associated with ERα over-expression in breast cancer." Molecular oncology 10.6 (2016): 850-865.

Pubmed: 27005559

DOI: 10.1016/j.molonc.2016.02.003

Research Highlights

Studies have shown that 20% of patients with metastatic ER-positive illness who were treated with endocrine treatments, such as tamoxifen and aromatase inhibitors, have gain-of-function mutations in ESR1, the gene encoding the ER.
Jeselsohn, Rinath, et al. "ESR1 mutations-a mechanism for acquired endocrine resistance in breast cancer." Nature reviews Clinical oncology 12.10 (2015): 573-583.
Pubmed: 26122181 DOI: 10.1038/nrclinonc.2015.117

Recent research has revealed that somatic ESR1 mutations are present in patients with metastatic breast cancer, and some of these changes support the receptor's activation without the need for estrogen. It is unknown to what extent all recurrent mutations can induce lower sensitivity to ER antagonists such as fulvestrant and estrogen-independent actions.
Toy, Weiyi, et al. "Activating ESR1 mutations differentially affect the efficacy of ER antagonists." Cancer discovery 7.3 (2017): 277-287.
Pubmed: 27986707 DOI: 10.1158/2159-8290.CD-15-1523