In Stock Cell Lines
The ESR1 Knockout HK-2 Cell Line is a CRISPR/Cas9-edited knockout cell line in an HK-2 human kidney proximal tubule epithelial background, disrupting the ESR1 gene encoding estrogen receptor alpha (ER??). This loss-of-function model abrogates ER??-mediated transcriptional regulation of targets such as Cyclin D1 and PGR, and eliminates interactions with cofactors like SRC-1. It is ideal for studying estrogen-independent signaling, investigating ER?? roles in nephrotoxicity and renal cell carcinoma, and screening estrogen receptor modulators using assays like ERE-luciferase reporter and cell proliferation analyses.
DDRGK1 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG16368
Blk Knockout RAW 264.7 Polyclonal Cells
Cat. No. ARG23529
ABCB10 Knockout A2780 Polyclonal Cells
Cat. No. ARG28524
DLG3 Knockout HAP1 Polyclonal Cells
Cat. No. ARG38893
DPP7 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG39679
SK-RC-42
Cat. No. ARC0845
The ESR1 Knockout HK-2 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from HK-2 human kidney proximal tubule epithelial cells, with targeted disruption of the ESR1 gene. This model eliminates estrogen receptor alpha (ER??) protein expression, enabling dissection of estrogen-dependent and -independent signaling pathways in a renal epithelial system.
HK-2 cells are an immortalized human proximal tubule epithelial line derived from normal adult kidney, immortalized with HPV-16 E6/E7. They retain key features of proximal tubule epithelia, including polarized morphology and transporter expression, and serve as a standard in vitro model for renal physiology, nephrotoxicity testing, and epithelial biology.
ESR1 encodes a nuclear hormone receptor that, upon binding 17??-estradiol, translocates to the nucleus and binds estrogen response elements (EREs) to regulate transcription of genes such as PGR, TFF1, GREB1, CTSD, and CCND1. ER?? transcriptional activity is modulated by cofactors including SRC-1, CBP/p300, NCoR, and SMRT, and by tethering to transcription factors SP1, AP-1, and NF-??B. Ligand-independent activation occurs via phosphorylation by kinases downstream of EGF and IGF-1, including MAPK, PKA, and SRC, integrating ER?? into broader signaling networks such as MAPK/ERK and PI3K-AKT pathways. In the knockout, loss of ER?? abrogates estrogen-mediated transcription and allows study of non-genomic estrogen effects or receptor-independent signaling.
In renal proximal tubule cells, ER?? has been implicated in responses to injury and carcinogenesis, though its specific roles remain poorly defined. The ESR1 Knockout HK-2 Cell Line provides a defined genetic background to investigate ER?? contributions to nephrotoxicity, renal cell carcinoma, and proximal tubule homeostasis, distinguishing direct receptor effects from off-target or estrogen-independent mechanisms.
Researchers can employ this cell line in applications ranging from mechanistic studies of estrogen signaling to drug screening of selective estrogen receptor modulators (SERMs) like tamoxifen. Typical assays include ERE-luciferase reporter analysis for transcriptional activity, Western blotting and RT-qPCR for target gene expression, immunofluorescence for ER??, and cell proliferation or apoptosis assays. For further information, please contact Ascent Research.
