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Cyagen's Knockout Cell Library provides researchers with rapid access to a wide range of knockout (KO) cell models and high-quality cell strains. To expand the availability of cell research tools, Cyagen has launched a plan to construct nearly 20,000 knockout (KO) cell models. Relying on our mature Smart-CRISPR™ cell gene editing platform and cell culture systems, the Knockout Cell Library will eventually cover all genes. We are committed to providing robust cell lines for basic research, antibody validation, drug screening, disease diagnosis, treatment, and detection. Now you can order RAW 264.7, HEK293T, A549, HCT 116, Hela, and other KO cells in stock, and get monoclonal homozygotes with prices as low as $2,000. Contact us at 800-921-8930 or email animal-service@cyagen.com for more information.

*If you cannot find the desired cell/gene, we recommend our custom KO cell service, starting at $5,999 and shipped in as fast as 8 weeks to meet your research needs. Click to inquire now.
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*The cell/gene that you searched for is currently not included in the KO Cell Library, we recommend our custom KO cell service, starting at $5,999 and shipped in as fast as 8 weeks to meet your research needs. Fill out the form below to contact us immediately.
Three Major Advantages to Safeguard Your Success
Original Smart-CRISPR™ Technology
The intelligent Smart-CRISPR™ cell gene editing system enables easy implementation of various strategies such as gene knockouts and knock-ins, achieving an editing efficiency as high as 90%.
Mature Gene Editing Technology Platform
From in vitro cell experiments to in vivo animal experiments, we have completed tens of thousands of successful gene editing projects, over 1,000 cases of successfully established cell lines, and have received numerous citations in peer-reviewed publications. We can provide full-process services ranging from cell gene expression regulation, cell function verification, mouse disease model construction, and phenotype analysis.
Large-Scale and Comprehensive Scientific Cell Library
Our newly upgraded delivery vector has an HDR efficiency of up to 50%, transfection efficiency of >50%, and transfection viability of >80%. We offer a wide variety of cell strains for scientific research purposes.
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Smart-CRISPR™Cell Gene Editing System

Service Case - THP-1 Gene Editing

Di-(2-ethylhexyl) phthalate (DEHP) exposure leads to ferroptosis via the HIF-1α/HO-1 signaling pathway in mouse testes.

Research Plan:
1. Validate that DEHP stimulation can cause testicular damage in vivo and in vitro.
2. Omics analysis and experimental validation indicate abnormal signaling pathways such as HIF-1α.
3. Explore the mechanism of action of the HIF-1α signaling pathway.
4. Further validate the role of HIF-1α by knocking out HIF-1α in vitro.

Conducting rigorous research requires a complete experimental workflow that validates findings at each step of the process. Generally, omics analysis is used to scientifically screen genes, and multiple experimental results must be cross-validated. Gene knockout (KO) is still one of the conventional strategies for gene function studies. A successful gene KO cell line is crucial for the accuracy of the validation results.

In this study, the authors used phenotype analysis, RNA-Seq analysis, and ChIP-qPCR analysis after MEHP stimulation to identify the regulatory gene associated with testicular dysfunction: HIF-1α. They also found the preliminary regulation mechanism: MEHP (the main biological metabolite of DEHP in vivo) can inhibit PHDs, affect HIF-1α accumulation and stability, cause HIF-1α to translocate to the nucleus, and induce the binding of HIF-1/Hmox1 in Leydig and Sertoli cells, leading to an upregulation in HO-1 expression. Overexpression of HO-1 leads to ferrous overload (hypoferraemia), ROS accumulation, and ultimately causes ferroptosis, damaging the viability of Leydig and Sertoli cells.

To further confirm these results, the researchers used Leydig and Sertoli cells with HIF-1α gene KO (HIF-1α gene KO Leydig and Sertoli cells provided by Cyagen) for subsequent experiments. Sanger sequencing and Western blotting were used to confirm the successful knocking out of HIF-1α in the KO cell lines. Compared with wild-type cells, the HIF-1α-KO cell lines showed significant improvement in the degree of cell viability damage under MEHP stimulation.

Meanwhile, lipid peroxidation (Figure 1B, I) and ferrous overload (Figure 1C, J) were inhibited. Expressions of Hmox1 and HO-1 were evaluated using qPCR and Western blotting respectively, demonstrating that knocking out Hif-1α can reverse the up-regulation of Hmox1 (Figure 1D, K) and HO-1 (Figure 1G, N) expression levels under MEHP stimulation.

Furthermore, the ROS burst (Figure 1E, L) and cell death (Figure 1F, M) levels after MEHP stimulation were also reduced after knockdown HIF-1α.

Western blotting showed that knockdown HIF-1α restored the expression of ACSL4, FTH1, and SLC7A11, and suppressed the expression of GPX4 (Figure 1G, N). Overall, these findings suggest that MEHP stimulation leads to ferroptosis in testicular Leydig and Sertoli cells in a HIF-1α-dependent manner.