Gene: DHFR2
Official Full Name: dihydrofolate reductase 2provided by HGNC
Gene Summary: Enables dihydrofolate reductase activity and mRNA binding activity. Involved in tetrahydrofolate metabolic process and thymidine biosynthetic process. Located in mitochondrial inner membrane and mitochondrial matrix. [provided by Alliance of Genome Resources, Apr 2025]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO37815 | DHFR2 Knockout cell line (HeLa) | Human | DHFR2 | 1:3~1:6 | Negative | Online Inquiry |
KO37816 | DHFR2 Knockout cell line (HCT 116) | Human | DHFR2 | 1:2~1:4 | Negative | Online Inquiry |
KO37817 | DHFR2 Knockout cell line (HEK293) | Human | DHFR2 | 1:3~1:6 | Negative | Online Inquiry |
KO37818 | DHFR2 Knockout cell line (A549) | Human | DHFR2 | 1:3~1:4 | Negative | Online Inquiry |
DHFR2 Gene Knockout Cell Lines are specifically engineered cell lines that have had the dihydrofolate reductase 2 (DHFR2) gene disrupted or removed. This targeted gene editing creates a powerful tool for researchers studying the role of DHFR2 in various biological processes, such as folate metabolism, cellular differentiation, and various disease states. The knockout of this gene provides insights into its function and elucidates its influence on pathways involved in cell proliferation and response to antifolate drugs.
The primary function of DHFR2 is to catalyze the reduction of dihydrofolate to tetrahydrofolate, a crucial cofactor in nucleotide synthesis. By knocking out this critical gene, researchers can investigate the downstream effects on cellular metabolism and growth. These cell lines facilitate the study of resistance mechanisms in cancer therapies and the exploration of novel drug targets, especially in the context of diseases that exhibit altered DHFR2 expression.
The scientific importance of DHFR2 Gene Knockout Cell Lines extends into both research and clinical applications. In research settings, they serve as models for understanding the molecular mechanisms of diseases such as cancer and autoimmune disorders, where DHFR2 dysregulation plays a significant role. Clinically, insights gained from these models can inform treatment strategies that utilize antifolate agents, enhancing the effectiveness of cancer therapies.
A key advantage of our DHFR2 Gene Knockout Cell Lines compared to traditional cell lines is their precision and specificity. By utilizing CRISPR-Cas9 technology, these cell lines are created with high efficiency and minimal off-target effects, ensuring that researchers receive reliable data that can be reproduced. Additionally, these lines come validated for consistency in laboratory performance, providing users with confidence in their reproducibility across various experimental conditions.
For researchers and clinicians alike, the value of DHFR2 Gene Knockout Cell Lines lies in their ability to unlock critical biological insights and enhance therapeutic strategies in the fight against diseases influenced by folate metabolism. By integrating this powerful tool into experimental designs, users position themselves at the forefront of innovative biological research.
Our company prides itself on its commitment to delivering state-of-the-art biological products backed by rigorous scientific validation and expert support. With a focus on advancing research capabilities, our DHFR2 Gene Knockout Cell Lines exemplify our dedication to empowering the scientific community with essential tools for discovery and advancement.
Please note that all services are for research use only. Not intended for any clinical use.
If your question is not addressed through these resources, you can fill out the online form below and we will answer your question as soon as possible.
There is no product in your cart. |
CD Biosynsis is a leading customer-focused biotechnology company dedicated to providing high-quality products, comprehensive service packages, and tailored solutions to support and facilitate the applications of synthetic biology in a wide range of areas.