Gene: ATF2
Official Full Name: activating transcription factor 2provided by HGNC
Gene Summary: This gene encodes a transcription factor that is a member of the leucine zipper family of DNA binding proteins. The encoded protein has been identified as a moonlighting protein based on its ability to perform mechanistically distinct functions This protein binds to the cAMP-responsive element (CRE), an octameric palindrome. It forms a homodimer or a heterodimer with c-Jun and stimulates CRE-dependent transcription. This protein is also a histone acetyltransferase (HAT) that specifically acetylates histones H2B and H4 in vitro; thus it may represent a class of sequence-specific factors that activate transcription by direct effects on chromatin components. The encoded protein may also be involved in cell's DNA damage response independent of its role in transcriptional regulation. Several alternatively spliced transcript variants have been found for this gene [provided by RefSeq, Jan 2014]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO10932 | ATF2 Knockout cell line (HeLa) | Human | ATF2 | 1:3~1:6 | Negative | Online Inquiry |
KO10933 | ATF2 Knockout cell line (HCT 116) | Human | ATF2 | 1:2~1:4 | Negative | Online Inquiry |
KO10934 | ATF2 Knockout cell line (HEK293) | Human | ATF2 | 1:3~1:6 | Negative | Online Inquiry |
KO10935 | ATF2 Knockout cell line (A549) | Human | ATF2 | 1:3~1:4 | Negative | Online Inquiry |
ATF2 Gene Knockout Cell Lines are specially designed cellular models in which the Activating Transcription Factor 2 (ATF2) gene has been inactivated or disrupted. The ATF2 protein plays a crucial role in regulating various cellular responses, including stress response, cell cycle regulation, and apoptosis. By providing a means to explore the functions of the ATF2 gene in a controlled environment, these knockout cell lines allow researchers to dissect the molecular mechanisms underlying numerous biological processes.
The primary function of these cell lines lies in their ability to model the effects of ATF2 deficiency, enabling the study of its role in gene expression regulation and signal transduction pathways. The knockout mechanism typically involves CRISPR-Cas9 technology or similar gene editing approaches, ensuring precise and reproducible results. This specificity provides researchers with insights into how ATF2 influences cellular behavior under various conditions, such as oxidative stress, inflammation, or cancer progression.
The scientific importance of ATF2 Gene Knockout Cell Lines is evident in both research and clinical settings. They are instrumental in elucidating the intricacies of diseases where ATF2 is implicated, including cancer, neurodegenerative disorders, and metabolic diseases. Their applications also extend to drug discovery, where understanding ATF2's role can lead to the development of targeted therapies that modulate its pathway to enhance treatment efficacy.
Compared to other gene knockout models, our ATF2 knockout cell lines offer well-characterized genetic backgrounds and robust performance, ensuring reliable experimental outcomes. They eliminate background variability often associated with other models, thus enhancing data reproducibility. Additionally, these cell lines are readily adaptable for high-throughput screening applications, facilitating the identification of novel therapeutic targets.
For researchers and clinicians seeking to deepen their understanding of ATF2's biological roles, our product serves as a valuable tool. Its ease of use, alongside the comprehensive support and guidance from our experienced team, positions it as an essential resource in modern biological research.
Our company, with a strong background in genetic engineering and cell biology, is committed to providing high-quality biological products. We strive to empower researchers with innovative tools that push the boundaries of scientific discovery.
Please note that all services are for research use only. Not intended for any clinical use.
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