Gene: RAD23B
Official Full Name: RAD23 homolog B, nucleotide excision repair proteinprovided by HGNC
Gene Summary: The protein encoded by this gene is one of two human homologs of Saccharomyces cerevisiae Rad23, a protein involved in the nucleotide excision repair (NER). This protein was found to be a component of the protein complex that specifically complements the NER defect of xeroderma pigmentosum group C (XP-c) cell extracts in vitro. This protein was also shown to interact with, and elevate the nucleotide excision activity of 3-methyladenine-DNA glycosylase (MPG), which suggested a role in DNA damage recognition in base excision repair. This protein contains an N-terminal ubiquitin-like domain, which was reported to interact with 26S proteasome, and thus this protein may be involved in the ubiquitin mediated proteolytic pathway in cells. Alternative splicing results in multiple transcript variants encoding distinct isoforms. [provided by RefSeq, Sep 2011]
Catalog Number | Product Name | Species | Gene | Passage ratio | Mycoplasma testing | Price |
---|---|---|---|---|---|---|
KO35716 | RAD23B Knockout cell line (HeLa) | Human | RAD23B | 1:3~1:6 | Negative | Online Inquiry |
KO35717 | RAD23B Knockout cell line (HCT 116) | Human | RAD23B | 1:2~1:4 | Negative | Online Inquiry |
KO35718 | RAD23B Knockout cell line (HEK293) | Human | RAD23B | 1:3~1:6 | Negative | Online Inquiry |
KO35719 | RAD23B Knockout cell line (A549) | Human | RAD23B | 1:3~1:4 | Negative | Online Inquiry |
RAD23B Gene Knockout Cell Lines are specifically engineered cellular models that have undergone the process of gene knockout, specifically targeting the RAD23B gene, which plays a critical role in DNA repair and cellular stress response mechanisms. By disabling the RAD23B gene, these cell lines serve as a valuable tool for scientists to investigate the physiological and pathological consequences of impaired DNA repair pathways, providing insight into cancer biology and other genetic disorders.
These cell lines function by lacking the RAD23B protein, which is involved in the nucleotide excision repair (NER) pathway. In its absence, researchers can evaluate changes in cellular response to DNA damage, assess alterations in cell cycle regulation, and determine how these impacts influence susceptibility to various chemotherapeutic agents. The use of RAD23B knockout cells enables a deeper understanding of the biological significance of DNA repair processes, making it an indispensable model for research on genomic stability and tumorigenesis.
The scientific importance of RAD23B Gene Knockout Cell Lines extends into both research and clinical applications. They provide a platform for studying the effectiveness of novel therapeutic strategies in cancer treatment, particularly those that exploit deficiencies in DNA repair mechanisms. This is crucial for developing precision medicine approaches that enhance treatment efficacy while minimizing off-target effects.
What sets our RAD23B Gene Knockout Cell Lines apart from alternative models is their extensive validation and characterization, ensuring reliability and reproducibility in experimental results. The uniqueness of these cell lines lies in their carefully controlled knockout of the RAD23B gene, allowing for specific investigations into DNA repair deficiencies that are highly relevant to current cancer research.
For researchers and clinicians, the availability of RAD23B Gene Knockout Cell Lines offers a robust tool for advancing knowledge in the field of genetics and cancer biology. The ability to manipulate DNA repair pathways opens up potential avenues for innovative therapies, fostering breakthroughs that can significantly impact patient care.
Our company prides itself on its commitment to producing high-quality biological products backed by rigorous scientific validation and a thorough understanding of cellular mechanisms, empowering researchers and clinicians to achieve their investigative goals with confidence.
Please note that all services are for research use only. Not intended for any clinical use.
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