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XPA Knockout Cell Lines

Gene: XPA

Official Full Name: XPA, DNA damage recognition and repair factorprovided by HGNC

Gene Summary: This gene encodes a zinc finger protein plays a central role in nucleotide excision repair (NER), a specialized type of DNA repair. NER is responsible for repair of UV radiation-induced photoproducts and DNA adducts induced by chemical carcinogens and chemotherapeutic drugs. The encoded protein interacts with DNA and several NER proteins, acting as a scaffold to assemble the NER incision complex at sites of DNA damage. Mutations in this gene cause Xeroderma pigmentosum complementation group A (XP-A), an autosomal recessive skin disorder featuring hypersensitivity to sunlight and increased risk for skin cancer. [provided by RefSeq, Aug 2017]

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Products Background

Products

Catalog Number Product Name Species Gene Passage ratio Mycoplasma testing Price
KO34801 XPA Knockout cell line (HeLa) Human XPA 1:3~1:6 Negative Online Inquiry
KO34802 XPA Knockout cell line (HCT 116) Human XPA 1:2~1:4 Negative Online Inquiry
KO34803 XPA Knockout cell line (HEK293) Human XPA 1:3~1:6 Negative Online Inquiry
KO34804 XPA Knockout cell line (A549) Human XPA 1:3~1:4 Negative Online Inquiry

Background

XPA Gene Knockout Cell Lines are meticulously engineered cell cultures that have undergone targeted gene disruption of the XPA gene, which plays a crucial role in nucleotide excision repair (NER). This gene is vital for the cellular response to DNA damage, particularly damage induced by ultraviolet (UV) light and various chemical agents. By creating these knockout lines, researchers can study the implications of impaired DNA repair mechanisms, elucidate pathways of cellular responses to genotoxic stress, and explore therapeutic vulnerabilities in cancer cells.

The key function of XPA Gene Knockout Cell Lines lies in their ability to model specific genetic deficiencies, allowing scientists to directly observe the effects of the loss of the XPA gene on cellular behavior and metabolic processes. Mechanistically, these cell lines serve as a powerful platform for investigating the consequences of defective NER, including increased mutation rates, genomic instability, and altered sensitivity to chemotherapeutic agents. They are invaluable for screening potential drug formulations and understanding the interplay between DNA repair mechanisms and cancer progression.

In research and clinical settings, XPA Gene Knockout Cell Lines are instrumental in advancing our understanding of hereditary diseases such as xeroderma pigmentosum, which is linked to mutations in the XPA gene. This product facilitates studies aimed at identifying novel therapeutic strategies and biomarkers in precision medicine, thereby ultimately improving patient outcomes.

One of the specific advantages of using XPA Gene Knockout Cell Lines is the high level of specificity and control they afford researchers compared to traditional models. They represent a clear distinction from wild-type cell lines, which may mask the effects of specific genetic alterations in drug response or sensitivity to environmental stressors. This specificity enables more accurate modeling of human disease, thereby enhancing the quality and relevance of experimental data.

The value of XPA Gene Knockout Cell Lines to researchers and clinicians is underscored by the significant insights they provide into the intersection of DNA damage response and human health. By facilitating a deeper understanding of how the loss of XPA function influences cellular processes and disease states, these cell lines act as critical tools in the quest for innovative treatments and diagnostic approaches.

At [Your Company Name], we pride ourselves on our commitment to delivering high-quality, reliable biological products. With our extensive expertise in gene editing technologies and cellular biology, we ensure that our XPA Gene Knockout Cell Lines meet the rigorous standards required for cutting-edge research and clinical applications.

Please note that all services are for research use only. Not intended for any clinical use.

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