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TXNRD2 Knockout Cell Lines

Gene: TXNRD2

Official Full Name: thioredoxin reductase 2provided by HGNC

Gene Summary: The protein encoded by this gene belongs to the pyridine nucleotide-disulfide oxidoreductase family, and is a member of the thioredoxin (Trx) system. Three thioredoxin reductase (TrxR) isozymes are found in mammals. TrxRs are selenocysteine-containing flavoenzymes, which reduce thioredoxins, as well as other substrates, and play a key role in redox homoeostasis. This gene encodes a mitochondrial form important for scavenging reactive oxygen species in mitochondria. It functions as a homodimer containing FAD, and selenocysteine (Sec) at the active site. Sec is encoded by UGA codon that normally signals translation termination. The 3' UTRs of selenoprotein mRNAs contain a conserved stem-loop structure, the Sec insertion sequence (SECIS) element, which is necessary for the recognition of UGA as a Sec codon rather than as a stop signal. Alternatively spliced transcript variants encoding different isoforms, including a few localized in the cytosol and some lacking the C-terminal Sec residue, have been found for this gene. [provided by RefSeq, Jun 2017]

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Products Background

Products

Catalog Number Product Name Species Gene Passage ratio Mycoplasma testing Price
KO31700 TXNRD2 Knockout cell line (HeLa) Human TXNRD2 1:3~1:6 Negative Online Inquiry
KO31701 TXNRD2 Knockout cell line (HCT 116) Human TXNRD2 1:2~1:4 Negative Online Inquiry
KO31702 TXNRD2 Knockout cell line (HEK293) Human TXNRD2 1:3~1:6 Negative Online Inquiry
KO31703 TXNRD2 Knockout cell line (A549) Human TXNRD2 1:3~1:4 Negative Online Inquiry

Background

TXNRD2 Gene Knockout Cell Lines are genetically engineered cell lines in which the TXNRD2 gene (thioredoxin reductase 2) has been deliberately disrupted. This specific genetic manipulation allows researchers to study the effects of the absence of this gene on cellular processes, metabolic pathways, and disease mechanisms. Thioredoxin reductase 2 plays a critical role in maintaining redox homeostasis and protecting cells from oxidative stress, making its study crucial for understanding various physiological and pathological conditions.

The primary mechanism of these knockout cell lines involves the gene editing approach through CRISPR/Cas9 or similar techniques, effectively rendering the TXNRD2 gene nonfunctional. By depleting the function of TXNRD2, researchers can investigate the compensatory mechanisms activated during oxidative stress and explore alterations in signaling pathways that are pivotal in cancer, neurodegeneration, and cardiovascular diseases. This makes the knockout cell lines invaluable for elucidating the gene's role in a myriad of biological contexts.

From a scientific perspective, these cell lines hold immense importance in both research and clinical settings. In research, they can be employed to identify drug targets, elucidate disease mechanisms, and develop novel therapeutic strategies. Clinically, understanding the implications of TXNRD2 dysfunction can aid in the development of biomarkers for disease progression or treatment response, ultimately paving the way for personalized medicine approaches.

Compared to conventional cell lines or more generalized knockout models, TXNRD2 Gene Knockout Cell Lines provide a specific focus on redox biology, enabling targeted investigations that can lead to faster breakthroughs. Their unique applications extend beyond mere academic inquiry, actively contributing to advancements in therapeutic development and mechanistic insights into oxidative stress-related diseases.

For researchers and clinicians aiming to deepen their understanding of redox biology and its consequences in health and disease, TXNRD2 Gene Knockout Cell Lines are an indispensable tool. Our company specializes in high-quality biological products, leveraging cutting-edge genetic engineering techniques to deliver reliable models that push the boundaries of scientific discovery and innovation.

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

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