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SDHB Knockout Cell Lines

Gene: SDHB

Official Full Name: succinate dehydrogenase complex iron sulfur subunit Bprovided by HGNC

Gene Summary: This tumor suppressor gene encodes the iron-sulfur protein subunit of the succinate dehydrogenase (SDH) enzyme complex which plays a critical role in mitochondria. The SDH enzyme complex is composed of four nuclear-encoded subunits. This enzyme complex converts succinate to fumarate which releases electrons as part of the citric acid cycle, and the enzyme complex additionally provides an attachment site for released electrons to be transferred to the oxidative phosphorylation pathway. The SDH enzyme complex plays a role in oxygen-related gene regulation through its conversion of succinate, which is an oxygen sensor that stabilizes the hypoxia-inducible factor 1 (HIF1) transcription factor. Sporadic and familial mutations in this gene result in paragangliomas, pheochromocytoma, and gastrointestinal stromal tumors, supporting a link between mitochondrial dysfunction and tumorigenesis. Mutations in this gene are also implicated in nuclear type 4 mitochondrial complex II deficiency. [provided by RefSeq, Jun 2022]

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Products Background

Products

Catalog Number Product Name Species Gene Passage ratio Mycoplasma testing Price
GP00267 SDHB gRNA1-gRNA7 KO plasmid SDHB $850
KO00674 SDHB Knockout cell line(A549) Human SDHB 1:3~1:4 Negative Online Inquiry
KO00891 SDHB Knockout cell line (HeLa) Human SDHB 1:3~1:6 Negative Online Inquiry

Background

SDHB Gene Knockout Cell Lines are genetically engineered cellular models specifically designed to study the effects of the succinate dehydrogenase B (SDHB) gene deficiency, which is critical in cellular energy metabolism and tumorigenesis. These cell lines provide a powerful tool for researchers focusing on the role of SDHB in the tricarboxylic acid (TCA) cycle and its implications in various hereditary and sporadic cancers, particularly paragangliomas and pheochromocytomas.

The primary function of these knockout cell lines is to enable the examination of metabolic reprogramming in the absence of SDHB, allowing for a better understanding of the biochemical pathways influenced by this gene mutation. By utilizing CRISPR/Cas9 gene-editing technology, the SDHB gene is precisely disrupted, leading to a loss of its associated enzymatic function. The resultant phenotype provides insights into succinate accumulation, oxidative stress, and downstream signaling pathways, offering a robust platform to investigate therapeutic interventions.

The scientific importance of SDHB Gene Knockout Cell Lines lies in their wide-ranging applications in both research and clinical settings. They serve not only as models for cancer research but also as valuable tools in drug discovery and the evaluation of metabolic inhibitors. By uncovering the molecular mechanisms behind SDHB-related diseases, researchers can develop targeted therapies that may enhance patient outcomes.

What sets our SDHB Gene Knockout Cell Lines apart from alternative models is the high specificity and reliability of the genetic modification, coupled with extensive validation of the resulting phenotypic characteristics. Additionally, these cell lines offer a complete compatibility with various assays and experimental protocols, ensuring ease of integration into existing research workflows.

For researchers and clinicians alike, the value of these cell lines is profound; they provide an innovative approach to unravel complex metabolic disorders and cancer biology. By delineating the pathways influenced by SDHB deficiency, they pave the way for novel therapeutic strategies that target metabolic dysregulation in tumors.

Our company specializes in the development of advanced genetic models, ensuring high-quality products backed by rigorous scientific research and validation. With a commitment to supporting the scientific community, we are dedicated to helping you unlock new discoveries in the field of biology and medicine.

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

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