CSAD Antibodies

Structure of CSAD

The molecular weight of cysteine sulfonic acid decarboxylase encoded by the CSAD gene is approximately 53 kDa. Its precise molecular weight varies slightly among different species, mainly due to specie-specific variations in amino acid sequences.

This enzyme is composed of approximately 480 amino acid residues and adopts a typical pyridoxal phosphate (PLP) -dependent enzyme folding pattern. Its tertiary structure forms a tight α/β folded barrel, with a PLP cofactor binding cavity at the center, covalently linked to Lys247 through a Schiff base. The active site is composed of a charge relay system formed by the arginine triad (Arg71, Arg97, Arg413), which is responsible for stabilizing the carboxyl group of the substrate. The side chains of Thr322 and Ser156 form a hydrogen bond network, precisely regulating the substrate orientation and catalytic process.

Fig. 1 The mechanisms of CSAD regulate the strength of the NF-κB signaling pathway.¹

Key structural properties of CSAD:

• Typical pyridoxal phosphate (PLP) -dependent enzyme folding architecture
• The conservative active pocket is composed of arginine triplets
• PLP cofactors are covalently linked through Schiff's base
• Substrate channel gating mechanisms ensure catalytic specificity

Functions of CSAD

The core function of the cysteine sulfonic acid decarboxylase encoded by the CSAD gene is a key step in catalyzing the biosynthesis of taurine, and it is also involved in multiple physiological regulatory networks.

The reaction catalyzed by this enzyme follows the ping-pong double displacement mechanism, with a Mie constant (Km value) of 0.8mM and an optimal pH of 7.4. These kinetic characteristics ensure that it can efficiently catalyze substrate transformation in the cytoplasm of hepatocytes. Enzyme activity is inhibited by product feedback and regulated by phosphorylation. This precise regulatory mechanism maintains the dynamic balance of taurine metabolism in the body.

Applications of CSAD and CSAD Antibody in Literature

1. Tan, Rongrong, et al. "CSAD ameliorates lipid accumulation in high-fat diet-fed mice." International Journal of Molecular Sciences 23.24 (2022): 15931.https://doi.org/10.3390/ijms232415931

This study, through the analysis of the GEO database and animal models, found that the expression of CSAD was significantly reduced in non-alcoholic fatty liver disease. Overexpression of CSAD in the liver can alleviate the pathological changes of fatty liver. The mechanism may be related to promoting β -oxidation of fatty acids and improving mitochondrial damage, and it is not dependent on the taurine pathway. Studies have shown that CSAD is a potential therapeutic target for NAFLD.

2. Zhang, Yufan, et al. "CSAD inhibits excessive inflammation during viral infections through the NF-κB signaling pathway." Journal of Virology (2025): e00706-25. https://doi.org/10.1128/jvi.00706-25

Research has found that CSAD is a key negative regulatory factor of the innate immune response. It prevents harmful excessive inflammation after viral infection by directly binding to IKKα and inhibiting the excessive activation of the NF-κB signaling pathway. This explains the differences in the intensity of immune responses among different individuals in terms of mechanisms.

3. Wang, Zengbin, et al. "RBM17 promotes hepatocellular carcinoma progression by regulating lipid metabolism and immune microenvironment: implications for therapeutic targeting." Cell Death Discovery 11.1 (2025): 338. https://doi.org/10.1038/s41420-025-02642-2

This study reveals that RBM17, which is highly expressed in liver cancer, promotes exon skipping of the CSAD gene by regulating alternative splicing, thereby facilitating the production of taurocholic acid (T-CA) and the infiltration of M2-type macrophages, and accelerating tumor progression. This indicates that targeting the RBM17-CSAD axis is a potential therapeutic strategy.

4. Abbasian, Nima, et al. "Hepatic cysteine sulphinic acid decarboxylase depletion and defective taurine metabolism in a rat partial nephrectomy model of chronic kidney disease." BMC nephrology 22.1 (2021): 250. https://doi.org/10.1186/s12882-021-02442-7

This study found that in a rat model of chronic kidney disease (CKD), although the mRNA levels of related genes did not change significantly, the expression of the key taurine synthase CSAD protein in the liver was significantly decreased, leading to impaired systemic taurine biosynthesis. Supplementation with L-glutamine failed to improve this condition. This indicates that the loss of CSAD protein is a key link in the reduction of taurine synthesis in CKD.

5. Ma, Hui-fen, et al. "Metabolomic profiling of brain protective effect of edaravone on cerebral ischemia-reperfusion injury in mice." Frontiers in pharmacology 13 (2022): 814942. https://doi.org/10.3389/fphar.2022.814942

This study reveals that edaravone promotes taurine production in the brain by up-regulating CSAD, a key rate-limiting enzyme in taurine synthesis, and thereby inhibits apoptosis of brain endothelial cells, exerting a therapeutic effect on ischemic stroke. CSAD has been confirmed as the target of edalafoxin.

Creative Biolabs: CSAD Antibodies for Research

Creative Biolabs specializes in the production of high-quality CSAD antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

• Custom CSAD Antibody Development: Tailor-made solutions to meet specific research requirements.
• Bulk Production: Large-scale antibody manufacturing for industry partners.
• Technical Support: Expert consultation for protocol optimization and troubleshooting.
• Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our CSAD antibodies, custom preparations, or technical support, contact us at email.