CDSN Antibodies

Structure of CDSN

The Corneodesmosin protein encoded by the CDSN gene is a secreted glycoprotein with a molecular weight of approximately 52-66 kDa. The size difference mainly stems from post-translational glycosylation modifications.

This protein is composed of 690 amino acids, and its primary structure includes an N-terminal signaling peptide, a conserved "G" domain, and a repeating region rich in glutamic acid/glutamine. Its secondary structure is mainly β -folded and coiled helices, and these structures form stable cores through disulfide bonds. The hydrophobic core is responsible for maintaining structural integrity, while the hydrophilic glutamate-rich region binds to keratinized envelope proteins through transglutaminase-mediated covalent cross-linking in the extracellular matrix, thereby forming strong intercellular bonding bonds between keratinocytes, which is the key molecular basis of the skin's physical barrier.

Fig. 1 Structural Localization of CdsL Binding Domains on the CdsN Monomer.¹

Key structural properties of CDSN:

• Rich in β-fold and coiled helix modular structure
• Crosslinking function of hydrophilic glutamic acid rich regions
• Calcium ion-dependent regulatory domain of cell adhesion

Functions of CDSN

The main function of the keratinized desmosin encoded by the CDSN gene is to construct and maintain the intercellular adhesion and barrier integrity of the stratum corneum of the skin. Its specific functions include:

The functional realization of this protein depends on its fine spatiotemporal regulation from synthesis, secretion to orderly degradation. Once the dynamic balance between its expression and degradation is disrupted, it will disrupt the homeostasis of the skin barrier, which is one of the key pathological bases for many common inflammatory and desquamation skin diseases.

Applications of CDSN and CDSN Antibody in Literature

1. van der Velden, Jaap JAJ, et al. "Mutations in the CDSN gene cause peeling skin disease and hypotrichosis simplex of the scalp." The Journal of dermatology 47.1 (2020): 3-7. https://doi.org/10.1111/1346-8138.15136

This article reports a rare skin disease caused by compound heterozygous mutations in the CDSN gene. The patient presented with generalized skin abruption. His mother carried a nonsense mutation of the same gene (c.598C>T), and the clinical manifestation was early hair thinning. This study confirmed the association between CDSN gene mutations and exfoliative skin diseases as well as simple oligotrichosis of the scalp.

2. Zingkou, Eleni, et al. "Deletion of the Epidermal Protease KLK5 Aggravates the Symptoms of Congenital Ichthyosis CDSN-nEDD." International Journal of Molecular Sciences 26.17 (2025): 8605. https://doi.org/10.3390/ijms26178605

This study explores the treatment strategies for ichthyosis caused by CDSN gene mutations. By constructing equivalent models of mouse and human skin, the study found that inhibiting the KLK5 serine protease not only failed to alleviate excessive desquamation but also exacerbated the disease phenotype. This indicates that a single targeted elimination of proteolysis cannot effectively treat this disease, and more precise regulation of enzyme activity is required.

3. Stone, Chris B., et al. "Chlamydia pneumoniae CdsL regulates CdsN ATPase activity, and disruption with a peptide mimetic prevents bacterial invasion." Frontiers in microbiology 2 (2011): 21. https://doi.org/10.3389/fmicb.2011.00021 

This article found that the secretory system protein CdsL of Chlamydia pneumoniae type III can inhibit the activity of ATPase CdsN, and two key binding domains were identified through epitope scanning. The treatment with CdsN peptide mimics can effectively inhibit chlamydia from invading cells, providing a basis for the development of new anti-virulence therapies.

4. Wiśniewski, Andrzej, et al. "HLA-C* 06: 02-independent, gender-related association of PSORS1C3 and PSORS1C1/CDSN single-nucleotide polymorphisms with risk and severity of psoriasis." Molecular Genetics and Genomics 293.4 (2018): 957-966. https://doi.org/10.1007/s00438-018-1435-4  

This study found in 461 patients with psoriasis that multiple SNPS in the PSORS1 region were significantly associated with disease risk. The results revealed for the first time that variations in the PSORS1C3 and CDSN genes have male-specific effects on the risk and severity of psoriasis, and are independent of the HLA-C*06:02 allele.

5. Fan, Xing, et al. "Fine mapping of the psoriasis susceptibility locus PSORS1 supports HLA-C as the susceptibility gene in the Han Chinese population." PLoS genetics 4.3 (2008): e1000038. https://doi.org/10.1371/journal.pgen.1000038

In this study, through family analysis of the Chinese population, the PSORS1 psoriasis susceptibility gene was located in the key regions near HLA-C. Analysis shows that HLA-Cw6 is the main risk allele, while the CDSN*TTC allele itself does not independently increase the risk of disease in the absence of HLA-Cw6, and does not support its status as the primary gene of PSORS1.

Creative Biolabs: CDSN Antibodies for Research

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

• Custom CDSN 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 CDSN antibodies, custom preparations, or technical support, contact us at email.