Mouse SPINK4 Protein

Produkt-Information von SPINK4 Protein

QC Testing von SPINK4 Protein

Purity	> 97 % as determined by SDS-PAGE	SDS-PAGE: SPINK4 protein
Endotoxin	< 1.0 EU per μg of the protein as determined by the LAL method
Stability	Samples are stable for up to twelve months from date of receipt at -70℃
Predicted N terminal	Gly 27
Molecular Mass	The secreted recombinant mouse SPINK4/Fc is a disulfide-linked homodimer. The reduced monomer comprises 301 amino acids and has a calculated molecular mass of 34.5 kDa. The apparent molecular mass of the monomer is approximately 35 kDa in SDS-PAGE under reducing conditions.
Formulation	Lyophilized from 0.2μm filtered solution of PBS, pH7.4 Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.

SPINK4 Protein Usage Guide

Verwandte Produkte & Themen von SPINK4 Protein

Enzyme>>Protease & Regulator>>Serine Protease & Regulator>>SPINK4

Beschreibung von SPINK4 Protein

Serine protease inhibitor Kazal-type 4, also known as Peptide PEC-60 homolog and SPINK4, is a secreted protein which contains one Kazal-like domain. SPINK4 is a member of the SPINK protein family. The gene family of serine protease inhibitors of the Kazal type (SPINK) are functional and positional candidate genes for celiac disease (CD). SPINK1 plays an important role in protecting the pancreas against excessive trypsinogen activation. It is a potent natural inhibitor of pancreatic trypsin activity. SPINK1 mutations are associated with the development of acute and chronic pancreatitis and have been detected in all forms of chronic pancreatitis. SPINK2 functions as a trypsin/acrosin inhibitor and is synthesized mainly in the testis and seminal vesicle where its activity is engaged in fertility. The SPINK2 protein contains a typical Kazal domain composed by six cysteine residues forming three disulfide bridges. SPINK9 was identified in human skin. Its expression was strong in palmar epidermis, but not detectable or very low in non palmoplantar skin.

References

1. Schneider, A. et al., 2004,Gastroenterol Clin North Am. 33 (4): 789-806.
2. Wapenaar, MC. et al., 2007, Immunogenetics. 59 (5): 349-57.
3. Brattsand, M. et al., 2009, J Invest Dermatol. 129 (7): 1656-65.
4. Chen, T. et al., 2009, Proteins. 77 (1): 209-19.
5. Noah, TK. et al., 2010, Exp Cell Res. 316 (3): 452-65.

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