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Human SPINK4 Gene cDNA clone plasmid

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Human SPINK4 cDNA Clone Product Information
Gene_bank_ref_id:NM_014471.1
RefSeq ORF Size:261bp
cDNA Description:Full length Clone DNA of Homo sapiens serine peptidase inhibitor, Kazal type 4.
Gene Synonym:PEC-60, MGC133107, SPINK4
Species:Human
Vector:pMD18-T Simple Vector
Plasmid:pMD-SPINK4
Restriction Site:
Tag Sequence:
Sequence Description:Identical with the Gene Bank Ref. ID sequence.
Sequencing primers:
Promoter:
Application:
Antibiotic in E.coli:
Antibiotic in mammalian cell:
Shipping_carrier:Each tube contains lyophilized plasmid.
Storage:The lyophilized plasmid can be stored at room temperature for three months.
pMD18-T Vector Information

pMD18-T Vector is a high-efficiency TA cloning vector constructed from pUC18, of which multiple cloning sites as shown below. The pMD18-T Vector is 2.6kb in size and contains the amplicin resistance gene for selection. The coding sequence was inserted by TA cloning at site 425.

pMD18-T vector Usage Suggestion:

The coding sequence can be amplified by PCR with M13-47 and RV-M primers.

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Background

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
  • Schneider, A. et al., 2004,Gastroenterol Clin North Am. 33 (4): 789-806.
  • Wapenaar, MC. et al., 2007, Immunogenetics. 59 (5): 349-57.
  • Brattsand, M. et al., 2009, J Invest Dermatol. 129 (7): 1656-65.
  • Chen, T. et al., 2009, Proteins. 77 (1): 209-19.
  • Noah, TK. et al., 2010, Exp Cell Res. 316 (3): 452-65.
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    Catalog: HG11669-M
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