Recombinant Human KLK1

Cat.No. : KLK1-29686TH
Product Overview : Recombinant full length Human KLK1 , a single, glycosylated, polypeptide chain, predicted Mwt: 28-32 kDa.
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Species : Human
Source : Yeast
Tag : Non
Protein Length : 238 amino acids
Description : Kallikreins are a subgroup of serine proteases having diverse physiological functions. Growing evidence suggests that many kallikreins are implicated in carcinogenesis and some have potential as novel cancer and other disease biomarkers. This gene is one of the fifteen kallikrein subfamily members located in a cluster on chromosome 19. This protein is functionally conserved in its capacity to release the vasoactive peptide, Lys-bradykinin, from low molecular weight kininogen.
Molecular Weight : 28.000kDa
Tissue specificity : Isoform 2 is expressed in pancreas, salivary glands, kidney, colon, prostate gland, testis, spleen and the colon adenocarcinoma cell line T84.
Biological activity : Human Kallikrein 1 active. Unit Definitin: 1 unit will hydrolize 1 umole of H-D-Val-Leu-Arg-pNA per minute at pH 8.0 at 37°C Human Kallikrein 1 measured biological activity of no less than 5 Units/mg
Form : Liquid
Purity : by SDS-PAGE
Storage buffer : Constituent:100% PBS
Storage : Please see Notes section
Sequence Similarities : Belongs to the peptidase S1 family. Kallikrein subfamily.Contains 1 peptidase S1 domain.
Gene Name KLK1 kallikrein 1 [ Homo sapiens ]
Official Symbol KLK1
Synonyms KLK1; kallikrein 1; kallikrein 1, renal/pancreas/salivary; kallikrein-1; Klk6;
Gene ID 3816
mRNA Refseq NM_002257
Protein Refseq NP_002248
Uniprot ID P06870
Chromosome Location 19q13.3
Pathway Blood Clotting Cascade, organism-specific biosystem; Endocrine and other factor-regulated calcium reabsorption, organism-specific biosystem; Endocrine and other factor-regulated calcium reabsorption, conserved biosystem;
Function peptidase activity; serine-type endopeptidase activity;

Kallikrein–Kinin System Suppresses Type I Interferon Responses: A Novel Pathway of Interferon Regulation

Journal: Frontiers in Immunology    PubMed ID: 29456540    Data: 2018/2/2

Authors: Alecia Seliga, Michael Hweemoon Lee, Uma Sriram

Article Snippet:The following reagents were used to stimulate cells: Recombinant human IFN-α (1,000 U/ml, PBL Assay Science, Piscataway, NJ, USA), mouse IFN-α (1,000 U/ml, PBL Assay Science), CpG-B 1826 (10 μg/ml), CpG-A-2336 (5 μg/ml) (IDT Biotechnologies, Coralville, IA, USA), CpG-A-1585 (1 μg/ml) (Invivogen, San Diego, CA, USA), resiquimod (1 μg/ml) (R848; Invivogen) ( , – ), bradykinin peptide (10 μM), Lys-des-Arg(9)-bradykinin, which is a kinin breakdown product and a selective bradykinin B1 receptor agonist (10 μM), Arg–Pro–Hyp–Gly–Phe–Ser–Pro–Phe–Arg B2 receptor agonist (10 μM), B1 receptor antagonist ([des-Arg 10 -HOE140]- DH-1 μg/ml), B2 receptor antagonist (HOE140–H–10 μM) (all bradykinin agonists and antagonists were purchased from Sigma-Aldrich, St. Louis, MO, USA) , recombinant human klk1 (1 μg/ml) (Creative BioMart, Shirley, NY, USA), captopril (20 μM)(Sigma) , and indomethacin (indo) (1 μg/ml) (Sigma) ( ).

klk1 and captopril also suppress interferon-stimulated genes. (A) Murine bone-marrow-derived dendritic cells (BMDCs) were stimulated with CpG-A for 2.5 h treated with antagonists for 30 min to block both B1 (DH—1 μg/ml) and B2 (H—10 μM) receptors and then stimulated with klk1 (1 μg/ml) or captopril (20 μM) for a further 4 h. Irf7 gene expression was analyzed by qPCR. Percent fold change was calculated by normalizing to CpG-A stimulation alone. (B) Human PBMCs were first treated with IFN-α for 3 h, 20 μM captopril was added and harvested after further 3 h and IRF7 and CXCL10 gene expression was analyzed by qPCR. Percent fold change was calculated by normalizing with IFN-α stimulation alone. Panels (A,B) represent average (mean + SEM) of at least three independent experiments, performed with independent BMDC cultures from each mouse or PBMCs from each donor; * p < 0.05, ** p < 0.01, *** p < 0.001.

klk1 and captopril also suppress interferon-stimulated genes. (A) Murine bone-marrow-derived dendritic cells (BMDCs) were stimulated with CpG-A for 2.5 h treated with antagonists for 30 min to block both B1 (DH—1 μg/ml) and B2 (H—10 μM) receptors and then stimulated with klk1 (1 μg/ml) or captopril (20 μM) for a further 4 h. Irf7 gene expression was analyzed by qPCR. Percent fold change was calculated by normalizing to CpG-A stimulation alone. (B) Human PBMCs were first treated with IFN-α for 3 h, 20 μM captopril was added and harvested after further 3 h and IRF7 and CXCL10 gene expression was analyzed by qPCR. Percent fold change was calculated by normalizing with IFN-α stimulation alone. Panels (A,B) represent average (mean + SEM) of at least three independent experiments, performed with independent BMDC cultures from each mouse or PBMCs from each donor; * p < 0.05, ** p < 0.01, *** p < 0.001.

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