serine Peptidase Inhibitor, Kazal Type 1 (SPINK1) ELISA Kits

Human serine Peptidase Inhibitor, Kazal Type 1 (SPINK1) interaction partners

1. PRSS1 and SPINK1 mutations serve as genetic background for hereditary pancreatitis in Japan

2. SPINK1 is both a targetable senescence-associated secretory phenotype factor and a novel noninvasive biomarker of therapeutically damaged tumor microenvironment.

3. 3 siblings with near identical clinical manifestations of early onset acute recurrent pancreatitis (ARP), all possessing the same heterozygous for serine protease inhibitor, Kazal type 1 (SPINK1) mutation c.55+1G>A.

4. We demonstrate for the first time a significant decrease of SPINK1 levels after surgical decompression of pancreatic duct and a reduction of trypsin activity analysis after endoscopic decompression

5. SPINK1 over expression is associated with prostate cancer specific mortality in at risk men with biochemical and clinical recurrence after prostatectomy

6. Data show that alteration in beta-catenin expression, a core component of the CDH17/beta-catenin axis, in tumors affects serine peptidase inhibitor Kazal type 1 (SPINK1) serum levels in hepatocellular carcinoma (HCC) patients.

7. Findings indicate that the serine protease inhibitor, Kazal type 1 (SPINK1) p.N34S allele may cause reduced SPINK1 expression.

8. Having correlated our findings with current knowledge of SPINK1's role in exocrine pancreas pathophysiology, we propose that complete and partial functional losses of the SPINK1 gene are associated with quite distinct phenotypes, the former causing a new pediatric disease entity of severe infantile isolated exocrine pancreatic insufficiency (EPI) .

9. results suggest that rs142703147:C>A, which disrupts a PTF1L-binding site within an evolutionarily conserved HNF1A-PTF1L cis-regulatory module located upstream of the SPINK1 promoter, contributes to the chronic pancreatitis risk haplotype.

10. Studied mutations in cationic trypsinogen (PRSS1) and serine protease inhibitor Kazal type 1 (SPINK1) and their association with alcoholic chronic pancreatitis (ACP) and idiopathic chronic pancreatitis.

11. Studies indicate that serine peptidase inhibitor Kazal type 1 (SPINK1) gene, particularly the N34S mutation, has a genetic association with the development of pancreatitis [Meta-analysis].

12. association between SPINK1 p.N34S gene variation and chronic pancreatitis [review, meta-analysis]

13. We present the case of a child with a homozygous mutation N34S in the SPINK1 gene, leading to acute recurrent pancreatitis and ultimately to chronic pancreatitis

14. Used in silico splicing prediction programs to prioritize SPINK1 intronic variants for further quantitative RT-PCR analysis the non-pathological c.194 + 13T > G variant was predicted by different programs to generate a new & viable donor splice site, the prediction scores being comparable to those for the physiological c.194 + 2T donor splice site & even higher than those for the physiological c.87 + 1G donor splice site.

15. Gene mutations were present in PRSS1 in 26 patients with acute recurrent and chronic pancreatitis, SPINK1 in 23, CTRC in 3, and CPA1 in 5. In the 31 patients with mutations in SPINK1, CTRC, or CPA1, 16 (51.6%) had homozygous or heterozygous mutations with other mutations.

16. SPINK1 can associate with EGFR to promote the expression of cell proliferation-related and anti-apoptosis-related genes/proteins; inhibit the expression of pro-apoptosis-related genes/proteins via p38, ERK, and JNK pathways; and consequently promote the proliferation of BRL-3A cells.

17. The present study demonstrates for the first time that both fibroblast-derived and recombinant IL-6 induces SPINK1 expression and secretion in in colorectal adenocarcinoma.

18. Absolute exclusivity between SPINK1 overexpression and homozygous PTEN deletion in localized PCA.

19. It is the first time to simultaneously detect SPINK1 and ERG expression in initially diagnosed bone metastatic prostate cancer. The over-expression of SPINK1 was not only related to poor PSA response, but also significantly associated with the occurrence of castration-resistant prostate cancer, especially in those with much more aggressive phenotype

20. We describe a case of malignant pancreatic cancer diagnosed in a young patient with chronic pancreatitis who is a SPINK 1 heterozygote gene mutation carrier

Cow (Bovine) serine Peptidase Inhibitor, Kazal Type 1 (SPINK1) interaction partners

1. Partially folded bovine pancreatic trypsin inhibitor analogues attain fully native structures when co-crystallized with S195A rat trypsin.

Mouse (Murine) serine Peptidase Inhibitor, Kazal Type 1 (SPINK1) interaction partners

1. It is a trypsin-specific inhibitor in the pancreas.

2. IFN regulatory factor 2 (Irf2) has a regulatory role in trypsinogen5 gene transcription, which is resistant to a major endogenous trypsin inhibitor, Spink3

3. SPINK3 modulates sperm physiology through a downstream reduction of endogenous NO concentration and independently of SPINK3 trypsin inhibitory activity.

4. uterine-gland-derived SPINK3, as a new paracrine modulator, might play an important role in embryo implantation through its influence on stromal decidualization in mice.

5. Spink3 may act as a growth factor, leading to cell proliferation and regeneration of tissue structure.

6. Results suggest that regulation of Prss1 and Spink3 expression is involved in the susceptibility to experimentally induced pancreatitis.

7. Spink3 trypsin inhibitor is required for normal pancreatic development. Data indicate an important relationship between endogenous pancreatic trypsin and Spink3 and the development of pancreatitis.

8. SPINK3 mRNA is upregulated in chronic pancreatitis.

9. Spink3 may play important roles in proliferation and/or differentiation of various cell types during development.