Human Pancreatic secretory trypsin inhibitor(SPINK1) ELISA kit

Instructions
Code CSB-EL022575HU
Size 96T,5×96T,10×96T
Trial Size 24T ELISA kits trial application
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Product Details

Alternative Names ISK1_HUMAN ELISA Kit; Pancreatic secretory trypsin inhibitor ELISA Kit; Pancreatic serine protease inhibitor Kazal ELISA Kit; PCTT ELISA Kit; PSTI ELISA Kit; Serine protease inhibitor Kazal type 1 ELISA Kit; Serine protease inhibitor Kazal-type 1 ELISA Kit; Spink 3 ELISA Kit; SPINK1 ELISA Kit; Spink3 ELISA Kit; TaTI ELISA Kit; TCP ELISA Kit; Tumor associated trypsin inhibitor ELISA Kit; Tumor-associated trypsin inhibitor ELISA Kit
Abbreviation SPINK1
Uniprot No. P00995
Species Homo sapiens (Human)
Sample Types serum, plasma, tissue homogenates
Detection Range 78 pg/ml - 5000 pg/ml
Sensitivity 19.5 pg/ml
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Cell Biology
Assay Principle quantitative
Measurement Sandwich
Troubleshooting
and FAQs
ELISA kit FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 7-14 working days

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Target Background

Function
(From Uniprot)
Serine protease inhibitor which exhibits anti-trypsin activity
Gene References into Functions
  1. 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. PMID: 29346218
  2. 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 PMID: 29525377
  3. SPINK1 over expression is associated with prostate cancer specific mortality in at risk men with biochemical and clinical recurrence after prostatectomy PMID: 27238617
  4. 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. PMID: 28631187
  5. Findings indicate that the serine protease inhibitor, Kazal type 1 (SPINK1) p.N34S allele may cause reduced SPINK1 expression. PMID: 28609377
  6. 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) . PMID: 28945313
  7. 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. PMID: 28556356
  8. 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. PMID: 29641165
  9. 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]. PMID: 28984793
  10. association between SPINK1 p.N34S gene variation and chronic pancreatitis [review, meta-analysis] PMID: 28546062
  11. 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 PMID: 28229614
  12. 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. PMID: 28472998
  13. 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. PMID: 27409067
  14. 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. PMID: 28845526
  15. 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. PMID: 26663388
  16. Absolute exclusivity between SPINK1 overexpression and homozygous PTEN deletion in localized PCA. PMID: 27738792
  17. 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 PMID: 27159572
  18. 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 PMID: 27358244
  19. Mutations in CFTR, SPINK1 or PRSS1 are present in one third of pediatric acute recurrent (ARP) or chronic (CP) pancreatitis with no other cause. PMID: 26692446
  20. TATI proved to be a sensitive indicator of disease recurrence and distant metastasis, with a sensitivity of 84.4% and 75.7%, respectively. PMID: 26350184
  21. Sixteen patients exhibited heterozygous pathogenic variants of SPINK1, including c.194+2T>C (n=12), p.N34S (n=3), and a novel pathogenic splicing variation c.194+1G>A. PMID: 27578509
  22. Data indicate that SPINK1 expression status shows a lower rate of concordance between primary prostate cancer (PCA) site and nodule metastases, than those of ERG and PTEN. PMID: 26725250
  23. Approx 25% of discontinuously involved prostate biopsy cores showed tumor foci with discordant ERG/SPINK1 status, consistent with multiclonal disease. PMID: 26743468
  24. Letter/Case Report: high penetrance of the PRSS1 A16V mutation caused by SPINK1 N34S and CFTR TG11-5T co-mutations associated with pancreatitis. PMID: 26658045
  25. Identify SPINK1 promoter variants exhibiting significant functional defects that should be considered potential risk factors for chronic pancreatitis. PMID: 26348468
  26. expression represents an independent prognostic factor for poor survival in ovarian carcinoma patients PMID: 26437224
  27. The SPINK1 protein seems to play a role in tumor proliferation. PMID: 26037168
  28. neither ERG nor SPINK1 appear to be useful biomarkers for prognostication of early stage prostate cancer PMID: 26172920
  29. The majority of children with genetic predisposition to idiopathic acute and acute recurrent pancreatitis have the SPINK1 mutation. PMID: 25981744
  30. Patients with SPINK1 N34S mutations were more likely to develop a Dilated duct, Calcifications, and Diabetes as Long-term Outcome of Endoscopic Treatments in Idiopathic Chronic Pancreatitis. PMID: 26632706
  31. Evidence suggests that SPINK1 is an important growth factor that connects chronic inflammation and cancer. PMID: 25804623
  32. Over-expression of FOXP1 and SPINK1 may participate in the carcinogenesis of hepatitis B virus related cirrhosis. PMID: 26054682
  33. SPINK1 plays a role as a growth factor, signaling through the EGFR pathway in pancreatic ductal adenocarcinoma and neoplasms, and that the EGFR is involved in the malignant transformation of IPMN. PMID: 23475261
  34. In Israel, pediatric as well as adult recurrent acute pancreatitis and chronic pancreatitis are often associated with cationic trypsinogen, SPINK1, chymotrypsin C, or Cystic Fibrosis Transmembrane Conductance Regulator mutations. PMID: 25383785
  35. Mutation p.N34S in SPINK1 may predispose patients to acute pancreatitis, especially in those abusing alcohol, and may promote a more severe course of the disease. PMID: 26100556
  36. This study shows that PRSS1, SPINK1 and CFTR mutations do not play a role in alcoholic and idiopathic chronic pancreatitis patients. PMID: 25835118
  37. no mutation associated with pancreatitis PMID: 26376395
  38. OPN, SPINK1, GPC3 and KNPA2 were significantly over-expressed in HCC tissues. These genes may be useful in developing future biomarkers and therapeutic strategies for HCC PMID: 25862856
  39. SPINK1 promoter variants are likely to be associated with the risk of BPH. PMID: 26124326
  40. These data highlight the importance of SPINK1/TATI as a tumor marker for HCV-induced HCC and may lead to a better understanding of HCV-induced hepatocarcinogenesis. PMID: 25531719
  41. Our results suggest that SPINK1 protein expression may not be a predictor of recurrence or lethal prostate cancer amongst men treated by radical prostatectomy PMID: 24687926
  42. One novel SPINK1 mutation was identified in Mexican patients with early onset idiopathic recurrent acute pancreatitis. PMID: 25206283
  43. Results suggest that sequence evaluation of the SPINK1 promoter region in patients with chronic pancreatitis is justified as part of the etiological investigation. PMID: 25792561
  44. ERG and TFF3 expression characterize 2 distinct subsets of prostate cancer, with a more aggressive subgroup of TFF3-expressing tumors that express SPINK1. PMID: 25639219
  45. The p.N34S mutation in SPINK1 gene was found more frequently in patients with AP in the Indian population, irrespective of disease etiology and whether the disease was recurrent or not, and with earlier age of onset. PMID: 24844923
  46. The SPINK1 mutation frequency was significantly decreased in patients with pancreatic cancer in comparison with patients with idiopathic pancreatitis but varied not significantly in comparison with healthy controls. PMID: 25003218
  47. study found a significant association of SPINK1 (N34S) gene polymorphism with chronic pancreatitis PMID: 24616641
  48. An association between strong claudin-5 expression and higher serum levels of TATI (p=0.04) and CA125 (p=0.008) were found PMID: 25667483
  49. Over-expression of TATI predicts an unfavorable outcome in several cancers and serum TATI can be used to identify patients at increased risk of aggressive disease--{REVIEW} PMID: 24583226
  50. Data indicate epidermal growth factor receptor (EGFR)+/tumor-associated trypsinogen inhibitor (TATI)+ patients showed better survival. PMID: 24204699

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Involvement in disease Pancreatitis, hereditary (PCTT); Tropical calcific pancreatitis (TCP)
Subcellular Location Secreted
Database Links

HGNC: 11244

OMIM: 167790

KEGG: hsa:6690

STRING: 9606.ENSP00000296695

UniGene: Hs.407856

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