# |
PMID |
Sentence |
1 |
10777670
|
Proximal to Lyp are the genes caspase-2 (Casp2) and pancreatic trypsin 1 (Prss1), while neuropeptide Y (Npy) is the closest distally positioned gene.
|
2 |
10777670
|
In human, the three genes are syntenic on HSA7, but they are not on a conserved segment: CASP2 and PRSS1 are localized to 7q35, while NPY is localized to 7p15.1.
|
3 |
10777670
|
This raises the question whether the human homologue of Lyp is linked to CASP2/PRSS1 or to NPY.
|
4 |
10777670
|
We present a comparative map of the Lyp region in rat and human, assigning the gene to a 1.3-Mb segment between RNY3 and ABP1 at 7q35.
|
5 |
10777670
|
Proximal to Lyp are the genes caspase-2 (Casp2) and pancreatic trypsin 1 (Prss1), while neuropeptide Y (Npy) is the closest distally positioned gene.
|
6 |
10777670
|
In human, the three genes are syntenic on HSA7, but they are not on a conserved segment: CASP2 and PRSS1 are localized to 7q35, while NPY is localized to 7p15.1.
|
7 |
10777670
|
This raises the question whether the human homologue of Lyp is linked to CASP2/PRSS1 or to NPY.
|
8 |
10777670
|
We present a comparative map of the Lyp region in rat and human, assigning the gene to a 1.3-Mb segment between RNY3 and ABP1 at 7q35.
|
9 |
10777670
|
Proximal to Lyp are the genes caspase-2 (Casp2) and pancreatic trypsin 1 (Prss1), while neuropeptide Y (Npy) is the closest distally positioned gene.
|
10 |
10777670
|
In human, the three genes are syntenic on HSA7, but they are not on a conserved segment: CASP2 and PRSS1 are localized to 7q35, while NPY is localized to 7p15.1.
|
11 |
10777670
|
This raises the question whether the human homologue of Lyp is linked to CASP2/PRSS1 or to NPY.
|
12 |
10777670
|
We present a comparative map of the Lyp region in rat and human, assigning the gene to a 1.3-Mb segment between RNY3 and ABP1 at 7q35.
|
13 |
11414764
|
These QTLs were located on completely different chromosomal regions from those of causative genes that have been reported for human chronic pancreatitis: PRSS1, CFTR, and SPINK1.
|
14 |
12011155
|
Mutations in the pancreatic secretory trypsin inhibitor gene (PSTI/SPINK1) rather than the cationic trypsinogen gene (PRSS1) are significantly associated with tropical calcific pancreatitis.
|
15 |
12452372
|
Germline mutations in CFTR and PSTI genes in chronic pancreatitis patients.
|
16 |
12452372
|
Mutations in the cationic trypsinogen, cystic fibrosis transmembrane conductance regulator (CFTR) and pancreatic secretory trypsinogen inhibitor (PSTI) genes have recently been associated with chronic pancreatitis.
|
17 |
12452372
|
This paper investigates the frequency of CFTR and PSTI gene mutation in patients with idiopathic and alcoholic chronic pancreatitis, the clinical course of patients with these two kinds of disease, and examines the clinical differences between carriers and noncarriers of mutation.
|
18 |
12452372
|
In idiopathic pancreatitis a significant increase was found in mutation frequency both in the CFTR gene (13%) and N34S mutation in the PSTI gene (3.9%), as well as an increase in familial disposition to pancreatic disorders.
|
19 |
16054982
|
Alcohol and its metabolites (acetaldehyde and fatty acid ethyl esters) can alter metabolic pathways involved in the inflammatory response and carcinogenesis, and they are mediated by one or more of the following mechanisms: (1) premature activation of zymogens; (2) induction of the inflammatory response through activation of nuclear transcription factors, including nuclear factor-kappa and activation protein 1; (3) increased production of reactive oxygen species, resulting in oxidative DNA damage and altered effect of dietary antioxidants; (4) activation of pancreatic stellate cells, which leads to fibrosis; (5) gene mutation in enzymes related to cytochrome P450, glutathione S-transferase, aldehyde dehydrogenase, cationic trypsinogen, and pancreatic secretory trypsin inhibitor; (6) synergistic effects of ethanol and tobacco carcinogen on NNK [nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone] metabolism; and (7) dysregulation of proliferation and apoptosis.
|
20 |
16111090
|
Strong variants were the rare autosomal-dominant mutations N29I and R122H of PRSS1 (cationic trypsinogen) and homozygous N34S of SPINK1 (pancreatic secretory trypsin inhibitor).
|
21 |
17031196
|
Some cause a high-penetrance, autosomal dominant type of clinical picture (eg, mutations at codons 29 and 122 of the cationic trypsinogen gene), whereas others have a low penetrance or are frequent in the general population (eg, mutations in Kazal type 1 [SPINK1] and in codons 16, 22, and 23 of the cationic trypsinogen gene) and act as disease modifiers.
|
22 |
17082646
|
DRlyp/lyp PLN mast cell gene expression profiling revealed an activated population and included significant overrepresentation of transcripts for mast cell protease 1, cationic trypsinogen, carboxypeptidase A, IL-5, and phospholipase Cgamma.
|
23 |
17082646
|
In the DR(+/+) rat, which develops T1DM upon depletion of T regulator cells, mast cells displayed gene expression consistent with the negative regulation of degranulation, including significant overrepresentation of transcripts encoding tyrosine phosphatase SHP-1, lipid phosphatase SHIP, and E3 ubiquitin ligase c-Cbl.
|
24 |
18428024
|
Urinary matrix metalloproteinase -8, -9, -14 and their regulators (TRY-1, TRY-2, TATI) in patients with diabetic nephropathy.
|
25 |
18428024
|
We studied the levels, molecular forms, and degree of activation of urinary MMP-8, -9, -14, trypsin-1 and -2, as well as tumor-associated trypsin inhibitor (TATI) of DNP patients and healthy controls.
|
26 |
18428024
|
Urinary samples were analyzed for MMPs by Western blotting and gelatin zymography and for trypsin-1, -2, and TATI by time-resolved immunofluorometric assays.
|
27 |
18428024
|
Total MMP-8 immunoreactivity, the proportion of active MMP-9, and gelatinolytic activity in urine were significantly higher in DNP patients than in controls.
|
28 |
18428024
|
MMP-8 and MMP-9 were found to form high molecular weight complexes in DNP urine.
|
29 |
18428024
|
Total immunoreactivity of soluble urinary MMP-14 and the levels of trypsin (TRY)-1 and TRY-2, but not of TATI, were also significantly increased in DNP.
|
30 |
18428024
|
Zymography, Western blotting, and immunofluorometric analysis of DNP urine showed a significant association especially between activation of MMP-9 as well as PMN-type MMP-8 and TRY-2.
|
31 |
18428024
|
Urinary matrix metalloproteinase -8, -9, -14 and their regulators (TRY-1, TRY-2, TATI) in patients with diabetic nephropathy.
|
32 |
18428024
|
We studied the levels, molecular forms, and degree of activation of urinary MMP-8, -9, -14, trypsin-1 and -2, as well as tumor-associated trypsin inhibitor (TATI) of DNP patients and healthy controls.
|
33 |
18428024
|
Urinary samples were analyzed for MMPs by Western blotting and gelatin zymography and for trypsin-1, -2, and TATI by time-resolved immunofluorometric assays.
|
34 |
18428024
|
Total MMP-8 immunoreactivity, the proportion of active MMP-9, and gelatinolytic activity in urine were significantly higher in DNP patients than in controls.
|
35 |
18428024
|
MMP-8 and MMP-9 were found to form high molecular weight complexes in DNP urine.
|
36 |
18428024
|
Total immunoreactivity of soluble urinary MMP-14 and the levels of trypsin (TRY)-1 and TRY-2, but not of TATI, were also significantly increased in DNP.
|
37 |
18428024
|
Zymography, Western blotting, and immunofluorometric analysis of DNP urine showed a significant association especially between activation of MMP-9 as well as PMN-type MMP-8 and TRY-2.
|
38 |
18428024
|
Urinary matrix metalloproteinase -8, -9, -14 and their regulators (TRY-1, TRY-2, TATI) in patients with diabetic nephropathy.
|
39 |
18428024
|
We studied the levels, molecular forms, and degree of activation of urinary MMP-8, -9, -14, trypsin-1 and -2, as well as tumor-associated trypsin inhibitor (TATI) of DNP patients and healthy controls.
|
40 |
18428024
|
Urinary samples were analyzed for MMPs by Western blotting and gelatin zymography and for trypsin-1, -2, and TATI by time-resolved immunofluorometric assays.
|
41 |
18428024
|
Total MMP-8 immunoreactivity, the proportion of active MMP-9, and gelatinolytic activity in urine were significantly higher in DNP patients than in controls.
|
42 |
18428024
|
MMP-8 and MMP-9 were found to form high molecular weight complexes in DNP urine.
|
43 |
18428024
|
Total immunoreactivity of soluble urinary MMP-14 and the levels of trypsin (TRY)-1 and TRY-2, but not of TATI, were also significantly increased in DNP.
|
44 |
18428024
|
Zymography, Western blotting, and immunofluorometric analysis of DNP urine showed a significant association especially between activation of MMP-9 as well as PMN-type MMP-8 and TRY-2.
|
45 |
18604651
|
These include alterations in genes coding for trypsinogens, the most abundant digestive enzymes (PRSS1 and PRSS2), the trypsin inhibitor (SPINK1) and the trypsin-degrading enzyme, chymotrypsinogen C (CTRC).
|
46 |
18604651
|
Indeed, alterations in at least two genes, SPINK1 and CTRC, are strongly associated with TCP.
|
47 |
23721890
|
Variants in four chronic pancreatitis genes, PRSS1, SPINK1, CTRC and CFTR, were systematically analyzed in the studied cases.
|
48 |
23721890
|
A heterozygous CTRC-deleting complex rearrangement, which was co-inherited with different trans variants in SPINK1, CFTR or PRSS1, is associated with variable phenotypes (chronic pancreatitis; pancreatic cancer and chronic pancreatitis; and type 1 diabetes).
|
49 |
23721890
|
Variants in four chronic pancreatitis genes, PRSS1, SPINK1, CTRC and CFTR, were systematically analyzed in the studied cases.
|
50 |
23721890
|
A heterozygous CTRC-deleting complex rearrangement, which was co-inherited with different trans variants in SPINK1, CFTR or PRSS1, is associated with variable phenotypes (chronic pancreatitis; pancreatic cancer and chronic pancreatitis; and type 1 diabetes).
|