Publication for PRSS1 and PRSS2

Species	Symbol	Function*	Entrez Gene ID*	Other ID	Gene coexpression	CoexViewer
hsa	PRSS1	serine protease 1	5644			[link]
hsa	PRSS2	serine protease 2	5645

Pubmed ID	Priority	Text
28096305	0.98	PRSS1 encodes trypsinogen-1 (cationic trypsin), PRSS2 encodes trypsinogen-2 (anionic trypsin) and PRSS3 encodes trypsinogen-3, where at least two isoforms with overlapping mature peptide sequences, formerly designated as mesotrypsinogen and trypsinogen IV, have been functionally characterised.
	0.97	PRSS1 and PRSS2 expression in IBS tissues versus healthy controls (see online supplementary figure S2A, B).
	0.97	PRSS1 (cationic trypsin: trypsin-1 precursor), PRSS2 (anionic trypsin: trypsin-2 precursor) and PRSS3 (trypsin-3 precursor) in control, lipopolysaccharide (LPS)-treated or epinephrine-treated Caco-2 cell monolayers.
	0.54	PRSS1, PRSS2 and PRSS3 forms were present in intestinal epithelial cells (figure 3A, B), and in human colonic tissues (figure 3B).
23987515	0.97	try 2 compared to try 1 for autologous fresh cycles, averaging 7.7 percentage points higher over five cycles.
	0.97	try 1, 38% also had a single embryo transfer in try 2, and 62% had more than one embryo transferred.
	0.97	try 2 compared to try 1 for fresh autologous cycles, averaging 7.7 percentage points higher.
	0.97	try 2 and try 1, nor did fresh or thawed donor cycles.
	0.97	try 1 returned for try 2, compared to 33.2% with singletons).
	0.96	Try 1 are more likely to return for Try 2.
	0.96	try 2 were more likely to have had an ART singleton versus multiple birth (33.2% after a try 1 singleton versus 8.1% after twins and 4.9% after triplets), and less likely to have a diagnosis of diminished ovarian reserve or tubal factors.
	0.96	try 2 versus try 1.
	0.96	try 1, 40% had fewer transferred in try 2.
	0.95	try 2 versus try 1 with thawed autologous cycles, or either fresh or thawed donor cycles.
	0.95	try 1 and try 2 for thawed cycles.
	0.82	try 1 and 49-56% for try 2.
	0.75	try 1 and 25,541 women in try 2 (see Table 1).
23143602	0.97	PRSS1-PRSS2 locus (Fig. 1; Table 2; Supplementary Figs. 4-5, Supplementary Table 2).
	0.97	PRSS1-PRSS2 and CLDN2 loci, although we also conducted a joint analysis of Stage 1 and Stage 2 data to uncover any new risk loci.
	0.97	PRSS1-PRSS2 locus exert a similar effect in patients with recurrent acute pancreatitis or chronic pancreatitis, it is reasonable to conjecture that variation at rs10273639 or variation in linkage disequilibrium with it directly affects risk for chronic pancreatitis and recurrent acute pancreatitis through its impact on trypsinogen expression.
	0.96	PRSS1-PRSS2 locus is associated with lower PRSS1 gene expression and that this effect is independent of the previously reported rare gain-of-function PRSS1 variants that increase susceptibility to both recurrent acute pancreatitis and chronic pancreatitis.
	0.95	PRSS1-PRSS2 loci (Figure 1; Supplementary Table 2-3; Supplementary Figs. 6-7).
	0.91	PRSS1 encodes cationic trypsinogen, and PRSS2 encodes anionic trypsinogen.
	0.65	PRSS1-PRSS2 locus), with the minor T allele reducing risk, and 0.26 for the T allele at rs12688220 (CLDN2 locus).
	0.52	PRSS1-PRSS2 loci alter risk for alcohol-related and sporadic pancreatitis
30524475	0.97	PRSS1-PRSS2 and MORC4 Loci and the Risk of Post-ERCP Pancreatitis
	0.96	PRSS1-PRSS2 (rs10273639) and MORC4 (rs12688220) are associated with recurrent acute pancreatitis and chronic pancreatitis.
	0.96	PRSS1-PRSS2 rs10273739 and MORC4 rs12688220 and PEP.
	0.95	PRSS1-PRSS2 (T and C) are 59 and 13 vs. 6 and 2 in mild and moderate/severe cases, respectively (p = 0.633).
	0.95	PRSS1-PRSS2 (T and C) are 59 and 13 versus 6 and 2 in mild and moderate/severe cases, respectively (p = 0.63).
	0.93	PRSS1-PRSS2 (TT, TC, and CC) are 26, 13, and 1 vs. 67, 25, and 1 in cases and controls, respectively (p = 0.642).
	0.93	PRSS1-PRSS2 (rs10273639) and MORC4 (rs12688220) are not associated with the risk or severity of post-ERCP pancreatitis.
	0.91	PRSS1-PRSS2 and MORC4 are not associated with the risk or severity of post-ERCP pancreatitis.
26820620	0.97	PRSS1-PRSS2 locus with OR 0.60 (95% CI [0.48-0.76], P = 9.92 x 10-06) as protective for CP.
	0.96	PRSS1-PRSS2 locus (OR 0.60; P = 9.92 x 10-06) and SAMD12-TNFRSF11B (OR 0.49, 95% CI [0.31-0.78], P = 0.0027).
	0.96	PRSS1-PRSS2 and SMAD12-TNFRSF11B loci with CP in Indians subjects of Indo-European origin and showed significant association particularly with variants in the MORC4/CLDN2 locus.
	0.95	PRSS1-PRSS2 locus in all three categorical analyses i.e. ICP and ACP combined as well as only ICP/ ACP versus controls suggesting a role of PRSS1-PRSS2 locus in Indian patients.
	0.93	PRSS1-PRSS2 locus with OR 0.55 (95% CI [0.39-0.79], P = 0.001) was present in ACP patients.
	0.90	PRSS1-PRSS2 locus was significantly associated in ICP patients similar to its status in the combined analysis (OR 0.63, 95% CI [0.49-0.82]; P = 5.78 x 10-04).
28536777	0.97	PRSS1-PRSS2 locus in subjects with idiopathic chronic pancreatitis with no family history.
	0.95	PRSS1-PRSS2 Copy Number Mutations
	0.93	PRSS1-PRSS2 locus was associated with hereditary pancreatitis.
	0.84	PRSS1 (c.-204C>A) which is part of a larger haplotype in the PRSS1-PRSS2 locus confers a small (1.4-fold to 1.6-fold) protective effect against chronic pancreatitis.
	0.84	cationic trypsinogen (PRSS1) and anionic trypsinogen (PRSS2).
28754779	0.97	PRSS1-PRSS2 and SPINK1 in alcoholic CP patients.
	0.94	PRSS1-PRSS2 and SPINK1 locus variants in ACP indicates that this mechanism is also relevant for ACP.
	0.90	PRSS1-PRSS2 reported in a previous GWAS.
	0.87	PRSS1-PRSS2 and SPINK1
	0.63	PRSS1-PRSS2 locus (rs2855983) were in linkage disequilibrium (LD) with the previously identified lead SNPs in these loci (see online supplementary table S3).
18986305	0.97	cationic trypsinogen from conditioned media of HEK 293T cells transfected with PRSS1 and PRSS2 plasmids with or without TPST2 plasmid.
	0.91	PRSS1) and serine protease 2 (PRSS2) genes on chromosome 7 and the serine protease 3 (PRSS3) gene on chromosome 9.
	0.52	PRSS1 gene were shown to cause hereditary chronic pancreatitis and a variant of the PRSS2 gene was shown to afford protection against chronic pancreatitis.
21631589	0.97	cationic trypsinogen, CTRC cleaves human anionic trypsinogen and human mesotrypsinogen at multiple sites.
	0.96	PRSS1, PRSS2, SPINK1 and CFTR mutations in chronic pancreatitis has been the subject of excellent reviews.
	0.94	PRSS1 and SPINK1 mutations, we found that the p.G191R variant in PRSS2 results in rapid autodegradation of anionic trypsinogen and thereby affords protection against chronic pancreatitis.
30134826	0.97	PRSS1, PRSS2, SPINK1, CTRC, CASR, CFTR, CTSB and KRT8 and 23 additional genes implicated in the PSP.
	0.97	PRSS1 in cis, 4 patients were heterozygous for CTRC mutations, 3 patients were heterozygous for PRSS2 mutations, 2 patients were heterozygous for CASR mutations and 2 patients were heterozygous for KRT8 mutations; 1 patient had a splicing mutation in PRSS1 and a missense mutation in KRT8 (Table 2).
	0.92	PRSS1/PRSS2 hybrid mutation and a heterozygous missense mutation of CTRC, respectively (Table 3).
21084314	0.97	trypsin1- and trypsin2-knockdown, particularly the latter, in H9c2 cardiomyoblasts significantly suppressed viral replication, up-regulation of MMPs, and production of active MMP-9 and cytokines, resulting in marked protection against cellular damage, ATP depletion, and apoptosis.
	0.95	trypsin1 (cationic trypsin, T1), trypsin2 (anionic trypsin, T2), and trypsin3 (mesotrypsin, T3).
23882137	0.97	Trypsin-1 and trypsin-2 appear to have a function in the degradation of vitreous type II collagen.
	0.96	Trypsin-1 was present as a double band and trypsin-2 as a single band (arrowheads).
24007357	0.97	Try2) case and (c) 90% (Try4) case.
	0.92	Try2, and Try4, respectively.
20950468	0.97	PRSS2 (cationic trypsinogen type 2) gene protects against chronic pancreatitis.
23035638	0.97	cationic trypsinogen (serine protease 1, PRSS1), anionic trypsinogen (PRSS2) and mesotrypsinogen (PRSS3).
25838820	0.97	PRSS1 and PRSS2 genes using genomic DNA from patients with hereditary pancreatitis (HP).
27555793	0.97	PRSS1 gene, as well as two exons on PRSS2 (which codes for anionic trypsinogen, a protein with functions similar to cationic trypsinogen), were found to be duplicated in patients with HP, causing gain-of-function mutations that increase the amount of trypsinogen produced.
20407433	0.96	PRSS1 and PRSS2 (Figure 1a).
	0.93	cationic trypsinogen (PRSS1), anionic trypsinogen (PRSS2), mesotrypsinogen (PRSS3), chymotrypsinogen B and (pro)elastase 3B (CELA3B) (Figure 3).
	0.91	PRSS1) and anionic trypsinogen (PRSS2) (Figure 4a).
	0.61	PRSS1, and PRSS2 but not against PRSS3.
	0.55	PRSS1, anti-PRSS2 and anti-PSTI in AIP patients.
22586407	0.96	PRSS1 and PRSS2 genes using genomic DNA from patients with HP.
	0.93	cationic trypsinogen (protease serine 1; PRSS1), anionic trypsinogen (protease serine 2; PRSS2), pancreatic secretory trypsin inhibitor (PSTI; serine protease inhibitor Kazal type 1; SPINK1), cystic fibrosis transmembrane conductance regulator (CFTR), chymotrypsinogen C (CTRC), and calcium-sensing receptor (CASR) have been shown to be associated with HP (Whitcomb,).
	0.90	PRSS1 gene mutations enhances the risk for CP, it was thought that mutations in the PRSS2 gene may predispose to disease (Witt et al.,).
27802312	0.96	PRSS1-PRSS2 and CLDN2-MORC4 locus.
	0.84	PRSS1 (cationic trypsinogen), CFTR (cystic fibrosis transmembrane conductance regulator), SPINK1 (serine protease, kazal type 1), CTRC (chymotrypsinogen C), CPA1 (carboxypeptidase A1) and the CLDN2-MORC4 locus have been identified to increase risk of CP development, a rare variant in PRSS2 (anionic trypsinogen) and a common variant in the PRSS1-PRSS2 locus are protective.
20452997	0.96	PRSS1 and PRSS2, the gene encoding human anionic trypsinogen.
29118810	0.96	PRSS1-PRSS2 locus account for an increased risk for alcoholic and sporadic CP, but rare PRSS1 gene variants, including three known diseases that were also screened and identified, were not associated with the observed phenotype.
29193645	0.95	Trypsin-1 levels were not affected by inhibitors (Fig. 4C, right panel) and trypsin-2 was not detected in the Caco-2 cell conditioned media by IFMA.
	0.79	trypsin-1 and trypsin-2 in a panel of CRC and melanoma cell lines harboring either wild-type or V600E BRAF.
	0.73	trypsin-1 (Fig. 4A, mid-panel) and trypsin-2 (Fig. 4A, bottom panel) levels at 72-h time point, suggesting inverse regulation between SPINK1 and its target proteases.
	0.69	trypsin-1, and trypsin-2 at 72-h time point in a panel of cell lines and their respective BRAF status.
31911942	0.95	PRSS1, PRSS2, and PRSS3 on cetuximab efficacy, we compared the expression data of the following six colon cancer cell lines: DiFi, LoVo, Caco-2, HT-29, HCT-8, and SW480.
	0.88	PRSS1, PRSS2, and PRSS3 mRNA expression in the cell lines.
	0.60	PRSS1 was significantly more highly expressed in the cetuximab-resistant cell lines than in the cetuximab-sensitive cell lines (Fig. 1B); PRSS2 and PRSS3 expression levels showed almost no differences between the cetuximab-resistant and cetuximab-sensitive cell lines.
30467200	0.95	PRSS1-PRSS2 top SNPs in the AALL0232 cohort strengthens the credibility of this result.
	0.53	PRSS1-PRSS2 variant (rs13228878) was modified by rs17107315 (SPINK1), rs10436957 (CTRC) and rs4409525 (CLDN2), no significant interactions were identified (P=0.48, P=0.95 and P=0.93, respectively).
23622139	0.94	PRSS1-PRSS2 locus significantly reduces expression of PRSS1 and reduces the risk of pancreatitis .
26228362	0.94	Anionic trypsinogen (PRSS2) shares the same physiological activity with cationic trypsinogen (PRSS1) but is synthesized in lower amounts and auto-activates less but autolyzes more rapidly.
28497564	0.93	PRSS1, PRSS2 (encoding anionic trypsinogen; MIM# 601564), SPINK1 (encoding pancreatic secretory trypsin inhibitor; MIM# 167790) and CTRC (encoding chymotrypsin C, which specifically degrades all human trypsinogen/trypsin isoforms; MIM# 601405) - have established the importance of a balance between the activation and inactivation of trypsinogen within the pancreas, thereby defining a trypsin-dependent pathway as a key component of the pathogenesis of chronic pancreatitis.
22885947	0.91	PRSS1 and PRSS2 expression appear to reduce the risk of pancreatitis from both Trypsin Pathways.
	0.81	PRSS1 haplotype that reduces PRSS1 and PRSS2 gene expression.
18665081	0.91	cationic trypsinogen (solid squares), and human anionic trypsinogen (solid triangles) were activated at 2 microM concentration with enteropeptidase for 60 min at 37 C in the presence of 1 mM CaCl2.
27341355	0.90	PRSS1-PRSS2 SNP, and an increased risk in variants of the CLDN2-MORC2 loci in alcoholic CP.
25546417	0.89	PRSS1-PRSS2 hybrid allele carried both p.N29I and p.N54S mutations.
	0.88	PRSS1 and PRSS2.
	0.60	PRSS1 and PRSS2, the present study confirms and extends the importance of gene conversions between trypsinogen genes in the generation of new pathogenic alleles in chronic pancreatitis.
29629340	0.88	PRSS1 and PRSS2 produced marginal results, unlike that with PRSS3 (Figures 6D,E).
	0.87	PRSS1, PRSS2, PRSS3, or vector only) for the indicated periods.
	0.52	PRSS1, PRSS2, and PRSS3 in human cells), PRSS1 and PRSS3 were expressed ubiquitously, but the expression profile of PRSS2 was low in A549, H292, and HT1080 cells (Figure 2B).
	0.51	PRSS1, PRSS2, and PRSS3) are expressed in non-pancreatic cells in humans (Wang et al.,; Yamamoto-Tanaka et al.,; Ghilardi et al.,), and some ectopic trypsins can enhance IAV proliferation in rat cardiomyoblasts and the lungs (Pan et al.,; Indalao et al.,).
19690177	0.87	PRSS1, and PRSS2 were selected.
24146905	0.87	PRSS1, NM_002769) and type 2 (gene ID: PRSS2, NM_002770) trypsinogen sequences were observed (figure S1).
30305676	0.84	cationic trypsinogen (PRSS1, serine protease 1) and anionic trypsinogen (PRSS2), and the minor isoform mesotrypsinogen (PRSS3).
19191323	0.80	PRSS1 and SPINK1 mutations, the p.G191R variant in the PRSS2 gene (MIM# 601564) was found to afford protection against chronic pancreatitis.
25010489	0.79	cationic trypsinogen was somewhat increased by sulfation but a similar effect was not observed with anionic trypsinogen.
26376395	0.76	PRSS2 = anionic trypsinogen, PRSS1 = cationic trypsinogen, SPINK1 = serine protease inhibitor Kazal type 1.
25774637	0.73	cationic trypsinogen (PRSS1, MIM276000), serine protease inhibitor Kazal type 1 (SPINK1, MIM167790), chymotrypsinogen C (CTRC, MIM601405), carboxypeptidase A1 (CPA1, MIM114850), and anionic trypsinogen (PRSS2, MIM601564).
29333155	0.62	PRSS1-PRSS2 Locus
	0.59	Cationic trypsinogen and anionic trypsinogen (encoded by PRSS1 and PRSS2, resp.) are the most abundant forms of trypsinogen in the pancreas.
27999401	0.53	PRSS1 and PRSS2 or between PRSS1 and the pseudogene PRSS3P2 were shown to generate pathogenic alleles that cause hereditary pancreatitis.
23872486	0.51	PRSS1-PRSS2 low-risk genotype however, should likely undergo a more thorough evaluation for other putative etiologies of AP.