Ignet

Gene Information

Gene symbol: KLK3

Gene name: kallikrein-related peptidase 3

HGNC ID: 6364

Synonyms: PSA

Related Genes

#	Gene Symbol	Number of hits
1	ACCS	1 hits
2	ACPP	1 hits
3	ADIPOQ	1 hits
4	AFP	1 hits
5	AIRE	1 hits
6	AKT1	1 hits
7	ALOX5	1 hits
8	ALX4	1 hits
9	CBL	1 hits
10	CCL2	1 hits
11	CEACAM5	1 hits
12	CLEC7A	1 hits
13	CRP	1 hits
14	GAA	1 hits
15	GAD1	1 hits
16	GAD2	1 hits
17	GPT	1 hits
18	GRB10	1 hits
19	HBB	1 hits
20	HLA-DRB1	1 hits
21	HMOX1	1 hits
22	HPT	1 hits
23	IDDM2	1 hits
24	IGF1R	1 hits
25	IL10	1 hits
26	IL1B	1 hits
27	IL6	1 hits
28	INS	1 hits
29	INSR	1 hits
30	IRS1	1 hits
31	IRS2	1 hits
32	ITGAX	1 hits
33	JAK2	1 hits
34	LEP	1 hits
35	MAPK3	1 hits
36	NOS2A	1 hits
37	PHKA1	1 hits
38	PRL	1 hits
39	SH2B1	1 hits
40	SH2B3	1 hits
41	SHC1	1 hits
42	SLC27A1	1 hits
43	SLC2A4	1 hits
44	SMCR	1 hits
45	STAT1	1 hits
46	STAT3	1 hits
47	TGFA	1 hits
48	TNF	1 hits

Related Sentences

#	PMID	Sentence
1	7505244	GAD autoantibodies in IDDM, stiff-man syndrome, and autoimmune polyendocrine syndrome type I recognize different epitopes.
2	7505244	Glutamic acid decarboxylase (GAD) is a major islet cell autoantigen in insulin-dependent diabetes mellitus (IDDM), and autoantibodies are found in high frequencies in patients with recent-onset IDDM, stiff-man syndrome (SMS), and autoimmune polyendocrine syndrome type I (APS I).
3	7505244	In this study, we examined the reactivity of anti-GAD-containing sera from 7 patients with IDDM, 4 patients with SMS, and 5 patients with APS I.
4	7505244	All sera immunoprecipitated GAD from [35S]methionine-labeled rat islet lysates and the sera from patients with SMS and APS I, but none of the IDDM patients' sera, identified the GAD protein in Western blots.
5	7505244	Two of four SMS patients' sera and 5 of 5 APS I patients' sera, in contrast to 0 of 7 IDDM patients' sera, inhibited the enzymatic activity of GAD.
6	7505244	When the various sera were tested with the GAD65 and GAD67 isoforms, produced separately by transient expression in COS cells, the enzymatic activity of GAD65 was inhibited by sera from patients with SMS and APS I, whereas no effect on the GAD67 activity was observed.
7	7505244	GAD autoantibodies in IDDM, stiff-man syndrome, and autoimmune polyendocrine syndrome type I recognize different epitopes.
8	7505244	Glutamic acid decarboxylase (GAD) is a major islet cell autoantigen in insulin-dependent diabetes mellitus (IDDM), and autoantibodies are found in high frequencies in patients with recent-onset IDDM, stiff-man syndrome (SMS), and autoimmune polyendocrine syndrome type I (APS I).
9	7505244	In this study, we examined the reactivity of anti-GAD-containing sera from 7 patients with IDDM, 4 patients with SMS, and 5 patients with APS I.
10	7505244	All sera immunoprecipitated GAD from [35S]methionine-labeled rat islet lysates and the sera from patients with SMS and APS I, but none of the IDDM patients' sera, identified the GAD protein in Western blots.
11	7505244	Two of four SMS patients' sera and 5 of 5 APS I patients' sera, in contrast to 0 of 7 IDDM patients' sera, inhibited the enzymatic activity of GAD.
12	7505244	When the various sera were tested with the GAD65 and GAD67 isoforms, produced separately by transient expression in COS cells, the enzymatic activity of GAD65 was inhibited by sera from patients with SMS and APS I, whereas no effect on the GAD67 activity was observed.
13	7578849	Association between antibodies to the MR 67,000 isoform of glutamate decarboxylase (GAD) and type 1 (insulin-dependent) diabetes mellitus with coexisting autoimmune polyendocrine syndrome type II.
14	7578849	By using an immunoprecipitation assay, we analysed reactivity of autoantibodies to human recombinant GAD65 and GAD67 in sera from patients with autoimmune polyendocrine syndrome Type II (APS II) with and without Type 1 (insulin-dependent) diabetes mellitus (IDDM) compared to patients with organ-specific autoimmunity.
15	7578849	Overall antibodies to GAD65 were correlated with IDDM in all study groups, whereas GAD67 antibodies were associated with IDDM when APS II coexists.
16	7578849	Antibodies to GAD65 and GAD67 were detected in 13 (44.8%) and 7 (24.1%) out of 29 APS II patients with IDDM, but in only 4 (13.8%) and 2 (6.9%) out of 29 APS II patients without IDDM, respectively (p < 0.05).
17	7578849	In short-standing IDDM (< 1 year), antibodies to GAD67 were significantly more frequent in patients with APS II (5 of 9 [55.6%] subjects) compared to matched diabetic patients without coexisting polyendocrinopathy (1 of 18 [5.6%] subjects) (p < 0.02).
18	7578849	The levels of GAD65 (142 +/- 90 AU) and GAD67 antibodies (178 +/- 95 AU) were significantly higher in patients with polyglandular disease than in patients with isolated IDDM (91 +/- 85 AU and 93 +/- 57 AU) (p < 0.02).
19	7578849	No correlation was observed between GAD antibodies and age, sex or any particular associated autoimmune disease, besides IDDM.
20	7681242	In these same subjects serum prostate-specific antigen (PSA), prostatic acid phosphatase (PAP), testosterone, prolactin and cortisol concentrations were assessed.
21	7681242	The use of NK activity data as a probe for tumor metastases was found to be statistically as reliable as was the application of the PSA serotest (but not serum PAP concentrations).
22	7681242	In these same subjects serum prostate-specific antigen (PSA), prostatic acid phosphatase (PAP), testosterone, prolactin and cortisol concentrations were assessed.
23	7681242	The use of NK activity data as a probe for tumor metastases was found to be statistically as reliable as was the application of the PSA serotest (but not serum PAP concentrations).
24	7686362	Serial measurements of tissue polypeptide specific antigen (TPS), PSA, PAP and CEA serotest values in treated patients with primary and metastatic prostate cancer.
25	7686362	Serum TPS values were compared with respective blood prostate specific antigen (PSA), prostatic acid phosphatase (PAP), carcinoembryonic antigen (CEA) and testosterone levels in a retrospective manner.
26	7686362	Serial measurements of tissue polypeptide specific antigen (TPS), PSA, PAP and CEA serotest values in treated patients with primary and metastatic prostate cancer.
27	7686362	Serum TPS values were compared with respective blood prostate specific antigen (PSA), prostatic acid phosphatase (PAP), carcinoembryonic antigen (CEA) and testosterone levels in a retrospective manner.
28	9228514	Neutral alpha-glucosidase levels as epididymal marker, fructose levels as vesicular marker, zinc, citric acid and prostate specific antigen levels as prostatic markers were measured in the seminal plasma of eight transfusion-dependent beta-thalassemic patients in order to study epididymal and sex accessory gland secretions (eighteen subjects served as controls).
29	9228514	Ejaculate of patients showed normal sperm count and low sperm motility, in the meantime seminal plasma exhibited unaltered both neutral alpha-glucosidase and fructose values but low levels of zinc, citric acid and prostate specific antigen were noticed as well.
30	9228514	Neutral alpha-glucosidase levels as epididymal marker, fructose levels as vesicular marker, zinc, citric acid and prostate specific antigen levels as prostatic markers were measured in the seminal plasma of eight transfusion-dependent beta-thalassemic patients in order to study epididymal and sex accessory gland secretions (eighteen subjects served as controls).
31	9228514	Ejaculate of patients showed normal sperm count and low sperm motility, in the meantime seminal plasma exhibited unaltered both neutral alpha-glucosidase and fructose values but low levels of zinc, citric acid and prostate specific antigen were noticed as well.
32	10412880	Blood samples were drawn from fasting patients to determine insulin, total cholesterol, triglycerides, HDL and LDL cholesterol, uric acid, alanine aminotransferase (ALAT) and prostate-specific antigen (PSA).
33	11223374	In patients with the rare, recessively inherited type 1 APS (APS-1), characterized by the triad of chronic mucocutaneous moniliasis, hypoparathyroidism, and Addison's disease, primary amenorrhea (elevated pituitary gonadotropins) or oligomenorrhea and infertility are constant features.
34	11223374	These autoantibodies react with 3 P450 enzymes involved with steroidogenesis, namely, 21-hydroxylase (adrenal specific), 17 alpha-hydroxylase, and the side chain cleavage enzyme.
35	15378031	The APS, SH2-B and LNK proteins are adapters that activate and modulate receptor tyrosine kinase and JAK/STAT signaling.
36	15378031	A newly developed bridging yeast tri-hybrid assay showed that APS dimerizes JAK2, insulin receptor and IGF1 receptor kinases using its SH2 and dimerization domains.
37	15378031	The APS, SH2-B and LNK proteins are adapters that activate and modulate receptor tyrosine kinase and JAK/STAT signaling.
38	15378031	A newly developed bridging yeast tri-hybrid assay showed that APS dimerizes JAK2, insulin receptor and IGF1 receptor kinases using its SH2 and dimerization domains.
39	15472233	The DNA of the phagotopes selected from the FPP and APS sera revealed consensus amino acid sequences of GRG and LGKRS, respectively.
40	15664450	Distinct Grb10 domain requirements for effects on glucose uptake and insulin signaling.
41	15664450	The adapter protein Grb10 binds to phosphotyrosine residues in insulin receptors via its C-terminal region and regulates insulin signaling.
42	15664450	Overexpression of FL-Grb10 inhibited insulin-stimulated receptor autophosphorylation and glucose uptake.
43	15664450	In spite of these differences, both FL-Grb10 and the BPS-SH2 fragment inhibited insulin-stimulated phosphorylation of IRS1, IRS2, Akt/PKB, Shc, ERK1/2, APS, and c-Cbl to a similar extent.
44	15664450	Co-precipitation studies demonstrated more sustained binding of the BPS-SH2 fragment than FL-Grb10 to insulin receptors.
45	15664450	Although receptor binding domains of Grb10 are sufficient to inhibit insulin effects on proximal post-receptor signaling responses, N-terminal domains of Grb10 are essential for the effects of this adapter protein on receptor phosphorylation and glucose uptake.
46	15767667	The isoforms of SH2-B, APS, and Lnk form a family of signaling proteins that have been described as activators, mediators, or inhibitors of cytokine and growth factor signaling.
47	15767667	Consistent with previous reports, we further show that the SH2 domains of SH2-B and APS bind JAK2 at Tyr813.
48	15767667	These findings suggested a model in which two molecules of SH2-B or APS homodimerize with their SH2 domains bound to two JAK2 molecules, creating heterotetrameric JAK2-(SH2-B)2-JAK2 or JAK2-(APS)2-JAK2 complexes.
49	15767667	We further show that APS and SH2-B isoforms heterodimerize.
50	15767667	At lower levels of SH2-B or APS expression, dimerization approximates two JAK2 molecules to induce transactivation.
51	15767667	At higher relative concentrations of SH2-B or APS, kinase activation is blocked.
52	15767667	SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present.
53	15767667	The isoforms of SH2-B, APS, and Lnk form a family of signaling proteins that have been described as activators, mediators, or inhibitors of cytokine and growth factor signaling.
54	15767667	Consistent with previous reports, we further show that the SH2 domains of SH2-B and APS bind JAK2 at Tyr813.
55	15767667	These findings suggested a model in which two molecules of SH2-B or APS homodimerize with their SH2 domains bound to two JAK2 molecules, creating heterotetrameric JAK2-(SH2-B)2-JAK2 or JAK2-(APS)2-JAK2 complexes.
56	15767667	We further show that APS and SH2-B isoforms heterodimerize.
57	15767667	At lower levels of SH2-B or APS expression, dimerization approximates two JAK2 molecules to induce transactivation.
58	15767667	At higher relative concentrations of SH2-B or APS, kinase activation is blocked.
59	15767667	SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present.
60	15767667	The isoforms of SH2-B, APS, and Lnk form a family of signaling proteins that have been described as activators, mediators, or inhibitors of cytokine and growth factor signaling.
61	15767667	Consistent with previous reports, we further show that the SH2 domains of SH2-B and APS bind JAK2 at Tyr813.
62	15767667	These findings suggested a model in which two molecules of SH2-B or APS homodimerize with their SH2 domains bound to two JAK2 molecules, creating heterotetrameric JAK2-(SH2-B)2-JAK2 or JAK2-(APS)2-JAK2 complexes.
63	15767667	We further show that APS and SH2-B isoforms heterodimerize.
64	15767667	At lower levels of SH2-B or APS expression, dimerization approximates two JAK2 molecules to induce transactivation.
65	15767667	At higher relative concentrations of SH2-B or APS, kinase activation is blocked.
66	15767667	SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present.
67	15767667	The isoforms of SH2-B, APS, and Lnk form a family of signaling proteins that have been described as activators, mediators, or inhibitors of cytokine and growth factor signaling.
68	15767667	Consistent with previous reports, we further show that the SH2 domains of SH2-B and APS bind JAK2 at Tyr813.
69	15767667	These findings suggested a model in which two molecules of SH2-B or APS homodimerize with their SH2 domains bound to two JAK2 molecules, creating heterotetrameric JAK2-(SH2-B)2-JAK2 or JAK2-(APS)2-JAK2 complexes.
70	15767667	We further show that APS and SH2-B isoforms heterodimerize.
71	15767667	At lower levels of SH2-B or APS expression, dimerization approximates two JAK2 molecules to induce transactivation.
72	15767667	At higher relative concentrations of SH2-B or APS, kinase activation is blocked.
73	15767667	SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present.
74	15767667	The isoforms of SH2-B, APS, and Lnk form a family of signaling proteins that have been described as activators, mediators, or inhibitors of cytokine and growth factor signaling.
75	15767667	Consistent with previous reports, we further show that the SH2 domains of SH2-B and APS bind JAK2 at Tyr813.
76	15767667	These findings suggested a model in which two molecules of SH2-B or APS homodimerize with their SH2 domains bound to two JAK2 molecules, creating heterotetrameric JAK2-(SH2-B)2-JAK2 or JAK2-(APS)2-JAK2 complexes.
77	15767667	We further show that APS and SH2-B isoforms heterodimerize.
78	15767667	At lower levels of SH2-B or APS expression, dimerization approximates two JAK2 molecules to induce transactivation.
79	15767667	At higher relative concentrations of SH2-B or APS, kinase activation is blocked.
80	15767667	SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present.
81	15767667	The isoforms of SH2-B, APS, and Lnk form a family of signaling proteins that have been described as activators, mediators, or inhibitors of cytokine and growth factor signaling.
82	15767667	Consistent with previous reports, we further show that the SH2 domains of SH2-B and APS bind JAK2 at Tyr813.
83	15767667	These findings suggested a model in which two molecules of SH2-B or APS homodimerize with their SH2 domains bound to two JAK2 molecules, creating heterotetrameric JAK2-(SH2-B)2-JAK2 or JAK2-(APS)2-JAK2 complexes.
84	15767667	We further show that APS and SH2-B isoforms heterodimerize.
85	15767667	At lower levels of SH2-B or APS expression, dimerization approximates two JAK2 molecules to induce transactivation.
86	15767667	At higher relative concentrations of SH2-B or APS, kinase activation is blocked.
87	15767667	SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present.
88	15767667	The isoforms of SH2-B, APS, and Lnk form a family of signaling proteins that have been described as activators, mediators, or inhibitors of cytokine and growth factor signaling.
89	15767667	Consistent with previous reports, we further show that the SH2 domains of SH2-B and APS bind JAK2 at Tyr813.
90	15767667	These findings suggested a model in which two molecules of SH2-B or APS homodimerize with their SH2 domains bound to two JAK2 molecules, creating heterotetrameric JAK2-(SH2-B)2-JAK2 or JAK2-(APS)2-JAK2 complexes.
91	15767667	We further show that APS and SH2-B isoforms heterodimerize.
92	15767667	At lower levels of SH2-B or APS expression, dimerization approximates two JAK2 molecules to induce transactivation.
93	15767667	At higher relative concentrations of SH2-B or APS, kinase activation is blocked.
94	15767667	SH2-B or APS homodimerization and SH2-B/APS heterodimerization thus provide direct mechanisms for activating and inhibiting JAK2 and other kinases from the inside of the cell and for potentiating or attenuating cytokine and growth factor receptor signaling when ligands are present.
95	16243513	Blood samples were collected to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, alanine aminotransferase and fasting plasma insulin level.
96	16243513	Eliminating the effect on mortality of higher stage and grade of the clinical prostate cancer and PSA at baseline, the following statistically significant correlations remained: a higher fasting plasma insulin level (P = 0.010) and a lower HDL-cholesterol level of borderline significance (P = 0.065).
97	16243513	Furthermore, our data suggest that the insulin level could be used as a marker of prostate cancer prognosis and tumour aggressiveness, regardless of the patient's prostate cancer stage, cancer grade and PSA level.
98	16243513	Blood samples were collected to determine triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol, low-density lipoprotein (LDL)-cholesterol, uric acid, alanine aminotransferase and fasting plasma insulin level.
99	16243513	Eliminating the effect on mortality of higher stage and grade of the clinical prostate cancer and PSA at baseline, the following statistically significant correlations remained: a higher fasting plasma insulin level (P = 0.010) and a lower HDL-cholesterol level of borderline significance (P = 0.065).
100	16243513	Furthermore, our data suggest that the insulin level could be used as a marker of prostate cancer prognosis and tumour aggressiveness, regardless of the patient's prostate cancer stage, cancer grade and PSA level.
101	17938644	Association between prostate-specific antigen and leptin, adiponectin, HbA1c or C-peptide among African-American and Caucasian men.
102	17938644	To understand this effect, we investigated the association between PSA and blood HbA1c, C-peptide, leptin and adiponectin levels in African-American (AA) (n=121) and Caucasian (CA) (n=121) men.
103	17938644	Association between prostate-specific antigen and leptin, adiponectin, HbA1c or C-peptide among African-American and Caucasian men.
104	17938644	To understand this effect, we investigated the association between PSA and blood HbA1c, C-peptide, leptin and adiponectin levels in African-American (AA) (n=121) and Caucasian (CA) (n=121) men.
105	18204460	Dok1 mediates high-fat diet-induced adipocyte hypertrophy and obesity through modulation of PPAR-gamma phosphorylation.
106	18204460	Insulin receptor substrate (IRS)-1 and IRS-2 have dominant roles in the action of insulin, but other substrates of the insulin receptor kinase, such as Gab1, c-Cbl, SH2-B and APS, are also of physiological relevance.
107	18204460	Embryonic fibroblasts from Dok1-deficient mice were impaired in adipogenic differentiation, and this defect was accompanied by an increased activity of the protein kinase ERK and a consequent increase in the phosphorylation of peroxisome proliferator-activated receptor (PPAR)-gamma on Ser112.
108	18204460	These results indicate that Dok1 promotes adipocyte hypertrophy by counteracting the inhibitory effect of ERK on PPAR-gamma and may thus confer predisposition to diet-induced obesity.
109	20112889	Testosterone supplementation in men with hypogonadism improves ED and libido, but requires interval monitoring of hemoglobin, serum transaminase, and prostate-specific antigen levels because of an increased risk of prostate adenocarcinoma.
110	20445731	Ca 19.9, CEA, AFP and PSA negative.
111	21136852	The decreased proteins were the prostatic acid phosphatase precursor, the ribonuclease and the kallikrein-3.
112	21388354	In this controlled study, 98 patients with APS type 2, 96 patients with type 1 diabetes (T1D), and 92 patients with autoimmune thyroid disease, both as a single autoimmune endocrinopathy, were tested for association with alleles of the human leukocyte antigen (HLA) class II loci DRB1, DQA1, and DQB1.
113	21949470	Prostate size correlated positively with age (r = 0.227, P < 0.001), PSA (r = 0.510, P < 0.001), and fasting glucose level (r = 0.186, P = 0.007), but not with BMI, testosterone, insulin level, or insulin resistance (each P > 0.05).
114	21949470	Testosterone level inversely correlated with BMI (r = -0.327, P < 0.001), insulin level (r = -0.207, P = 0.003), and insulin resistance (r = -0.221, P = 0.001), but not with age, prostate size, PSA, or fasting glucose level (each P > 0.05).
115	21949470	Prostate size correlated positively with age (r = 0.227, P < 0.001), PSA (r = 0.510, P < 0.001), and fasting glucose level (r = 0.186, P = 0.007), but not with BMI, testosterone, insulin level, or insulin resistance (each P > 0.05).
116	21949470	Testosterone level inversely correlated with BMI (r = -0.327, P < 0.001), insulin level (r = -0.207, P = 0.003), and insulin resistance (r = -0.221, P = 0.001), but not with age, prostate size, PSA, or fasting glucose level (each P > 0.05).
117	22426864	We measure blood glucose, serum lipid, insulin, C-peptide, myocardial enzyme levels, myocardial glycogen staining, myocardial ultrastructure, fluorescence quantitative RT-PCR detection of myocardial PPAR-α and the target genes (FATP, ACS) and GLUT4 mRNA expression in normal control group, DM group and APS treatment group hamsters.
118	22426864	Gene expression of myocardial PPAR-α and its target genes (FATP, ACS) in APS group were significantly lower than in DM group, while gene expression of GLUT4 in APS group was higher than DM group.
119	23143785	Curcumin's pleiotropic activities emanate from its ability to modulate numerous signaling molecules such as pro-inflammatory cytokines, apoptotic proteins, NF-κB, cyclooxygenase-2, 5-LOX, STAT3, C-reactive protein, prostaglandin E(2), prostate-specific antigen, adhesion molecules, phosphorylase kinase, transforming growth factor-β, triglyceride, ET-1, creatinine, HO-1, AST, and ALT in human participants.
120	23563695	Interleukin (IL)-10 protein levels and expression of most of the anti-inflammatory genes, including IL-10, macrophage mannose receptor (MMR), arginase, Dectin-1, YM-1 and YM-2, were significantly increased after treatment with APS for 24 h.
121	23563695	Furthermore, APS induced IL-10 protein production and anti-inflammatory gene expression of IL-10, MMR, Dectin-1, arginase, YM-1 and YM-2.
122	23563695	Additionally, APS inhibited IL-1β protein production and expression of most of the pro-inflammatory genes, such as IL-1β, iNOS, MCP-1, IL-6 and CD11c but not tumor necrosis factor (TNF)-α.
123	23563695	Interleukin (IL)-10 protein levels and expression of most of the anti-inflammatory genes, including IL-10, macrophage mannose receptor (MMR), arginase, Dectin-1, YM-1 and YM-2, were significantly increased after treatment with APS for 24 h.
124	23563695	Furthermore, APS induced IL-10 protein production and anti-inflammatory gene expression of IL-10, MMR, Dectin-1, arginase, YM-1 and YM-2.
125	23563695	Additionally, APS inhibited IL-1β protein production and expression of most of the pro-inflammatory genes, such as IL-1β, iNOS, MCP-1, IL-6 and CD11c but not tumor necrosis factor (TNF)-α.
126	23786295	Genetic analyses of patients and their families with APS type 1 (autoimmune polyendocrinopathy candidiasis, ectodermal dystrophy) identified the autoimmune regulator (AIRE) gene, which drives the expression of peripheral tissue-specific antigens in thymic cells and is critical in the development of self-tolerance.