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PMID |
Sentence |
1 |
9388271
|
Activation of protein kinase C stimulates tyrosine phosphorylation and activation of ErbB2 and ErbB3.
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2 |
9388271
|
Purification of the 190-kDa tyrosine-phosphorylated protein revealed that it consists of both ErbB2 and ErbB3.
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3 |
9388271
|
Following PMA-induced tyrosine phosphorylation, ErbB2 and ErbB3 were able to associate with the SH2 domains of several signaling proteins including the p85alpha subunit of phosphatidylinositol 3-kinase, Syp, and Grb2.
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4 |
9388271
|
Both ErbB2 and paxillin also exhibit reduced migration on SDS-polyacrylamide gel electrophoresis following PMA treatment, suggesting that they are also phosphorylated on serine/threonine residues.
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5 |
9388271
|
The activation of ErbB2 and ErbB3 that is initiated by PMA may contribute to the tumor promoting activity of these compounds.
|
6 |
9388271
|
Activation of protein kinase C stimulates tyrosine phosphorylation and activation of ErbB2 and ErbB3.
|
7 |
9388271
|
Purification of the 190-kDa tyrosine-phosphorylated protein revealed that it consists of both ErbB2 and ErbB3.
|
8 |
9388271
|
Following PMA-induced tyrosine phosphorylation, ErbB2 and ErbB3 were able to associate with the SH2 domains of several signaling proteins including the p85alpha subunit of phosphatidylinositol 3-kinase, Syp, and Grb2.
|
9 |
9388271
|
Both ErbB2 and paxillin also exhibit reduced migration on SDS-polyacrylamide gel electrophoresis following PMA treatment, suggesting that they are also phosphorylated on serine/threonine residues.
|
10 |
9388271
|
The activation of ErbB2 and ErbB3 that is initiated by PMA may contribute to the tumor promoting activity of these compounds.
|
11 |
9388271
|
Activation of protein kinase C stimulates tyrosine phosphorylation and activation of ErbB2 and ErbB3.
|
12 |
9388271
|
Purification of the 190-kDa tyrosine-phosphorylated protein revealed that it consists of both ErbB2 and ErbB3.
|
13 |
9388271
|
Following PMA-induced tyrosine phosphorylation, ErbB2 and ErbB3 were able to associate with the SH2 domains of several signaling proteins including the p85alpha subunit of phosphatidylinositol 3-kinase, Syp, and Grb2.
|
14 |
9388271
|
Both ErbB2 and paxillin also exhibit reduced migration on SDS-polyacrylamide gel electrophoresis following PMA treatment, suggesting that they are also phosphorylated on serine/threonine residues.
|
15 |
9388271
|
The activation of ErbB2 and ErbB3 that is initiated by PMA may contribute to the tumor promoting activity of these compounds.
|
16 |
9388271
|
Activation of protein kinase C stimulates tyrosine phosphorylation and activation of ErbB2 and ErbB3.
|
17 |
9388271
|
Purification of the 190-kDa tyrosine-phosphorylated protein revealed that it consists of both ErbB2 and ErbB3.
|
18 |
9388271
|
Following PMA-induced tyrosine phosphorylation, ErbB2 and ErbB3 were able to associate with the SH2 domains of several signaling proteins including the p85alpha subunit of phosphatidylinositol 3-kinase, Syp, and Grb2.
|
19 |
9388271
|
Both ErbB2 and paxillin also exhibit reduced migration on SDS-polyacrylamide gel electrophoresis following PMA treatment, suggesting that they are also phosphorylated on serine/threonine residues.
|
20 |
9388271
|
The activation of ErbB2 and ErbB3 that is initiated by PMA may contribute to the tumor promoting activity of these compounds.
|
21 |
9388272
|
Comparison of phorbol ester and sphingomyelinase-induced phosphorylation of ErbB2 and ErbB3.
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22 |
9388272
|
Chem. 272, 31172-31181), we demonstrated that phorbol 12-myristate 13-acetate (PMA) treatment of Fao cells induces tyrosine phosphorylation of several proteins including ErbB2 and ErbB3.
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23 |
9388272
|
In the present study we show that sphingomyelinase also results in the enhanced tyrosine phosphorylation of ErbB2 and ErbB3 in these cells.
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24 |
9388272
|
Prolonged insulin treatment resulted in decreased expression of both ErbB2 and ErbB3.
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25 |
9388272
|
Insulin also appears to negatively regulate the protein tyrosine kinase responsible for phosphorylating ErbB2 in PMA-stimulated cells.
|
26 |
9388272
|
The former effect of insulin was relieved by treatment with inhibitors of phosphatidylinositol 3-kinase.
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27 |
9388272
|
Comparison of phorbol ester and sphingomyelinase-induced phosphorylation of ErbB2 and ErbB3.
|
28 |
9388272
|
Chem. 272, 31172-31181), we demonstrated that phorbol 12-myristate 13-acetate (PMA) treatment of Fao cells induces tyrosine phosphorylation of several proteins including ErbB2 and ErbB3.
|
29 |
9388272
|
In the present study we show that sphingomyelinase also results in the enhanced tyrosine phosphorylation of ErbB2 and ErbB3 in these cells.
|
30 |
9388272
|
Prolonged insulin treatment resulted in decreased expression of both ErbB2 and ErbB3.
|
31 |
9388272
|
Insulin also appears to negatively regulate the protein tyrosine kinase responsible for phosphorylating ErbB2 in PMA-stimulated cells.
|
32 |
9388272
|
The former effect of insulin was relieved by treatment with inhibitors of phosphatidylinositol 3-kinase.
|
33 |
9388272
|
Comparison of phorbol ester and sphingomyelinase-induced phosphorylation of ErbB2 and ErbB3.
|
34 |
9388272
|
Chem. 272, 31172-31181), we demonstrated that phorbol 12-myristate 13-acetate (PMA) treatment of Fao cells induces tyrosine phosphorylation of several proteins including ErbB2 and ErbB3.
|
35 |
9388272
|
In the present study we show that sphingomyelinase also results in the enhanced tyrosine phosphorylation of ErbB2 and ErbB3 in these cells.
|
36 |
9388272
|
Prolonged insulin treatment resulted in decreased expression of both ErbB2 and ErbB3.
|
37 |
9388272
|
Insulin also appears to negatively regulate the protein tyrosine kinase responsible for phosphorylating ErbB2 in PMA-stimulated cells.
|
38 |
9388272
|
The former effect of insulin was relieved by treatment with inhibitors of phosphatidylinositol 3-kinase.
|
39 |
9388272
|
Comparison of phorbol ester and sphingomyelinase-induced phosphorylation of ErbB2 and ErbB3.
|
40 |
9388272
|
Chem. 272, 31172-31181), we demonstrated that phorbol 12-myristate 13-acetate (PMA) treatment of Fao cells induces tyrosine phosphorylation of several proteins including ErbB2 and ErbB3.
|
41 |
9388272
|
In the present study we show that sphingomyelinase also results in the enhanced tyrosine phosphorylation of ErbB2 and ErbB3 in these cells.
|
42 |
9388272
|
Prolonged insulin treatment resulted in decreased expression of both ErbB2 and ErbB3.
|
43 |
9388272
|
Insulin also appears to negatively regulate the protein tyrosine kinase responsible for phosphorylating ErbB2 in PMA-stimulated cells.
|
44 |
9388272
|
The former effect of insulin was relieved by treatment with inhibitors of phosphatidylinositol 3-kinase.
|
45 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
46 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
47 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
48 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
49 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
50 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
51 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
52 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
53 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
54 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
55 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
56 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
57 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
58 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
59 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
60 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
61 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
62 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
63 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
64 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
65 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
66 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
67 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
68 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
69 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
70 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
71 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
72 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
73 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
74 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
75 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
76 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
77 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
78 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
79 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
80 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
81 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
82 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
83 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
84 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
85 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
86 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
87 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
88 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
89 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
90 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
91 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
92 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
93 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
94 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
95 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
96 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
97 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
98 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
99 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
100 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
101 |
9389501
|
Hepatic expression of ErbB3 is repressed by insulin in a pathway sensitive to PI-3 kinase inhibitors.
|
102 |
9389501
|
ErbB3 is an epidermal growth factor receptor-related type I tyrosine kinase receptor capable, in conjunction with ErbB2 or epidermal growth factor receptor, of transmitting proliferative and differentiative signals in a variety of cell types.
|
103 |
9389501
|
Insulin inhibits the increase in heregulin beta1 binding, as well as the increase in ErbB3 messenger RNA and protein.
|
104 |
9389501
|
Two models of insulin deficiency in vivo (diabetes and fasting) demonstrated elevated levels of hepatic ErbB3 protein, strengthening the relevance of our observations in vitro.
|
105 |
9389501
|
Using chemical activators or antagonists, we sought to identify the signaling pathways that link insulin to ErbB3 expression.
|
106 |
9389501
|
The PI-3 kinase inhibitors, wortmannin and LY294002, completely blocked the inhibition of ErbB3 protein expression by insulin, suggesting a role for PI-3 kinase in the regulation of this growth factor receptor.
|
107 |
9389501
|
Rapamycin, an inhibitor of p70 S6 kinase, an enzyme downstream of PI-3 kinase, failed to block the effect of insulin on ErbB3 expression.
|
108 |
9389501
|
These results suggest a complex regulatory paradign for ErbB3 that includes PI-3 kinase and may be linked, via insulin, to the metabolic status of the animal.
|
109 |
9815939
|
The erbB-3 gene encodes a transmembrane protein that is related to the epidermal growth factor (EGF) receptor and erbB-2.
|
110 |
9815939
|
Four of six pancreatic cancer cell lines exhibited the 6.2-kb erbB-3 mRNA transcript, and all four cell lines coexpressed the epidermal growth factor receptor and erbB-2.
|
111 |
9815939
|
The erbB-3 gene encodes a transmembrane protein that is related to the epidermal growth factor (EGF) receptor and erbB-2.
|
112 |
9815939
|
Four of six pancreatic cancer cell lines exhibited the 6.2-kb erbB-3 mRNA transcript, and all four cell lines coexpressed the epidermal growth factor receptor and erbB-2.
|
113 |
17704947
|
Enhancement of erbB2 and erbB3 expression during oral oncogenesis in diabetic rats.
|
114 |
18225590
|
The expression of EGFR, erbB2, erbB3, FGFR-2, FGFR-3, c-myc, N-ras, ets-1, H-ras, c-fos and c-jun, the tumor suppressor genes p53 and p16, apoptosis markers Bax and Bcl-2, and the cell proliferation marker Ki-67 in the sequential stages of rat oral oncogenesis was investigated.
|
115 |
18225590
|
Diabetes seems to promote the activation of the Ras/Raf/MAPK signal transduction pathway mainly by induction of erbB2 and erbB3 receptors, leading to increased cell proliferation, while there was no difference in apoptosis levels during oncogenesis.
|
116 |
18225590
|
The expression of EGFR, erbB2, erbB3, FGFR-2, FGFR-3, c-myc, N-ras, ets-1, H-ras, c-fos and c-jun, the tumor suppressor genes p53 and p16, apoptosis markers Bax and Bcl-2, and the cell proliferation marker Ki-67 in the sequential stages of rat oral oncogenesis was investigated.
|
117 |
18225590
|
Diabetes seems to promote the activation of the Ras/Raf/MAPK signal transduction pathway mainly by induction of erbB2 and erbB3 receptors, leading to increased cell proliferation, while there was no difference in apoptosis levels during oncogenesis.
|
118 |
18462017
|
By using an integrative genomics approach, we highlight how the gene RPS26 and not ERBB3 is supported by our data as the most likely susceptibility gene for a novel type 1 diabetes locus recently identified in a large-scale, genome-wide association study.
|
119 |
18462017
|
We also identify SORT1 and CELSR2 as candidate susceptibility genes for a locus recently associated with coronary artery disease and plasma low-density lipoprotein cholesterol levels in the process.
|
120 |
19956107
|
In addition to the support for previously identified loci (PTPN22/1p13; ERBB3/12q13; SH2B3/12q24; CLEC16A/16p13; UBASH3A/21q22), evidence supporting two new and distinct chromosome locations associated with T1D was observed: FHOD3/18q12 (rs2644261, P=5.9 x 10(-4)) and Xp22 (rs5979785, P=6.8 x 10(-3); http://www.T1DBase.org).
|
121 |
19956107
|
In contrast, the Xp22 SNP is located 30 kb centromeric of the functional candidate genes TLR8 and TLR7 genes.
|
122 |
19956107
|
Both TLR8 and TLR7 are functional candidate genes owing to their key roles as pathogen recognition receptors and, in the case of TLR7, overexpression has been associated directly with murine autoimmune disease.
|
123 |
20586186
|
[Association of the polymorphisms of the ERBB3 and SH2B3 genes with type 1 diabetes].
|
124 |
20586186
|
To study the association with diabetes mellitus type 1 we performed analysis of the distribution of frequencies of alleles and genotypes of polymorphic marker rs2292239 of ERBB3 gene, encoding epidermal growth factor receptor type 3 and polymorphic marker rs3184504 of SH2B3 gene, encoding adaptor protein LNK.
|
125 |
20586186
|
For the polymorphic marker rs2292239 of ERBB3 gene was not found statistically significant associations with type 1 diabetes, while analysis of the distribution of frequencies of alleles and genotypes of the polymorphic marker rs3184504 of SH2B3 gene showed the presence of association with T1DM in Russian population.
|
126 |
20586186
|
[Association of the polymorphisms of the ERBB3 and SH2B3 genes with type 1 diabetes].
|
127 |
20586186
|
To study the association with diabetes mellitus type 1 we performed analysis of the distribution of frequencies of alleles and genotypes of polymorphic marker rs2292239 of ERBB3 gene, encoding epidermal growth factor receptor type 3 and polymorphic marker rs3184504 of SH2B3 gene, encoding adaptor protein LNK.
|
128 |
20586186
|
For the polymorphic marker rs2292239 of ERBB3 gene was not found statistically significant associations with type 1 diabetes, while analysis of the distribution of frequencies of alleles and genotypes of the polymorphic marker rs3184504 of SH2B3 gene showed the presence of association with T1DM in Russian population.
|
129 |
20586186
|
[Association of the polymorphisms of the ERBB3 and SH2B3 genes with type 1 diabetes].
|
130 |
20586186
|
To study the association with diabetes mellitus type 1 we performed analysis of the distribution of frequencies of alleles and genotypes of polymorphic marker rs2292239 of ERBB3 gene, encoding epidermal growth factor receptor type 3 and polymorphic marker rs3184504 of SH2B3 gene, encoding adaptor protein LNK.
|
131 |
20586186
|
For the polymorphic marker rs2292239 of ERBB3 gene was not found statistically significant associations with type 1 diabetes, while analysis of the distribution of frequencies of alleles and genotypes of the polymorphic marker rs3184504 of SH2B3 gene showed the presence of association with T1DM in Russian population.
|
132 |
20962850
|
Our results replicate previously reported associations to alleles of interferon regulatory factor 5 (IRF5), major histocompatibility complex (MHC), tumor necrosis factor (ligand) superfamily member 4 (TNFSF4), Kell blood group complex subunit-related family member 6 (XKR6), B-cell scaffold protein with ankyrin repeats 1 (BANK1), protein tyrosine phosphatase non-receptor type 22 (PTPN22), ubiquitin-conjugating enzyme E2L 3 (UBE2L3) and islet cell autoantigen 1 (ICA1).
|
133 |
20962850
|
We also identify putative associations to cytotoxic T-lymphocyte-associated protein 4 (CTLA4), a gene associated with several autoimmune disorders, and ERBB3, a locus on 12q13 that was previously reported to be associated with type 1 diabetes.
|
134 |
21270831
|
Analysis of the samples identified 18 SNPs (PTPN22, INS, IFIH1, SH2B3, ERBB3, CTLA4, C14orf181, CTSH, CLEC16A, CD69, ITPR3, C6orf173, SKAP2, PRKCQ, RNLS, IL27, SIRPG and CTRB2) with putative association.
|
135 |
23755131
|
The model consists of two components: (1) A pattern of declining residual β-cell function positively associated with young age, presence of diabetic ketoacidosis and long duration of disease symptoms (P = 0.0004), and with risk alleles of WFS1, CDKN2A/2B and RNLS (P = 0.006). (2) A second pattern of high ZnT8 autoantibody levels and low postprandial glucagon levels associated with risk alleles of IFIH1, TCF2, TAF5L, IL2RA and PTPN2 and protective alleles of ERBB3 gene (P = 0.0005).
|