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PMID |
Sentence |
1 |
2000701
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Amyloid protein in somatostatinoma differs from human islet amyloid polypeptide.
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2 |
2000701
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To examine the characteristics of this amyloid, we compared amyloid deposits in a somatostatinoma to those found in pancreatic tissue in patients with Type II diabetes mellitus and in insulinomas, using immunohistochemical techniques and specific antibodies to islet amyloid polypeptide or other pancreatic hormones, as well as electron-microscopy.
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3 |
2000701
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Antibodies to islet amyloid polypeptide regions 8-17 or 25-37 were confirmed to be specific.
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4 |
2000701
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Amyloid deposits in patients with Type II diabetes mellitus and in insulinomas, but not those in the somatostatinoma strongly reacted with these antibodies, or to an antibody to amyloid P component.
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5 |
2000701
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As amyloid in somatostatinomas is unlike that consisting of islet amyloid polypeptide or other mature pancreatic hormones, it may be a novel type of local amyloid in pancreatic islets.
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6 |
6159507
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Serum amyloid P-component (SAP) is a normal plasma protein and is a constituent of normal human glomerular basement membrane.
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7 |
7753801
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Serum amyloid P component prevents proteolysis of the amyloid fibrils of Alzheimer disease and systemic amyloidosis.
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8 |
7753801
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Serum amyloid P component (SAP) binds to all types of amyloid fibrils and is a universal constituent of amyloid deposits, including the plaques, amorphous amyloid beta protein deposits and neurofibrillary tangles of Alzheimer disease [Coria, F., Castano, E., Prelli, F., Larrondo-Lillo, M., van Duinen, S., Shelanski, M.
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9 |
7753801
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Here we show that SAP prevents proteolysis of the amyloid fibrils of Alzheimer disease, of systemic amyloid A amyloidosis and of systemic monoclonal light chain amyloidosis and may thereby contribute to their persistence in vivo.
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10 |
7753801
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Interference with binding of SAP to amyloid fibrils in vivo is thus an attractive therapeutic objective, achievement of which should promote regression of the deposits.
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11 |
7753801
|
Serum amyloid P component prevents proteolysis of the amyloid fibrils of Alzheimer disease and systemic amyloidosis.
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12 |
7753801
|
Serum amyloid P component (SAP) binds to all types of amyloid fibrils and is a universal constituent of amyloid deposits, including the plaques, amorphous amyloid beta protein deposits and neurofibrillary tangles of Alzheimer disease [Coria, F., Castano, E., Prelli, F., Larrondo-Lillo, M., van Duinen, S., Shelanski, M.
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13 |
7753801
|
Here we show that SAP prevents proteolysis of the amyloid fibrils of Alzheimer disease, of systemic amyloid A amyloidosis and of systemic monoclonal light chain amyloidosis and may thereby contribute to their persistence in vivo.
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14 |
7753801
|
Interference with binding of SAP to amyloid fibrils in vivo is thus an attractive therapeutic objective, achievement of which should promote regression of the deposits.
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15 |
7753801
|
Serum amyloid P component prevents proteolysis of the amyloid fibrils of Alzheimer disease and systemic amyloidosis.
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16 |
7753801
|
Serum amyloid P component (SAP) binds to all types of amyloid fibrils and is a universal constituent of amyloid deposits, including the plaques, amorphous amyloid beta protein deposits and neurofibrillary tangles of Alzheimer disease [Coria, F., Castano, E., Prelli, F., Larrondo-Lillo, M., van Duinen, S., Shelanski, M.
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17 |
7753801
|
Here we show that SAP prevents proteolysis of the amyloid fibrils of Alzheimer disease, of systemic amyloid A amyloidosis and of systemic monoclonal light chain amyloidosis and may thereby contribute to their persistence in vivo.
|
18 |
7753801
|
Interference with binding of SAP to amyloid fibrils in vivo is thus an attractive therapeutic objective, achievement of which should promote regression of the deposits.
|
19 |
7753801
|
Serum amyloid P component prevents proteolysis of the amyloid fibrils of Alzheimer disease and systemic amyloidosis.
|
20 |
7753801
|
Serum amyloid P component (SAP) binds to all types of amyloid fibrils and is a universal constituent of amyloid deposits, including the plaques, amorphous amyloid beta protein deposits and neurofibrillary tangles of Alzheimer disease [Coria, F., Castano, E., Prelli, F., Larrondo-Lillo, M., van Duinen, S., Shelanski, M.
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21 |
7753801
|
Here we show that SAP prevents proteolysis of the amyloid fibrils of Alzheimer disease, of systemic amyloid A amyloidosis and of systemic monoclonal light chain amyloidosis and may thereby contribute to their persistence in vivo.
|
22 |
7753801
|
Interference with binding of SAP to amyloid fibrils in vivo is thus an attractive therapeutic objective, achievement of which should promote regression of the deposits.
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23 |
7868080
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Intracerebral and cerebrovascular beta-protein amyloid deposits are a hallmark of the pathology of both sporadic and familial Alzheimer's disease, beta 2-microglobulin-derived amyloid is a common complication of long term haemodialysis, and islet amyloid polypeptide is the fibril protein in the universal islet amyloidosis of type II diabetes mellitus.
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24 |
7868080
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New fibril proteins have lately been identified in hereditary amyloidosis, including variants of gelsolin, apolipoprotein AI, lysozyme and fibrinogen.
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25 |
7868080
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The development of radiolabelled serum amyloid P component (SAP) scintigraphy has allowed amyloid to be diagnosed non-invasively in vivo for the first time, provided unique insight into the distribution and size of amyloid deposits, and yielded novel information on the natural history and the effects of treatment.
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26 |
8175664
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A fusion protein containing the full-length sequences of the mitogen, basic fibroblast growth factor (FGF-2), and the ribosome-inactivating protein, saporin (SAP), has been expressed in E. coli.
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27 |
9375734
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Amyloid fibrils are derived from different unrelated proteins in the different forms of the disease but share many common properties, including the capacity to bind the normal plasma protein serum amyloid P component (SAP).
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28 |
9375734
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This is the basis for our development of radiolabelled SAP as a nuclear medicine tracer for the diagnosis and quantitative monitoring of amyloid.
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29 |
9375734
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Amyloid fibrils are derived from different unrelated proteins in the different forms of the disease but share many common properties, including the capacity to bind the normal plasma protein serum amyloid P component (SAP).
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30 |
9375734
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This is the basis for our development of radiolabelled SAP as a nuclear medicine tracer for the diagnosis and quantitative monitoring of amyloid.
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31 |
12015594
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Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis.
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32 |
12015594
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The normal plasma protein serum amyloid P component (SAP) binds to fibrils in all types of amyloid deposits, and contributes to the pathogenesis of amyloidosis.
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33 |
12015594
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In order to intervene in this process we have developed a drug, R-1-[6-[R-2-carboxy-pyrrolidin-1-yl]-6-oxo-hexanoyl]pyrrolidine-2-carboxylic acid, that is a competitive inhibitor of SAP binding to amyloid fibrils.
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34 |
12015594
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This mechanism of drug action potently removes SAP from human amyloid deposits in the tissues and may provide a new therapeutic approach to both systemic amyloidosis and diseases associated with local amyloid, including Alzheimer's disease and type 2 diabetes.
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35 |
12015594
|
Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis.
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36 |
12015594
|
The normal plasma protein serum amyloid P component (SAP) binds to fibrils in all types of amyloid deposits, and contributes to the pathogenesis of amyloidosis.
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37 |
12015594
|
In order to intervene in this process we have developed a drug, R-1-[6-[R-2-carboxy-pyrrolidin-1-yl]-6-oxo-hexanoyl]pyrrolidine-2-carboxylic acid, that is a competitive inhibitor of SAP binding to amyloid fibrils.
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38 |
12015594
|
This mechanism of drug action potently removes SAP from human amyloid deposits in the tissues and may provide a new therapeutic approach to both systemic amyloidosis and diseases associated with local amyloid, including Alzheimer's disease and type 2 diabetes.
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39 |
12015594
|
Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis.
|
40 |
12015594
|
The normal plasma protein serum amyloid P component (SAP) binds to fibrils in all types of amyloid deposits, and contributes to the pathogenesis of amyloidosis.
|
41 |
12015594
|
In order to intervene in this process we have developed a drug, R-1-[6-[R-2-carboxy-pyrrolidin-1-yl]-6-oxo-hexanoyl]pyrrolidine-2-carboxylic acid, that is a competitive inhibitor of SAP binding to amyloid fibrils.
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42 |
12015594
|
This mechanism of drug action potently removes SAP from human amyloid deposits in the tissues and may provide a new therapeutic approach to both systemic amyloidosis and diseases associated with local amyloid, including Alzheimer's disease and type 2 diabetes.
|
43 |
12015594
|
Targeted pharmacological depletion of serum amyloid P component for treatment of human amyloidosis.
|
44 |
12015594
|
The normal plasma protein serum amyloid P component (SAP) binds to fibrils in all types of amyloid deposits, and contributes to the pathogenesis of amyloidosis.
|
45 |
12015594
|
In order to intervene in this process we have developed a drug, R-1-[6-[R-2-carboxy-pyrrolidin-1-yl]-6-oxo-hexanoyl]pyrrolidine-2-carboxylic acid, that is a competitive inhibitor of SAP binding to amyloid fibrils.
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46 |
12015594
|
This mechanism of drug action potently removes SAP from human amyloid deposits in the tissues and may provide a new therapeutic approach to both systemic amyloidosis and diseases associated with local amyloid, including Alzheimer's disease and type 2 diabetes.
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47 |
12618085
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We therefore evaluated CRP and the nearby serum amyloid P-component, APCS, which is structurally similar to CRP, as candidate diabetes susceptibility genes.
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48 |
12618085
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We genotyped representative SNPs in approximately 1300 Pima samples and found a single variant in the CRP promoter (SNP 133552) that was associated with T2DM (P=0.014), as well as a common haplotype (CGCG) that was associated with both T2DM (P=0.029) and corrected insulin response, a surrogate measure of insulin secretion in non-diabetic subjects (P=0.050).
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49 |
12962700
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Glycosaminoglycans (GAG) and the pentraxin protein, serum amyloid P (SAP) component, are universal non-fibrillar constituents of amyloid deposits that contribute to fibrillogenesis.
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50 |
12962700
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We review potential therapies for amyloidosis, which include measures to reduce the production of amyloidogenic precursor proteins, interference with fibrillogenesis, and enhancement of amyloid clearance, either by active or passive immunisation or by destabilising deposits through removal of serum amyloid P component.
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51 |
12962700
|
Glycosaminoglycans (GAG) and the pentraxin protein, serum amyloid P (SAP) component, are universal non-fibrillar constituents of amyloid deposits that contribute to fibrillogenesis.
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52 |
12962700
|
We review potential therapies for amyloidosis, which include measures to reduce the production of amyloidogenic precursor proteins, interference with fibrillogenesis, and enhancement of amyloid clearance, either by active or passive immunisation or by destabilising deposits through removal of serum amyloid P component.
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53 |
16595606
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Fasting plasma levels of glucose, insulin and serum amyloid-P (SAP) and body weight in 234 female F2 mice were measured after being fed the western diet for 12 weeks.
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54 |
16595606
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Thus, these results demonstrate genetic linkages of hyperglycemia and body weight with SAP, a marker of the acute-phase response, in hyperlipidemic apoE(-/-) mice and suggest a probability for the Sap gene to be a positional candidate of Bglu3.
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55 |
16595606
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Fasting plasma levels of glucose, insulin and serum amyloid-P (SAP) and body weight in 234 female F2 mice were measured after being fed the western diet for 12 weeks.
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56 |
16595606
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Thus, these results demonstrate genetic linkages of hyperglycemia and body weight with SAP, a marker of the acute-phase response, in hyperlipidemic apoE(-/-) mice and suggest a probability for the Sap gene to be a positional candidate of Bglu3.
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57 |
16823976
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Multiplexed affinity retrieval devices and methodology were developed to simultaneously target retinol binding protein, C-reactive protein, serum amyloid P component, as well as an added exogenous internal reference standard (staphylococcal enterotoxin B) for subsequent MALDI-TOF MS analysis.
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58 |
16823976
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This approach allows for semiquantitative analysis of both retinol binding protein and serum amyloid P component while performing absolute quantitative measurements of C-reactive protein.
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59 |
16823976
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Multiplexed affinity retrieval devices and methodology were developed to simultaneously target retinol binding protein, C-reactive protein, serum amyloid P component, as well as an added exogenous internal reference standard (staphylococcal enterotoxin B) for subsequent MALDI-TOF MS analysis.
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60 |
16823976
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This approach allows for semiquantitative analysis of both retinol binding protein and serum amyloid P component while performing absolute quantitative measurements of C-reactive protein.
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61 |
17110595
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A nuclear receptor corepressor-dependent pathway mediates suppression of cytokine-induced C-reactive protein gene expression by liver X receptor.
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62 |
17110595
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We demonstrate herein that 2 synthetic LXR ligands, T0901317 and GW3965, inhibit interleukin-1beta/interleukin-6-induced CRP mRNA and protein expression in human hepatocytes.
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63 |
17110595
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Knockdown of LXRalpha/beta by short interfering RNAs completely abolished the inhibitory effect of the LXR agonist T0901317 on cytokine-induced CRP gene transcription.
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64 |
17110595
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Finally, treatment of C57Bl6/J mice with LXR ligands attenuated lipopolysaccharide-induced mouse CRP and serum amyloid P component gene expression in the liver, whereas no effect was observed in LXRalphabeta knockout mice.
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65 |
18193704
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Work on the pentraxin proteins, C-reactive protein (CRP) and serum amyloid P component (SAP), and on amyloidosis, has benefited from abundant serendipity, leading to routine clinical use of CRP measurements, the invention of SAP scintigraphy for amyloidosis, the establishment of the NHS National Amyloidosis Centre providing superior patient care, and latterly the invention of a novel pharmacological mechanism for therapeutic depletion of pathogenic proteins.
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66 |
20674218
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The distinct effect of T2DM induction on the pattern of rat serum includes the down-regulation of Apolipoprotein E, Apolipoprotein A-I, Ig gamma-2A chain C region, and up-regulation of Transthyretin (TTR), Haptoglobin (Hp), Serum amyloid P-componen (SAP), Prothrombin.
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67 |
22274563
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Apcs, encoding an acute phase response protein serum amyloid P (SAP), is located underneath the linkage peak of Bglu3.
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68 |
22274563
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The Western diet consumption led to a gradual rise in plasma SAP levels, which was accompanied by rising fasting glucose in both B6 and C3H apoE(-/-) mice.
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69 |
22274563
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Apcs, encoding an acute phase response protein serum amyloid P (SAP), is located underneath the linkage peak of Bglu3.
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70 |
22274563
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The Western diet consumption led to a gradual rise in plasma SAP levels, which was accompanied by rising fasting glucose in both B6 and C3H apoE(-/-) mice.
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71 |
23776068
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In addition, for the first time, we identified several differentially regulated plasma proteins between healthy control and diabetic rats, including apolipoprotein E, fetuin B, α-1-acid glycoprotein, β-2-glycoprotein 1, 3-hydroxyanthranilate 3,4-dioxygenase, and serum amyloid P-component.
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