+ |
CRP | up-regulates quantity by expression
transcriptional regulation
|
CCL2 |
0.454 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252144 |
|
|
Homo sapiens |
Retinal Pigment Epithelium Cell |
pmid |
sentence |
26961257 |
In this study, we provide mechanistic insight into how CRP contributes to the development of AMD. In particular, we show that monomeric CRP (mCRP) but not the pentameric form (pCRP) upregulates IL-8 and CCL2 levels in retinal pigment epithelial cells. Further, we show that complement factor H (FH) binds mCRP to dampen its proinflammatory activity. FH from AMD patients carrying the “risk” His402 polymorphism displays impaired binding to mCRP, and therefore proinflammatory effects of mCRP remain unrestrained. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CRP | up-regulates quantity by expression
transcriptional regulation
|
CXCL8 |
0.492 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252143 |
|
|
Homo sapiens |
Retinal Pigment Epithelium Cell |
pmid |
sentence |
26961257 |
In this study, we provide mechanistic insight into how CRP contributes to the development of AMD. In particular, we show that monomeric CRP (mCRP) but not the pentameric form (pCRP) upregulates IL-8 and CCL2 levels in retinal pigment epithelial cells. Further, we show that complement factor H (FH) binds mCRP to dampen its proinflammatory activity. FH from AMD patients carrying the “risk” His402 polymorphism displays impaired binding to mCRP, and therefore proinflammatory effects of mCRP remain unrestrained. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CFH | down-regulates activity
binding
|
CRP |
0.568 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252145 |
|
|
Homo sapiens |
Retinal Pigment Epithelium Cell |
pmid |
sentence |
26961257 |
In this study, we provide mechanistic insight into how CRP contributes to the development of AMD. In particular, we show that monomeric CRP (mCRP) but not the pentameric form (pCRP) upregulates IL-8 and CCL2 levels in retinal pigment epithelial cells. Further, we show that complement factor H (FH) binds mCRP to dampen its proinflammatory activity. FH from AMD patients carrying the “risk” His402 polymorphism displays impaired binding to mCRP, and therefore proinflammatory effects of mCRP remain unrestrained. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CRP | down-regulates quantity by repression
transcriptional regulation
|
GCH1 |
0.282 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252216 |
|
|
Homo sapiens |
Human Aortic Endothelial Cell |
pmid |
sentence |
17942113 |
The gene expression and enzymatic activity of GTPCH1, the first enzyme in the de novo biosynthesis of BH(4), were significantly inhibited by CRP. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CRP | up-regulates quantity by expression
transcriptional regulation
|
LPL |
0.381 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251852 |
|
|
Homo sapiens |
|
pmid |
sentence |
18708524 |
C-reactive protein enhances macrophage lipoprotein lipase expression. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CRP | down-regulates quantity by repression
translation regulation
|
IL10 |
0.481 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251824 |
|
|
Homo sapiens |
Macrophage |
pmid |
sentence |
16917108 |
CRP significantly decreased IL-10 mRNA stability |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CRP | down-regulates activity
|
GCH1 |
0.282 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252215 |
|
|
Homo sapiens |
Human Aortic Endothelial Cell |
pmid |
sentence |
17942113 |
The gene expression and enzymatic activity of GTPCH1, the first enzyme in the de novo biosynthesis of BH(4), were significantly inhibited by CRP. Importantly, GTPCH1 is known to be regulated by cAMP-mediated pathway. In the present study, CRP-mediated inhibition of GTPCH1 activity was reversed by pretreatment with cAMP analogues. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CRP | down-regulates quantity by destabilization
|
NOS3 |
0.477 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-252217 |
|
|
|
|
pmid |
sentence |
17942113 |
C-reactive protein (CRP), a cardiovascular risk marker, induces endothelial dysfunction. CRP decreases endothelial nitric oxide synthase (eNOS) expression and bioactivity in human aortic endothelial cells (HAECs). CRP treatment significantly decreased levels of BH4 thereby promoting eNOS uncoupling. we found that CRP decreased the eNOS dimer/monomer ratio further supporting eNOS uncoupling. |
|
Publications: |
1 |
+ |
CRP | down-regulates quantity
post transcriptional regulation
|
IL10 |
0.481 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251825 |
|
|
Homo sapiens |
|
pmid |
sentence |
16917108 |
CRP significantly decreased IL-10 mRNA stability |
|
Publications: |
1 |
Organism: |
Homo Sapiens |