| + |
Amyloid_fibril_formation | up-regulates 
|
calcium(2+) |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255481 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15621017 |
It has been reported that Aβ can result in an increase in intracellular Ca2+, which in turn can activates CaMK. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
Amyloid_fibril_formation | down-regulates 
|
AKT |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255493 |
|
|
|
|
| pmid |
sentence |
| 26721223 |
Excessive accumulation of Aβ protein in the AD brain may lead to a decrease in the levels of phosphatidylinositol-3 kinase (PI3K) and the serine/threonine protein kinase B (Akt) activity. |
|
| Publications: |
1 |
| + |
APP | up-regulates
|
Amyloid_fibril_formation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251638 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11578751 |
Neurodegeneration in Alzheimer's disease is a pathologic condition of cells rather than an accelerated way of aging. The senile plaques are generated by a deposition in the human brain of fibrils of the β-amyloid peptide (Aβ), a fragment derived from the proteolytic processing of the amyloid precursor protein (APP). Tau protein is the major component of paired helical filaments (PHFs), which form a compact filamentous network described as neurofibrillary tangles (NFTs). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer |
| + |
Amyloid_fibril_formation | up-regulates activity
|
DKK1 |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255482 |
|
|
|
|
| pmid |
sentence |
| 15229249 |
Exposure of the cultures to beta-amyloid peptide (βAP) induced the expression of the secreted glycoprotein Dickkopf-1 (DKK1). |
|
| Publications: |
1 |
| + |
Amyloid_fibril_formation | down-regulates
|
PI3K |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255492 |
|
|
|
|
| pmid |
sentence |
| 26721223 |
Excessive accumulation of Aβ protein in the AD brain may lead to a decrease in the levels of phosphatidylinositol-3 kinase (PI3K) and the serine/threonine protein kinase B (Akt) activity. |
|
| Publications: |
1 |
| + |
Amyloid_fibril_formation | up-regulates
|
Apoptosis |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-251640 |
|
|
Homo sapiens |
Alzheimer Disease Specific Cell Type |
| pmid |
sentence |
| 11578751 |
Alzheimer's disease, the cause of one of the most common types of dementia, is a brain disorder affecting the elderly and is characterized by the formation of two main protein aggregates: senile plaques and neurofibrillary tangles, which are involved in the process leading to progressive neuronal degeneration and death |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer |
3.0
Amyloid_fibril_formation