| + |
ROS | up-regulates 
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263828 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32454942 |
Next to their interaction with adaptive immune cells, activated microglia can secrete cytotoxic cytokines and oxidative products, such as ROS and NO radicals in MS lesions thereby promoting oxidative stress and contributing to myelin destruction |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
nitric oxide | up-regulates
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263829 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32454942 |
Next to their interaction with adaptive immune cells, activated microglia can secrete cytotoxic cytokines and oxidative products, such as ROS and NO radicals in MS lesions thereby promoting oxidative stress and contributing to myelin destruction |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
TNF | up-regulates
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263834 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24507514 |
TNF-a is the most comprehensively studied cytokine in both EAE and MS. Most TNF-a overexpressing transgenic animals showed spontaneous pathology, characterized by progressive demyelination and macrophage infiltration |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
IFNG | up-regulates
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263833 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 24507514 |
Beside its wellknown antiviral and proinflammatory action, overexpression of IFN-g in the CNS could participate in demyelination. Transgenic overexpression of IFN-g in the mouse by CNS oligodendrocytes led to chronic demyelination that may be severe |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Tissue: |
Central Nervous System |
| Pathways: | Multiple sclerosis |
| + |
TNFRSF21 | down-regulates 
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263832 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32454942 |
Next to inhibition of sTNF/TNFR1 signaling, specific activation of TNFR2 may hold promise as a new MS therapy. Indeed, TNF promotes proliferation of oligodendrocyte progenitors and remyelination via TNFR2 |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Multiple sclerosis |
| + |
MYT1L | down-regulates
|
Demyelination |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266779 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 29397565 |
Myt1L (myelin transcription factor 1-like), mainly expressed in neurons, has been associated with intellectual disability, schizophrenia, and depression. In the present study, we found that Myt1L was expressed in oligodendrocyte lineage cells during myelination and remyelination. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
Demyelination