| + |
AKT3 | down-regulates activity 
phosphorylation
|
CYCS |
0.268 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277235 |
Tyr47 |
KTGQAPGySYTAANK |
in vitro |
|
| pmid |
sentence |
| 32781572 |
Finally, we propose that pro-survival kinase Akt (protein kinase B) is a likely mediator of the S47 phosphorylation of Cytc in the brain. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
AKT2 | down-regulates activity
phosphorylation
|
CYCS |
0.298 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277236 |
Tyr47 |
KTGQAPGySYTAANK |
in vitro |
|
| pmid |
sentence |
| 32781572 |
Finally, we propose that pro-survival kinase Akt (protein kinase B) is a likely mediator of the S47 phosphorylation of Cytc in the brain. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
AKT1 | down-regulates activity
phosphorylation
|
CYCS |
0.48 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277237 |
Tyr47 |
KTGQAPGySYTAANK |
in vitro |
|
| pmid |
sentence |
| 32781572 |
Finally, we propose that pro-survival kinase Akt (protein kinase B) is a likely mediator of the S47 phosphorylation of Cytc in the brain. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Parkinson |
| + |
3a | up-regulates activity 
|
CYCS |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260214 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18632968 |
Thus, caspase-9 activation and cytochrome c release in cells expressing the 3a protein indicated that this viral protein also activates the intrinsic pathway of apoptosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-COV APOPTOSIS |
| + |
BID | up-regulates activity
|
CYCS |
0.575 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-59224 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9727492 |
TBID induces first the clustering of mitochondria around the nuclei and release of cytochrome c. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
PRKAA1 | up-regulates quantity by expression
transcriptional regulation
|
CYCS |
0.356 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-156772 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 17609368 |
Severalin vivostudies using aicar to activate ampk chronically determined that mitochondrial enzymes [e.g., cytochromec, uncoupling protein 3 (ucp-3)] (1518) and proteins involved in glucose uptake (glut4) (1820) are increased at the transcriptional level in skeletal muscle. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Tissue: |
Muscle, Skeletal Muscle |
| + |
CYCS | up-regulates
|
Oxidative_phosphorylation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253100 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 23021218 |
PGC1a is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cyto- chrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
BAX | up-regulates
|
CYCS |
0.687 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-160039 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18097445 |
This process of mitochondrial outer membrane permeabilization (momp) results in the release of cycs.it is commonly thought that bax and bak form pores in membranes |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
CYCS | form complex 
binding
|
Apoptosome |
0.831 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256430 |
|
|
in vitro |
|
| pmid |
sentence |
| 10206961 |
APAF-1 binds and hydrolyzes ATP or dATP to ADP or dADP, respectively. The hydrolysis of ATP/dATP and the binding of cytochrome c promote APAF-1 oligomerization, forming a large multimeric APAF-1.cytochrome c complex. Such a complex can be isolated using gel filtration chromatography and is by itself sufficient to recruit and activate procaspase-9. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | Alzheimer |
| + |
CYCS | up-regulates activity 
binding
|
APAF1 |
0.786 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-135384 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15829969 |
During apoptosis, Apaf-1 binds to cytochrome c and in the presence of ATP/dATP forms an apoptosome, leading to the recruitment and activation of the initiator caspase, caspase-9. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-149574 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16977332 |
Apaf-1 exists in an inactive conformation in cells and is activated through binding to cytochrome c and dATP. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-50585 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9267021 |
Once released from mitochondria, cytochrome c binds to Apaf-1, which may trigger the activation of caspase-3 in the presence of dATP. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-137295 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15907471 |
Cytochrome c (Cyt c) is then released from the intermembrane space of the mitochondrion into the cytosol, where it binds to apoptotic protease-activating factor 1 (Apaf-1) in the presence of ATP/dATP to form the apoptosome. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
GHITM | down-regulates quantity
relocalization
|
CYCS |
0.258 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260294 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 18417609 |
MICS1 was clearly coprecipitated with cytochrome c-3FLAG and the amount was DSP concentration-dependent (Figure 6A). Together with the finding that overexpression of exogenous MICS1 delayed the apoptotic release of cytochrome c in normal-serum level medium (Figure 4A), these results suggest that MICS1 helps to retain cytochrome c in the inner membrane, apart from the morphological changes. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
BAX | up-regulates
relocalization
|
CYCS |
0.687 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-73898 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10629050 |
The integration of bax oligomers in the outer mitochondrial membrane is followed by cytochrome crelease |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
CYCS | up-regulates activity
binding
|
CASP9 |
0.876 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-53585 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 9390557 |
Caspase-9 and apaf-1 bind to each other via their respective nh2-terminal ced-3 homologous domains in the presence of cytochrome c and datp, an event that leads to caspase-9 activation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, Parkinson, SARS-COV APOPTOSIS |
| + |
BAK1 | up-regulates
relocalization
|
CYCS |
0.549 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-105206 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11175253 |
Allosteric activation of bak induces its intramembranous oligomerization into a proposed pore for cytochrome c efflux |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
PPARGC1A | up-regulates quantity by expression
transcriptional regulation
|
CYCS |
0.391 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253097 |
|
|
Mus musculus |
Adipocyte |
| pmid |
sentence |
| 23021218 |
PGC1a is known to drive the expression of many genes involved in mitochondrial oxidative phosphorylation, including cytochrome c (CytC) and the cyto- chrome C oxidative (COX) subunits (CoxIII, Cox4il, Cox5b, Cox7a, and Cox8b). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
BAK1 | up-regulates
|
CYCS |
0.549 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-160036 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18097445 |
This process of mitochondrial outer membrane permeabilization (momp) results in the release of cycs. It is commonly thought that bax and bak form pores in membranes |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CASP8 | up-regulates activity
|
CYCS |
0.495 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-68225 |
|
|
Homo sapiens |
JURKAT Cell |
| pmid |
sentence |
| 10364179 |
Caspase-8 triggered rapid cytochrome c release from mitochondria. The effect was indirect. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
TP53 | up-regulates
|
CYCS |
0.47 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-140251 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19007744 |
P53 translocation precedes changes of mitochondrial membrane potential, cytochrome c release and caspase activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Mitochondrial Control of Apoptosis |
| + |
PINK1 | down-regulates quantity
|
CYCS |
0.393 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-249704 |
|
|
Homo sapiens |
Neuron |
| pmid |
sentence |
| 20012177 |
There is a strong cyto-protective role of PINK1 in maintaining mitochondrial homeostasis via different mechanisms. Overexpression of wild-type PINK1 in SH-SY5Y neuroblastoma cells stabilizes respiring mitochondrial networks through various mechanisms that include maintaining mitochondrial membrane potential, reducing basal and neurotoxin-induced ROS, suppression of cytochrome c release, reversal of toxin-induced fission, and suppression of autophagy |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Parkinson |
| + |
BCL2 | down-regulates activity 
|
CYCS |
0.63 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-99063 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 12624108 |
Bcl-2 blocked the release of mitochondrial cytochrome c |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Alzheimer, COVID-19 Causal Network, Death Receptor Signaling, Mitochondrial Control of Apoptosis, SARS-COV APOPTOSIS |
| + |
Caspase 8 complex | up-regulates activity
|
CYCS |
0.495 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256473 |
|
|
Homo sapiens |
JURKAT Cell |
| pmid |
sentence |
| 10364179 |
Caspase-8 triggered rapid cytochrome c release from mitochondria. The effect was indirect. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
CYCS
- 
- 