+ |
FSTL1 | up-regulates activity
binding
|
DIP2A |
0.494 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266603 |
|
|
Homo sapiens |
Cardiac Microvascular Endothelial Cell |
pmid |
sentence |
20054002 |
We identified DIP2A as a novel FSTL1-binding partner from the membrane fraction of endothelial cells. Co-immunoprecipitation assays revealed a direct physical interaction between FSTL1 and DIP2A. The work in the current study identifies DIP2A as a novel receptor for FSTL1 that mediates Akt activation and cell survival and function in cardiovascular cells in vitro. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
DIP2A | up-regulates activity
binding
|
SOD2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266592 |
|
|
Mus musculus |
Brain |
pmid |
sentence |
33781892 |
DIP2a is associated with SOD in the mitochondria of mouse brain. DIP2a knockout inhibited SOD activity. In this paper, we analyzed the interacting proteins of DIP2A by mass spectrum analysis and found that DIP2A was correlated with superoxide dismutase (SOD), SOD1 and SOD2. Knockout of DIP2A decreased SOD activity and increased the level of ROS in the mouse brain. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
DIP2A | up-regulates quantity
chemical modification
|
acetyl-CoA |
0.8 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266590 |
|
|
in vitro |
|
pmid |
sentence |
30672040 |
In this paper, we summarized the conservation of gene sequences and protein domains of DIP2 family members and predicted that they may have a similar functional role in acetyl-coenzyme A (acetyl-CoA) synthesis. We then used the most characterized member, disconnected interacting protein 2 homolog A (DIP2A), for further study. DIP2A is a cytoplasmic protein that is preferentially localized to mitochondria, and its acetyl-CoA synthetase activity has been demonstrated in vitro. Furthermore, the level of acetyl-CoA in HEK293 cells overexpressing DIP2A was increased, which is consistent with its metabolically related function. |
|
Publications: |
1 |
Organism: |
In Vitro |
+ |
DIP2A | up-regulates activity
acetylation
|
CTTN |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266589 |
|
|
Mus musculus |
Brain |
pmid |
sentence |
31600191 |
DIP2A binds to cortactin and modulates cortactin acetylation. Autism candidate gene disconnected-interacting protein homolog 2 A (DIP2A) is known to be involved in acetylated coenzyme A (Ac-CoA) synthesis and is primarily expressed in the brain regions with abundant pyramidal neurons. We further identified that DIP2A interacted with cortactin, an activity-dependent spine remodeling protein. The binding activity of DIP2A-PXXP motifs (P, proline; X, any residue) with the cortactin-Src homology 3 (SH3) domain was critical for maintaining the level of acetylated cortactin. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
DIP2A | up-regulates activity
binding
|
SOD1 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266591 |
|
|
Mus musculus |
Brain |
pmid |
sentence |
33781892 |
DIP2a is associated with SOD in the mitochondria of mouse brain. DIP2a knockout inhibited SOD activity. In this paper, we analyzed the interacting proteins of DIP2A by mass spectrum analysis and found that DIP2A was correlated with superoxide dismutase (SOD), SOD1 and SOD2. Knockout of DIP2A decreased SOD activity and increased the level of ROS in the mouse brain. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
DIP2A | up-regulates activity
binding
|
ABL2 |
0.2 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266593 |
|
|
Mus musculus |
Pyramidal Neuron |
pmid |
sentence |
33622779 |
Here, using cultured hippocampal neurons pooled from both sexes of mice, we provide evidence that binding to cortactin tethers Abl2 in spines, where Abl2 and cortactin maintain the small pool of stable actin required for dendritic spine stability. |
|
Publications: |
1 |
Organism: |
Mus Musculus |