| + |
USP45 | up-regulates activity 
deubiquitination
|
ERCC4/ERCC1 |
0.541 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268504 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 25538220 |
USP45 associates with the ERCC1–XPF endonuclease. USP45 interacts specifically with ERCC1–XPF via its N-terminal 61 residues. USP45 deubiquitylates ERCC1. USP45 promotes survival of cells exposed to agents that induce DNA damage responses controlled by ERCC1–XPF endonuclease |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SLX4 | up-regulates
binding
|
ERCC4/ERCC1 |
0.813 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-217652 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24726326 |
Slx4 is a tumor suppressor that stimulates the activity of the nuclease xpf-ercc1 in dna crosslink repair. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | DNA repair in cancer |
| + |
ERCC1 | form complex 
binding
|
ERCC4/ERCC1 |
0.952 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-142989 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16338413 |
Human ercc1/xpf interaction domains reveals a complementary role for the two proteins in nucleotide excision repair. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ERCC4 | form complex
binding
|
ERCC4/ERCC1 |
0.952 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-142992 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16338413 |
Human ercc1/xpf interaction domains reveals a complementary role for the two proteins in nucleotide excision repair. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ERCC4/ERCC1 | up-regulates 
|
DNA_repair |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259064 |
|
|
in vitro |
|
| pmid |
sentence |
| 10542278 |
HMLH1 and hPMS2 function in postreplicative mismatch repair in the form of a heterodimer referred to as hMutLα. Tumors or cell lines lacking this factor display mutator phenotypes and microsatellite instability, and mutations in the hMLH1 andhPMS2 genes predispose to hereditary non-polyposis colon cancer. Recombinant hMutLα and hMutLβ, expressed in the baculovirus system, were tested for their activity in an in vitro mismatch repair assay. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | DNA repair in cancer |
3.0
ERCC4/ERCC1
CPX-478