| + |
SIRT1 | up-regulates activity 
deacetylation
|
XPA |
0.526 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258986 |
Lys215 |
QENREKMkQKKFDKK |
Homo sapiens |
|
| pmid |
sentence |
| 30327428 |
SIRT1 deacetylates XPA at residues K63, K67, and K215 to promote interactions with ATR |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262293 |
Lys63 |
TGGMANVkAAPKIID |
Homo sapiens |
A-375 Cell |
| pmid |
sentence |
| 30327428 |
SIRT1 deacetylates XPA at residues K63, K67, and K215 to promote interactions with ATR |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-262294 |
Lys67 |
ANVKAAPkIIDTGGG |
Homo sapiens |
A-375 Cell |
| pmid |
sentence |
| 30327428 |
SIRT1 deacetylates XPA at residues K63, K67, and K215 to promote interactions with ATR |
|
| Publications: |
3 |
Organism: |
Homo Sapiens |
| + |
ATR | up-regulates activity
phosphorylation
|
XPA |
0.505 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250584 |
Ser173 |
VKKNPHHsQWGDMKL |
Homo sapiens |
A-549 Cell |
| pmid |
sentence |
| 16540648 |
Defects in ATR-dependent XPA phosphorylation increases the cell sensitivity to UV irradiation. | The XPA-deficient cells complemented with XPA-S196A mutant, in which Ser196 was substituted with an alanine, displayed significantly higher UV sensitivity compared with the XPA cells complemented with wild-type XPA. Moreover, substitution of Ser196 with aspartic acid for mimicking the phosphorylation of XPA increased the cell survival to UV irradiation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258985 |
Ser196 |
RSLEVWGsQEALEEA |
Homo sapiens |
|
| pmid |
sentence |
| 30327428 |
ATR mediated phosphorylation of XPA on S196 enhances cAMP-mediated optimization of NER, and is promoted by SIRT1-mediated deacetylation of XPA on K63, K67 and K215. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
ATM |
phosphorylation
|
XPA |
0.61 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250579 |
Ser173 |
VKKNPHHsQWGDMKL |
in vitro |
|
| pmid |
sentence |
| 16540648 |
Kinase phosphorylation assays were done with synthesized short peptides (20-mer) with the sequences at Ser173 and Ser196 of XPA, respectively. Both peptides seemed to be good substrates for DNA-PK, ATR ( Fig. 2D), and ATM (data not shown). |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250580 |
Ser196 |
RSLEVWGsQEALEEA |
in vitro |
|
| pmid |
sentence |
| 16540648 |
Kinase phosphorylation assays were done with synthesized short peptides (20-mer) with the sequences at Ser173 and Ser196 of XPA, respectively. Both peptides seemed to be good substrates for DNA-PK, ATR ( Fig. 2D), and ATM (data not shown). |
|
| Publications: |
2 |
Organism: |
In Vitro |
| + |
ATR | up-regulates
phosphorylation
|
XPA |
0.505 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-199802 |
Ser196 |
RSLEVWGsQEALEEA |
Homo sapiens |
|
| pmid |
sentence |
| 23178497 |
Atr phosphorylates xpa. at serine 196. Atr-mediated xpa phosphorylation enhances xpa stability by inhibiting herc2-mediated ubiquitination and subsequent degradation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-145190 |
Ser196 |
RSLEVWGsQEALEEA |
Homo sapiens |
|
| pmid |
sentence |
| 16540648 |
Atr was the major kinase responsible for the cellular phosphorylation of xpa following uv irradiation / we propose that the phosphorylation of xpa by atr checkpoint may positively regulate ner activity and thus may facilitate the cells to recover from ner-related dna damages. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
HERC2 | down-regulates 
ubiquitination
|
XPA |
0.394 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-164595 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 20304803 |
Herc2 may ubiquitinate xpa and thus target it for proteolytic degradation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
XPA | up-regulates activity 
|
DNA_repair |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-258984 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 30327428 |
A coordinated repair process mediated by the xeroderma pigmentosum complementation group proteins (XPs), which include XPA through XPG. XPA is indispensable in this pathway and has reported functions in DNA damage verification, stabilization of repair intermediates and positioning of NER factors |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
XPA | up-regulates
|
Nucleotide-excision_repair |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275704 |
|
|
|
|
| pmid |
sentence |
| 24086043 |
The core NER dual incision reaction has been reconstituted in vitro with purified factors using XPC-RAD23B, TFIIH, XPA, RPA, XPG, and ERCC1-XPF (Aboussekhra et al. 1995; Mu et al. 1995; Araujo et al. 2000). Functional studies revealed that XPC-RAD23B is the initial damage recognition factor in this system, as the presence of XPC-RAD23B is required for assembly of the other core NER factors and progression through the NER pathway both in vitro and in vivo |
|
| Publications: |
1 |
| + |
RAD23B | up-regulates activity
binding
|
XPA |
0.761 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275697 |
|
|
|
|
| pmid |
sentence |
| 24086043 |
GG-NER is initiated by the GG-NER specific factor XPC-RAD23B, in some cases with the help of UV-DDB (UV-damaged DNA-binding protein). TC-NER is initiated by RNA polymerase stalled at a lesion with the help of TC-NER specific factors CSA, CSB, and XAB2. Both pathways require the core NER factors to complete the excision process|The core NER dual incision reaction has been reconstituted in vitro with purified factors using XPC-RAD23B, TFIIH, XPA, RPA, XPG, and ERCC1-XPF (Aboussekhra et al. 1995; Mu et al. 1995; Araujo et al. 2000).|The core NER dual incision reaction has been reconstituted in vitro with purified factors using XPC-RAD23B, TFIIH, XPA, RPA, XPG, and ERCC1-XPF (Aboussekhra et al. 1995; Mu et al. 1995; Araujo et al. 2000). Functional studies revealed that XPC-RAD23B is the initial damage recognition factor in this system, as the presence of XPC-RAD23B is required for assembly of the other core NER factors and progression through the NER pathway both in vitro and in vivo |
|
| Publications: |
1 |
3.0
XPA
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