| + |
CHD2 | up-regulates quantity 
relocalization
|
H3-3A |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264527 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26895424 |
Non-homologous end-joining (NHEJ) is the dominant DSB repair pathway in human cells, but our understanding of how it operates in chromatin is limited. Here, we define a mechanism that plays a crucial role in regulating NHEJ in chromatin. This mechanism is initiated by DNA damage-associated poly(ADP-ribose) polymerase 1 (PARP1), which recruits the chromatin remodeler CHD2 through a poly(ADP-ribose)-binding domain. CHD2 in turn triggers rapid chromatin expansion and the deposition of histone variant H3.3 at sites of DNA damage. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHD2 | up-regulates quantity
relocalization
|
XRCC4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264528 |
|
|
Homo sapiens |
U2-OS Cell |
| pmid |
sentence |
| 26895424 |
CHD2 Promotes the Recruitment of Core NHEJ Factors. overexpression of ATPase-dead CHD2 (K515R; Figure S5F), but not wild-type CHD2, also reduced the recruitment of XRCC4 (Figure 5E). Together, these findings suggest that the chromatin remodeling activity of CHD2 promotes the efficient assembly of NHEJ complexes at DSBs. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHD2 | up-regulates activity
binding
|
MYOD1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264525 |
|
|
|
|
| pmid |
sentence |
| 29962935 |
CHD2 also showed an interaction with MyoD, a master regulator of skeletal muscle differentiation, and together MyoD and CHD2 bind to myogenic gene promoters. |
|
| Publications: |
1 |
| + |
PARP1 | up-regulates quantity
binding
|
CHD2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264526 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26895424 |
Non-homologous end-joining (NHEJ) is the dominant DSB repair pathway in human cells, but our understanding of how it operates in chromatin is limited. Here, we define a mechanism that plays a crucial role in regulating NHEJ in chromatin. This mechanism is initiated by DNA damage-associated poly(ADP-ribose) polymerase 1 (PARP1), which recruits the chromatin remodeler CHD2 through a poly(ADP-ribose)-binding domain. CHD2 in turn triggers rapid chromatin expansion and the deposition of histone variant H3.3 at sites of DNA damage. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CHD2 | up-regulates 
|
DNA_repair |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-264529 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 26895424 |
We show in mouse cells that the cNHEJ-dependent fusion of chromosomes containing uncapped telomeres requires the activity of CHD2. Together, these findings argue that the chromatin response mediated by CHD2 is triggered by the presence of DSBs and promotes repair of these lesions by the canonical KU-dependent NHEJ pathway. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
3.0
CHD2
- 
- 