| + |
PLK1 | down-regulates quantity by destabilization 
dephosphorylation
|
RAD21 |
0.727 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275535 |
Ser175 |
REIMREGsAFEDDDM |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 15737063 |
We suspected that the observed enhancement of Scc1's cleavability in the presence of Plk1 might be due to phosphorylation at two sites that are directly adjacent to the cleavage sites, Ser175 and Ser454, which we had found to be phosphorylated in mitosis in vivo (Table 1). We therefore mutated these two residues to alanine, thereby creating mutant Scc1-S175A/S454A (see Figure 1C), and tested the cleavability of this mutant in the absence or presence of Plk1 in vitro. |Scc1 phosphorylation is dispensable for cohesin dissociation from chromosomes in early mitosis but enhances the cleavability of Scc1 by separase. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275536 |
Ser454 |
EPSRLQEsVMEASRT |
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 15737063 |
We suspected that the observed enhancement of Scc1's cleavability in the presence of Plk1 might be due to phosphorylation at two sites that are directly adjacent to the cleavage sites, Ser175 and Ser454, which we had found to be phosphorylated in mitosis in vivo (Table 1). We therefore mutated these two residues to alanine, thereby creating mutant Scc1-S175A/S454A (see Figure 1C), and tested the cleavability of this mutant in the absence or presence of Plk1 in vitro. |Scc1 phosphorylation is dispensable for cohesin dissociation from chromosomes in early mitosis but enhances the cleavability of Scc1 by separase. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
RAD21 | down-regulates quantity
transcriptional regulation
|
APOB |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259974 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25575569 |
The promoter region of APOB bound RAD21 but not RAD21 p.622 Ala>Thr; expression of wild-type RAD21 in HEK293 cells repressed expression of APOB, compared with control vector. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
STAG2 | up-regulates quantity by stabilization 
binding
|
RAD21 |
0.964 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261511 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 28430577 |
Cohesin is an evolutionarily conserved complex composed of four core proteins (SMC1A, SMC3, RAD21 and either STAG2 or STAG1) that form a ring-shaped structure able to encircle chromatin |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ESPL1 | down-regulates quantity by destabilization
cleavage
|
RAD21 |
0.772 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-275537 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 15737063 |
In order to segregate sister chromatids to opposite poles in anaphase, cohesin has to be removed from chromosomes. In budding yeast, the prevalent mode of cohesin removal is by proteolytic cleavage of the Scc1 subunit at the onset of anaphase by the endopeptidase separase |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CC2D1A | up-regulates activity
binding
|
RAD21 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268294 |
|
|
|
|
| pmid |
sentence |
| 20171170 |
Akt kinase-interacting protein 1 (Aki1)/Freud-1/CC2D1A is localized in the cytosol, nucleus, and centrosome. Aki1 plays distinct roles depending on its localization. | In the centrosome, it regulates spindle pole localization of the cohesin subunit Scc1, thereby mediating centriole cohesion during mitosis. |
|
| Publications: |
1 |
| + |
RAD21 | form complex 
binding
|
Cohesin complex |
0.966 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263311 |
|
|
|
|
| pmid |
sentence |
| 28430577 |
Cohesin is an evolutionarily conserved complex composed of four core proteins (SMC1A, SMC3, RAD21 and either STAG2 or STAG1) that form a ring-shaped structure able to encircle chromatin |
|
| Publications: |
1 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-115426 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 11875078 |
Rad21 is a component of the cohesin complex that holds sister chromatids together during mitosis and repairs double-strand dna breaks. Interestingly, rad21 is cleaved by a caspase-like esp1/separase at the onset of anaphase to trigger sister chromatid separation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RAD21 | down-regulates activity
relocalization
|
RUNX1 |
0.288 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261514 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
| pmid |
sentence |
| 26607380 |
Large-scale AML genome re-sequencing efforts have identified novel recurrently mutated genes, including the members of the cohesin complex (RAD21, SMC3, SMC1A, and STAG2), implicated in the pathogenesis of this disease.Using ATAC-seq, we determined that mutant cohesin lead to a state of elevated chromatin accessibility and higher predicted binding at transcription factor binding sites for ERG, GATA2, and RUNX1. Moreover, using ChIP-Seq, we formally demonstrated increased binding of GATA2 and RUNX1 to these sites. Finally, we demonstrated that knockdown of these three TFs in human HSPC can revert the differentiation block induced by mutant cohesin. These results support a model in which mutant cohesin impairs hematopoietic differentiation and enforces stem cell programs through the modulation of ERG, GATA2, and RUNX1 chromatin accessibility, expression, and activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML, NPM1_new |
| + |
RAD21 | up-regulates activity 
|
DNA_repair |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259975 |
|
|
Mus musculus |
|
| pmid |
sentence |
| 20711430 |
Rad21-cohesin haploinsufficiency impedes DNA repair and enhances gastrointestinal radiosensitivity in mice |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| Pathways: | Acute Myeloid Leukemia |
| + |
RAD21 | down-regulates activity
relocalization
|
GATA2 |
0.332 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261513 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
| pmid |
sentence |
| 26607380 |
Large-scale AML genome re-sequencing efforts have identified novel recurrently mutated genes, including the members of the cohesin complex (RAD21, SMC3, SMC1A, and STAG2), implicated in the pathogenesis of this disease.Using ATAC-seq, we determined that mutant cohesin lead to a state of elevated chromatin accessibility and higher predicted binding at transcription factor binding sites for ERG, GATA2, and RUNX1. Moreover, using ChIP-Seq, we formally demonstrated increased binding of GATA2 and RUNX1 to these sites. Finally, we demonstrated that knockdown of these three TFs in human HSPC can revert the differentiation block induced by mutant cohesin. These results support a model in which mutant cohesin impairs hematopoietic differentiation and enforces stem cell programs through the modulation of ERG, GATA2, and RUNX1 chromatin accessibility, expression, and activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RAD21 | down-regulates activity
relocalization
|
ERG |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261515 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell |
| pmid |
sentence |
| 26607380 |
Large-scale AML genome re-sequencing efforts have identified novel recurrently mutated genes, including the members of the cohesin complex (RAD21, SMC3, SMC1A, and STAG2), implicated in the pathogenesis of this disease.Using ATAC-seq, we determined that mutant cohesin lead to a state of elevated chromatin accessibility and higher predicted binding at transcription factor binding sites for ERG, GATA2, and RUNX1. Moreover, using ChIP-Seq, we formally demonstrated increased binding of GATA2 and RUNX1 to these sites. Finally, we demonstrated that knockdown of these three TFs in human HSPC can revert the differentiation block induced by mutant cohesin. These results support a model in which mutant cohesin impairs hematopoietic differentiation and enforces stem cell programs through the modulation of ERG, GATA2, and RUNX1 chromatin accessibility, expression, and activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
RAD21 | down-regulates quantity by repression
transcriptional regulation
|
RUNX1 |
0.288 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-259973 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24321385 |
We observed that depletion of RAD21 (but not CTCF) enhanced RUNX1 transcription in human HL-60 myelocytic leukemia cells |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, MLL fusion protein in AML, NPM1_new |
3.0
RAD21
- 
- 