| + |
SALL4 | up-regulates quantity by expression 
transcriptional regulation
|
NANOG |
0.803 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266079 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16840789 |
We conclude that the Nanog enhancer activity is regulated by both Sall4 and Nanog. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SALL4 | down-regulates quantity by repression 
transcriptional regulation
|
PTEN |
0.398 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255126 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19440552 |
Stem cell factor SALL4 represses the transcriptions of PTEN and SALL1 through an epigenetic repressor complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SOX2/POU5F1 | up-regulates quantity by expression
transcriptional regulation
|
SALL4 |
0.757 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269252 |
|
|
|
|
| pmid |
sentence |
| 31583686 |
Both SOX2 and SOX17 are able to partner with OCT4 and, as a consequence, recognize and bind specific binding motifs.6, 7 In human and mouse ESCs, SOX2/OCT4 bind to canonical motifs (CTTTGTCATGCAAAT-like), which are composite SOX (CATTGTC-like) and OCT (ATGCAAAT-like) motifs|This way SOX17 and SOX2 regulate a common set of pluripotency and GC-related genes (PRDM14, DPPA4, TDGF1, NANOG, LIN28A, TRIM71, OTX2, PIM2) (Fig. 6). Additionally, in TCam-2 cells SOX17 binds to compressed motifs or SOX motifs (not bound by SOX2 in ECs), thereby regulating the PGC specifiers PRDM1 and TFAP2C, the GC-related genes NANOS3 and BMP7 and the cancer-related genes MYC and IGF1 (Fig. 6). In 2102EP cells, SOX2 further binds canonical elements or SOX motifs (not bound by SOX17 in TCam-2), regulating additional pluripotency genes (GDF3, LEFTY2, SALL4, SOX2 and POU5F1) (Fig. 6). |
|
| Publications: |
1 |
| + |
CRBN | down-regulates quantity by destabilization 
ubiquitination, binding
|
SALL4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272206 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32071327 |
Thalidomide-induced teratogenicity is dependent on its binding to cereblon (CRBN), the substrate receptor of the Cul4A-DDB1-CRBN-RBX1 E3 ubiquitin ligase complex. Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-272208 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32071327 |
Thalidomide-induced teratogenicity is dependent on its binding to cereblon (CRBN), the substrate receptor of the Cul4A-DDB1-CRBN-RBX1 E3 ubiquitin ligase complex. Thalidomide binding to CRBN elicits subsequent ubiquitination and proteasomal degradation of CRBN neosubstrates including SALL4, a transcription factor of which polymorphisms phenocopy thalidomide-induced limb defects in humans. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
STAT3 | up-regulates quantity by expression 
transcriptional regulation
|
SALL4 |
0.603 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255244 |
|
|
Homo sapiens |
MDA-MB-231 Cell |
| pmid |
sentence |
| 19151334 |
We further tested the functional relationship between STAT3 and SALL4 using MDA-MB-231, a breast cell line carrying constitutive SALL4 expression and STAT3 activity. Down-regulation of the STAT3 activity using a dominant-negative construct resulted in a significant decrease in the expression of SALL4. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SALL4 | up-regulates quantity by expression
transcriptional regulation
|
HOXA9 |
0.375 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255125 |
|
|
Homo sapiens |
Acute Myeloid Leukemia Cell Line |
| pmid |
sentence |
| 24051379 |
In primary human AML cells, downregulation of SALL4 led to decreased HOXA9 expression and enhanced apoptosis. We found that SALL4 bound a specific region of the HOXA9 promoter in leukemic cells. SALL4 overexpression led to enhanced binding of histone activation markers at the HOXA9 promoter region, as well as increased HOXA9 expression in these cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SALL4 | down-regulates quantity by repression
transcriptional regulation
|
SALL1 |
0.478 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255127 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19440552 |
Stem cell factor SALL4 represses the transcriptions of PTEN and SALL1 through an epigenetic repressor complex. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SALL4 | up-regulates quantity by expression
transcriptional regulation
|
ABCA3 |
0.279 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255121 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21526180 |
we demonstrated that SALL4 was able to bind to the promoter region of ABCA3 and activate its expression while regulating the expression of ABCG2 indirectly. SALL4 expression was positively correlated to those of ABCG2 and ABCA3 in primary leukemic patient samples |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SALL4 | down-regulates quantity by repression
transcriptional regulation
|
CDH1 |
0.302 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255124 |
|
|
Homo sapiens |
Breast Cancer Cell Line |
| pmid |
sentence |
| 23954296 |
Our shRNA-mediated SALL4 knockdown system and SALL4 overexpression system revealed that SALL4 suppresses the expression of adhesion gene CDH1, and positively regulates the CDH1 suppressor ZEB1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SALL4 | up-regulates quantity by expression
transcriptional regulation
|
ZEB1 |
0.251 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255123 |
|
|
Homo sapiens |
Breast Cancer Cell Line |
| pmid |
sentence |
| 23954296 |
Our shRNA-mediated SALL4 knockdown system and SALL4 overexpression system revealed that SALL4 suppresses the expression of adhesion gene CDH1, and positively regulates the CDH1 suppressor ZEB1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SALL4 | up-regulates quantity by expression
transcriptional regulation
|
CECR2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263893 |
|
|
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 33144328 |
SALL4 activates Cecr2 by directly binging to its promotor region and CECR2 in turn promotes reprogramming through forming a SMARCA1-contained chromatin remodeling complex with its DTT domain. |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
SALL4 | up-regulates quantity by expression
transcriptional regulation
|
ABCG2 |
0.264 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-255122 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21526180 |
we demonstrated that SALL4 was able to bind to the promoter region of ABCA3 and activate its expression while regulating the expression of ABCG2 indirectly. SALL4 expression was positively correlated to those of ABCG2 and ABCA3 in primary leukemic patient samples |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
4.0
SALL4
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