+ |
CSNK2A1 | up-regulates activity
phosphorylation
|
NKX2-5 |
0.338 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-250924 |
Ser164 |
FKQQRYLsAPERDQL |
Chlorocebus aethiops |
COS Cell |
pmid |
sentence |
9858576 |
Mutational analysis and in vitro kinase assays suggested that this 40-kDa Csx/Nkx2.5 kinase is a catalytic subunit of casein kinase II (CKII) that phosphorylates the serine residue between the first and second helix of the homeodomain. This CKII site is phosphorylated in vivo. CKII-dependent phosphorylation of the homeodomain increased Csx/Nkx2. 5 DNA binding. Serine-to-alanine mutation at the CKII phosphorylation site reduced transcriptional activity when the carboxyl-terminal repressor domain was deleted. |
|
Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
+ |
NKX2-5 | up-regulates quantity by expression
transcriptional regulation
|
LYL1 |
0.319 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253655 |
|
|
Homo sapiens |
|
pmid |
sentence |
19608273 |
Sequence analysis of the LYL1 promoter region revealed potential binding sites for transcription factors HOXA10, LMO2 and NKX2-5. Overexpression analysis, reporter gene assays and chromatin immuno-precipitation confirmed their activating impact on LYL1 expression. In conclusion, we identified multiple mechanisms which activate LYL1 in leukemic cells, including structural genomic alterations, namely microdeletion or amplification, together with the involvement of prominent oncogenic transcription factors. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NKX2-5 | down-regulates quantity by repression
transcriptional regulation
|
CTNNB1 |
0.353 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253653 |
|
|
Homo sapiens |
Cardiac Muscle Cell Line |
pmid |
sentence |
19479054 |
Using antisense inhibition we disrupted the expression of NKX2-5 and studied changes in expression of cardiac-associated genes. Down-regulation of NKX2-5 resulted in increased beta-catenin while GATA4 was decreased. We demonstrated that this regulation was conferred by binding of NKX2-5 to specific elements (NKEs) in the promoter region of the beta-catenin and GATA4 genes. Using promoter-luciferase reporter assay combined with mutational analysis of the NKEs we demonstrated that the identified NKX2-5 binding sites were essential for the suppression of beta-catenin, and upregulation of GATA4 by NKX2-5. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NKX2-5 | up-regulates quantity by expression
transcriptional regulation
|
ANKRD1 |
0.343 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253646 |
|
|
Rattus norvegicus |
Cardiac Muscle Cell Line |
pmid |
sentence |
9043061 |
Finally, a carp promoter-lacZ transgene, which displays cardiac-specific expression in wild-type and Nkx2-5(+/-) background, was also significantly reduced in Nkx2-5(-/-) embryos, indicating that Nkx2-5 either directly or indirectly regulates carp promoter activity during in vivo cardiogenesis as well as in cultured cardiac myocytes |
|
Publications: |
1 |
Organism: |
Rattus Norvegicus |
+ |
NKX2-5 | up-regulates quantity by expression
transcriptional regulation
|
GATA4 |
0.844 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253654 |
|
|
Homo sapiens |
|
pmid |
sentence |
19479054 |
Using antisense inhibition we disrupted the expression of NKX2-5 and studied changes in expression of cardiac-associated genes. Down-regulation of NKX2-5 resulted in increased beta-catenin while GATA4 was decreased. We demonstrated that this regulation was conferred by binding of NKX2-5 to specific elements (NKEs) in the promoter region of the beta-catenin and GATA4 genes. Using promoter-luciferase reporter assay combined with mutational analysis of the NKEs we demonstrated that the identified NKX2-5 binding sites were essential for the suppression of beta-catenin, and upregulation of GATA4 by NKX2-5. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NKX2-5 | up-regulates quantity by expression
transcriptional regulation
|
TBX5 |
0.795 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253650 |
|
|
|
|
pmid |
sentence |
15095414 |
Mutation at the potential TBE-B and -C sites, and at the GC box and NKX2.5 sites significantly decreased luciferase activity, suggesting that the GC box and the potential TBE-B, -C, and NKX2.5 sites are functionally important for the activation of the promoter function. |
|
Publications: |
1 |
+ |
JARID2 | down-regulates activity
binding
|
NKX2-5 |
0.467 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-224787 |
|
|
Rattus norvegicus |
Cardiomyocyte Cell Line |
pmid |
sentence |
15542826 |
JMJ physically associates with Nkx2.5 and GATA4 in vitro and in vivo as determined by glutathione S-transferase pull-down and immunoprecipitation assays. we show that JMJ represses ANF gene expression by inhibiting transcriptional activities of Nkx2.5 and GATA4. |
|
Publications: |
1 |
Organism: |
Rattus Norvegicus |
+ |
NKX2-5 | up-regulates quantity by expression
transcriptional regulation
|
MYL2 |
0.606 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253645 |
|
|
Rattus norvegicus |
Cardiac Muscle Cell Line |
pmid |
sentence |
9043061 |
The mammalian homolog of the Drosophila tinman homeobox gene, Nkx2-5, is specifi- cally required for ventricular chamber-specific myosin light chain-2 (MLC-2v) expression and looping morphogenesis during mammalian heart development. |
|
Publications: |
1 |
Organism: |
Rattus Norvegicus |
+ |
NKX2-5 | up-regulates quantity by expression
transcriptional regulation
|
MEF2C |
0.731 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253656 |
|
|
Homo sapiens |
|
pmid |
sentence |
21261500 |
Taken together, our results indicate that the expression of MEF2C in T-ALL cells is principally deregulated via activating leukemic transcription factors GFI1B or NKX2-5 and by escaping inhibitory developmental STAT5 signaling. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
NKX2-5 |
transcriptional regulation
|
NPPB |
0.334 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-253649 |
|
|
|
|
pmid |
sentence |
15837525 |
In comparison to the ANF gene, less is known about BNP promoter consensus elements that regulate gene expression by mechanical or neurohumoral agonists. A number of cis-acting elements for GATA, Nkx2.5, NF-kappaB and TEF transcription factors have recently been identified within the BNP promoter that regulate BNP expression in response to specific agonists. This review focuses on the information available regarding cis-acting determinants responsible for inducible BNP transcription. |
|
Publications: |
1 |