+ |
CREBBP | up-regulates activity
acetylation
|
KLF1 |
0.504 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251826 |
Lys288 |
CAHPGCGkSYTKSSH |
Homo sapiens |
|
pmid |
sentence |
11259590 |
EKLF residues acetylated by CREB binding protein (CBP) in vitro map to Lys-288 in its transactivation domain and Lys-302 in its zinc finger domain. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
CSNK2A1 | up-regulates activity
phosphorylation
|
KLF1 |
0.349 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-241361 |
Thr23 |
ALGPFPDtQDDFLKW |
Mus musculus |
MEL Cell |
pmid |
sentence |
9722526 |
Regulation of erythroid Krppel-like factor (EKLF) transcriptional activity by phosphorylation of a protein kinase casein kinase II site within its interaction domain. the transactivation capability of EKLF is augmented by co-transfection of CKIIalpha. in vitro assays demonstrate that CKIIalpha interacts with EKLF, and that the EKLF interaction domain is phosphorylated by CKII only at Thr-41 |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
CSNK2A2 | up-regulates activity
phosphorylation
|
KLF1 |
0.348 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-241365 |
Thr23 |
ALGPFPDtQDDFLKW |
Mus musculus |
MEL Cell |
pmid |
sentence |
9722526 |
Regulation of erythroid Krppel-like factor (EKLF) transcriptional activity by phosphorylation of a protein kinase casein kinase II site within its interaction domain. the transactivation capability of EKLF is augmented by co-transfection of CKIIalpha. in vitro assays demonstrate that CKIIalpha interacts with EKLF, and that the EKLF interaction domain is phosphorylated by CKII only at Thr-41 |
|
Publications: |
1 |
Organism: |
Mus Musculus |
+ |
CBP/p300 | up-regulates activity
acetylation
|
KLF1 |
0.472 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251789 |
|
|
Homo sapiens |
Erythroid Cell |
pmid |
sentence |
9707565 |
CBP and p300, but Not P/CAF, Enhance EKLF Trans-activation in Erythroid Cells. We find that EKLF is an acetylated transcription factor, and that it interacts in vivo with CBP, p300, and P/CAF. However, its interactions with these histone acetyltransferases are not equivalent, as CBP and p300, but not P/CAF, utilize EKLF as a substrate for in vitro acetylation within its trans-activation region. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
KLF1 | up-regulates
|
Erythrocyte_differentiation |
0.7 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256086 |
|
|
Homo sapiens |
Hematopoietic Stem Cell |
pmid |
sentence |
28026072 |
Activation of KLF1 at day 10 of the differentiation process when hematopoietic progenitor cells were present, enhanced erythroid commitment and differentiation. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Pathways: | HaematopoiesisTranscriptionalControl |
+ |
FLI1 | down-regulates activity
binding
|
KLF1 |
0.378 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256044 |
|
|
Mus musculus |
MEL Cell |
pmid |
sentence |
12556498 |
FLI-1 represses the transcriptional activity of EKLF.Our data indicate that the ETS domain of FLI-1 is absolutely required to inhibit EKLF activity. Since the FLI-1 ETS domain interacts with the DNA binding domain of EKLF, one possibility could be that FLI-1 inhibits the binding of EKLF to its DNA targets |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | HaematopoiesisTranscriptionalControl |
+ |
KLF1 | up-regulates quantity by expression
transcriptional regulation
|
KLF8 |
0.253 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266050 |
|
|
Mus musculus |
|
pmid |
sentence |
18687676 |
Here we report that Klf8 is repressed by Klf3 in vivo and is up-regulated by Klf1. Transcript analysis indicates that Klf8 has two promoters, both containing multiple CACCC elements. Transactivation assays and chromatin immunoprecipitation experiments indicate that Klf3 represses Klf8 directly and that Klf1 activates Klf8 directly. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Tissue: |
Liver |
+ |
KLF1 | down-regulates activity
binding
|
FLI1 |
0.378 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256046 |
|
|
Mus musculus |
MEL Cell |
pmid |
sentence |
12556498 |
The present study also shows that EKLF itself inhibits FLI-1 activity. As suggested above for the inhibition of EKLF activity, the inhibition of FLI-1 activity most probably involves the indirect recruitment of EKLF to FLI-1 target promoters by protein-protein interaction. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | HaematopoiesisTranscriptionalControl |
+ |
GATA1 | up-regulates quantity by expression
transcriptional regulation
|
KLF1 |
0.517 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256051 |
|
|
Mus musculus |
|
pmid |
sentence |
8195185 |
Regulation of the Erythroid Kruppel-like Factor (EKLF) Gene Promoter by the Erythroid Transcription Factor GATA-l.Accordingly,we have also demonstrated that GATA-2, like GATA-1, is able to activate the EKLF promoter in NIH3T3. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | HaematopoiesisTranscriptionalControl |
+ |
GATA2 | up-regulates quantity by expression
transcriptional regulation
|
KLF1 |
0.442 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-256052 |
|
|
Mus musculus |
|
pmid |
sentence |
8195185 |
Regulation of the Erythroid Kruppel-like Factor (EKLF) Gene Promoter by the Erythroid Transcription Factor GATA-l.Accordingly,we have also demonstrated that GATA-2, like GATA-1, is able to activate the EKLF promoter in NIH3T3. |
|
Publications: |
1 |
Organism: |
Mus Musculus |
Pathways: | HaematopoiesisTranscriptionalControl |
+ |
KLF1 | up-regulates quantity by expression
transcriptional regulation
|
HBB |
0.415 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251790 |
|
|
Homo sapiens |
Erythroid Cell |
pmid |
sentence |
9707565 |
EKLF is an acetylated transcription factor, and that it interacts in vivo with CBP, p300, and P/CAF. However, its interactions with these histone acetyltransferases are not equivalent, as CBP and p300, but not P/CAF, utilize EKLF as a substrate for in vitro acetylation within its trans-activation region. The functional effects of these interactions are that CBP and p300, but not P/CAF, enhance EKLF's transcriptional activation of the beta-globin promoter in erythroid cells. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
KLF1 | up-regulates quantity by expression
transcriptional regulation
|
CDKN2C |
0.269 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-266046 |
|
|
Drosophila melanogaster |
SCHNEIDER-2 Cell |
pmid |
sentence |
17442339 |
Thus, EKLF is a direct regulator of p18INK4c gene expression, and much of EKLF's role in driving erythroid cell differentiation may occur via p18INK4c. |
|
Publications: |
1 |
Organism: |
Drosophila Melanogaster |