+ |
GSK3B | down-regulates activity
phosphorylation
|
MYOCD |
0.406 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251245 |
Ser451 |
NGFYHFGsTSSSPPI |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251244 |
Ser455 |
HFGSTSSsPPISPAS |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251243 |
Ser459 |
TSSSPPIsPASSDLS |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251246 |
Ser463 |
PPISPASsDLSVAGS |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251247 |
Ser626 |
DQTNVLSsTFLSPQC |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251248 |
Ser630 |
VLSSTFLsPQCSPQH |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251249 |
Ser634 |
TFLSPQCsPQHSPLG |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-251250 |
Ser638 |
PQCSPQHsPLGAVKS |
Homo sapiens |
HEK-293 Cell |
pmid |
sentence |
16141410 |
In vitro and in vivo (HEK 293 cells) kinase assays with synthetic peptides and full-length myocardin demonstrated that myocardin was a primed GSK3beta substrate, with serines 455 to 467 and 624 to 636 being the major GSK3beta phosphorylation sites. GSK3β phosphorylation at the sites identified inhibits myocardin intrinsic transcriptional activity |
|
Publications: |
8 |
Organism: |
Homo Sapiens |
+ |
MYOCD | up-regulates
binding
|
SRF |
0.79 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-174322 |
|
|
Homo sapiens |
|
pmid |
sentence |
21673106 |
A coactivator of srf, myocd, interacts with srf and activates vsmc expression of contractile genes. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle, Smooth Muscle |
+ |
TGFB1 | up-regulates quantity by expression
transcriptional regulation
|
MYOCD |
0.271 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-174396 |
|
|
Homo sapiens |
|
pmid |
sentence |
21673106 |
These results indicate that (i) tgf- and klf4 regulate myocd transcription positively and negatively, respectively. When __90% of smad4 was down-regulated myocd mrna induction by tgf- was abolished, suggesting that smad4 plays a critical role in transcriptional activation of the myocd gene |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle, Smooth Muscle |
+ |
KLF4 | down-regulates
|
MYOCD |
0.479 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-174255 |
|
|
Homo sapiens |
|
pmid |
sentence |
21673106 |
Finally, we demonstrate that the basal expression of both myocd and mrtf-a is negatively regulated by klf4. . The mechanism of inhibition of myocd or mrtf-a by klf4 is currently unclear and warrants future study. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
Tissue: |
Muscle, Smooth Muscle |
+ |
MYOCD | down-regulates
|
KLF4 |
0.479 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-174319 |
|
|
Homo sapiens |
|
pmid |
sentence |
21673106 |
These results further confirm that bmp4 requires mrtf-a, whereas tgf-_ requires myocd for the induction of pri-mir-143/145 and down-regulation of klf4. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |
+ |
MYOCD | up-regulates quantity by expression
transcriptional regulation
|
ACTG2 |
0.436 |
Identifier |
Residue |
Sequence |
Organism |
Cell Line |
SIGNOR-254620 |
|
|
Homo sapiens |
|
pmid |
sentence |
19797053 |
These results demonstrate the ability of MYOCD to discriminate among several juxtaposed CArG elements, presumably through its novel partnership with NKX3.1, to optimally transactivate the human ACTG2 promoter. |
|
Publications: |
1 |
Organism: |
Homo Sapiens |