| + |
ATM | up-regulates 
phosphorylation
|
ATF2 |
0.584 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-137619 |
Ser490 |
QSTEPALsQIVMAPS |
Homo sapiens |
|
| pmid |
sentence |
| 15916964 |
Here, we demonstrate that the protein kinase atm phosphorylates atf2 on serines 490 and 498 following ionizing radiation (ir). dose- and time-dependent phosphorylation of atf2 by atm that results in its rapid colocalization with gamma-h2ax and mrn components into ir-induced foci (irif) |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-137623 |
Ser498 |
QIVMAPSsQSQPSGS |
Homo sapiens |
|
| pmid |
sentence |
| 15916964 |
Here, we demonstrate that the protein kinase atm phosphorylates atf2 on serines 490 and 498 following ionizing radiation (ir). dose- and time-dependent phosphorylation of atf2 by atm that results in its rapid colocalization with gamma-h2ax and mrn components into ir-induced foci (irif) |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
VRK1 | up-regulates
phosphorylation
|
ATF2 |
0.379 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124330 |
Ser62 |
FGPARNDsVIVADQT |
Homo sapiens |
|
| pmid |
sentence |
| 15105425 |
Vrk1 phosphorylates atf2 mainly on thr-73, stabilizing the atf2 protein and increasing its intracellular level. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-124334 |
Thr73 |
ADQTPTPtRFLKNCE |
Homo sapiens |
|
| pmid |
sentence |
| 15105425 |
Vrk1 phosphorylates atf2 mainly on thr-73, stabilizing the atf2 protein and increasing its intracellular level. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
MAPK14 | up-regulates activity
phosphorylation
|
ATF2 |
0.786 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-250090 |
Ser90 |
GLFNELAsPFENEFK |
Homo sapiens |
Hep-G2 Cell |
| pmid |
sentence |
| 10085140 |
P38 directly phosphorylates ATF-2 at Thr-69, Thr-71, and Ser-90, resulting in stimulation of its trans-activating capacity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-65593 |
|
|
Homo sapiens |
HEK-293 Cell |
| pmid |
sentence |
| 10085140 |
On the other hand, sapks such as jnks and p38 phosphorylate atf-2 at thr-69, thr-71, and ser-90 which lie close to the n-terminal transcriptional activation domain and stimulate itstrans-activating capacity our results indicate that atf-2 not only directly binds to smad3/4 hetero-oligomers but also that atf-2 is phosphorylated by tgf- signaling via tak1 and p38. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
PRKCE | up-regulates
phosphorylation
|
ATF2 |
0.292 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-195761 |
Thr52 |
HKHKHEMtLKFGPAR |
Homo sapiens |
Melanoma Cell, Skin Cancer Cell |
| pmid |
sentence |
| 22304920 |
Pkc_ phosphorylation of atf2 on thr52. Pkc_ promotes oncogenic functions of atf2 in the nucleus while blocking its apoptotic function at mitochondria |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
MAPK9 | up-regulates
phosphorylation
|
ATF2 |
0.686 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163262 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32429 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 7737130 |
Stimulation of atf-2-dependent transactivation by genotoxic agents requires the presence of threonines 69 and 71 located in the n-terminal transactivation domain. These sites are the target of p54 and p46 stress-activated protein kinases (sapks) which bind to, and phosphorylate atf-2 in vitro. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32433 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 7737130 |
Stimulation of atf-2-dependent transactivation by genotoxic agents requires the presence of threonines 69 and 71 located in the n-terminal transactivation domain. These sites are the target of p54 and p46 stress-activated protein kinases (sapks) which bind to, and phosphorylate atf-2 in vitro. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163266 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
ROBO | up-regulates
phosphorylation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-137635 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 15916964 |
Phosphorylation of atf2 by jnk/p38 on thr69/71 is prerequisite to its transcriptional activities |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-137639 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 15916964 |
Phosphorylation of atf2 by jnk/p38 on thr69/71 is prerequisite to its transcriptional activities |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
MAPK8 | up-regulates
phosphorylation
|
ATF2 |
0.771 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32421 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 7737130 |
Stimulation of atf-2-dependent transactivation by genotoxic agents requires the presence of threonines 69 and 71 located in the n-terminal transactivation domain. These sites are the target of p54 and p46 stress-activated protein kinases (sapks) which bind to, and phosphorylate atf-2 in vitro. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-33914 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 7824938 |
Activating transcription factor-2 (atf2) was found to be a target of the jnk signal transduction pathway. Atf2 was phosphorylated by jnk on two closely spaced threonine residues within the nh2-terminal activation domain. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-33918 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 7824938 |
Activating transcription factor-2 (atf2) was found to be a target of the jnk signal transduction pathway. Atf2 was phosphorylated by jnk on two closely spaced threonine residues within the nh2-terminal activation domain. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-32425 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 7737130 |
Stimulation of atf-2-dependent transactivation by genotoxic agents requires the presence of threonines 69 and 71 located in the n-terminal transactivation domain. These sites are the target of p54 and p46 stress-activated protein kinases (sapks) which bind to, and phosphorylate atf-2 in vitro. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SAPK/JNK Signaling |
| + |
MAPK14 | up-regulates
phosphorylation
|
ATF2 |
0.786 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90521 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 12110590 |
Here, we show that in fibroblasts, insulin, epidermal growth factor (egf) and serum activate atf2 via a so far unknown two-step mechanism involving two distinct ras effector pathways: the raf-mek-erk pathway induces phosphorylation of atf2 thr71, whereas subsequent atf2 thr69 phosphorylation requires the ral-ralgds-src-p38 pathway. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163246 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-65597 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 10085140 |
On the other hand, sapks such as jnks and p38 phosphorylate atf-2 at thr-69, thr-71, and ser-90 which lie close to the n-terminal transcriptional activation domain and stimulate itstrans-activating capacity our results indicate that atf-2 not only directly binds to smad3/4 hetero-oligomers but also that atf-2 is phosphorylated by tgf- signaling via tak1 and p38. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-65601 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 10085140 |
On the other hand, sapks such as jnks and p38 phosphorylate atf-2 at thr-69, thr-71, and ser-90 which lie close to the n-terminal transcriptional activation domain and stimulate itstrans-activating capacity our results indicate that atf-2 not only directly binds to smad3/4 hetero-oligomers but also that atf-2 is phosphorylated by tgf- signaling via tak1 and p38. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90525 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 12110590 |
Here, we show that in fibroblasts, insulin, epidermal growth factor (egf) and serum activate atf2 via a so far unknown two-step mechanism involving two distinct ras effector pathways: the raf-mek-erk pathway induces phosphorylation of atf2 thr71, whereas subsequent atf2 thr69 phosphorylation requires the ral-ralgds-src-p38 pathway. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163250 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Publications: |
6 |
Organism: |
Homo Sapiens |
| Pathways: | TGF-beta Signaling |
| + |
JNK | up-regulates
phosphorylation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-137627 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 15916964 |
Phosphorylation of atf2 by jnk/p38 on thr69/71 is prerequisite to its transcriptional activities |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-137631 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 15916964 |
Phosphorylation of atf2 by jnk/p38 on thr69/71 is prerequisite to its transcriptional activities |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling |
| + |
MAPK3 | up-regulates
phosphorylation
|
ATF2 |
0.728 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163254 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90529 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 12110590 |
Here, we show that in fibroblasts, insulin, epidermal growth factor (egf) and serum activate atf2 via a so far unknown two-step mechanism involving two distinct ras effector pathways: the raf-mek-erk pathway induces phosphorylation of atf2 thr71, whereas subsequent atf2 thr69 phosphorylation requires the ral-ralgds-src-p38 pathway. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90533 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 12110590 |
Here, we show that in fibroblasts, insulin, epidermal growth factor (egf) and serum activate atf2 via a so far unknown two-step mechanism involving two distinct ras effector pathways: the raf-mek-erk pathway induces phosphorylation of atf2 thr71, whereas subsequent atf2 thr69 phosphorylation requires the ral-ralgds-src-p38 pathway. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163258 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
PLK3 | up-regulates
phosphorylation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170004 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 21098032 |
Kinase activity of plk3 was significantly activated by hyperosmotic stimulation. Further downstream, active plk3 phosphorylated atf-2 at the thr-71 site in vivo and in vitro. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163270 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163274 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-170008 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 21098032 |
Kinase activity of plk3 was significantly activated by hyperosmotic stimulation. Further downstream, active plk3 phosphorylated atf-2 at the thr-71 site in vivo and in vitro. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| + |
ERK1/2 | up-regulates
phosphorylation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260755 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
MAPK1 | up-regulates
phosphorylation
|
ATF2 |
0.722 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-163242 |
Thr69 |
SVIVADQtPTPTRFL |
Homo sapiens |
|
| pmid |
sentence |
| 20068231 |
Phosphorylation of thr-69 by mapk14 and mapk11, and at thr-71 by mapk1/erk2, mapk3/erk1, mapk11, mapk12 and mapk14 in response to external stimulus like insulin causes increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-90517 |
Thr71 |
IVADQTPtPTRFLKN |
Homo sapiens |
|
| pmid |
sentence |
| 12110590 |
Here, we show that in fibroblasts, insulin, epidermal growth factor (egf) and serum activate atf2 via a so far unknown two-step mechanism involving two distinct ras effector pathways: the raf-mek-erk pathway induces phosphorylation of atf2 thr71, whereas subsequent atf2 thr69 phosphorylation requires the ral-ralgds-src-p38 pathway. |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| + |
ATF2 | up-regulates quantity by expression 
transcriptional regulation
|
PLAT |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253724 |
|
|
Homo sapiens |
HeLa Cell |
| pmid |
sentence |
| 8647095 |
We suggest that the mechanism for the transcriptional down-regulation of t-PA by PMA in HT-1080 cells requires CREB-1 binding to the t-PACRE while ATF-2, by associating with the same site, plays a role in PMA-mediated induction of t-PA in HeLa cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF2 | up-regulates
transcriptional regulation
|
IL6 |
0.303 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254512 |
|
|
Homo sapiens |
Macrophage |
| pmid |
sentence |
| 20086235 |
JNK phosphorylates proteins that are part of AP-1, in particular c-Jun and activating transcription factor 2 (ATF-2). With dominant-negative mutants, antisense RNA, inhibitors, and genetic ablation, it has been shown that JNK and c-Jun play a major role in IL-1–induced expression of genes encoding IL-6 and IL-8 and other IL-1–responsive genes |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
ATF2 | up-regulates quantity by expression
transcriptional regulation
|
GCH1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252226 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16149046 |
Constitutively active mutants of activating transcription factor 2 (ATF2) and c-Jun additionally stimulated GTP cyclohydrolase I promoter activity, but to a lesser extent than the constitutively active CREB mutant. Enzymatic reactions that require tetrahydrobiopterin as cofactor are therefore indirectly controlled by signaling cascades involving the signal-responsive transcription factors CREB, c-Jun, and ATF2. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF2 | down-regulates quantity by repression 
transcriptional regulation
|
SIRT4 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267831 |
|
|
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 33861966 |
Our data suggest that mTORC1 promotes the binding of the E3 ligase, βTrCP, to CREB2 (Figure 4D), promoting CREB2 degradation by the proteasome (Figure 4E). Here, we show that mTORC1 promotes glutamine anaplerosis by activating glutamate dehydrogenase (GDH). This regulation requires transcriptional repression of SIRT4, the mitochondrial-localized sirtuin that inhibits GDH. Mechanistically, mTORC1 represses SIRT4 by promoting the proteasome-mediated destabilization of cAMP-responsive element binding 2 (CREB2). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
BTRC | down-regulates quantity by destabilization
ubiquitination
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267830 |
|
|
Mus musculus |
MEF Cell |
| pmid |
sentence |
| 33861966 |
Our data suggest that mTORC1 promotes the binding of the E3 ligase, βTrCP, to CREB2 (Figure 4D), promoting CREB2 degradation by the proteasome (Figure 4E). Here, we show that mTORC1 promotes glutamine anaplerosis by activating glutamate dehydrogenase (GDH). This regulation requires transcriptional repression of SIRT4, the mitochondrial-localized sirtuin that inhibits GDH. Mechanistically, mTORC1 represses SIRT4 by promoting the proteasome-mediated destabilization of cAMP-responsive element binding 2 (CREB2). |
|
| Publications: |
1 |
Organism: |
Mus Musculus |
| + |
N | up-regulates quantity by expression
transcriptional regulation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260727 |
|
|
in vitro |
|
| pmid |
sentence |
| 14623261 |
The transcription factors c-Fos, FosB, CREB-1, and ATF2 were all activated by the addition of SARS-CoV N protein to the sample well |
|
| Publications: |
1 |
Organism: |
In Vitro |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
ATF2 | up-regulates quantity by expression
transcriptional regulation
|
YTHDC2 |
0.278 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269001 |
|
|
Homo sapiens |
Lung Adenocarcinoma Cell Line |
| pmid |
sentence |
| 24269672 |
Collectively, these data show that YTHDC2 plays an important role in tumor cells growth and activation/recruitment of c-Jun and ATF-2 to the YTHDC2 promoter is necessary for the transcription of YTHDC2, and that HDAC activity is required for the efficient expression of YTHDC2 in both of hepatocyte and HCC cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF2 | up-regulates quantity by expression
transcriptional regulation
|
FGF21 |
0.353 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253743 |
|
|
Homo sapiens |
Skeletal Muscle Satellite Cell |
| pmid |
sentence |
| 25055037 |
The increased production of reactive oxygen species, subsequent induction of p38 MAPK (mitogen-activated protein kinase) and activation of an ATF2 (activating transcription factor 2)-binding site at the proximal promoter region of the FGF21 gene was found to be a major mechanism linking mitochondrial dysfunction with enhanced FGF21 gene transcription in myogenic cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
CREB5 | up-regulates activity
binding
|
ATF2 |
0.618 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-219655 |
|
|
Chlorocebus aethiops |
CV-1 Cell |
| pmid |
sentence |
| 8378084 |
CRE-BPa specifically binds to CRE as a homodimer or heterodimer with c-Jun or CRE-BP1. In CAT cotransfection experiments using CV-1 cells, transient expression of each of four CRE-BPa proteins caused a 1.6- to 3.4-fold increase of CRE-dependent transcription |
|
| Publications: |
1 |
Organism: |
Chlorocebus Aethiops |
| + |
ATF2 | up-regulates quantity by expression
transcriptional regulation
|
POLB |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253744 |
|
|
Homo sapiens |
Peripheral Blood Mononuclear Cell |
| pmid |
sentence |
| 10518804 |
We identified the heterodimeric transcription factor ATF2/CREB as constitutively binding to the essential cAMP response element (CRE) site within the Ca2+-regulated DNA polymerase beta promoter and contributing to the activation of this promoter. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
JDP2 | down-regulates activity
binding
|
ATF2 |
0.537 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-226395 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18671972 |
JDP2 dimerizes with other AP-1 proteins such as activating transcription factor-2 (ATF2) and Jun to repress transcription from promoters that contain a cyclic AMP-responsive element (CRE). |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF2 | up-regulates quantity by expression
transcriptional regulation
|
ST3GAL5 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253745 |
|
|
Homo sapiens |
ARPE-19 Cell |
| pmid |
sentence |
| 21699754 |
Our results identified the core promoter region in the hST3Gal V promoter and for the first time demonstrated that ATF2 binding to the CREB/ATF binding site at -143 is essential for transcriptional activation of hST3Gal V in VPA-induced ARPE-19 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
ATF2 | up-regulates
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261324 |
|
|
|
|
| pmid |
sentence |
| 22685333 |
ATF2 contributes to global transcription and the DNA damage response, in addition to specific transcriptional activities that are related to cell development, proliferation and death. |
|
| Publications: |
1 |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling |
| + |
Gbeta | up-regulates
phosphorylation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270073 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 12110590 |
Here, we show that in fibroblasts, insulin, epidermal growth factor (egf) and serum activate atf2 via a so far unknown two-step mechanism involving two distinct ras effector pathways: the raf-mek-erk pathway induces phosphorylation of atf2 thr71, whereas subsequent atf2 thr69 phosphorylation requires the ral-ralgds-src-p38 pathway. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
SMAD3/SMAD4 | up-regulates activity
binding
|
ATF2 |
0.58 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-65583 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10085140 |
Here we report that the transcription factor atf-2 (also called cre-bp1) is bound by a hetero-oligomer of smad3 and smad4 upon tgf-beta stimulation. Both of these actions are shown to be responsible for the synergistic stimulation of ATF-2 trans-activating capacity. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, TGF-beta Signaling |
| + |
FH | up-regulates activity
binding
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-266314 |
|
|
in vitro |
|
| pmid |
sentence |
| 28628081 |
Glucose deficiency induces AMPK activation, which phosphorylates FH at Ser75 and promotes its binding to ATF2 and the enrichment of the FH–ATF2 complex on the promoter regions of ATF2-targeted genes. |
|
| Publications: |
1 |
Organism: |
In Vitro |
| + |
MAPK12 | up-regulates
phosphorylation
|
ATF2 |
0.522 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-65589 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10085140 |
Our results indicate that atf-2 not only directly binds to smad3/4 hetero-oligomers but also that atf-2 is phosphorylated by tgf-beta signaling via tak1 and p38. The two pathways, smad and tak1, synergistically enhance the activity of atf-2 which acts as their common nuclear target |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
p38 | up-regulates
phosphorylation
|
ATF2 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-270124 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10085140 |
Our results indicate that atf-2 not only directly binds to smad3/4 hetero-oligomers but also that atf-2 is phosphorylated by tgf-beta signaling via tak1 and p38. The two pathways, smad and tak1, synergistically enhance the activity of atf-2 which acts as their common nuclear target |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION |
| + |
MAPK11 | up-regulates
phosphorylation
|
ATF2 |
0.747 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-65586 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 10085140 |
Our results indicate that atf-2 not only directly binds to smad3/4 hetero-oligomers but also that atf-2 is phosphorylated by tgf-beta signaling via tak1 and p38. The two pathways, smad and tak1, synergistically enhance the activity of atf-2 which acts as their common nuclear target |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
3.0
ATF2
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