| + |
ERK1/2 | up-regulates 
phosphorylation
|
AP1 |
0.784 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252358 |
Ser374 |
PSSDSLSsPTLLAL |
Homo sapiens |
|
| pmid |
sentence |
| 12972619 |
In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252359 |
Thr232 |
GGLPEVAtPESEEAF |
Homo sapiens |
|
| pmid |
sentence |
| 7816602 |
Phosphorylation of the c-fos and c-jun hob1 motif stimulates its activation capacity here we show that the hob1-containing activation domain of c-fos is stimulated by ha-ras in vivo and phosphorylated by a map kinase family member in vitro and that mutating t232 to ala abolishes both functions. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252357 |
Thr325 |
TELEPLCtPVVTCTP |
Homo sapiens |
|
| pmid |
sentence |
| 12972619 |
In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252353 |
Thr331 |
CTPVVTCtPSCTAYT |
Homo sapiens |
|
| pmid |
sentence |
| 12972619 |
In a previous study we have observed that exposure of nih 3t3 cells to pdgf or serum leads to c-fos phosphorylation by erk on specific residues, thr232, thr325, thr331, and ser374, within the cooh-terminal c-fos tad we have recently shown that erk phosphorylates multiple residues within the carboxylterminal transactivation domain (tad) of c-fos, thus resulting in its increased transcriptional activity. |
|
| Publications: |
4 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, B-cell activation, COVID-19 Causal Network, FLT3-ITD signaling, Hepatocellular Tumor, Luminal Breast Cancer, Leptin Signaling, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, T cell activation, Toll like receptors |
| + |
MAPK8 | up-regulates activity
phosphorylation
|
AP1 |
0.811 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252354 |
Ser63 |
KNSDLLTsPDVGLLK |
Chlorocebus aethiops |
COS Cell |
| pmid |
sentence |
| 8137421 |
The jnk-mediated phosphorylation of both ser63 and ser73 within the transactivation domain of c-jun potentiates its transcriptional activity. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252355 |
Ser73 |
VGLLKLAsPELERLI |
Chlorocebus aethiops |
COS-7 Cell |
| pmid |
sentence |
| 8137421 |
JNK1 binds to the c-Jun transactivation domain and phosphorylates it on Ser-63 and Ser-73. The effect on AP-1 transcriptional activity results, in part, from enhanced phosphorylation of the c-Jun NH2-terminal activation domain. |
|
| Publications: |
2 |
Organism: |
Chlorocebus Aethiops |
| Pathways: | Acute Myeloid Leukemia, COVID-19 Causal Network, Toll like receptors |
| + |
AP1 | up-regulates activity
transcriptional regulation
|
CCL2 |
0.601 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260764 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21561061 |
3b Potentiates AP-1-Dependent MCP-1 Promoter Activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM |
| + |
AP1 | up-regulates activity
binding
|
CD3 |
0.327 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-267994 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 16473826 |
When T cells encounter antigens via the T cell antigen receptor (TCR), information about the quantity and quality of antigen engagement is relayed to the intracellular signal transduction machinery. The TCR itself lacks a significant intracellular domain. Instead, it is associated with CD3 molecules that contain intracellular signaling domains that couple the TCR/CD3 complex to the downstream signaling machinery. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | T cell activation |
| + |
AP1 | up-regulates quantity by expression 
transcriptional regulation
|
CXCL8 |
0.563 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261029 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 32446778 |
The up-regulation of the CXCL8 gene expression, could be due to a direct effect of the virus at the cellular level. Indeed, intestinal and lung cells lines infected by SARS-CoV, promptly increase their secretion of CXCL8 [88]. This observation would fit with the notion that the expression of CXCL8 is dependent on the tran-scription factor Activator protein 1 (AP-1), which was shown to bestrongly up-regulated by SARS-CoV |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | SARS-CoV CYTOKINE STORM |
| + |
JUN | form complex 
binding
|
AP1 |
0.951 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256365 |
|
|
in vitro |
|
| pmid |
sentence |
| 3142692 |
The c-Jun and c-fos proto-oncogenes encode proteins that form a complex which regulates transcription from promoters containing AP-1 activation elements. c-Jun has specific DNA binding activity, while c-Fos has homology to the putative DNA binding domain of c-Jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256361 |
|
|
in vitro |
|
| pmid |
sentence |
| 2467839 |
The protein products of the fos (Fos) and jun (Jun) proto-oncogenes have been shown to associate with a DNA element known as the transcription factor activator protein-1 (AP-1) binding site. Jun (previously known as the Fos-binding protein p39) and Fos form a protein complex in the nucleus. These data demonstrate a cooperative interaction between the protein products of two proto-oncogenes with a DNA element involved in transcriptional regulation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256363 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1904542 |
The proteins encoded by the proto-oncogenes c-fos and c-jun (Fos and Jun, respectively) form a heterodimeric complex that regulates transcription by interacting with the DNA-regulatory element known as the activator protein 1 (AP-1) binding site. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256367 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25875593 |
C-Fos dimerizes with c-Jun to form the transcription activator protein-1 (AP-1) which binds to the specific recognition site. |
|
| Publications: |
4 |
Organism: |
In Vitro, Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, Luminal Breast Cancer, SARS-CoV CYTOKINE STORM, TGF-beta Signaling |
| + |
ESR1 | up-regulates activity
binding
|
AP1 |
0.71 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-263656 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 18247370 |
The primary conclusion of the results reported here is that ERα and c‐jun, c‐fos and ATF‐2, but not Fra‐2 AP‐1 factors interact “in vivo” with specific estrogen‐responsive regulatory sequences and AP‐1 cis‐elements within the F promoter of the human ERα gene in osteoblast‐like SaOS‐2 cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Luminal Breast Cancer |
| + |
SMAD2/SMAD4 | up-regulates activity
binding
|
AP1 |
0.526 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256180 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22926518 |
The activated TGFβ type I receptor kinase propagates the signal within the cell through phosphorylation of the receptor-regulated (R-)Smad proteins Smad2 and Smad3 at their extreme carboxyl-terminal serine residues.1, 2 The activated R-Smads then form heteromeric complexes with the common-partner (Co-)Smad, Smad4, and accumulate in the nucleus, where they can bind DNA and regulate gene expression. The Smads control gene expression in a cell type-specific manner by interacting with other proteins, such as AP-1, AP-2 and Ets transcription factors and specific co-activators and co-repressors. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
EPAS1 | down-regulates activity 
binding
|
AP1 |
0.351 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269042 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 24383088 |
Co-transfection experiments revealed that HIF-2α had greater potency on the GLIS1 promoter activation than HIF-1α. Subsequent studies using wild-type and mutant HIF-2α demonstrated that DNA binding activity was not necessary but TADs were critical for GLIS1 induction. Finally, co-transfection experiments indicated that HIF-2α cooperated with AP-1 family members in upregulating GLIS1 transcription. These results suggest that the hypoxic signaling pathway may play a pivotal role in regulating the reprogramming factor GLIS1, via non-canonical mechanisms involving partner transcription factor rather than by direct HIF transactivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AP1 | up-regulates
|
Proliferation |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-252356 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9878062 |
AP‐1 proteins, including c‐Fos and c‐Jun, are prominent nuclear targets of growth factor induced signaling, making AP‐1 a candidate nuclear effector of growth factor induced proliferation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, FLT3 in AML, Onco-fusion proteins in AML, miRNA in AML, B-cell activation, COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, Hepatocellular Tumor, Luminal Breast Cancer, Leptin Signaling, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, TGF-beta Signaling, TGFb in cancer |
| + |
SMAD3/SMAD4 | up-regulates activity
binding
|
AP1 |
0.63 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256181 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 22926518 |
The activated TGFβ type I receptor kinase propagates the signal within the cell through phosphorylation of the receptor-regulated (R-)Smad proteins Smad2 and Smad3 at their extreme carboxyl-terminal serine residues.1, 2 The activated R-Smads then form heteromeric complexes with the common-partner (Co-)Smad, Smad4, and accumulate in the nucleus, where they can bind DNA and regulate gene expression. The Smads control gene expression in a cell type-specific manner by interacting with other proteins, such as AP-1, AP-2 and Ets transcription factors and specific co-activators and co-repressors. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253332 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 9732876 |
Smad3 and smad4 also act together with c-jun and c-fos to activate transcription in response to tgf-beta, through a tgf-beta-inducible association of c-jun with smad3 and an interaction of smad3 and c-fos |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, Hepatocellular Tumor, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), TGF-beta Signaling, TGFb in cancer |
| + |
FOS | form complex
binding
|
AP1 |
0.951 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256366 |
|
|
in vitro |
|
| pmid |
sentence |
| 3142692 |
The c-Jun and c-fos proto-oncogenes encode proteins that form a complex which regulates transcription from promoters containing AP-1 activation elements. c-Jun has specific DNA binding activity, while c-Fos has homology to the putative DNA binding domain of c-Jun. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256362 |
|
|
in vitro |
|
| pmid |
sentence |
| 2467839 |
The protein products of the fos (Fos) and jun (Jun) proto-oncogenes have been shown to associate with a DNA element known as the transcription factor activator protein-1 (AP-1) binding site. Jun (previously known as the Fos-binding protein p39) and Fos form a protein complex in the nucleus. These data demonstrate a cooperative interaction between the protein products of two proto-oncogenes with a DNA element involved in transcriptional regulation. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256364 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 1904542 |
The proteins encoded by the proto-oncogenes c-fos and c-jun (Fos and Jun, respectively) form a heterodimeric complex that regulates transcription by interacting with the DNA-regulatory element known as the activator protein 1 (AP-1) binding site. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-256368 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 25875593 |
C-Fos dimerizes with c-Jun to form the transcription activator protein-1 (AP-1) which binds to the specific recognition site. |
|
| Publications: |
4 |
Organism: |
In Vitro, Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML, Leptin Signaling, T cell activation |
| + |
PML-RARalpha | up-regulates activity
|
AP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-261507 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 8415704 |
PML-RAR alpha chimera cooperates with c-Jun and, strikingly, with c-Fos to stimulate the transcription of both synthetic and natural reporter genes containing an AP-1 site |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, FLT3 in AML, Onco-fusion proteins in AML |
| + |
AP1 | up-regulates activity
binding
|
NFATC1 |
0.649 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253004 |
|
|
Homo sapiens |
T-lymphocyte |
| pmid |
sentence |
| 15928679 |
Activator protein 1 (AP1) proteins are the main transcriptional partners of NFAT during T-cell activation |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | B-cell activation, T cell activation |
| + |
3b | up-regulates activity
|
AP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260757 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21561061 |
SARS-CoV Accessory Protein 3b Induces AP-1 TranscriptionalActivity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM |
| + |
miR-155 | up-regulates quantity by expression
post transcriptional regulation
|
AP1 |
0.4 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-268039 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 19219026 |
Here we report that the c-Myc (hereafter referred to as Myc) oncogenic transcription factor, which is known to regulate microRNAs and stimulate cell proliferation, transcriptionally represses miR-23a and miR-23b, resulting in greater expression of their target protein, mitochondrial glutaminase, in human P-493 B lymphoma cells and PC3 prostate cancer cells. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, miRNA in AML |
| + |
JNK | up-regulates activity
binding
|
AP1 |
0.811 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253340 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 24315690 |
In addition to the possible regulation of the transcription factor c-Jun by phosphorylation via the c-Jun N-terminal kinase (JNK) or the kinases ERK1, ERK2 and GSK3β, further signaling pathways lead to an up-regulation of c-Jun protein and thus AP-1 activity |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, EBV infection, FLT3-ITD signaling, SARS-CoV MAPK PERTURBATION, TGF-beta Signaling |
| + |
AML1-ETO | up-regulates activity
binding
|
AP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260094 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 10208431 |
The AML1/ETO fusion protein is essential to the development of t(8;21) acute myeloid leukemia (AML) and is well recognized for its dominant-negative effect on the coexisting wild-type protein AML1. On physical interaction, AML1/ETO can form a complex with wild-type AML1 on chromatin, and the runt homology domain of both proteins are responsible for their interactions. More importantly, the relative binding signals of AML1 and AML1/ETO on chromatin determine which genes are repressed or activated by AML1/ETO. Further analysis of coregulators indicates that AML1/ETO transactivates gene expression through recruiting AP-1 to the AML1/ETO-AML1 complex. AML1/ETO transactivates gene expression through recruiting AP-1 to the AML1/ETO-AML1 complex |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, Onco-fusion proteins in AML |
| + |
AP1 | up-regulates
transcriptional regulation
|
IL6 |
0.628 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-254513 |
|
|
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, Multiple sclerosis, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM |
| + |
TEAD | up-regulates activity
binding
|
AP1 |
0.36 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-277658 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 26258633 |
YAP/TAZ/TEAD and AP-1 form a complex that synergistically activates target genes directly involved in the control of S-phase entry and mitosis. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AP1 | up-regulates quantity by expression
transcriptional regulation
|
GLIS1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-269041 |
|
|
Homo sapiens |
MCF-7 Cell |
| pmid |
sentence |
| 24383088 |
Co-transfection experiments revealed that HIF-2α had greater potency on the GLIS1 promoter activation than HIF-1α. Subsequent studies using wild-type and mutant HIF-2α demonstrated that DNA binding activity was not necessary but TADs were critical for GLIS1 induction. Finally, co-transfection experiments indicated that HIF-2α cooperated with AP-1 family members in upregulating GLIS1 transcription. These results suggest that the hypoxic signaling pathway may play a pivotal role in regulating the reprogramming factor GLIS1, via non-canonical mechanisms involving partner transcription factor rather than by direct HIF transactivation. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| + |
AP1 | up-regulates
transcriptional regulation
|
CCND1 |
0.606 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-253215 |
|
|
Homo sapiens |
Lung Cancer Cell Line |
| pmid |
sentence |
| 12509763 |
Substrates for ERK1/2 include nuclear proteins such as C-JUN, this leads to activation of the AP-1 transcription factor, which is made up of FOS-JUN heterodimers.|As a result of stimulating these transcriptional regulators, key cell-cycle regulatory proteins, such as D-type cyclins, are expressed, which enables the cell to progress through the G1 phase of the cell-cycle. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia |
| + |
AP1 | up-regulates activity
binding
|
SPI1 |
0.525 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260098 |
|
|
Homo sapiens |
Kasumi-1 Cell |
| pmid |
sentence |
| 12393465 |
These results indicate that AML1-ETO competes c-Jun away from binding to the β3β4 domain of PU.1. Thus, the c-Jun coactivation function of PU.1 is down-regulated and this in turn down-regulates transcriptional activity of PU.1. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | Acute Myeloid Leukemia, AML1-ETO in AML, miRNA in AML |
| + |
AP1 | up-regulates activity
|
Immune_response |
0.7 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260765 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 21561061 |
AP-1 regulates transcription of many genes involved in viralpathogenesis, including pro-inflammatory and antiviral cytokineslike IL-6,33IL-8,34RANTES,35MCP-1,19interferons,9etc., thatare characteristic of an infection. SARS pathology is the result ofan exacerbated pro-inflammatory immune response by cytokinesin the lungs of patients and in infected animal models. |
|
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260766 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 31340499 |
AP-1 Transcription Factors as Regulators of Immune Responses in Cancer |
|
| Publications: |
2 |
Organism: |
Homo Sapiens |
| Pathways: | B-cell activation, COVID-19 Causal Network, EBV infection, Multiple sclerosis, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM, T cell activation, Toll like receptors |
| + |
N | up-regulates activity
|
AP1 |
0.2 |
| Identifier |
Residue |
Sequence |
Organism |
Cell Line |
| SIGNOR-260725 |
|
|
Homo sapiens |
|
| pmid |
sentence |
| 14623261 |
Taken together, we have shown that the coronavirus N protein can activate AP-1 signal transduction pathway. |
|
| Publications: |
1 |
Organism: |
Homo Sapiens |
| Pathways: | COVID-19 Causal Network, SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM |
3.0
AP1
CPX-486