Relation Results

Identifier	Residue	Sequence	Organism
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
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
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
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

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

Identifier	Residue	Organism
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	Organism
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	Organism
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.

Identifier	Residue	Organism
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.

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

Identifier	Residue	Organism
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

Identifier	Residue	Organism
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	Organism
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

Identifier	Residue	Organism
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

Identifier	Residue	Organism
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	Organism
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.

Identifier	Residue	Organism
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	Organism
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.

Publications:

4

Organism:

In Vitro, Homo Sapiens

Pathways:

Acute Myeloid Leukemia, miRNA in AML, Leptin Signaling, T cell activation

Identifier	Residue	Organism
SIGNOR-260766		Homo sapiens
pmid	sentence
31340499	AP-1 Transcription Factors as Regulators of Immune Responses in Cancer

Identifier	Residue	Organism
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.

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

Identifier	Residue	Organism
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

Identifier	Residue	Organism
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

Identifier	Residue	Organism
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

Identifier	Residue	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

Identifier	Residue	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

Identifier	Residue	Organism
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

Identifier	Residue	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

Identifier	Residue	Organism
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

Identifier	Residue	Organism
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

Identifier	Residue	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

Identifier	Residue	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

Identifier	Residue	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

Identifier	Residue	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

Identifier	Residue	Organism
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

Identifier	Residue	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

Identifier	Residue	Organism
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

Name	AP1 View Modifications
Primary ID	SIGNOR-C154
Links	CPX-486
Type	complex
Formed by	JUN, FOS
Relations	36
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, Macrophage: IL1 beta, Mitochondrial dynamics in T cell exhaustion, Multiple sclerosis, Pancreatic ductal adenocarcinoma (PDA), SARS-CoV MAPK PERTURBATION, SARS-CoV CYTOKINE STORM, T cell activation, TGF-beta Signaling, Toll like receptors, TGFb in cancer

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