Crosstalk from NF-kappa B signaling pathway to TNF signaling pathway
TNF-α decreases VEGF secretion in highly polarized RPE cells but increases it in non-polarized RPE cells related to crosstalk between JNK and NF-κB pathways.
- Molecule in TNF signaling pathway: MAPK8
- Tissue : retinal pigment epithelium cell
- Regulation type : Inhibiting
- Sentence from paper : In polarized RPE cells, JNK was already activated and NF-κB was inactivated, thus activation of NF-κB became significant after TNF-α exposure compared to control leading to inhibition of JNK and down-regulation of the VEGF expression.
β-agonists selectively modulate proinflammatory gene expression in skeletal muscle cells via non-canonical nuclear crosstalk mechanisms.
- Molecule in TNF signaling pathway: Il6
- Tissue : C2C12 cell
- Regulation type : Activating
- Sentence from paper : Using the IL-6 promoter as a model, we demonstrated that TNF-α/isoproterenol cotreatment provoked phosphorylation of histone H3 at serine 10, concomitant with enhanced promoter accessibility and recruitment of the NF-κB p65 subunit, cAMP-response element-binding protein (CREB), CREB-binding protein (CBP) and RNA polymerase II.
LPS Down-Regulates Specificity Protein 1 Activity by Activating NF-κB Pathway in Endotoxemic Mice.
- Sentence from paper : Enhancing tissue level of Sp1 activity by inhibiting NF-κB-mediated Sp1 down-regulation increased tissue level of IL-10 and decreased tissue level of TNF- αin the lungs.
|Molecule in NF-kappa B signaling pathway||Molecule in TNF signaling pathway||Tissue||Species||PubMed Identifier|
|RELA||MAPK8||retinal pigment epithelium cell||Sus scrofa||23922887|
|Rela||Il6||C2C12 cell||Mus musculus||24603712|
Note: "Unknown" indicates that the molecule has not been identified.
Note: We direct each interaction from the molecule in the first pathway to the molecule in the second pathway. The direction of the interaction does not imply that the first molecule regulates the second molecule or that they directly interact. Hence, the interactions in this network may be indirect and may not indicate any mechanism.
XTalkDB does not contain any molecules mediating the crosstalk.
The name of the upstream (first) pathway in a pair of crosstalking pathways.
The name of the downstream (second) pathway in a pair of crosstalking pathways.
The string used as a structured query in PubMed that returned the recorded PMID as a result.
The PubMed identifier for the reported publication.
yes, if Pathway A elicits a downstream transcriptional response in Pathway B.
yes, if the crosstalk is transcriptional.
The downstream effect on Pathway B. This attribute can take one of the following two values:
The molecule in Pathway A responsible for mediating crosstalk to Pathway B.
|Molecule A Identifier|
Unique identifier for Molecule A in the namespace recorded in "Molecule A Source", e.g., the UniProt ID of a protein.
|Molecule A Source|
The name of database that the value in "Molecule A Identifier" comes from, e.g., "UniProt" if the molecule is a protein.
The molecule in Pathway B responsible for mediating crosstalk from Pathway A.
|Molecule B Identifier|
Unique identifier for Molecule B in the namespace recorded in "Molecule B Source", e.g., the UniProt ID of a protein.
|Molecule B Source|
The name of database that the value in "Molecule B Identifier" comes from, e.g., "UniProt" if the molecule is a protein.
The name of the species in which the crosstalk was observed.
The name of the tissue or cell line in which the crosstalk was observed.
The BRENDA Tissue Ontology (BTO) Identifier of the tissue or cell line in which the crosstalk was observed.
Notes on the experimental condition in the publication.
|Sentence from paper|
The sentence in the publication supporting the crosstalk. We record a sentence only if it states that Pathway A increases or decreases Pathway B signaling. The sentence may also include information about the proteins or genes responsible for mediating the crosstalk.
|Misleading evidence for crosstalk|
A sentence in the paper that appears to support evidence for crosstalk when the study does not conclude there is crosstalk.
A curator's notes that may provide rationale for the values recorded for the attributes.
*This attribute may represent either an individual molecule or several molecules. We use the following syntax for this attribute.
- colon (:): The molecules participate in the complex, e.g., SMAD3:SMAD4 in the case of crosstalk from the TGF-beta signaling pathway to the Hippo signaling pathway (the complex consisting of SMAD3 and SMAD4 mediates this crosstalk).
- slash (/): Either of the molecules can mediate the crosstalk, e.g., YAP1/WWTR1 for the same pair of pathways (YAP1 or WWTR1 can mediate the crosstalk).
- comma (,): All the molecules are required for the crosstalk but they do not form a complex, e.g., TSC2,RPTOR for the crosstalk from the MAPK signaling pathway to the mTOR signaling pathway (both TSC2 and RPTOR act as mediators).
- brackets (): If we cannot identify the specific molecule, we record all molecules in the family, e.g., [TEAD1/TEAD2/TEAD3/TEAD4]. In this case, the publication only listed the protein TEAD as mediating the crosstalk (from the Hippo signaling pathway to the Wnt signaling pathway).