Crosstalk from Hedgehog signaling pathway to NF-kappa B signaling pathway

List of curated literature with evidence for crosstalk from Hedgehog signaling pathway to NF-kappa B signaling pathway

  • Folate deprivation enhances invasiveness of human colon cancer cells mediated by activation of sonic hedgehog signaling through promoter hypomethylation and cross action with transcription nuclear factor-kappa B pathway.

    • PubMed ID : 22461522
    • Molecule in Hedgehog signaling pathway: SHH
    • Species : Homo sapiens
    • Transcription : no
    • Sentence from paper : The data suggest that regulation of NF-κB activation by Shh signaling could be compartmentalized in the cytosol, at least, at the IκBα degradation and subject to the FD-associated multistep regulatory process

  • Trimeric G protein-CARMA1 axis links smoothened, the hedgehog receptor transducer, to NF-κB activation in diffuse large B-cell lymphoma.

    • PubMed ID : 23632891
    • Molecule in Hedgehog signaling pathway: SMO
    • Species : Homo sapiens
    • Transcription : no

    • Molecule in NF-kappa B signaling pathway: PRKCB
    • Tissue : B-lymphocyte
    • Regulation type : Activating
    • Sentence from paper : In addition, our data indicate that the mechanistic link between SMO and NF-κB involves activation of PKCβ-1 and PKCβ-2 and the recruitment of CARMA1, BCL10, and MALT1 (CBM signalosome) to the SMO receptor complex

Molecules mediating the crosstalk
Molecule in Hedgehog signaling pathwayMolecule in NF-kappa B signaling pathwayTissueSpeciesPubMed Identifier
SHHNFKBIAcolonic cancer cellHomo sapiens22461522
SMOPRKCBB-lymphocyteHomo sapiens23632891

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.

Attribute NameDescription
Pathway A

The name of the upstream (first) pathway in a pair of crosstalking pathways.

Pathway B

The name of the downstream (second) pathway in a pair of crosstalking pathways.

Pubmed Query

The string used as a structured query in PubMed that returned the recorded PMID as a result.

PMID

The PubMed identifier for the reported publication.
We recorded "NO_RESULTS_FOR_PUBMED_QUERY" as a dummy PMID when the PubMed query returned no results.

Crosstalk

yes, if Pathway A elicits a downstream transcriptional response in Pathway B.
no, otherwise.

Transcriptional

yes, if the crosstalk is transcriptional.
no, otherwise.

Regulation type

The downstream effect on Pathway B. This attribute can take one of the following two values:

  • Activating: Stimulation of Pathway A up-regulates a gene or activates a protein that is representative of Pathway B.
  • Inhibiting: Stimulation of Pathway A down-regulates a gene or inhibits a protein that is representative of Pathway B.
Molecule A*

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.

Molecule B*

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.

Species

The name of the species in which the crosstalk was observed.

Tissue

The name of the tissue or cell line in which the crosstalk was observed.

BTO ID

The BRENDA Tissue Ontology (BTO) Identifier of the tissue or cell line in which the crosstalk was observed.

Condition

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.

Additional notes

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).