Crosstalk from Insulin signaling pathway to Wnt signaling pathway
New insights into the role of cAMP in the production and function of the incretin hormone glucagon-like peptide-1 (GLP-1).
- Sentence from paper : GLP-1 also stimulated β-cat phosphorylation at Ser675, and this is likely mediated by PKA activation
Modulation of β-catenin signaling by glucagon receptor activation.
- Molecule in Wnt signaling pathway: Lrp5/Lrp6
- Tissue : hepatocyte
- Regulation type : Activating
- Sentence from paper : So activation of GCGR upon ligand binding can directly cross-talk to Lrp5/6 to transmit downstream β-catenin signaling whereas phosphorylation and activation of Lrp5/6 on the other hand can communicate back to GCGR to boost GCGR mediated cAMP/PKA pathway
Metformin enhances glucagon-like peptide 1 via cooperation between insulin and Wnt signaling.
- Sentence from paper : In addition, insulin receptor substrate 2 gene depletion blocked metformin-enhanced B-catenin translocation.
Wnt-independent role of β-catenin in thyroid cell proliferation and differentiation.
- Molecule in Wnt signaling pathway: Ctnnb1
- Tissue : PCCL-3 cell, FRTL-5 cell
- Regulation type : Activating
- Sentence from paper : This effect takes place in a Wnt-independent manner because TSH and IGF-1, through the activation of protein kinase A and protein kinase B/Akt, phosphorylate β-catenin at S552 and S675, which results in β-catenin release from E-cadherin at the adherens junctions.
|Molecule in Insulin signaling pathway||Molecule in Wnt signaling pathway||Tissue||Species||PubMed Identifier|
|Igf1||Ctnnb1||PCCL-3 cell, FRTL-5 cell||Rattus norvegicus||24645679|
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).