General Information:
Id: | 11,431 |
Diseases: |
Cardiovascular disease
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Mus musculus | |
article | |
Reference: | Trinath J et al.(2014) The WNT signaling pathway contributes to dectin-1-dependent inhibition of Toll-like receptor-induced inflammatory signature Mol. Cell. Biol. 34: 4301-4314 [PMID: 25246634] |
Interaction Information:
Comment | Dectin-1 activation robustly dampens TLR-induced proinflammatory signature in macrophages. |
Formal Description Interaction-ID: 114202 |
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Comment | Dectin-1-induced PIAS-1 and SOCS-1 negatively influence TLR signaling by targeting IRAK-1, IRAK-4, and MyD88. While SOCS-1 targeted IRAK-1, IRAK-4, and MyD88 for proteasomal degradation, PIAS-1 was found to target IRAK-1 and MyD88. |
Formal Description Interaction-ID: 114260 |
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Comment | Dectin-1-induced PIAS-1 and SOCS-1 negatively influence TLR signaling by targeting IRAK-1, IRAK-4, and MyD88. While SOCS-1 targeted IRAK-1, IRAK-4, and MyD88 for proteasomal degradation, PIAS-1 was found to target IRAK-1 and MyD88. |
Formal Description Interaction-ID: 114261 |
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Comment | Dectin-1-induced PIAS-1 and SOCS-1 negatively influence TLR signaling by targeting IRAK-1, IRAK-4, and MyD88. While SOCS-1 targeted IRAK-1, IRAK-4, and MyD88 for proteasomal degradation, PIAS-1 was found to target IRAK-1 and MyD88. |
Formal Description Interaction-ID: 114262 |
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Comment | Dectin-1-induced PIAS-1 and SOCS-1 negatively influence TLR signaling by targeting IRAK-1, IRAK-4, and MyD88. While SOCS-1 targeted IRAK-1, IRAK-4, and MyD88 for proteasomal degradation, PIAS-1 was found to target IRAK-1 and MyD88. |
Formal Description Interaction-ID: 114263 |
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Drugbank entries | Show/Hide entries for IRAK4 |
Comment | Dectin-1-induced PIAS-1 and SOCS-1 negatively influence TLR signaling by targeting IRAK-1, IRAK-4, and MyD88. While SOCS-1 targeted IRAK-1, IRAK-4, and MyD88 for proteasomal degradation, PIAS-1 was found to target IRAK-1 and MyD88. |
Formal Description Interaction-ID: 114264 |
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Comment | Dectin-1-induced PIAS-1 and SOCS-1 negatively influence TLR signaling by targeting IRAK-1, IRAK-4, and MyD88. While SOCS-1 targeted IRAK-1, IRAK-4, and MyD88 for proteasomal degradation, PIAS-1 was found to target IRAK-1 and MyD88. |
Formal Description Interaction-ID: 114265 |
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Comment | Dectin-1-induced PIAS-1 and SOCS-1 negatively influence TLR signaling by targeting IRAK-1, IRAK-4, and MyD88. While SOCS-1 targeted IRAK-1, IRAK-4, and MyD88 for proteasomal degradation, PIAS-1 was found to target IRAK-1 and MyD88. |
Formal Description Interaction-ID: 114266 |
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Comment | Activation of dectin-1 receptor with curdlan led to an increase in phosphorylation of Syk and subsequently induced production of ROS and led to the expression of PIAS-1 and SOCS-1. |
Formal Description Interaction-ID: 114267 |
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Drugbank entries | Show/Hide entries for SYK |
Comment | Dectin-1 receptor was essential for curdlan-induced expression of WNT5A. |
Formal Description Interaction-ID: 114268 |
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Comment | Overexpression of WNT5A led to augmented expression of curdlan-induced PIAS-1 and SOCS-1. |
Formal Description Interaction-ID: 114269 |
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Comment | Overexpression of WNT5A led to augmented expression of curdlan-induced PIAS-1 and SOCS-1. |
Formal Description Interaction-ID: 114270 |
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Comment | Dectin-1-induced expression of WNT5A led to the activation of CAMKII, TAK1, and Pyk2, which was further validated by genetic knock-down of WNT5A by specific siRNA. |
Formal Description Interaction-ID: 114271 |
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Comment | Dectin-1-induced expression of WNT5A led to the activation of CAMKII, TAK1, and Pyk2, which was further validated by genetic knock-down of WNT5A by specific siRNA. |
Formal Description Interaction-ID: 114272 |
gene/protein increases_activity of complex/PPI Calcium/calmodulin-dependent protein kinase type II |
Comment | Dectin-1-induced expression of WNT5A led to the activation of CAMKII, TAK1, and Pyk2, which was further validated by genetic knock-down of WNT5A by specific siRNA. |
Formal Description Interaction-ID: 114273 |
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Drugbank entries | Show/Hide entries for PTK2B |
Comment | There is increased nuclear translocation of NF-kappaB in macrophages upon engagement of dectin-1 receptor with curdlan via the WNT-Ca2+/CAMKII-TAK1 axis. |
Formal Description Interaction-ID: 114274 |
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