Smad6-specific recruitment of Smurf E3 ligases mediates TGF-β1-induced degradation of MyD88 in TLR4 signalling (Q39478664)

12 September 2017

Smad6-specific recruitment of Smurf E3 ligases mediates TGF-β1-induced degradation of MyD88 in TLR4 signalling (English)

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12 September 2017

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2

Jin Seok Park

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12 September 2017

7

Seok Hee Park

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12 September 2017

1

Youn Sook Lee

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12 September 2017

4

Su Myung Jung

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12 September 2017

3

Jun Hwan Kim

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12 September 2017

Jae Young Lee

5

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PubMed ID

21897371

12 September 2017

Seong-Jin Kim

series ordinal

6

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PubMed ID

21897371

12 September 2017

language of work or name

English

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publication date

6 September 2011

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12 September 2017

Nature Communications

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12 September 2017

2

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12 September 2017

460

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https://scigraph.springernature.com/pub.10.1038/ncomms1469

12 September 2017

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Transforming growth factor-beta differentially inhibits MyD88-dependent, but not TRAM- and TRIF-dependent, lipopolysaccharide-induced TLR4 signaling.

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Smad6 negatively regulates interleukin 1-receptor-Toll-like receptor signaling through direct interaction with the adaptor Pellino-1.

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Smad7 binds to the adaptors TAB2 and TAB3 to block recruitment of the kinase TAK1 to the adaptor TRAF2.

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Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF beta receptor for degradation

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Identification of Smad7, a TGFbeta-inducible antagonist of TGF-beta signalling

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Smurf1 interacts with transforming growth factor-beta type I receptor through Smad7 and induces receptor degradation

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Cooperative inhibition of bone morphogenetic protein signaling by Smurf1 and inhibitory Smads

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Smad6 inhibits signalling by the TGF-beta superfamily.

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The cloning and characterization of human MyD88: a member of an IL-1 receptor related family

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MyD88 is an adaptor protein in the hToll/IL-1 receptor family signaling pathways

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Signaling to NF-kappaB by Toll-like receptors

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Relevance of mutations in the TLR4 receptor in patients with gram-negative septic shock

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Toll-like receptor 4-deficient mice have reduced bone destruction following mixed anaerobic infection

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IRAK-M is a negative regulator of Toll-like receptor signaling

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Inhibition of interleukin 1 receptor/Toll-like receptor signaling through the alternatively spliced, short form of MyD88 is due to its failure to recruit IRAK-4

21 January 2018

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Regulation of TGF-beta family signaling by E3 ubiquitin ligases

21 January 2018

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Smurf2 induces ubiquitin-dependent degradation of Smurf1 to prevent migration of breast cancer cells

21 January 2018

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Smad7 and Smad6 bind to discrete regions of Pellino-1 via their MH2 domains to mediate TGF-beta1-induced negative regulation of IL-1R/TLR signaling

21 January 2018

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Pattern recognition receptors and inflammation

21 January 2018

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Immunity, Inflammation, and Cancer

21 January 2018

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Nonresolving inflammation

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Immune and inflammatory mechanisms of atherosclerosis (*)

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Ubiquitin ligase Smurf1 targets TRAF family proteins for ubiquitination and degradation

21 January 2018

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Regulation of planar cell polarity by Smurf ubiquitin ligases

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The role of TBK1 and IKKε in the expression and activation of Pellino 1.

21 January 2018

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IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway

21 January 2018

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The type I TGF-beta receptor engages TRAF6 to activate TAK1 in a receptor kinase-independent manner

21 January 2018

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The E3 ubiquitin ligase Triad3A negatively regulates the RIG-I/MAVS signaling pathway by targeting TRAF3 for degradation

21 January 2018

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A two-tiered mechanism of EGFR inhibition by RALT/MIG6 via kinase suppression and receptor degradation.

21 January 2018

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The IL-1 receptor/toll-like receptor superfamily: crucial receptors for inflammation and host defense

21 January 2018

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12 December 2020

A mechanism of suppression of TGF-beta/SMAD signaling by NF-kappa B/RelA

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12 December 2020

Epidemic inflammation: pondering obesity

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12 December 2020

Biologic basis for interleukin-1 in disease

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12 December 2020

SOCS1/JAB is a negative regulator of LPS-induced macrophage activation

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12 December 2020

Identifiers

DOI

10.1038/NCOMMS1469

1 reference

12 September 2017

0 references

1 reference

PubMed ID

21897371