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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...

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Related Experiment Video

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Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

MLK4 has negative effect on TLR4 signaling.

Alim Seit-Nebi1, Wei Cheng, Hong Xu

  • 1Key Laboratory of the Ministry of Education for Cell Biology and Tumor Cell Engineering, School of Life Sciences, Xiamen University, Xiamen, China.

Cellular & Molecular Immunology
|May 24, 2011
PubMed
Summary
This summary is machine-generated.

Mixed-lineage kinase 4 (MLK4) negatively regulates Toll-like receptor 4 (TLR4) signaling. MLK4 inhibits lipopolysaccharide-induced activation of JNK and ERK pathways, reducing pro-inflammatory cytokine production.

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Published on: July 26, 2017

Area of Science:

  • Immunology
  • Cell Signaling
  • Molecular Biology

Background:

  • Toll-like receptors (TLRs) on macrophages initiate inflammatory responses by producing cytokines like tumor-necrosis factor-α (TNF-α).
  • Proper termination of TLR signaling is crucial to prevent immune disorders caused by sustained cytokine expression.

Purpose of the Study:

  • To identify novel proteins interacting with TLR4.
  • To elucidate the role of mixed-lineage kinase (MLK) 4 in TLR4-mediated signaling pathways.

Main Methods:

  • Identified MLK4 as a TLR4-interacting protein.
  • Investigated MLK4's effect on mitogen-activated protein kinase (MAPK) pathways (JNK, p38, ERK) and NF-κB activation following lipopolysaccharide (LPS) stimulation.
  • Analyzed TNF-α production in cells with altered MLK4 expression (knockdown and overexpression).

Main Results:

  • MLK4 interacts with TLR4 but does not function as a MAP3K.
  • MLK4 inhibits LPS-induced JNK and ERK activation, but not p38 or NF-κB activation.
  • MLK4 knockdown increased, while overexpression reduced, LPS-induced TNF-α production.

Conclusions:

  • MLK4 acts as a negative regulator of TLR4 signaling.
  • MLK4 plays a critical role in controlling the magnitude and duration of the inflammatory response initiated by TLR4 stimulation.