Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

The RNA-binding protein Tristetraprolin (TTP) is a critical negative regulator of the NLRP3 inflammasome.

The Journal of biological chemistry - 28 Apr 2017

Haneklaus Moritz, O'Neil John D, Clark Andrew R, Masters Seth L, O'Neill Luke A J

Abstract excerpt

The NLRP3 inflammasome is a central regulator of inflammation in many common diseases, including atherosclerosis and type 2 diabetes, driving the production of pro-inflammatory mediators such as IL-1β and IL-18. Due to its function as an inflammatory gatekeeper, expression and activation of NLRP3 need to be tightly regulated. In this study, we highlight novel post-transcriptional mechanisms that can modulate...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to 3' Untranslated Regions
Share to Caspase 1

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Genes, Reporter

Share to Inflammasomes

Share to Interleukin-18

Share to Interleukin-1beta

Share to NLR Family, Pyrin Domain-Containing 3 Protein

Share to RNA-Binding Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 28302726
DOI: 10.1074/jbc.M116.772947
PMCID: PMC5409458

Genes

NLRP3
AIM2
NLRC4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

The RNA-binding protein Tristetraprolin (TTP) is a critical negative regulator of the NLRP3 inflammasome.PMID 28302726Read ↗

Evidence that tristetraprolin is a physiological regulator of granulocyte-macrophage colony-stimulating factor messenger RNA deadenylation and stabilitySemantic proximity Read ↗

Identification of the anti-inflammatory protein tristetraprolin as a hyperphosphorylated protein by mass spectrometry and site-directed mutagenesis.Semantic proximity Read ↗

Tristetraprolin regulates interleukin-6 expression through p38 MAPK-dependent affinity changes with mRNA 3' untranslated region.Semantic proximity Read ↗

Tristetraprolin Regulates TH17 Cell Function and Ameliorates DSS-Induced Colitis in MiceSemantic proximity Read ↗

Multiple functions of tristetraprolin/TIS11 RNA-binding proteins in the regulation of mRNA biogenesis and degradation.Semantic proximity Read ↗

Enhanced stability of tristetraprolin mRNA protects mice against immune-mediated inflammatory pathologies.Semantic proximity Read ↗

Nuclear Receptors as Multiple Regulators of NLRP3 Inflammasome FunctionSemantic proximity Read ↗

Tristetraprolin expression by keratinocytes controls local and systemic inflammationSemantic proximity Read ↗

Gain-of-Function Mutation of Tristetraprolin Impairs Negative Feedback Control of Macrophages In Vitro yet Has Overwhelmingly Anti-Inflammatory Consequences In Vivo.Semantic proximity Read ↗

Regulation of the NLRP3 Inflammasome by Post-Translational Modifications and Small MoleculesSemantic proximity Read ↗

Tristetraprolin Overexpression in Non-hematopoietic Cells Protects Against Acute Lung Injury in MiceSemantic proximity Read ↗

MK2-induced tristetraprolin:14-3-3 complexes prevent stress granule association and ARE-mRNA decay.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.