Evidence map›Paper›PMID 39519307›Full record

ArticleInternational journal of molecular sciences2024

RIPK2 Is Crucial for the Microglial Inflammatory Response to Bacterial Muramyl Dipeptide but Not to Lipopolysaccharide.

Changjun Yang, Maria Carolina Machado da Silva, John Aaron Howell, Jonathan Larochelle, Lei Liu, Rachel E Gunraj, Antônio Carlos Pinheiro de Oliveira, Eduardo Candelario-Jalil

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Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Changjun YangDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.ORCID 0000-0001-6253-7207
Maria Carolina Machado da SilvaDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.ORCID 0000-0002-0200-2902
John Aaron HowellDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.ORCID 0000-0001-9875-6022
Jonathan LarochelleDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.
Lei LiuDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.
Rachel E GunrajDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.
Antônio Carlos Pinheiro de OliveiraDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.ORCID 0000-0003-3217-4294
Eduardo Candelario-JalilDepartment of Neuroscience, McKnight Brain Institute, University of Florida, 1149 SW Newell Drive, Gainesville, FL 32610, USA.ORCID 0000-0003-3631-1989

Funding

Role of RIPK2 in the neuroinflammatory response to ischemic strokeR01NS129136 · NINDS · UNIVERSITY OF FLORIDA · PI Eduardo Jesus Candelario-Jalil · 2023 to 2026
$1.6M
American Heart Association 971058American Heart Association-American Stroke Association 971058NIH/NINDS R01NS129136NINDS NIH HHS R01 NS129136
6 · The paper itself

Abstract

Receptor-interacting serine/threonine protein kinase 2 (RIPK2) is a kinase that is essential in modulating innate and adaptive immune responses. As a downstream signaling molecule for nucleotide-binding oligomerization domain 1 (NOD1), NOD2, and Toll-like receptors (TLRs), it is implicated in the signaling triggered by recognition of microbe-associated molecular patterns by NOD1/2 and TLRs. Upon activation of these innate immune receptors, RIPK2 mediates the release of pro-inflammatory factors by activating mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB). However, whether RIPK2 is essential for downstream inflammatory signaling following the activation of NOD1/2, TLRs, or both remains controversial. In this study, we examined the role of RIPK2 in NOD2- and TLR4-dependent signaling cascades following stimulation of microglial cells with bacterial muramyl dipeptide (MDP), a NOD2 agonist, or lipopolysaccharide (LPS), a TLR4 agonist. We utilized a highly specific proteolysis targeting chimera (PROTAC) molecule, GSK3728857A, and found dramatic degradation of RIPK2 in a concentration- and time-dependent manner. Importantly, the PROTAC completely abolished MDP-induced increases in iNOS and COX-2 protein levels and pro-inflammatory gene transcription of

Indexed as

Acetylmuramyl-Alanyl-IsoglutamineInflammationLipopolysaccharidesMicrogliaNod2 Signaling Adaptor ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Toll-Like Receptor 4AnimalsCell LineCyclooxygenase 2MiceNF-kappa BSignal TransductionAcetylmuramyl-Alanyl-IsoglutamineCyclooxygenase 2LipopolysaccharidesNF-kappa BNod2 Signaling Adaptor ProteinReceptor-Interacting Protein Serine-Threonine Kinase 2Ripk2 protein, mouseToll-Like Receptor 4inflammatory responselipopolysaccharidemicrogliamitogen-activated protein kinasemuramyl dipeptidenuclear factor-kappa Bnucleotide-binding oligomerization domain-like receptorreceptor-interacting serine/threonine protein kinase 2Toll-like receptor

Identifiers

PMID39519307
PMCPMC11546996

What Socratic holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.