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

A missense mutation in the MLKL brace region promotes lethal neonatal inflammation and hematopoietic dysfunction

19 Jun 2020

Abstract excerpt

Abstract MLKL is the essential effector of necroptosis, a form of programmed lytic cell death. We have isolated a mouse strain with a single missense mutation,MlklD139V, that alters the two-helix ‘brace’ that connects the killer four-helix bundle and regulatory pseudokinase domains. This confers constitutive, RIPK3 independent killing activity to MLKL. Homozygous mutant mice develop lethal postnatal inflammation...

Read the complete abstract on PubMed

Topics

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

Share to Cell death mechanisms and regulation
Share to interferon and immune responses
Share to Viral Infections and Immunology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 32561755
DOI: 10.1038/s41467-020-16819-z

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

A missense mutation in the MLKL brace region promotes lethal neonatal inflammation and hematopoietic dysfunctionPMID 32561755Read ↗

Missense mutations in the MLKL ‘brace’ region lead to lethal neonatal inflammation in mice and are present in high frequency in humansSemantic proximity Read ↗

The Role of the Key Effector of Necroptotic Cell Death, Mlkl, in Mouse Models of DiseaseSemantic proximity Read ↗

The Role of the Key Effector of Necroptotic Cell Death, MLKL, in Mouse Models of DiseaseSemantic proximity Read ↗

A common human MLKL polymorphism confers resistance to negative regulation by phosphorylation.Semantic proximity Read ↗

A common human <i>MLKL</i> polymorphism confers resistance to negative regulation by phosphorylationSemantic proximity Read ↗

Somatic Mosaic NLRC4 Variants in Autoinflammatory Diseases: Functional Characterization and Correlation of Mosaicism Levels with Disease Age of Onset and Severity.Semantic proximity Read ↗

MLKL deficiency protects against low-grade, sterile inflammation in aged miceSemantic proximity Read ↗

Depicting pathogenesis of osteomyelitis by single cell RNA-sequencing and an involvement of <i>Morrbid</i> in the autoinflammatory diseaseSemantic proximity Read ↗

Mutations that prevent caspase cleavage of RIPK1 cause autoinflammatory disease.Semantic proximity Read ↗

Case Report: Infantile Urticaria as a Herald of Neonatal Onset Multisystem Inflammatory Disease With a Novel Mutation in NLRP3.Semantic proximity Read ↗

Infective, neoplastic, and homeostatic sequelae of the loss of perforin function in humans.Semantic proximity Read ↗

Pathogenic variants in MDFIC cause recessive central conducting lymphatic anomaly with lymphedemaSemantic proximity Read ↗

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