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

Disease-related mutations in PI3Kγ disrupt regulatory C-terminal dynamics and reveal a path to selective inhibitors.

eLife - 4 Mar 2021

Rathinaswamy Manoj K, Gaieb Zied, Fleming Kaelin D, Borsari Chiara, Harris Noah J, Moeller Brandon E, Wymann Matthias P, Amaro Rommie E, Burke John E

Abstract excerpt

Class I Phosphoinositide 3-kinases (PI3Ks) are master regulators of cellular functions, with the class IB PI3K catalytic subunit (p110γ) playing key roles in immune signalling. p110γ is a key factor in inflammatory diseases and has been identified as a therapeutic target for cancers due to its immunomodulatory role. Using a combined biochemical/biophysical approach, we have revealed insight into regulation of...

Read the complete abstract on PubMed

Topics

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

Share to Immunologic Deficiency Syndromes
Share to Mutation

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Open in PubMed Open full text

Identifiers

PMID: 33661099
DOI: 10.7554/eLife.64691
PMCID: PMC7955810

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. Graph snapshot: 2026-09-29.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Disease-related mutations in PI3Kγ disrupt regulatory C-terminal dynamics and reveal a path to selective inhibitors.PMID 33661099Read ↗

Disease related mutations in PI3Kγ disrupt regulatory C-terminal dynamics and reveals a path to selective inhibitorsSemantic proximity Read ↗

Structure of the phosphoinositide 3-kinase p110γ-p101 complex reveals molecular mechanism of GPCR activationSemantic proximity Read ↗

PI3Kδ is selectively inhibited by roginolisib through stabilizing of the C-terminal helix kα12Semantic proximity Read ↗

The Therapeutic Potential for PI3K Inhibitors in Autoimmune Rheumatic DiseasesSemantic proximity Read ↗

Function, Regulation and Biological Roles of PI3Kγ VariantsSemantic proximity Read ↗

Structural Insights into the Development of Inhibitors Against Cancer-Specific Mutations of PI3Kα.Semantic proximity Read ↗

Oncogenic mutations of PIK3CA lead to increased membrane recruitment driven by reorientation of the ABD, p85 and C-terminus.Semantic proximity Read ↗

Somatic mutations in PI3Kα: Structural basis for enzyme activation and drug designSemantic proximity Read ↗

Conformational disruption of PI3Kδ regulation by immunodeficiency mutations in PIK3CD and PIK3R1.Semantic proximity Read ↗

Structure, function and inhibition of the phosphoinositide 3-kinase p110α enzyme.Semantic proximity Read ↗

The structural basis of PI3K cancer mutations: from mechanism to therapy.Semantic proximity Read ↗

Identification of a chemical probe for lipid kinase phosphatidylinositol-5-phosphate 4-kinase gamma (PI5P4Kγ)Semantic proximity Read ↗

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