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

Insights into the pathological mechanisms of p85α mutations using a yeast-based phosphatidylinositol 3-kinase model.

Bioscience reports - 30 Apr 2017

Oliver María D, Fernández-Acero Teresa, Luna Sandra, Rodríguez-Escudero Isabel, Molina María, Pulido Rafael, Cid Víctor J

Abstract excerpt

In higher eukaryotes, cell proliferation is regulated by class I phosphatidylinositol 3-kinase (PI3K), which transduces stimuli received from neighboring receptors by local generation of PtdIns(3,4,5)P3 in cellular membranes. PI3K is a heterodimeric protein consisting of a regulatory and a catalytic subunit (p85 and p110 respectively). Heterologous expression of p110α in Saccharomyces cerevisiae leads to toxicity...

Read the complete abstract on PubMed

Topics

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

Share to Class Ia Phosphatidylinositol 3-Kinase
Share to Growth Disorders

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Hypercalcemia

Share to Immunoblotting

Share to Metabolic Diseases

Share to Nephrocalcinosis

Share to Protein Subunits

Share to Saccharomyces cerevisiae Proteins

Source

Open in PubMed Open full text

Identifiers

PMID: 28143957
DOI: 10.1042/BSR20160258
PMCID: PMC5350601

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

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

Insights into the pathological mechanisms of p85α mutations using a yeast-based phosphatidylinositol 3-kinase model.PMID 28143957Read ↗

Mechanistic investigation of genotype-phenotype correlations in PIK3R1-related diseasesSemantic proximity Read ↗

Molecular Mechanisms of Human Disease Mediated by Oncogenic and Primary Immunodeficiency Mutations in Class IA Phosphoinositide 3-Kinases.Semantic proximity Read ↗

Paradoxical dominant negative activity of an immunodeficiency-associated activating <i>PIK3R1</i> variantSemantic proximity Read ↗

Domain analysis reveals striking functional differences between the regulatory subunits of phosphatidylinositol 3-kinase (PI3K), p85α and p85βSemantic proximity Read ↗

Critical role for the p110alpha phosphoinositide-3-OH kinase in growth and metabolic regulation.Semantic proximity Read ↗

The p110α isoform of PI3K is essential for proper growth factor signaling and oncogenic transformationSemantic proximity Read ↗

p110δ PI3 kinase pathway: emerging roles in cancerSemantic proximity Read ↗

Class I PI3K in oncogenic cellular transformation.Semantic proximity Read ↗

p110δ PI3K as a therapeutic target of solid tumoursSemantic proximity Read ↗

Activated PI3Kinase Delta Syndrome—A Multifaceted DiseaseSemantic proximity Read ↗

Should individual PI3 kinase isoforms be targeted in cancer?Semantic proximity Read ↗

Phosphatidylinositol 3-kinase: the oncoprotein.Semantic proximity Read ↗

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