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

Suppressors of the egg-laying defective phenotype of sel-12 presenilin mutants implicate the CoREST corepressor complex in LIN-12/Notch signaling in C. elegans.

Genes & development - 15 Oct 2002

Jarriault Sophie, Greenwald Iva

Abstract excerpt

Presenilin is an essential component of the LIN-12/Notch signaling pathway and also plays a critical role in the genesis of Alzheimer's disease. Previously, a screen for suppressors of the egg-laying defective phenotype caused by partial loss of presenilin activity in Caenorhabditis elegans identified a number of new spr genes that are potentially involved in the regulation of LIN-12/Notch signaling or presenilin...

Read the complete abstract on PubMed

Topics

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

Share to Co-Repressor Proteins
Share to Eggs
Share to Embryo, Nonmammalian

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Helminth Proteins

Share to Lac Operon

Share to Receptors, Notch

Share to RNA Splice Sites

Share to Transgenes

Source

Open in PubMed Open full text

Identifiers

PMID: 12381669
DOI: 10.1101/gad.1022402
PMCID: PMC187465

Genes

SPR

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Suppressors of the egg-laying defective phenotype of sel-12 presenilin mutants implicate the CoREST corepressor complex in LIN-12/Notch signaling in C. elegans.PMID 12381669Read ↗

lin-35/Rb and the CoREST ortholog spr-1 coordinately regulate vulval morphogenesis and gonad development in C. elegans.Semantic proximity Read ↗

Loss of spr-5 bypasses the requirement for the C.elegans presenilin sel-12 by derepressing hop-1.Semantic proximity Read ↗

spr-2, a suppressor of the egg-laying defect caused by loss of sel-12 presenilin in Caenorhabditis elegans, is a member of the SET protein subfamily.Semantic proximity Read ↗

Two suppressors of sel-12 encode C2H2 zinc-finger proteins that regulate presenilin transcription in Caenorhabditis elegans.Semantic proximity Read ↗

Overlapping and non-overlapping roles of the class-I histone deacetylase-1 corepressors, LET-418, SIN-3, and SPR-1 in <i>Caenorhabditis elegans</i> embryonic developmentSemantic proximity Read ↗

Reverse genetic analysis of Caenorhabditis elegans presenilins reveals redundant but unequal roles for sel-12 and hop-1 in Notch-pathway signaling.Semantic proximity Read ↗

UBR-5, a Conserved HECT-Type E3 Ubiquitin Ligase, Negatively Regulates Notch-Type Signaling in Caenorhabditis elegans.Semantic proximity Read ↗

Mutations in genes involved in nonsense mediated decay ameliorate the phenotype of sel-12 mutants with amber stop mutations in Caenorhabditis elegans.Semantic proximity Read ↗

HOP-1, a Caenorhabditis elegans presenilin, appears to be functionally redundant with SEL-12 presenilin and to facilitate LIN-12 and GLP-1 signaling.Semantic proximity Read ↗

sel-10, a negative regulator of lin-12 activity in Caenorhabditis elegans, encodes a member of the CDC4 family of proteins.Semantic proximity Read ↗

sel-7, a positive regulator of lin-12 activity, encodes a novel nuclear protein in Caenorhabditis elegans.Semantic proximity Read ↗

Presenilin is required for proper morphology and function of neurons in C. elegans.Semantic proximity Read ↗

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