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

Defining the breakpoints of the quaking(viable) mouse mutation reveals a duplication from a Parkin intron.

Movement disorders : official journal of the Movement Disorder Society - 1 Oct 2005

Dapper Jason D, Justice Monica J

Abstract excerpt

The quakingviable (qkv) mutant mouse shows a recessive neurological phenotype that includes central nervous system (CNS) dysmyelination, seizures, and tremor associated with voluntary movement. The molecular defect of qkv has been previously reported to be a spontaneous approximately 1 megabase (Mb) deletion in the proximal region of mouse chromosome 17 that occurred in the DBA mouse strain more than four decades...

Read the complete abstract on PubMed

Topics

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

Share to Chromosomes, Mammalian
Share to Demyelinating Diseases

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

Share to DNA Fragmentation

Share to Gene Duplication

Share to Microfilament Proteins

Share to Molecular Chaperones

Share to Transcriptional Activation

Share to Ubiquitin-Protein Ligases

Source

Identifiers

PMID: 16001410
DOI: 10.1002/mds.20595

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

Defining the breakpoints of the quaking(viable) mouse mutation reveals a duplication from a Parkin intron.PMID 16001410Read ↗

It's a double knock-out! The quaking mouse is a spontaneous deletion of parkin and parkin co-regulated gene (PACRG).Semantic proximity Read ↗

Deletion of the Parkin coregulated gene causes male sterility in the quaking(viable) mouse mutant.Semantic proximity Read ↗

The quaking gene product necessary in embryogenesis and myelination combines features of RNA binding and signal transduction proteins.Semantic proximity Read ↗

A new ENU-induced allele of mouse quaking causes severe CNS dysmyelination.Semantic proximity Read ↗

A 1.2-Mb YAC contig spans the quaking region.Semantic proximity Read ↗

The proximal end of mouse chromosome 17: new molecular markers identify a deletion associated with quakingviable.Semantic proximity Read ↗

Dysmyelination with preservation of transverse bands in a long-lived allele of the quaking mouse.Semantic proximity Read ↗

Loss of p53 in quaking viable mice leads to Purkinje cell defects and reduced survival.Semantic proximity Read ↗

The quaking I-5 protein (QKI-5) has a novel nuclear localization signal and shuttles between the nucleus and the cytoplasm.Semantic proximity Read ↗

Generation and characterisation of a parkin-Pacrg knockout mouse line and a Pacrg knockout mouse lineSemantic proximity Read ↗

Prime editing-mediated correction of the leptin receptor in muscle cells of db/db mice.Semantic proximity Read ↗

Prime Editing in vivo: Correcting the Leptin Receptor of db/db MiceSemantic proximity Read ↗

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