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

New cerebellar phenotypes in YAC transgenic mouse in vivo library of human Down syndrome critical region-1.

Biochemical and biophysical research communications - 21 Dec 2007

Rachidi Mohammed, Lopes Carmela, Vayssettes Catherine, Smith Desmond J, Rubin Edward M, Delabar Jean-Maurice

Abstract excerpt

Down syndrome (DS) is the most frequent genetic cause of mental retardation (MR) associated with neurological alterations. To allow a genetic dissection of DS phenotype, we studied eight transgenic mouse lines carrying YACs containing human DNA fragments covering DS critical region (DCR-1), as an in vivo library. Herein, we found an increased brain size in the 152F7-mice containing DYRK1A gene. We also identified...

Read the complete abstract on PubMed

Topics

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

Share to Cerebellum
Share to Chromosomes, Artificial, Yeast

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Conserved Sequence

Share to DNA-Binding Proteins

Share to Intracellular Signaling Peptides and Proteins

Share to Mice, Transgenic

Share to Muscle Proteins

Share to Peptide Library

Source

Identifiers

PMID: 17963726
DOI: 10.1016/j.bbrc.2007.10.035

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

New cerebellar phenotypes in YAC transgenic mouse in vivo library of human Down syndrome critical region-1.PMID 17963726Read ↗

Transgenic mouse in vivo library of human Down syndrome critical region 1: association between DYRK1A overexpression, brain development abnormalities, and cell cycle protein alteration.Semantic proximity Read ↗

Neurodevelopmental delay, motor abnormalities and cognitive deficits in transgenic mice overexpressing Dyrk1A (minibrain), a murine model of Down's syndrome.Semantic proximity Read ↗

Genetic dissection of the Down syndrome critical regionSemantic proximity Read ↗

Dyrk1A haploinsufficiency affects viability and causes developmental delay and abnormal brain morphology in mice.Semantic proximity Read ↗

Dyrk1a from Gene Function in Development and Physiology to Dosage Correction across Life Span in Down SyndromeSemantic proximity Read ↗

DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down SyndromeSemantic proximity Read ↗

Mental retardation and associated neurological dysfunctions in Down syndrome: a consequence of dysregulation in critical chromosome 21 genes and associated molecular pathways.Semantic proximity Read ↗

Lifespan analysis of brain development, gene expression and behavioral phenotypes in the Ts1Cje, Ts65Dn and Dp(16)1/Yey mouse models of Down syndrome.Semantic proximity Read ↗

Triplication of DYRK1A causes retinal structural and functional alterations in Down syndromeSemantic proximity Read ↗

Molecular Cartography of the Human and Mouse Down Syndrome BrainSemantic proximity Read ↗

<i>Ripply3</i> overdosage induces mid-face shortening through <i>Tbx1</i> downregulation in Down syndrome modelsSemantic proximity Read ↗

The spatio‐temporal and subcellular expression of the candidate Down syndrome gene Mnb/Dyrk1A in the developing mouse brain suggests distinct sequential roles in neuronal developmentSemantic proximity Read ↗

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