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

Validation of microarray data in human lymphoblasts shows a role of the ubiquitin-proteasome system and NF-kB in the pathogenesis of Down syndrome

5 Jul 2013

Abstract excerpt

BACKGROUND: Down syndrome (DS) is a complex disorder caused by the trisomy of either the entire, or a critical region of chromosome 21 (21q22.1-22.3). Despite representing the most common cause of mental retardation, the molecular bases of the syndrome are still largely unknown. METHODS: To better understand the pathogenesis of DS, we analyzed the genome-wide transcription profiles of lymphoblastoid cell lines...

Read the complete abstract on PubMed

Topics

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

Share to Down syndrome and intellectual disability research
Share to Genetics and Neurodevelopmental Disorders
Share to Ubiquitin and proteasome pathways

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 23830204
DOI: 10.1186/1755-8794-6-24

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Validation of microarray data in human lymphoblasts shows a role of the ubiquitin-proteasome system and NF-kB in the pathogenesis of Down syndromePMID 23830204Read ↗

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 ↗

The cognitive phenotype of Down syndrome: insights from intracellular network analysis.Semantic proximity Read ↗

Transcriptome and Proteome Profiling of Neural Induced Pluripotent Stem Cells from Individuals with Down Syndrome Disclose Dynamic Dysregulations of Key Pathways and Cellular FunctionsSemantic proximity Read ↗

The burden of trisomy 21 disrupts the proteostasis network in Down syndromeSemantic proximity Read ↗

Single-cell atlas of the fetal Down syndrome cortex uncovers chromosome 21 regulators of intellectual disability gene networksSemantic proximity Read ↗

Genomic and functional profiling of human Down syndrome neural progenitors implicates S100B and aquaporin 4 in cell injurySemantic proximity Read ↗

NF-κB-inducing Kinase Phosphorylates and Blocks the Degradation of Down Syndrome Candidate Region 1Semantic proximity Read ↗

Proteomics Study of Peripheral Blood Mononuclear Cells in Down Syndrome ChildrenSemantic proximity Read ↗

An Integrated Human/Murine Transcriptome and Pathway Approach To Identify Prenatal Treatments For Down SyndromeSemantic proximity Read ↗

Concise review: new paradigms for Down syndrome research using induced pluripotent stem cells: tackling complex human genetic disease.Semantic proximity Read ↗

A New Approach to The Pathogenesis of Down Syndrome: An Integrated Quantitative Neuro-Transcriptome Analysis of Several Brain Areas in Human Trisomy 21.Semantic proximity Read ↗

Chr21 protein–protein interactions: enrichment in proteins involved in intellectual disability, autism, and late-onset Alzheimer’s diseaseSemantic proximity Read ↗

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