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

Special AT-rich binding protein-2 (SATB2) differentially affects disease-causing p63 mutant proteins.

The Journal of biological chemistry - 25 Nov 2011

Chung Jacky, Grant R Ian, Kaplan David R, Irwin Meredith S

Abstract excerpt

p63, a p53 family member, is critical for proper skin and limb development and directly regulates gene expression in the ectoderm. Mice lacking p63 exhibit skin and craniofacial defects including cleft palate. In humans p63 mutations are associated with several distinct developmental syndromes. p63 sterile-α-motif domain, AEC (ankyloblepharon-ectodermal dysplasia-clefting)-associated mutations are associated with...

Read the complete abstract on PubMed

Topics

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

Share to Cleft Lip
Share to Cleft Palate
Share to Ectodermal Dysplasia

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Eye Abnormalities

Share to Eyelids

Share to Matrix Attachment Region Binding Proteins

Share to Phosphoproteins

Share to Transcriptional Activation

Source

Open in PubMed Open full text

Identifiers

PMID: 21965674
DOI: 10.1074/jbc.M111.271189
PMCID: PMC3220488

Genes

SATB2

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

Special AT-rich binding protein-2 (SATB2) differentially affects disease-causing p63 mutant proteins.PMID 21965674Read ↗

Isoform-Specific Roles of Mutant p63 in Human DiseasesSemantic proximity Read ↗

Distinct interactors define the p63 transcriptional signature in epithelial development or cancerSemantic proximity Read ↗

Genome-wide analysis of p63 binding sites identifies AP-2 factors as co-regulators of epidermal differentiationSemantic proximity Read ↗

p63-associated disorders.Semantic proximity Read ↗

Protein aggregation of the p63 transcription factor underlies severe skin fragility in AEC syndrome.Semantic proximity Read ↗

The p53/p63/p73 family of transcription factors: overlapping and distinct functionsSemantic proximity Read ↗

Differential transcriptional activity of ΔNp63β is encoded by an isoform-specific C-terminusSemantic proximity Read ↗

Deletion of p63 exon 13 in mice reveals C-terminal isoform–specific functions in epithelial developmentSemantic proximity Read ↗

Mutations in the p53 homolog p63: allele-specific developmental syndromes in humans.Semantic proximity Read ↗

Targeted p63 isoform switch corrects dominant mutations in AEC syndrome without disrupting epidermal homeostasisSemantic proximity Read ↗

P63 in health and cancerSemantic proximity Read ↗

ASPP2 suppresses squamous cell carcinoma via RelA/p65–mediated repression of p63Semantic proximity Read ↗

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