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POU3F4 mutations can be predicted by incomplete partition type III anomaly by radiological examination of the inner ear. All six of the patients showed mixed hearing loss, but none showed fluctuations in hearing, which may be related to the lack of vestibular aqueduct enlargement at the operculum.
Sequencing of the entire POU3F4 gene is recommended in patients with characteristic temporal bone malformations. Results of POU3F4 mutation testing are important not only for a proper genetic counseling, but also for adequate preparation and conduction of a surgical procedure.
A nonsense mutation is identified in a family displaying the pedigree consistent with X-linked recessive pattern in POU3F4 gene.
POU3F4 mutation in profoundly deaf patients may have poorer prognosis after cochlear implantation, than other types.
findings may greatly contribute to the elucidation of the roles of the Oct (show Plxna2 Proteins) and Myc (show MYC Proteins) proteins in osteoblast direct reprogramming. The results may also lead to establishment of novel regenerative therapy for various bone resorption diseases
Audiological, medical, and family histories were collected and family members interviewed to compare hearing thresholds and case histories between cases with mutations in SMPX (show SMPX Proteins) versus POU3F4.
Our data suggest that different POU3F4 mutations might show different recurrence rate in siblings of the incomplete partition type III anomaly especially in East Asian population
POU3F4 mutations are associated with X-linked deafness
We concluded that the probable presence of the third window effect is not limited to the particular type of POU3F4 mutation.
Results show three novel mutations in the POU3F4 gene resulting in profound hearing loss in both humans and mice.
pou3f4 expression in inner ear might be under the control of distinct regulatory elements that fine-tune the spatio-temporal activity of this gene
Brn4 substantially contributes to cochlear gap junction properties to maintain the proper EP in cochleae, similar to connexin-related deafness.
Efnb2 (show EFNB2 Proteins) expression was attenuated in Pou3f4 hemizygous null mutants relative to control.
This study indicated a model whereby Pou3f4 in the otic mesenchyme establishes an Eph/ephrin-mediated fasciculation signal that promotes inner radial bundle formation.
The effects of Brn-4 on the neuronal differentiation and development of neural stem cells, were investigated.
a transcription factor targeted to the early mouse pancreas induces ectopic glucagon (show GCG Proteins) gene expression
late-onset effect of Brn-4 deficiency on the hearing organ of the mouse. About one third of heterozygous female mice revealed late-onset profound deafness at the age of 1 year.
lack of role in regulating Pax6 (show PAX6 Proteins) and Nkx2.2 (show Nkx2-2 Proteins)
Tbx1 (show TBX1 Proteins) and Brn4 function in signaling from the periotic mesenchyme to the otic vesicle to direct proper coiling of the cochlear duct.
This gene encodes a member of the POU-III class of neural transcription factors. This family member plays a role in inner ear development. The protein is thought to be involved in the mediation of epigenetic signals which induce striatal neuron-precursor differentiation. Mutations in this gene are associated with X chromosome-linked nonsyndromic mixed deafness.
POU domain, class 3, transcription factor 4
, POU class 3 homeobox 4
, POU domain, class 3, transcription factor 4-like
, brain-specific homeobox/POU domain protein 4
, octamer-binding transcription factor 9
, POU 2 transcription factor
, POU domain, class 3, transcription factor 4-A
, Transcription factor POU2
, XLPOU 2
, RHS2 class III POU protein
, octamer-binding protein 9
, Brain-specific homeobox/POU domain protein 4
, POU homeodomain protein
, brain-4 class III POU-domain protein
, sex linked fidget