Browse our anti-POU Domain, Class 3, Transcription Factor 4 (POU3F4) Antibodies

Human POU Domain, Class 3, Transcription Factor 4 (POU3F4) interaction partners

1. POU3F4 gene mutation analysis will increase the success rate of stapes operations and cochlear implantations.

2. 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.

3. 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.

4. A nonsense mutation is identified in a family displaying the pedigree consistent with X-linked recessive pattern in POU3F4 gene.

5. POU3F4 mutation in profoundly deaf patients may have poorer prognosis after cochlear implantation, than other types.

6. findings may greatly contribute to the elucidation of the roles of the Oct and Myc proteins in osteoblast direct reprogramming. The results may also lead to establishment of novel regenerative therapy for various bone resorption diseases

7. Audiological, medical, and family histories were collected and family members interviewed to compare hearing thresholds and case histories between cases with mutations in SMPX versus POU3F4.

8. 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

9. POU3F4 mutations are associated with X-linked deafness

10. We concluded that the probable presence of the third window effect is not limited to the particular type of POU3F4 mutation.

11. Results show three novel mutations in the POU3F4 gene resulting in profound hearing loss in both humans and mice.

12. Frameshift truncation and extension mutations in the C-terminus of POU3F4 lead to cytoplasmic localization and subsequent proteosomal degradation due to structural aberrations, which cause transcriptional inactivity and thus nonsyndromic hearing loss.

13. Study found no mutations in GJB6 or POU3F4 in nonsyndromic Tibetan Chinese patients with hearing impairment.

14. pou3f4 expression in inner ear might be under the control of distinct regulatory elements that fine-tune the spatio-temporal activity of this gene

15. DNA sequencing of the POU3F4 gene revealed a novel nucleotide variation, c.647G to A. The additional mutation confirms the crucial role of POU3F4 in auditory function.

16. POU3F4 did not contribute to Y linked familial deafness in a Chinese pedigree.

17. evaluation of DFN3 patients with deletions in the POU3F4 locus and detection of carrier female using MLPA.

18. novel mutations in the POU3F4 gene resulting in congenital X-linked deafness DFN3.

19. Data suggest that multiple enhancers control the expression of Pou3f4 in the inner ear and these may contribute to the phenotype observed in DFN3 patients.

20. Results strongly suggest that the deafness in DFN3 patients is largely due to the null function of POU3F4.

Xenopus laevis POU Domain, Class 3, Transcription Factor 4 (POU3F4) interaction partners

1. Xenopus pou3f genes were expressed in the forming neural tube and their expression was maintained in the brain, mostly in the dorsal part, at tailbud stages. The pou3f2, pou3f3, and pou3f4 genes were also expressed in the developing otic vesicle, and pou3f1 in some cells of the epidermis. Besides ectodermal derivatives, pou3f3 and pou3f4 were expressed in the developing kidney.

2. pou3f4 expression in inner ear might be under the control of distinct regulatory elements that fine-tune the spatio-temporal activity of this gene

Mouse (Murine) POU Domain, Class 3, Transcription Factor 4 (POU3F4) interaction partners

1. Brn4 substantially contributes to cochlear gap junction properties to maintain the proper EP in cochleae, similar to connexin-related deafness.

2. Efnb2 expression was attenuated in Pou3f4 hemizygous null mutants relative to control.

3. Results show three novel mutations in the POU3F4 gene resulting in profound hearing loss in both humans and mice.

4. This study indicated a model whereby Pou3f4 in the otic mesenchyme establishes an Eph/ephrin-mediated fasciculation signal that promotes inner radial bundle formation.

5. pou3f4 expression in inner ear might be under the control of distinct regulatory elements that fine-tune the spatio-temporal activity of this gene

6. The effects of Brn-4 on the neuronal differentiation and development of neural stem cells, were investigated.

7. a transcription factor targeted to the early mouse pancreas induces ectopic glucagon gene expression

8. 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.

9. lack of role in regulating Pax6 and Nkx2.2

10. Tbx1 and Brn4 function in signaling from the periotic mesenchyme to the otic vesicle to direct proper coiling of the cochlear duct.

11. Brn4 regulate retinoic acid metabolic genes during cochlear morphogenesis