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Human POU Domain, Class 4, Transcription Factor 3 (POU4F3) interaction partners

1. Findings expanded the mutation spectrum of POU4F3 and suggest the pathogenesis associated with aberrant POU4F3 localization.

2. POU4F3 c.602T>C (p.Leu201Pro) is related to midfrequency hearing loss.

3. report the first nonsense mutation of POU4F3 associated with progressive hearing loss and explored the possible underlying mechanism

4. DFNA52 were mapped between STR D5S2056 and D5S638 on chromosome, and analysis candidate genes in this region did not reveal any potentially pathogenic mutations segregating with congenital sensorineural hearing loss.

5. Mutations in POU4F3 are a relatively common cause of autosomal dominant nonsyndromic hearing loss in Chinese Hans.

6. Novel 12 POU4F3 likely pathogenic variants (six missense variants, three frameshift variants, and three nonsense variants) were successfully identified in 15 probands (2.5%) among 602 families exhibiting autosomal dominant hearing loss, whereas no variants were detected in the other 1,947 probands with autosomal recessive or inheritance pattern unknown hearing loss.

7. results indicated GRHL2 might be a noise-induced hearing loss (NIHL) susceptibility gene, but the effect of POU4F3 on NIHL could only be detected when taking noise exposure into account and their effects were enhanced by higher levels of noise exposure

8. this study identified a novel heterozygous mutation (c.602delT, p.L201fs) in the gene POU4F3 within a large hearing impaired Chinese family.

9. This study showed that Mendelian sensorineural hearing loss exhibits vestibular dysfunction, including DFNA9, DFNA11, DFNA15 and DFNA28.

10. The pou4f3 gene is regulated by ATOH1 and other transcription factors in cochlear hair cells.

11. These data demonstrate that Nr2f2 is a direct target of POU4F3 in vitro and that this regulatory relationship may be relevant to hair cell development and survival.

12. Data indicate that POUF4F3 deletion associated with hearing impairment.

13. new variants in genes such as POU4F3 is associated with nonsyndromic deafness and vestibular dysfunction

14. SNP linkage analysis and whole exome sequencing identify a novel POU4F3 mutation in autosomal dominant late-onset nonsyndromic hearing loss (DFNA15).

15. This is the first report of a POU4F3 mutation in Asia, and moreover our data suggest that further investigation will need to delineate ethnicity-specific genetic background for autosomal dominant non-syndromic hearing loss within Asian populations.

16. Molecular modelling is utilised to propose a mechanism of stability enhancement, via an interaction between the truncated POU(HD) domain and the POU(S) domain of the transcription factor.

17. Proneural and proneuroendocrine transcription factor expression in cutaneous mechanoreceptor (Merkel) cells and Merkel cell carcinoma

18. Mutant POU4F3 loses most of its transcriptional activity and most of its ability to bind to DNA. The mutation causes autosomal-dominant nonsyndromic hearing loss and eventually leads to hair cell morbidity in affected family H members.

19. Data show that Brn-3c is capable of activating both BDNF and NT-3 promoters in inner ear sensory epithelial cell lines.

20. our data show there are common sequence variants in the Brn-3c 5'-flanking region that affect transcriptional regulation in vitro

Mouse (Murine) POU Domain, Class 4, Transcription Factor 3 (POU4F3) interaction partners

1. identify separate enhancers at various locations of pou4f3 gene that direct expression to different inner ear hair cells types at different ages and determine that 0.4 kb of upstream sequence determines expression level

2. Atoh1 function in hair cell differentiation is modulated by interaction with other transcription factors, such as Gfi1 and Pou4f3. (Review)

3. These data illuminate a genetic pathway that initiates auditory HC regeneration and suggest p27(Kip1), GATA3, and POU4F3 as additional therapeutic targets for ATOH1-mediated auditory hair cells regeneration.

4. These data demonstrate that Nr2f2 is a direct target of POU4F3 in vitro and that this regulatory relationship may be relevant to hair cell development and survival.

5. Data indicate that Brn3 transcription factors Brn3b affects Brn3a and Brn3c positive Retinal Ganglion Cells (RGCs) in cell autonomous and non-cell autonomous fashion.

6. induction of POU4F3 by TFE2 and GATA3

7. neither Brn3a nor Brn3c are expressed in intrinsically photosensitive retinal ganglion cells

8. Data show that Ap-2delta occupies and activates the Pou4f3 and Bhlhb4 promoters.

9. Stress-granule-associated protein Caprin-1 is downregulated by Pou4f3.

10. Taken together, our data suggest that SHH plays an important role in the promotion of auditory hair cell differentiation via the Math1-Brn3.1 signaling pathway.

11. Brn3c null mice show severe compromised production of these neurotrophins and should therefore show a comparable pattern of nerve fiber loss.

12. Brn-3c was found to contain an independent N-terminal activation domain that is sufficient to activate gene transcription in the organ-of-Corti-derived cell lines.

13. Inner hair cells constitutively express alpha9alpha10 nicotinic cholinergic receptors into adulthood by expressing the alpha10 cDNA under the control of the Pou4f3 gene promoter.