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POU domain, class 4, transcription factor 3

Brn-3C, POU4F3, DFNA15, Brn-3.1
This gene encodes a member of the POU-domain family of transcription factors. POU-domain proteins have been observed to play important roles in control of cell identity in several systems. This protein is found in the retina and may play a role in determining or maintaining the identities of a small subset of visual system neurons. Defects in this gene are the cause of non-syndromic sensorineural deafness autosomal dominant type 15. [provided by RefSeq, Mar 2009] (from NCBI)
Top mentioned proteins: HAIR, Math1, CAN, Brn-3A, FATE
Papers using Brn-3C antibodies
A GFP-based genetic screen reveals mutations that disrupt the architecture of the zebrafish retinotectal projection
Baier Herwig et al., In Frontiers in Neural Circuits, 2004
... Pou4f3:gfp transgenic line has been described ...
Papers on Brn-3C
Transcriptome profiling of induced hair cells (iHCs) generated by combined expression of Gfi1, Pou4f3 and Atoh1 during embryonic stem cell differentiation.
Henrique et al., Lisbon, Portugal. In Genom Data, Dec 2015
We found that combined activity of three transcription factors, Gfi1, Pou4f3, and Atoh1, can program ESC-derived progenitors towards HC fate with efficiencies of 55%-80%.
Fractalkine Signaling Regulates Macrophage Recruitment into the Cochlea and Promotes the Survival of Spiral Ganglion Neurons after Selective Hair Cell Lesion.
Warchol et al., Saint Louis, United States. In J Neurosci, Dec 2015
We used a novel transgenic mouse model in which the human diphtheria toxin receptor (huDTR) is selectively expressed under the control of Pou4f3, a hair cell-specific transcription factor.
Short Report - Clinical Genetics Genomic copy number alterations in non-syndromic hearing loss.
Mingroni-Netto et al., São Paulo, Brazil. In Clin Genet, Nov 2015
Rare copy number variants (CNVs) were detected in 12 probands; four of the detected CNVs comprised genes previously associated with hearing loss (POU4F3, EYA4, USH2A, BCAP31) and were considered causative, stressing the contribution of genomic imbalance to non-syndromic deafness.
Neurog1 can partially substitute for Atoh1 function in hair cell differentiation and maintenance during organ of Corti development.
Fritzsch et al., Iowa City, United States. In Development, Sep 2015
Replacement of Atoh1 with Neurog1 maintains limited expression of Pou4f3 and Barhl1 and rescues HCs quantitatively, but not qualitatively.
Generation of sensory hair cells by genetic programming with a combination of transcription factors.
Henrique et al., Lisbon, Portugal. In Development, Jul 2015
Here, we show that combined expression of the transcription factors Gfi1, Pou4f3 and Atoh1 can induce direct programming towards HC fate, both during in vitro mouse embryonic stem cell differentiation and following ectopic expression in chick embryonic otic epithelium.
Triage of Atypical Glandular Cell by SOX1 and POU4F3 Methylation: A Taiwanese Gynecologic Oncology Group (TGOG) Study.
Lai et al., Taipei, Taiwan. In Plos One, 2014
INTRODUCTION: Invasive procedures including loop electrosurgical excision, cervical conization, and endometrial sampling are often recommended when atypical glandular cells (AGC) are detected on Pap smear with unsatisfactory colposcopy.
Opportunities and limits of the one gene approach: the ability of Atoh1 to differentiate and maintain hair cells depends on the molecular context.
Fritzsch et al., Iowa City, United States. In Front Cell Neurosci, 2014
However, other gene mutations also result in loss of initially forming HCs, notably null mutants for Pou4f3, Barhl1, and Gfi1.
Triage of high-risk human papillomavirus-positive women by methylated POU4F3.
Lai et al., Taipei, Taiwan. In Clin Epigenetics, 2014
Five genes, POU4F3, HS3ST2, AJAP1, PAX1, and SOX1, were prioritized for the clinical performance to triage hrHPV-positive women.
Genetics of dizziness: cerebellar and vestibular disorders.
Lopez-Escamez et al., Almería, Spain. In Curr Opin Neurol, 2014
Moreover, new variants in genes such as COCH, MYO7A and POU4F3 are associated with nonsyndromic deafness and vestibular dysfunction.
Differential expression of Brn3 transcription factors in intrinsically photosensitive retinal ganglion cells in mouse.
Dhingra et al., India. In J Comp Neurol, 2012
neither Brn3a nor Brn3c are expressed in intrinsically photosensitive retinal ganglion cells
Caprin-1 is a target of the deafness gene Pou4f3 and is recruited to stress granules in cochlear hair cells in response to ototoxic damage.
Dawson et al., London, United Kingdom. In J Cell Sci, 2011
Stress-granule-associated protein Caprin-1 is downregulated by Pou4f3.
AP-2δ is a crucial transcriptional regulator of the posterior midbrain.
Moser et al., Bonn, Germany. In Plos One, 2010
Data show that Ap-2delta occupies and activates the Pou4f3 and Bhlhb4 promoters.
A novel frameshift mutation of POU4F3 gene associated with autosomal dominant non-syndromic hearing loss.
Kim et al., Taegu, South Korea. In Biochem Biophys Res Commun, 2010
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.
Stem cells and molecular strategies to restore hearing.
Fritzsch et al., Omaha, United States. In Panminerva Med, 2008
In either of these strategies, hair cell specific genes known to be essential for hair cell differentiation or maintenance such as ATOH1, POU4F3, GFI1, and miRNA-183 will be utilized with the hope of completely restoring hearing to all patients with hearing loss.
Molecular modelling insights into DFNA15 mediated enhancement of POU4F3 stability.
Lefebvre et al., Liège, Belgium. In Int J Comput Biol Drug Des, 2007
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.
Inner ear proteomics of mouse models for deafness, a discovery strategy.
Alagramam et al., Bar Harbor, United States. In Brain Res, 2006
Here, we discuss the potential utility of SSUMM to unravel the protein expression profiles of hair cells using the Pou4f3 mouse mutant as an example.
Mutant mice reveal the molecular and cellular basis for specific sensory connections to inner ear epithelia and primary nuclei of the brain.
Tessarollo et al., Omaha, United States. In Hear Res, 2005
We directly tested the significance of hair cells or sensory epithelia for fiber guidance in mutants that lose hair cells (Pou4f3) or do not form a posterior crista (Fgf10).
Mutation in transcription factor POU4F3 associated with inherited progressive hearing loss in humans.
Avraham et al., Tel Aviv-Yafo, Israel. In Science, 1998
The human homolog of mouse Pou4f3, a member of the POU-domain family of transcription factors whose targeted inactivation causes profound deafness in mice, was physically mapped to the 25-centimorgan DFNA15-linked region.
Requirement for Brn-3.0 in differentiation and survival of sensory and motor neurons.
Rosenfeld et al., San Diego, United States. In Nature, 1997
Members of one such family, the class IV POU domain transcription factor Brn-3.0, and two highly related factors Brn-3.1 and Brn-3.2, are differentially expressed in the developing and mature mammalian nervous system.
Role of transcription factors Brn-3.1 and Brn-3.2 in auditory and visual system development.
Rosenfeld et al., San Diego, United States. In Nature, 1996
The neurally expressed genes Brn-3.1 and Brn-3.2 (refs 1-6) are mammalian orthologues of the Caenorhabditis elegans unc-86 gene that constitute, with Brn-3.0 (refs 1-3,8,9), the class IV POU-domain transcription factors.
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