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POU class 3 homeobox 2

Brn-2, POU3F2, Brain-2
This gene encodes a member of the POU-III class of neural transcription factors. The encoded protein is involved in neuronal differentiation and enhances the activation of corticotropin-releasing hormone regulated genes. Overexpression of this protein is associated with an increase in the proliferation of melanoma cells. [provided by RefSeq, Mar 2012] (from NCBI)
Top mentioned proteins: CAN, Sox2, OCT, Brn-1, Microphthalmia-Associated Transcription Factor
Papers on Brn-2
Deterministic transfection drives efficient nonviral reprogramming and uncovers reprogramming barriers.
Lee et al., Durham, United States. In Nanomedicine, Jan 2016
The superior capabilities of our technology are demonstrated by modification of the well-established direct neuronal reprogramming paradigm using overexpression of the transcription factors Brn2, Ascl1, and Myt1l (BAM).
Direct Conversion of Equine Adipose-Derived Stem Cells into Induced Neuronal Cells Is Enhanced in Three-Dimensional Culture.
Strappe et al., Wagga Wagga, Australia. In Cell Reprogram, Dec 2015
In this study, we demonstrate the generation of induced neuronal cells from equine adipose-derived stem cells (EADSCs) using a combination of lentiviral vector expression of the neuronal transcription factors Brn2, Ascl1, Myt1l (BAM) and NeuroD1 and a defined chemical induction medium, with βIII-tubulin-positive induced neuronal cells displaying a distinct neuronal morphology of rounded and compact cell bodies, extensive neurite outgrowth, and branching of processes.
Modeling Neurological Disease by Rapid Conversion of Human Urine Cells into Functional Neurons.
Wu et al., Shanghai, China. In Stem Cells Int, Dec 2015
In the current study, we provide a noninvasive approach to obtain directly reprogrammed functional neurons by overexpression of the transcription factors Ascl1, Brn2, NeuroD, c-Myc, and Myt1l in human urine cells.
Irradiation of primary human gliomas triggers dynamic and aggressive survival responses involving microvesicle signaling.
Limoli et al., Irvine, United States. In Environ Mol Mutagen, Dec 2015
Radiation-induced changes were exacerbated under chronic as compared to acute irradiation paradigms and promoted cellular reprogramming through enhanced expression of key transcription factors and regulators involved in differentiation and pluripotency (SOX2, POU3F2, SALL2, OLIG2, NANOG, POU5F1v1, MSI1).
FGF8 is Essential for Functionality of Induced Neural Precursor Cell-derived Dopaminergic Neurons.
Park et al., Seoul, South Korea. In Int J Stem Cells, Nov 2015
In the present study, we demonstrate that iNPCs can be generated by transducing Brn2, Ascl1, Myt1L and Bcl-xL in a culture supplemented with several mitogens and subsequently can be differentiated to dopaminergic neurons (DA).
Reconstructing and reprogramming the tumor-propagating potential of glioblastoma stem-like cells.
Bernstein et al., United States. In Cell, 2014
Here, we identify a core set of neurodevelopmental TFs (POU3F2, SOX2, SALL2, and OLIG2) essential for GBM propagation.
Hierarchical mechanisms for direct reprogramming of fibroblasts to neurons.
Wernig et al., Stanford, United States. In Cell, 2013
Here, we reveal a hierarchical mechanism in the direct conversion of fibroblasts into induced neuronal (iN) cells mediated by the transcription factors Ascl1, Brn2, and Myt1l.
MITF and PAX3 Play Distinct Roles in Melanoma Cell Migration; Outline of a "Genetic Switch" Theory Involving MITF and PAX3 in Proliferative and Invasive Phenotypes of Melanoma.
Baguley et al., Dunedin, New Zealand. In Front Oncol, 2012
However, recently the paired box transcription factor PAX3 was shown to transcriptionally activate POU3F2/BRN2, leading to direct repression of MITF expression.
Phosphorylation of BRN2 modulates its interaction with the Pax3 promoter to control melanocyte migration and proliferation.
Larue et al., Orsay, France. In Mol Cell Biol, 2012
Melanocyte migration and proliferation are controlled both through the regulation of Pax3 by nonphosphorylated Brn2 and through the regulation of MITF-M by the overall BRN2 level.
Induction of human neuronal cells by defined transcription factors.
Wernig et al., Stanford, United States. In Nature, 2011
We recently observed that forced expression of a combination of three transcription factors, Brn2 (also known as Pou3f2), Ascl1 and Myt1l, can efficiently convert mouse fibroblasts into functional induced neuronal (iN) cells.
Direct reprogramming of adult human fibroblasts to functional neurons under defined conditions.
Ding et al., Los Angeles, United States. In Cell Stem Cell, 2011
Here we show that a combination of a microRNA (miR-124) and two transcription factors (MYT1L and BRN2) is sufficient to directly reprogram postnatal and adult human primary dermal fibroblasts (mesoderm) to functional neurons (ectoderm) under precisely defined conditions.
Inverse expression states of the BRN2 and MITF transcription factors in melanoma spheres and tumour xenografts regulate the NOTCH pathway.
Sturm et al., Brisbane, Australia. In Oncogene, 2011
links BRN2 as an activator and MITF as a repressor of the NOTCH pathway in melanoma cells. Loss of the BRN2-MITF axis in antisense-ablated cell lines decreased the melanoma sphere-forming capability and cell adhesion
Melanoma cell invasiveness is regulated by miR-211 suppression of the BRN2 transcription factor.
Hayward et al., Brisbane, Australia. In Pigment Cell Melanoma Res, 2011
a model for the apparent non-overlapping expression levels of BRN2 and MITF in melanoma, mediated by miR-211 expression.
Hard times for oncogenic BRAF-expressing melanoma cells.
Houslay, Glasgow, United Kingdom. In Cancer Cell, 2011
describe that the oncogenic BRAF Val600Glu mutant, which occurs in about half of melanomas, downregulates the cGMP-hydrolysing phosphodiesterase PDE5A in melanoma cells through the ERK-MAPK cascade coupled to the POU-domain transcription factor BRN2, thereby increasing intracellular cGMP levels and promoting invasiveness.
Mutant huntingtin fragment selectively suppresses Brn-2 POU domain transcription factor to mediate hypothalamic cell dysfunction.
Nukina et al., Saitama, Japan. In Hum Mol Genet, 2010
In the brains of Huntington's disease model mice, Brn-2 loses its function through two pathways, its sequestration by mutant huntingtin and its reduced transcription, leading to reduced expression of hypothalamic neuropeptides.
Genome-wide analysis of POU3F2/BRN2 promoter occupancy in human melanoma cells reveals Kitl as a novel regulated target gene.
Davidson et al., Illkirch-Graffenstaden, France. In Pigment Cell Melanoma Res, 2010
POU3F2 may regulate the properties of melanoma cells via autocrine KIT ligand signalling.
POU domain transcription factors: BRN2 as a regulator of melanocytic growth and tumourigenesis.
Sturm et al., Brisbane, Australia. In Pigment Cell Melanoma Res, 2008
Here, we focus on the role of the BRN2 (POU3F2/N-Oct-3) transcription factor in the melanocytic lineage where it may co-ordinate normal developmental cues that can be re-activated in melanoma.
The WNT/Beta-catenin pathway in melanoma.
Delmas et al., Orsay, France. In Front Biosci, 2005
Beta-catenin can induce ubiquitous genes such as myc or cyclinD1, cell lineage-restricted genes such as Brn2 and melanocyte-specific genes such as Mitf-M and Dct.
Fibroblast growth factor homologous factors: evolution, structure, and function.
Goldfarb, New York City, United States. In Cytokine Growth Factor Rev, 2005
Whereas FGFs function through binding to the extracellular domains of FGF receptors (FGFRs), FHFs bind to intracellular domains of voltage-gated sodium channels (VGSCs) and to a neuronal MAP kinase scaffold protein, islet-brain-2 (IB2).
Interplay of Pax6 and SOX2 in lens development as a paradigm of genetic switch mechanisms for cell differentiation.
Kamachi et al., Suita, Japan. In Int J Dev Biol, 2003
More broadly, SOX1/2/3 interact with various partner transcription factors, and participate in defining distinct cell states that depend on the partner factors: Pax6 for lens differentiation, Oct3/4 for establishing the epiblast/ES cell state, and Brn2 for the neural primordia.
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