| http://purl.uniprot.org/citations/15492043 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15492043 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15492043 | http://www.w3.org/2000/01/rdf-schema#comment | "The Pit1-Oct1-Unc86 domain (POU domain) transcription factor Brn3a controls sensory neuron survival by regulating the expression of Trk receptors and members of the Bcl-2 family. Loss of Brn3a leads to a dramatic increase in apoptosis and severe loss of neurons in sensory ganglia. Although recent evidence suggests that Brn3a-mediated transcription can be modified by additional cofactors, the exact mechanisms are not known. Here, we report that homeodomain interacting protein kinase 2 (HIPK2) is a pro-apoptotic transcriptional cofactor that suppresses Brn3a-mediated gene expression. HIPK2 interacts with Brn3a, promotes Brn3a binding to DNA, but suppresses Brn3a-dependent transcription of brn3a, trkA, and bcl-xL. Overexpression of HIPK2 induces apoptosis in cultured sensory neurons. Conversely, targeted deletion of HIPK2 leads to increased expression of Brn3a, TrkA, and Bcl-xL, reduced apoptosis and increases in neuron numbers in the trigeminal ganglion. Together, these data indicate that HIPK2, through regulation of Brn3a-dependent gene expression, is a critical component in the transcriptional machinery that controls sensory neuron survival."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.org/dc/terms/identifier | "doi:10.1083/jcb.200406131"xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.org/dc/terms/identifier | "doi:10.1083/jcb.200406131"xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Wei G."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Wei G."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Wong C."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Wong C."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Neve R.L."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Neve R.L."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Huang E.J."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Huang E.J."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Reichardt L.F."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Reichardt L.F."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Doxakis E."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Doxakis E."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Luo E.J."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Luo E.J."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Tang A.A."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Tang A.A."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Wiggins A.K."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Wiggins A.K."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Zang K."xsd:string |
| http://purl.uniprot.org/citations/15492043 | http://purl.uniprot.org/core/author | "Zang K."xsd:string |