Mouse,Mus musculus,Oculorhombin,Paired box protein Pax-6,Pax6,Pax-6,Sey
- Known as:
- Mouse,Mus musculus,Oculorhombin,Paired box protein Pax-6,Pax6,Pax-6,Sey
- Catalog number:
- EIAAB29973
- Category:
- -
- Supplier:
- EIAab
- Gene target:
- Mouse Mus musculus Oculorhombin Paired box protein Pax-6 Pax6 Sey
Ask about this productRelated genes to: Mouse,Mus musculus,Oculorhombin,Paired box protein Pax-6,Pax6,Pax-6,Sey
- Gene:
- PAX6 NIH gene
- Name:
- paired box 6
- Previous symbol:
- AN2
- Synonyms:
- D11S812E, AN, WAGR
- Chromosome:
- 11p13
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: Mouse,Mus musculus,Oculorhombin,Paired box protein Pax-6,Pax6,Pax-6,Sey
Related articles to: Mouse,Mus musculus,Oculorhombin,Paired box protein Pax-6,Pax6,Pax-6,Sey
- To investigate the molecular diagnosis of a three-generation Chinese family affected with aniridia, and further to identify clinically a missense mutation in members with atypical aniridia. - Source: PubMed
Publication date: 2024/03/18
Lin Zhi-BoFeng Chun-YunLi JinPan An-PengSun Hai-SenYu A-YongChen Shi-Hao - Chaetognaths are a clade of marine worm-like invertebrates with a heavily debated phylogenetic position. Their nervous system superficially resembles the protostome type, however, knowledge regarding the molecular processes involved in neurogenesis is lacking. To better understand these processes, we examined the expression profiles of marker genes involved in bilaterian neurogenesis during post-embryonic stages of Spadella cephaloptera. We also investigated whether the transcription factor encoding genes involved in neural patterning are regionally expressed in a staggered fashion along the mediolateral axis of the nerve cord as it has been previously demonstrated in selected vertebrate, insect, and annelid models. - Source: PubMed
Publication date: 2024/05/08
Ordoñez June FWollesen Tim - During development, neural stem cells in the cerebral cortex, also known as radial glial cells (RGCs), generate excitatory neurons, followed by production of cortical macroglia and inhibitory neurons that migrate to the olfactory bulb (OB). Understanding the mechanisms for this lineage switch is fundamental for unraveling how proper numbers of diverse neuronal and glial cell types are controlled. We and others recently showed that Sonic Hedgehog (Shh) signaling promotes the cortical RGC lineage switch to generate cortical oligodendrocytes and OB interneurons. During this process, cortical RGCs generate intermediate progenitor cells that express critical gliogenesis genes , and . The increased expression and appearance of Egfr and Olig2 cortical progenitors are concurrent with the switch from excitatory neurogenesis to gliogenesis and OB interneuron neurogenesis in the cortex. While Shh signaling promotes expression in the developing spinal cord, the exact mechanism for this transcriptional regulation is not known. Furthermore, the transcriptional regulation of and has not been explored. Here, we show that in cortical progenitor cells, multiple regulatory programs, including Pax6 and Gli3, prevent precocious expression of , a gene essential for production of cortical oligodendrocytes and astrocytes. We identify multiple enhancers that control expression in cortical progenitors and show that the mechanisms for regulating expression are conserved between the mouse and human. Our study reveals evolutionarily conserved regulatory logic controlling the lineage switch of cortical neural stem cells. - Source: PubMed
Publication date: 2024/05/07
Liang Xiaoyi GHoang KendyMeyerink Brandon LKc PratikshaParaiso KittWang LiJones Ian RZhang YueKatzman SolFinn Thomas STsyporin JeremiahQu FangyuanChen ZhaoxuVisel AxelKriegstein ArnoldShen YinPilaz Louis-JanChen Bin - Mutations in human nonsense-mediated mRNA decay (NMD) factors are enriched in neurodevelopmental disorders. We show that deletion of key NMD factor Upf2 in mouse embryonic neural progenitor cells causes perinatal microcephaly but deletion in immature neurons does not, indicating NMD's critical roles in progenitors. Upf2 knockout (KO) prolongs the cell cycle of radial glia progenitor cells, promotes their transition into intermediate progenitors, and leads to reduced upper-layer neurons. CRISPRi screening identified Trp53 knockdown rescuing Upf2KO progenitors without globally reversing NMD inhibition, implying marginal contributions of most NMD targets to the cell cycle defect. Integrated functional genomics shows that NMD degrades selective TRP53 downstream targets, including Cdkn1a, which, without NMD suppression, slow the cell cycle. Trp53KO restores the progenitor cell pool and rescues the microcephaly of Upf2KO mice. Therefore, one physiological role of NMD in the developing brain is to degrade selective TRP53 targets to control progenitor cell cycle and brain size. - Source: PubMed
Publication date: 2024/04/22
Lin LinZhao JingrongKubota NaotoLi ZhelinLam Yi-LiNguyen Lauren PYang LuPokharel Sheela PBlue Steven MYee Brian AChen ReneeYeo Gene WChen Chun-WeiChen LiangZheng Sika - Stem cells are undifferentiated cells that possess the potential for self-renewal with the capacity to differentiate into multiple lineages. In humans, their limited numbers pose a challenge in fulfilling the necessary demands for the regeneration and repair of damaged tissues or organs. Studies suggested that mesenchymal stem cells (MSCs), necessary for repair and regeneration via transplantation, require doses ranging from 10 to 400 million cells. Furthermore, the limited expansion of MSCs restricts their therapeutic application. - Source: PubMed
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