Ask about this productRelated genes to: EMX1 antibody
- Gene:
- EMX1 NIH gene
- Name:
- empty spiracles homeobox 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 2p13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1994-02-08
- Date modifiied:
- 2015-08-25
Related products to: EMX1 antibody
Related articles to: EMX1 antibody
- Axon growth is an essential cellular process during neural development, and its dysregulation contributes to numerous neurodevelopmental disorders. During axon growth, extracellular signals direct neurons to extend projections that connect with their synaptic targets. Paxillin is a key member of adhesion sites that control motility by linking the intracellular actin cytoskeleton to the extracellular matrix. Paxillin also binds to the cytoskeletal protein, tubulin. However, little is known about the role of adhesion proteins in neurons. Here, we use conditional paxillin knockout mice to investigate how the loss of paxillin in pyramidal cortical neurons affects developing neuron morphology. Surprisingly, loss of paxillin in pyramidal cortical neurons caused no change in axon length or soma area between control ( ) and conditional paxillin knockout ( ) mice at basal conditions. Following brain-derived neurotrophic factor stimulation, the loss of paxillin resulted in no change in soma area or axonal β-tubulin levels, but did result in a significant increase in axon length, as compared to control. Finally, the corpus callosum size was not significantly different between and animals. In summary, these data suggest that paxillin is not required for axonal growth during neural development. - Source: PubMed
Publication date: 2026/05/21
Rygel KatelynGillespie KaseyWelshhans Kristy - Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by social communication deficits, restricted interests, and repetitive behaviors. Emerging evidence links several autism susceptibility genes to the nonsense-mediated decay (NMD) pathway, which maintains the homeostasis of gene transcription and protein translation in the nervous system. However, the role of Suppressor with morphogenetic effect on genitalia 7 (Smg7), an essential NMD factor, in brain function and ASD remains largely unknown. Here, we generated an Emx1-Cre-mediated conditional Smg7 knockout (Smg7cko) mouse model to investigate its neurological consequences. We found that both male and female Smg7cko mice exhibited autism-like behaviors, including impaired social interaction and communication, repetitive behaviors, anxiety-like traits, and learning and memory deficits. These phenotypes were accompanied by neuronal hyperexcitability and increased dendritic spine density in layer II/III pyramidal neurons of the hippocampus and the medial prefrontal cortex (mPFC). Notably, Smg7 deletion led to pronounced upregulation of Protein Kinase D1 (PKD1) transcripts, an NMD target, in these brain regions. Strikingly, adeno-associated virus (AAV)-mediated PKD1 knockdown (AAVsh-PKD1) in the hippocampus and mPFC significantly rescued social deficits in Smg7-deficient mice. Together, these findings identify Smg7 as a key regulator of neuronal function and behavior, and reveal PKD1 upregulation as a pathogenic mechanism underlying ASD-like phenotypes, providing new insight into NMD deficiency in ASD pathophysiology and a potential therapeutic target. - Source: PubMed
Publication date: 2026/06/06
Pang YayanHao AiweiHan HuiliYuan HaoChen ChengyanXue MengtongWang LuDai ChunfangWu BinLi TangliangTian XinDong Zhifang - Postnatal cortical myelination requires epigenetic activation of oligodendrocyte gene programs, but the role of histone demethylases remains unclear. - Source: PubMed
Publication date: 2026/05/19
Lambries RuthShen ZihanMias George IHe Jin - Modulation of neural activity is a promising strategy to influence the growth of axons and improve behavioral recovery after damage to the central nervous system. The benefits of neuromodulation likely depend on optimization across multiple input parameters. Here we used a chemogenetic approach to achieve continuous, long-term elevation of neural activity in murine corticospinal tract (CST) neurons. To specifically target CST neurons, AAV2-retro-DIO-hM3Dq-mCherry or matched mCherry control was injected to the cervical spinal cord of adult Emx1-Cre transgenic mice. Pilot studies verified efficient transgene expression in CST neurons and effective elevation of neural activity as assessed by cFos immunohistochemistry. In subsequent experiments mice were administered either DIO-hM3Dq-mCherry or control DIO-mCherry, were pre-trained on a pellet retrieval task, and then received unilateral pyramidotomy injury to selectively ablate the right CST. Mice then received continual clozapine via drinking water and weekly testing on the pellet retrieval task, followed by cortical injection of a viral tracer to assess cross-midline sprouting by the spared CST. After sacrifice at eight weeks post-injury immunohistochemistry for cFos verified elevated CST activity in hM3Dq-treated animals and immunohistochemistry for PKC-gamma verified unilateral ablation of the CST in all animals. Despite the chronic elevation of CST activity, however, both groups showed similar levels of cross-midline CST sprouting and similar success in the pellet retrieval task. These data indicate that continuous, long-term elevation of activity that is targeted specifically to CST neurons does not affect compensatory sprouting or directed forelimb movements. - Source: PubMed
Publication date: 2026/05/06
Wang ZimeiBrannigan MatthewFriedrich LoganBlackmore Murray G - Neural progenitor cell (NPC) proliferation is fundamental for population expansion and brain development. G phase control determines the cell cycle duration of NPCs and thereby affects their proliferation efficiency. However, the molecular mechanisms governing G phase progression in NPCs remain unclear. Here, we show that AKT gain-of-function mutations and pharmacological inhibition exert opposing effects on NPC proliferation. Consistently, Emx1-Cre-mediated deletion of Akt1/2/3 in mice impairs NPC proliferation and disrupts cortical development. We find that AKT deficiency induces G phase arrest and prolongs the cell cycle of NPCs. Mechanistically, we demonstrate that AKT-mediated phosphorylation inhibits the activity of CRL4 E3 ubiquitin ligase to safeguard cyclin D2 (CCND2) stability. Specifically, AKT phosphorylates DDB1, the adaptor of CRL4, which disrupts its interaction with CCND2 and reduces its degradation. These findings reveal a post-translational mechanism impacting NPC cell cycle and cortical morphogenesis, providing insight into the etiology of malformations of cortical development. - Source: PubMed
Publication date: 2026/04/27
Wang HeLiu PanmiaoWang RunminGu HanwenZhu TingtingChen GuiquanYang Jian-Jun