LHX6 antibody
- Known as:
- LHX6 (anti-)
- Catalog number:
- orb101798
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Biorbyt biorb
- Gene target:
- LHX6 antibody
Related genes to: LHX6 antibody
- Gene:
- LHX6 NIH gene
- Name:
- LIM homeobox 6
- Previous symbol:
- -
- Synonyms:
- LHX6.1
- Chromosome:
- 9q33.2
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-21
- Date modifiied:
- 2015-08-25
Related products to: LHX6 antibody
Related articles to: LHX6 antibody
- We applied transcriptome tomography to create a whole-brain model of early-stage Huntington's disease (HD) in R6/2 mice, which ubiquitously express truncated human mutant HTT containing approximately 150 CAG repeats. Medium spiny neuron (MSN)-related genes showed abnormal expression in the HD brain, in terms of expression similarity to wild-type Htt. Bdnf was the most probable upstream regulator of these genes. Smarca4, the Bdnf-regulator, was similarly expressed to wild-type Htt in the control brain; however, this was not observed in HD, implying a possible involvement of Smarca4 in glutamate excitotoxicity in HD. Lhx6, a master gene for MSN-related pathway development ordinarily conserved postnatally and in adulthood, was lost in the HD co-expression network. And a network hub node, Fcho1, was lost in connection involving Lhx6 and mitochondrial gene clusters. Loss of Smarca4, Lhx6, and Fcho1 in co-expression may contribute to spatiotemporally specific neuronal loss in HD. - Source: PubMed
Publication date: 2026/06/30
Okamura-Oho YukoShimokawa KazuroOota SatoshiYoshiki AtsushiMorita MasahikoNishimura MasaomiNakamura SakikoTsujimura YukiIshikawa ShumpeiYokota Hideo - Parkinson's disease (PD) is characterized by abnormal beta oscillations (13-30 Hz) within the basal ganglia, which contribute not only to motor symptoms but also to sleep disturbances. In this study, we developed a computational model of the basal ganglia-thalamocortical (BGTC) network that includes the pedunculopontine nucleus (PPN), to investigate the mechanism by which the abnormal oscillations disrupt sleep. The model incorporates key nuclei, neurotransmitter systems, and neural pathways to simulate sleep-related brain activity in Parkinsonian conditions. Our simulations show that abnormal beta oscillations impair sleep across all vigilance states. During wakefulness, elevated beta activity in the basal ganglia and cortex prolongs sleep latency. In rapid eye movement (REM) sleep, reduced firing in the pedunculopontine nucleus combined with enhanced beta oscillations underlies features of REM sleep behavior disorder (RBD). In Non-REM 2 (N2) sleep, the formation of sleep spindles is reduced and shifted toward higher frequencies, promoting sleep fragmentation. In Non-REM 3 (N3) sleep, slow-wave amplitude decreases, indicating reduced depth. Propagation analysis reveals that the neural pathways Lhx6-cortical inhibitory neurons (IN), PPN-thalamic reticular nucleus (RE), and globus pallidus internus (GPi)-thalamocortex (TC) can facilitate the propagation of beta oscillations to cortex, while the GPi-TC pathway suppresses it during wakefulness, REM, and N2 sleep. Additionally, the pathway Lhx6-cortical pyramidal neurons (PY) inhibits beta propagation during wakefulness but promotes it during other sleep stages. These findings identify specific pathways through which abnormal beta oscillations propagate and disrupt thalamocortical sleep rhythms, providing new insights into the mechanisms underlying sleep disturbances in Parkinson's disease and highlighting potential therapeutic targets. - Source: PubMed
Publication date: 2026/05/20
Wang HongbinAn ShunqiangLiu HanXu HuicongZhao QingZhang AiZhang ShuaiXu Guizhi - Sleep pressure is regulated not only by circadian rhythms, but also by sleep homeostasis, an activity-dependent process that dissipates during sleep. Recent work implicates -positive GABAergic neurons of the zona incerta (ZI) in regulating sleep pressure, but their precise role remains unclear. Using sleep deprivation and HiPlex single-molecule fISH, we show that -positive ZI neurons are broadly activated by both natural and induced increases in sleep pressure and remain active for more than 3 h into recovery sleep. Anterior -positive neurons showed stronger activation. induction differed across molecularly distinct subpopulations, with -positive cells showing robust responses and -positive cells showing reduced activation. We also identified distinct sleep pressure-responsive Lhx6-negative -positive GABAergic ZI subpopulations. Finally, intersectional genetic loss of reduced and redistributed -positive neurons, blunted their activation, and increased total sleep time. These findings reveal a central, heterogeneous role for -positive ZI neurons in sleep homeostasis. - Source: PubMed
Publication date: 2026/03/19
Chandler Parris WashingtonLee Sang SooDuncan Leighton HKim Dong WonWu MarkBlackshaw Seth - Mesial temporal lobe epilepsy (TLE) is the most common form of acquired epilepsy involving the hippocampus and is a frequent sequelae of head trauma. TLE is associated with refractory seizures and significant cognitive deficits. Yet, the gene expression patterns and cell types driving epileptogenesis and the associated cognitive deficits are poorly understood. To address this, we performed single nucleus RNA sequencing on hippocampal tissue from mice at 3 and 6 weeks following pilocarpine-induced status epilepticus, a robust model of TLE. At these early timepoints, epilepsy samples showed reductions in specific Cck and Lamp5-Lhx6 interneuron subclusters, alongside increases in Cajal-Retzius cells, dentate granule (DG) cell precursors, and a mature DG cell subcluster. Among glia, an astrocyte subcluster and a markedly expanded microglia sublcuster were increased. We term this microglia population epilepsy-associated microglia (EAM). The transcriptomic profile of EAM partially overlaps with microglia described in models of Alzheimer's disease and traumatic brain injury, with enrichment of genes including and . EAM display amoeboid morphology, can be found in dense clumps around pyramidal and granule cell body layers, and exhibit enlarged vesicles and mitochondria on electron microscopy. Cell-cell interaction analysis predict that DG cells are the main interaction partners of EAM. This dataset recapitulates known cellular alterations in TLE while defining their underlying transcriptomic programs, enabling mechanistic dissection of the key processes driving epileptogenesis. - Source: PubMed
Publication date: 2026/03/05
Ho VictoriaTjondropurnomo RuthNguyen JenniferBalkó EszterDepew SamanthaChen XingSingh RadhikaVan Veen J EdwardRácz BenceGolshani Peyman - Single-cell spatial transcriptomes have demonstrated molecular and cellular diversity in the brain, but gene regulatory mechanisms underlying transcriptomic profiles and disease pathogenesis remain largely unknown in primates. Here we performed single-nucleus Assay for Transposase-Accessible Chromatin followed by sequencing (snATAC-seq) for ~1.6 million cells from 142 cortical regions of two male cynomolgus monkeys (Macaca fascicularis), and identified distinct chromatin accessibility profiles of cis-regulatory elements (CREs) for various cell types. By integrative analysis with large-scale spatial transcriptome data, we found that these CREs showed laminar and regional preferences, with their regional accessibility exhibiting striking dependence on the region's hierarchical level. Cross-species comparison of snATAC-seq data revealed human/macaque-enriched layer-4 glutamatergic neurons and LAMP5/LHX6-expressing GABAergic neurons as well as human/macaque-biased CREs for genes related to neurodevelopment and psychiatric diseases. Importantly, risk single-nucleotide polymorphisms for many brain disorders strongly associated with human/macaque-biased CREs in glutamatergic neuronal types and those for Alzheimer's disease strongly associated with CREs exclusively in microglia. Our results provided the basis for understanding the spatial gene regulatory mechanisms underlying cellular diversity and disease pathogenesis in the primate cortex. - Source: PubMed
Publication date: 2026/03/17
Meng JuanChen ChengZhu ZhiyongSun YongkangHuang YimingHu KaijieFu JiqiangWu LuyanLi LingBai YiqinFei TianyiLiu ZhenLi ChaoShen ZhimingLiu LongqiLi ChengyuSong TaoLiu CirongPoo MumingLiu ShipingLei YingSun Yidi