Ask about this productRelated genes to: CUX2 antibody
- Gene:
- CUX2 NIH gene
- Name:
- cut like homeobox 2
- Previous symbol:
- CUTL2
- Synonyms:
- KIAA0293, CDP2
- Chromosome:
- 12q24.11-q24.12
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-08
- Date modifiied:
- 2018-02-13
Related products to: CUX2 antibody
Related articles to: CUX2 antibody
- This study integrates single-cell and bulk RNA-seq to investigate cell type-specific alterations in fatty acid metabolism-related genes in the dorsolateral prefrontal cortex (DLPFC) of schizophrenia (SCZ) patients and to evaluate their potential as diagnostic biomarkers. - Source: PubMed
Publication date: 2026/04/21
Zhao CuiZhang LiangYang PingLi LiangZeng WeiqiXie Weiqi - Prefrontal neurons exhibit diverse activity during cognitive functions such as working memory, attention, and timing; however, the importance of this heterogeneity is unclear. Our goal was to better understand the diversity of prefrontal activity through anatomical connectivity. We harnessed circuit-specific tools in mice to capture activity within prefrontal projections during interval timing, a highly translational cognitive process that requires working memory for temporal rules and attention to the passage of time to estimate a temporal interval of several seconds. We used neuronal recordings to capture prefrontal activity during interval timing, with major patterns characterized by monotonic time-dependent ramping over a temporal interval. We then leveraged retrograde viruses to interrogate prefrontal cortex (PFC) projections to the mediodorsal thalamus (PFC-MD) and the dorsomedial striatum (PFC-DMS). We report three main findings. First, circuit-specific fiber photometry revealed that PFC-MD and PFC-DMS activity encoded distinct temporal signals, with PFC-MD projections ramping down and PFC-DMS ramping up to interval timing response times. Second, circuit-specific inactivation revealed that suppressing PFC-DMS projections disrupted animals' internal estimates of time. Third, circuit-specific single-nucleus RNA sequencing of projection-defined prefrontal neurons revealed distinct transcriptomic profiles of PFC-MD and PFC-DMS projections, with enrichment of cortical layer-associated genes as well as genes such as and . These data suggest that differences in gene expression and connectivity distinguish prefrontal activity during interval timing. These findings advance our fundamental understanding of prefrontal function and dysfunction in human disease. - Source: PubMed
Publication date: 2026/05/06
Ding XinWeber Matthew AButler Trevor CBova Alexandra SGuerrero Stephanie GHunter Christopher MCole Rachel CStutt Hannah RMcMurrin Madison SSpicer Mackenzie MConlon Mackenzie MHeiney Shane AKim YoungchoResch Jon MNarayanan Nandakumar S - Most neurodevelopmental disorders (NDDs), including intellectual disability, epilepsy, and autism spectrum disorder (ASD), exhibit marked sex differences in risk, incidence, prognosis, and clinical presentation. Increasing evidence suggests that these disorders often originate from alterations in circuit formation that occur during critical developmental windows preceding the onset of symptoms. However, the extent to which sexual dimorphism emerges during neuronal differentiation remains largely underexplored in the context of NDD research. In the cerebral cortex, layer (L) 2/3 excitatory pyramidal neurons, which integrate information across cortical areas and hemispheres, have been broadly implicated in NDDs. In this study, we investigate the transcriptional expression dynamics of L2/3 neurons across three developmental stages-embryonic day (E) 19, postnatal day (P) 4, and P7-and identify a window of transient, sex-biased gene expression at P4, possibly related to the process of brain masculinization. Furthermore, gene expression analysis following knockout (KO) mutations of Cux1 and Cux2 in L2/3 neurons reveals sex-biased dysregulation, with male neurons exhibiting heightened susceptibility and amplified transcriptional disruption, resulting in a molecular fingerprint that is distinct from their WT counterparts. These findings underscore the need to incorporate studies of sex-dependent differentiation trajectories as a biological variable in NDD research and may inform the development of more targeted, sex-specific therapeutic strategies. - Source: PubMed
Publication date: 2026/04/08
Marcos-Grañeda EliaMartín-Fernández FernandoWeiss Linnea AOliveros Juan CNieto Marta - During mammalian evolution, excitatory neurons in upper cortical layer 2 and layer 3 (L2/3) have shown a disproportionate expansion compared with other layers. Replicative expansion of cortical neural progenitors is associated with considerable oxidative DNA damage. Here we show that activating transcription factor 4 (ATF4) has roles as a critical regulator of the DNA damage response, directly activating components of double-stranded DNA repair, including CIRBP, UBA52 and EBF1. Notably, pan-cortical knockout (Emx1-Cre;Atf4) demonstrates that ATF4 is required specifically for the development of upper layer 2/3 neurons, marked by the expression of cut-like homeobox 2 protein, CUX2. ATF4 functions to repair DNA damage and attenuate cell death of embryonic radial glial progenitors in a p53-dependent manner. In particular, we show that cold inducible RNA-binding protein (CIRBP) is a transcriptional target of ATF4 that is required for normal phosphorylation of the key double-strand DNA repair factor ataxia telangiectasia mutated (ATM). These findings establish that ATF4 is an essential regulator of the DNA damage response. They further indicate that there are extraordinary requirements for DNA repair after replicative stress in CUX2 neurons during mammalian brain development. - Source: PubMed
Publication date: 2026/04/01
Xia WenlongMorcom LauraXu ZhaoyangLu I-LingWang QingHoi Kimberly KWei MingmingZhu KeyingJordan GregoryTang Xiao-YanGonzalez-Maya JulioMattera Vanesa SPanigrahi Sophia MKawaguchi RikiEmery BenFranco Santos JGeschwind Daniel HPopko BrianRowitch David HFancy Stephen P J - Neurodegeneration shows regional and cell-type-specific patterns in ageing and disease, but the underlying mechanisms for cell-type-specific neuronal losses remain poorly understood. Previous studies have shown that upper cortical layer thinning occurs in progressive human multiple sclerosis (MS) and that cortical layer 2 and layer 3 (L2/3) excitatory neurons (L2/3ENs) that express CUT-like homeobox 2 (CUX2) are selectively vulnerable to degeneration. Here we report that L2/3ENs within MS cortical lesions have an elevated DNA damage burden. DNA damage and selective loss of L2/3ENs were recapitulated in diverse mouse models of demyelination and pan-cortical inflammation, confirming their intrinsic vulnerability. Functions of Cux2 and activating transcription factor 4 (Atf4) were essential for resilience of L2/3ENs during postnatal neuroinflammation, acting in neurons to enhance DNA double-strand break repair. Interferon-γ, a cytokine implicated in MS pathogenesis, was sufficient to elevate levels of reactive oxygen species, leading to DNA damage-mediated neuronal death in vitro, and caused selective depletion of L2/3 neurons in mice. These findings indicate that DNA damage burden and inadequate repair in CUX2 L2/3ENs contributes to selective vulnerability in neuroinflammatory injury. - Source: PubMed
Publication date: 2026/04/01
Morcom LauraXia WenlongXu ZhaoyangAwasthi YashikaGeywitz CelineEllis Matthew ONoli TomasZulji AmelYamamoto DanielGirdler Gemma CKai LiZhu KeyingWei MingmingTang Xiao-YanHoi Kimberly KGonzalez-Maya JulioDuncan Greg JVaquie Adrien MGold Diaz DianaKawaguchi RikiLiu ErdongSun YuYang DennyJordan Gregory DLu I-LingHolmqvist StaffanBartels TheresaRidley KatherineChoi Jennifer Ja-YoonFranco Santos JHuang Eric JEmery BenGeschwind DanielSchirmer LucasBalmus GabrielPopko BrianFancy Stephen P JRowitch David H