Ask about this productRelated genes to: Onecut1 Blocking Peptide
- Gene:
- ONECUT1 NIH gene
- Name:
- one cut homeobox 1
- Previous symbol:
- HNF6, HNF6A
- Synonyms:
- HNF-6
- Chromosome:
- 15q21.3
- Locus Type:
- gene with protein product
- Date approved:
- 2000-02-11
- Date modifiied:
- 2015-08-25
Related products to: Onecut1 Blocking Peptide
Related articles to: Onecut1 Blocking Peptide
- The CCR4-NOT complex is a central regulator of post-transcriptional gene expression that controls mRNA deadenylation and decay. Although the catalytic subunits have been well characterized, the physiological roles of several non-catalytic subunits including CNOT11 in mammalian tissues remain incompletely understood. Here, we investigate the physiological role of CNOT11 using genetic mouse models. No homozygous global Cnot11 knockout mice are obtained from heterozygous intercrosses, indicating that CNOT11 is required for early development. We generate hepatocyte-specific Cnot11 knockout mice (Cnot11-LKO) and find that Cnot11-LKO mice exhibit growth retardation and alterations in serum biochemical parameters during early postnatal stages, which are largely resolved by adulthood. Histological analysis does not reveal overt liver injury, while morphological differences in hepatocytes are observed. A marked increase in Ki67-positive cells was observed in the liver of Cnot11-LKO mice relative to control mice. Most Ki67-positive cells express HNF4A, suggesting that hepatocyte maturation is still in progress in the absence of CNOT11. Transcriptomic analyses of early postnatal livers reveal increased expression of cell cycle-related genes and reduced expression of metabolic genes, further supporting delayed liver maturation. These findings suggest that CNOT11 contributes to proper postnatal liver maturation and is required for the timely establishment of metabolically mature hepatocyte functions. - Source: PubMed
Nishijima SaoriSuzuki ToruAbe TakayaBando KanaYamamoto Tadashi - Strabismus, or misalignment of the eyes, is a heritable disorder frequently associated with vision loss and decreased quality of life. Incomitant strabismus, where the degree of misalignment differs based on gaze angle, can arise from mutations in genes that regulate the development of extraocular motor neurons. To date, few such genes have been identified. The extraocular motor system is highly conserved across vertebrates, suggesting a comparative transcriptomic discovery approach would be fruitful. Using bulk and single-cell sequencing in a small accessible vertebrate, the larval zebrafish, we identified genes expressed in subpopulations of extraocular motor neurons in cranial nuclei nIII/nIV. We next assessed extraocular motor neuron number and vestibulo-ocular reflex performance after CRISPR/Cas9-mediated mutagenesis of three genes with suggestive expression patterns: , , , and one known to disrupt nIII/nIV motor neuron specification: . Loss of impaired the vestibulo-ocular reflex without change to nIII/nIV motor neuron number. Our data suggest that constitutive disruptions to can impair nIII/nIV-dependent eye movements. More broadly, our work illuminates considerable transcriptomic diversity among extraocular motor neuron subpopulations, and establishes a pipeline to identify genes relevant to ocular motor disease etiology. - Source: PubMed
Publication date: 2026/04/08
Gershowitz EmilyHamling Kyla RoseRosti BaşakGelnaw HannahXiang GraceQuainoo CherylGoldblatt DenaLeary PaigeSchoppik David - Hepatoblastoma is the most common malignant liver tumor in children. Our previous work showed that enforced expression of the transcription factor One Cut Homeobox 1 (ONECUT1) suppresses the initiation of hepatoblastoma. However, it remains unclear whether increasing ONECUT1 expression can also inhibit tumor progression after tumors have already formed. The purpose of this study was to determine the effects of ONECUT1 induction on tumor cell behavior and tumor growth during established hepatoblastoma progression. - Source: PubMed
Publication date: 2026/04/05
Qiao YuXu MengWu YanhuiCui GuofeiDeng ShanshanBai LiangliangSong XiaoshuangZhong JianBian WeijieYu GangEvert MatthiasWang XueCalvisi Diego FChen XinLi LinLiao Weiting - Many vertebrates, including fish, amphibians, and reptiles, dynamically adjust their body color to the perceived brightness of the ambient background. This response takes tens of minutes and involves the aggregation or dispersion of pigment granules within the melanophores of the skin, resulting in the pale or dark appearance of the animal, respectively. In teleosts, ambient light detection depends on the retina, which transmits the signal to the hypothalamus, leading to the secretion of peptide hormones via the pituitary gland into the bloodstream. Melanin-concentrating hormone (MCH) is released upon light stimulation, resulting in the blanching of the skin. Alpha-melanocyte-stimulating hormone (α-MSH, encoded by the pomca gene and produced in the hypothalamus and pituitary) has the opposite effect: light inhibits its secretion, leading to melanin dispersion in the skin. Because "dark appearance" is an easy-to-score phenotype in larval zebrafish, defective visual background adaptation (VBA) has been used in genetic screens as a proxy for retinal defects, but the responsible neuroendocrine circuit remained elusive. Here, we identified the molecular and cellular components underlying this response. We found that intrinsically photosensitive retinal ganglion cells (ipRGCs), expressing the homeobox transcription factor Onecut1, project to the neuropil region of the preoptic area, where their axons overlap with the dendrites of pmchl-expressing hypothalamic neurons. Signals from these ipRGCs increase the transcription of pmchl, one of two genes encoding MCH isoforms, and repress pomca. Ablation of either onecut1-positive ipRGCs or pmchl-expressing hypothalamic neurons prevents the fish larva from adapting to a bright background. - Source: PubMed
Publication date: 2025/11/05
Slanchev KrasimirLaurell EvaArnold-Ammer IreneKuehn EnricoPandiarajan UyyashrinilaBaier Herwig - PD-1/PD-L1, a classic immune checkpoint commonly employed in targeted therapy, has proven to yield only limited benefits for patients with lung squamous cell carcinoma (LUSC). Unraveling the intrinsic mechanisms underlying the progression of LUSC serves as the foundation for discovering more effective treatment strategies. - Source: PubMed
Publication date: 2025/08/15
Huang XiaoyanYan JingweiPeng ShucongZhou YifanChen Shangwei