ATOH1, 158-354aa , Human, E.coli
- Known as:
- ATOH1, 158-354aa , Human, E.coli
- Catalog number:
- ATGP1485
- Product Quantity:
- 0.5mg
- Category:
- -
- Supplier:
- ATGen
- Gene target:
- ATOH1 158-354aa Human .coli
Related genes to: ATOH1, 158-354aa , Human, E.coli
- Gene:
- ATOH1 NIH gene
- Name:
- atonal bHLH transcription factor 1
- Previous symbol:
- -
- Synonyms:
- HATH1, MATH-1, Math1, bHLHa14
- Chromosome:
- 4q22.2
- Locus Type:
- gene with protein product
- Date approved:
- 1997-02-27
- Date modifiied:
- 2016-10-05
- Gene:
- FCN2 NIH gene
- Name:
- ficolin 2
- Previous symbol:
- -
- Synonyms:
- P35, FCNL, EBP-37, ficolin-2
- Chromosome:
- 9q34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1996-07-11
- Date modifiied:
- 2016-10-05
Related products to: ATOH1, 158-354aa , Human, E.coli
Related articles to: ATOH1, 158-354aa , Human, E.coli
- BACKGROUNDSmall-cell lung cancer (SCLC) is an aggressive malignancy with a poor prognosis and marked transcriptional heterogeneity that may drive distinct therapeutic vulnerabilities. Clinical translation of molecular subtyping has been limited by restricted access to tumor biopsies, particularly at relapse.METHODSWe applied chromatin immunoprecipitation of cell-free nucleosomes carrying active histone modifications followed by sequencing (cfChIP-seq) to 441 plasma samples from individuals with advanced SCLC, other neuroendocrine carcinomas, or non-SCLC cancers, as well as from healthy controls. Plasma cfChIP-seq profiles were integrated with matched tumor transcriptomes from 73 samples, including 41 time-matched pairs.RESULTScfChIP-seq captured the epigenetic and transcriptional landscape of tumor-derived cell-free DNA (cfDNA), including SCLC tissue- and cell-of-origin signatures. A quantitative cfChIP-seq-derived SCLC score tracked radiographic tumor burden and was associated with prognosis. Signals at promoters of lineage-defining transcription factor genes, including ASCL1, NEUROD1, POU2F3, and ATOH1, correlated strongly with matched tumor RNA expression and supported noninvasive inference of SCLC transcriptional subtypes directly from plasma.CONCLUSIONPlasma cfChIP-seq provides a practical liquid biopsy platform for real-time assessment of tumor burden, tumor state, and molecular subtype in SCLC. These findings support further development of cfChIP-seq for precision monitoring and subtype-informed therapeutic stratification in SCLC.TRIAL REGISTRATIONClinicalTrials.gov NCT02484404, NCT02487095, NCT02769962, NCT03554473, NCT03896503, and NCT02146170.FUNDINGCenter for Cancer Research; Intramural Program of the NCI (ZIA BC 011793); European Research Council (ERC) (Adg no. 101019560 "cfChIP"). - Source: PubMed
Publication date: 2026/10/01
Fialkoff GavrielTakahashi NobuyukiSharkia IsraaGutin JeniaHermoni NadavNirula MichaelKumar RajeshPongor LorincNichols SamanthaSciuto LindaParmar KanakDesai ParthSuresh PriyaAbel MelissaEl Meskini RajaaMaoz MyriamRottenberg YakirNevo ShoshanNechushtan HovavPeretz TamarRoame DianaHubert AyalaCohen Jonathan ESalah AzzamTemper MarkGrinshpun AlbertWeaver-Ohler ZoeRajan ArunFigg William DouglasZick AviadSadeh RonenFriedman NirThomas Anish - The modulation of Notch and Wnt signaling was evaluated for its ability to promote the differentiation and maturation of hair cell (HC)-like cells in otic organoids derived from mouse embryonic stem cells (mESCs). Using R1/E mESCs, we generated otic organoids and treated them with the Notch pathway inhibitor (γ-secretase inhibitor, DAPT) and the Wnt signaling agonist (CHIR99021) during two-time windows: days (D) D12-D18 (early treatment) or D28-D34 (late treatment). Among the late treatment conditions, lower concentration (5 μM DAPT and 2.5 μM CHIR99021) yielded greater expression of MyoVIIa and Atoh1 compared with higher doses (10 and 5 μM, respectively). Ultrastructural analysis by transmission electron microscopy further demonstrated that late treatment with lower-dose DAPT and CHIR99021 generated HC-like cells harboring longer and more prominent stereocilia-like bundles than those observed in other conditions. In contrast, early treatment produced HCs arranged in a typical otic organoid pattern, resulting in a more morphologically stable but less robustly induced HC-like population. These findings indicate that temporally and dose-controlled modulation of Notch and Wnt signaling efficiently enhances HC-like cell differentiation and stereocilia maturation in mESC-derived otic organoids, providing a useful platform for future studies in inner ear regeneration and cell-based therapies. - Source: PubMed
Publication date: 2026/09/25
Kim HantaiKim Yeon JuKim Young SunSo SeongjunSung SiungPark SunhoKim JanghoKim KyunghoonChoung Yun-HoonHa Jungho - : Intestinal mucosal function relies on the integrated contribution of multiple cell lineages, including secretory cells. Long noncoding RNA modulates many cell processes essential for human pathologies. Here, we investigated the role of in development and function of secretory lineage cells and elucidated the implication of altered ATOH1 by in dysfunction of the secretory cells. : Studies were conducted in -transgenic (H19-Tg) and -knockout (H19) mice, intestinal organoids, and Caco-2 cells. Secretory lineage cells were examined by fluorescent immunostaining with their specific cell markers, including Lysozyme, Mucin2, DCLK1, and Chromogranin A. Intestinal mucosal growth was measured by BrdU incorporation, and intestinal permeability was detected by paracellular tracer flux assay using FITC-Dextran. Single cell RNA-sequence, quantitative real-time PCR, and Western immunoblotting analyses were used to monitor changes in gene expression. : Tissue-specific transgenic expression of in the intestinal epithelium caused defects in Paneth, goblet, tuft, and enteroendocrine cells in mice, whereas targeted deletion of the gene increased the function of secretory lineage cells. Locally increasing the levels of in the epithelium impaired gut barrier function in H19-Tg mice, although it failed to alter mucosal growth. The intestinal mucosal tissues of H19-Tg mice exhibited a remarkable decrease in the levels of differentiation-associated transcription factors including ATOH1. Ectopically expressed ATOH1 in the -enriched intestinal organoids derived from H19-Tg mice rescued development of the secretory lineage cells. Mechanistically, inhibited ATOH1 expression via inhibition of its translation. : These findings indicate that functions as a negative regulator of differentiation and function of secretory lineage cells in the intestinal mucosa at least partially via the inhibition of ATOH1 translation. - Source: PubMed
Publication date: 2026/09/15
Kwon Min SChung Hee KChen HongxiaVanderStoep AmyWarner BridgetteZhao HaonanAtluri PrathikTesfayohannes EmnetTurner Douglas JXiao LanWang Jian-Ying - Merkel cells (MCs) are specialized mechanosensory receptor cells essential for touch sensation, exhibiting both epithelial and neuroendocrine characteristics. However, the regulatory processes that shape MC fate remain poorly defined. Using single-cell RNA sequencing, we construct a conserved, triphasic atlas of MC ontogeny comprising an epithelial-like stage, a transitional intermediate phase, and a terminal neuroendocrine state. Importantly, we identify as a priming factor essential for initiating MC differentiation, while acts as a driver of epithelial-neuroendocrine conversion and subsequent functional integration. Moreover, the gene regulatory network analysis further reveals that TUBB3 primed cells could differentiate into the MC lineage under the regulation of and . Genetic lineage tracing and cross-species analyses validate these mechanisms. Together, our work delineates the transcriptional network orchestrating MC fate determination and mechanosensory differentiation, providing not only mechanistic insights but also highlighting actionable targets relevant to MC carcinoma and sensory restoration. - Source: PubMed
Publication date: 2026/09/22
Zhang YajunYuan HuipuJiang YuyanWang TengRui ChenDing YuanyuanWang TuanWang ChaochenXiao Ying - Atoh1 is essential for the development of the cerebellum and inner ear, but the in vivo role of its promoter-proximal region remains incompletely understood. We generated deletion lines targeting the Atoh1 promoter-proximal region containing C sites and examined their phenotypes in the cerebellum and inner ear. - Source: PubMed
Publication date: 2026/09/18
Sakamoto SusumuKita TomokoYamada MayumiImayoshi ItaruTateya Tomoko