ATOH8
- Known as:
- ATOH8
- Catalog number:
- 002159A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ATOH8
Related genes to: ATOH8
- Gene:
- ATOH8 NIH gene
- Name:
- atonal bHLH transcription factor 8
- Previous symbol:
- -
- Synonyms:
- HATH6, FLJ14708, bHLHa21
- Chromosome:
- 2p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2004-02-11
- Date modifiied:
- 2015-06-19
Related products to: ATOH8
Related articles to: ATOH8
- Cardiac fibrosis is a major driver of heart failure and a key therapeutic target. Here, we demonstrated the role of atonal homologue 8 (ATOH8) in the modulation of cardiac fibrosis in heart failure. The expression of ATOH8 was significantly reduced in patients with heart failure and in the left ventricular tissues of model mice. ATOH8 silencing resulted in the worsening of fibrosis, and adenovirus- induced overexpression of ATOH8 attenuated the progression of cardiac fibrosis under conditions. RNA sequencing analysis demonstrated that ATOH8 potentially influences cardiac fibrosis by modulating the TGF-/Smad signaling pathway. This was verified through ATOH8 silencing experiments, which showed a marked reduction in the expression of Smad7-a known inhibitor of fibrosis. Further investigation into the molecular mechanisms via immunoprecipitation mass spectrometry indicated that ATOH8 can directly bind to the transcription factor RUNX2, which was found to directly interact with the promoter region of Smad7 to suppress its expression. Accordingly, ATOH8 silencing was found to enhance RUNX2-mediated transcriptional repression of Smad7. The findings collectively imply that ATOH8 attenuates cardiac fibrosis through the RUNX2/Smad7 axis, although interactions with other fibrotic proteins need to be explored further. Through experiments in model mice of heart failure, we were able to demonstrate that the targeted overexpression of ATOH8 in fibroblasts via adeno-associated virus-9 carrying periostin significantly alleviated cardiac fibrosis and dysfunction induced by transverse aortic constriction surgery. Thus, the findings presented here indicate that ATOH8 potentially represents a novel biomarker and therapeutic target for the attenuation of cardiac fibrosis. - Source: PubMed
Publication date: 2026/08/31
Chen ChongYang YapanYang ChengyingjieGao ChuanyuLiu YuhaoYang HonghuiWang XiaohuZhang YachenGe Zhuowang - - Source: PubMed
Publication date: 2026/06/18
Shankland Stuart JWessely Oliver - Atonal BHLH transcription factor 8 () is a basic helix-loop-helix (bHLH) transcription factor; however, its role in glomerular epithelial cells (podocytes) remains unclear. This study aimed to elucidate the function of ATOH8 in podocytes. First, ATOH8 expression in the mouse kidney was confirmed in podocytes by immunofluorescence staining and in situ hybridization. In cultured human podocytes, transforming growth factor-beta (TGF-β) treatment significantly reduced mRNA expression. To examine the functional consequences of ATOH8 downregulation, expression was knocked down with shRNA. Subsequent RNA sequencing analysis of -knockdown podocytes revealed increased extracellular matrix gene expression and activation of TGF-β signaling. -knockdown podocytes also showed SMAD2/3 nuclear translocation, increased SMAD transcriptional activity, as determined by a luciferase assay, and upregulated mRNA even without TGF-β stimulation, consistent with TGF-β signaling activation. In vivo, C57BL/6 -deficient mice showed no renal abnormalities at baseline. However, in an adriamycin (ADR)-induced focal segmental glomerulosclerosis (FSGS) model, -deficient mice developed significantly more severe glomerulosclerosis than wild-type mice, with higher renal cortical and mRNA levels. Reduced ATOH8 expression was also observed in ADR-induced nephropathy in mice and rats and in various human glomerular diseases. These findings suggest that ATOH8 downregulation enhances TGF-β signaling and glomerulosclerosis progression, indicating a protective role for ATOH8 in maintaining podocyte integrity and preventing kidney injury. This study identifies atonal transcription factor 8 (ATOH8) as a previously unexplored regulator of podocyte function. We demonstrate that ATOH8 knockdown activates TGF-β signaling and increases extracellular matrix gene expression. Notably, ATOH8 deficiency alone does not cause renal injury but exacerbates glomerulosclerosis in an adriamycin-induced nephropathy model, accompanied by increased mRNA expression in the renal cortex. These findings indicate that ATOH8 plays a protective role in podocyte function and limits glomerulosclerosis during kidney injury. - Source: PubMed
Publication date: 2026/01/16
Hamatani HirokoTabei AkifumiOgawa ShinichiroSuwa JunyaIshihara ReiMurakami YukiSakairi ToruIkeuchi HidekazuKaneko YoriakiHanda HiroshiMorikawa MasatoHiromura Keiju - The basic helix-loop-helix (bHLH) transcription factor 'Atoh8' is involved in the regulation of several developmental processes and pathologies. It regulates organogenesis, reprogramming, stem cell fate determination, and cancer development. However, the mechanisms underlying these observations remain unclear. Unlike many tissue-specific bHLH factors, Atoh8 is ubiquitously expressed during development as well as in adult tissues. In this study, we explored whether Atoh8 modulates basic cellular functions, which may reveal a common mechanism that could explain the diverse observations reported in the literature. Our findings demonstrate that the loss of Atoh8 impairs autophagy. In both primary myoblasts and mouse embryonic stem cells lacking Atoh8, we observed differential expression of LC3B-II, TFEB, and accumulation of p62, indicating impairment of autophagy. Furthermore, mass spectrometric analysis performed on C2C12 and Atoh8 overexpressing C2C12 myoblasts revealed significant alterations in the expression of proteins associated with mitochondrial and lysosomal functions. Finally, Cut&Tag sequencing performed in Atoh8 overexpressing C2C12 cells revealed that Atoh8 binds to multiple genes involved in autophagosome assembly. Overall, this study underscores that Atoh8 is a critical regulator of macroautophagy, and its reduction disrupts the autophagic process, whereas its overexpression results in increased autophagic flux. - Source: PubMed
Publication date: 2025/12/15
Divvela Satya Srirama KarthikOffei Eric BekoeKadr HawiHausherr MaximilianEggers BrittaRozanova SvitlanaEisenacher MartinNguyen Hoang DuyTuoc TranBader VerianYang XuesongZaehres HolmChen AnqiNguyen Huu PhucWinklhofer Konstanze FMarcus KatrinBrand-Saberi Beate - The transcription factor ATOH8 regulates cell fate and differentiation during development. Loss of ATOH8 leads to defects in murine placenta development, yet its specific functions in self-renewal and differentiation of human trophoblast stem cells (TSCs) remain poorly understood. Here, we reveal that ATOH8 is critical for extravillous trophoblasts (EVTs) formation while being dispensable for the self-renewal of TSCs. We show predominant ATOH8 expression in EVTs compared to syncytiotrophoblasts (STs) and TSCs. Knockdown (KD) of ATOH8 in TSCs does not alter their morphology, proliferation, or self-renewal marker expression, indicating that ATOH8 is not required for TSC maintenance. However, during EVT differentiation, ATOH8 expression gradually increases and its depletion results in pronounced morphological abnormalities, impaired expression of EVT markers, sustained TSC marker expression, and abolished invasive capacity. Conversely, ATOH8 overexpression (OE) under self-renewing conditions modestly induces EVT markers, whereas its OE during ST differentiation disrupts ST formation by reducing cell fusion and aberrantly activating EVT genes. Transcriptomic profiling reveals that the loss of ATOH8 during EVT differentiation disrupts pathways critical for placental development, including extracellular matrix organization and PI3K-AKT signaling. We also show that ATOH8 functions within a cooperative network of EVT regulators, reciprocally regulating their expression and maintaining a transcriptional circuit essential for EVT specification. Collectively, these findings establish ATOH8 as an indispensable regulator of EVT differentiation and invasive function, orchestrating EVT-specific gene programs and pathways alongside other key transcription factors to ensure proper EVT formation. - Source: PubMed
Publication date: 2025/11/04
Salamah JoudiSalamah MohamedLee Bum-Kyu