Ask about this productRelated genes to: Hoxd13 antibody
- Gene:
- HOXD13 NIH gene
- Name:
- homeobox D13
- Previous symbol:
- HOX4I, SPD
- Synonyms:
- -
- Chromosome:
- 2q31.1
- Locus Type:
- gene with protein product
- Date approved:
- 1991-05-08
- Date modifiied:
- 2015-08-25
Related products to: Hoxd13 antibody
Related articles to: Hoxd13 antibody
- While previous studies have indicated that H3K36me3, which is mediated by Setd2, may regulate the cell fate of mesenchymal stem cells (MSCs) both in vitro and in vivo, the specific role of MSCs in the onset and progression of MDS remains unclear. Thus, the histone methyltransferase Setd2 is implicated in MDS-associated leukemia. This study utilized NUP98-HOXD13 (NHD13) mice with targeted deletion of Setd2 in MSCs. Here, we found that Setd2-deficient mice undergo faster leukemia transformation than control mice do, as evidenced by the abnormal differentiation of hematopoietic stem progenitor cells in the bone marrow, abnormal hematopoiesis, and increased number of blast cells. Compared with that of control mice, the morphology of NHD13 mouse MSCs with Setd2 deficiency was irregular, and the support function of hematopoietic cells was compromised. This study demonstrated that targeted deletion of Setd2 in MSCs facilitates the advancement of MDS. Furthermore, we identified increased expression of coagulation factor XII as a key leukemic transformation mediator in Setd2-deficient MSCs. Moreover, we found that SETD2 expression is significantly lower in high-risk MDS patients than in low-risk MDS patients, further suggesting that the targeted deletion of Setd2 in MSCs is associated with MDS progression. Collectively, our results suggest that Setd2 in MSCs suppresses MDS progression to leukemia through coagulation factor XII-mediated suppression of the stem cell support capacity of MSCs. Overall, this study sheds light on the pathogenesis of MDS and provides a therapeutic strategy for regulating the microenvironment in patients with MDS who cannot be cured by haematopoietic stem cell transplantation. - Source: PubMed
Publication date: 2026/04/30
Wang Rou-JiaLi Zi-JuanChen Bing-YiGuo JuanTao YingLi Hong-PingFei Ming-YueChang Bin-HeZhao Mu-YingShi LeiZhao Si-DaZhang ZhengSu Ji-YingSong Lu-XiHe QiWu DongWu Ling-YunZhang Jia-YingZong Li-JuanSun Xiao-JianZhao You-ShanWang LanChang Chun-Kang - - Source: PubMed
Publication date: 2026/04/21
Zhao BinLi JiachengWang ZunxianZhou HairuiCheng ZhuoxinMa Shuxia - Myelodysplastic syndrome (MDS) is a heterogeneous group of myeloid neoplasms characterized by treatment difficulties and a propensity to progress to acute myeloid leukemia. Impaired natural killer (NK) cell surveillance is a hallmark of MDS, yet the underlying molecular mechanisms remain poorly understood. This study aims to elucidate the mechanism by which HIF-1α regulates NK cell differentiation disorders and its impact on NK cell cytotoxicity in MDS. Flow cytometry was employed to compare HIF-1α expression and NK cell differentiation between wild-type and NUP98/HOXD13 (NHD13) mice. Our results demonstrated a significant increase in HIF-1α expression in the bone marrow and peripheral blood of MDS mice, accompanied by a notable decrease in immature NK cell subsets and activating receptors (NKG2D, NKp44, and DNAM-1). Overexpression of HIF-1α in human NK cells or pharmacological stabilization with CoCl2 inhibits the differentiation into mature NK cells, suppresses the expression of degranulation molecules such as Granzyme B, and impairs NK cell cytotoxicity. Western blot analysis indicated that HIF-1α regulates NK cell differentiation and function via the JAK1/STAT5/SOCS2 signaling pathway. Collectively, these findings suggest that the hypoxic microenvironment in MDS enhances HIF-1α expression, which subsequently impairs NK cell maturation and inhibits their cytotoxicity. Targeting HIF-1α may delay MDS progression by enhancing NK cell function via the JAK1/STAT5/SOCS2 signaling pathway. - Source: PubMed
Xu ShujuanJiang YixiangWang ShengtaoChen BeiliLin WenyuanJiang FangWu XianyiTang RongfangNie YuweiChen TongtongWang Xiaotao - Alpha-terpineol (α-terpineol), a ubiquitous monoterpenoid alcohol found in numerous essential oils, is widely employed in cosmetics, perfumes, and aromatic therapies. Despite its extensive application, concerns regarding its potential reproductive and developmental toxicity remain inadequately characterized, particularly concerning specific teratogenic effects and underlying molecular mechanisms. This study presents novel findings, demonstrating that α-terpineol exposure during the critical organogenesis period significantly induces developmental toxicity in Wistar rat fetuses. α-terpineol was administered at the doses of 0, 75, 150, and 300 mg/kg with a dose volume of 5 mL/kg. We report dose-dependent embryotoxic and teratogenic effects, including reduced fetal weight and a spectrum of severe skeletal malformations such as anophthalmia, club foot, micrognathia, phocomelia, and irregularities in the vertebral column, ribs, and limb bones. Crucially, our comprehensive gene expression analysis revealed statistically significant alterations in the expression patterns of HOXD13 and GDF11, two pivotal genes essential for skeletal patterning and limb development. The observed downregulation of these genes suggests a potential molecular association into α-terpineol-induced teratogenesis. These findings underscore the significant developmental risks associated with α-terpineol exposure during pregnancy and provides insights into potential molecular changes underlying its teratogenic potential, warranting further investigation into human health implications and the establishment of safe exposure limits for this widely used compound. - Source: PubMed
Publication date: 2026/04/01
Hegde Sneha SumaMalashetty Vijaykumar B - Soft tissue sarcomas are rare malignant mesenchymal tumors for which accurate diagnosis, prognostic stratification, and therapeutic decision-making remain challenging. Although histopathology and immunohistochemistry are essential diagnostic tools, they frequently fail to capture the molecular complexity underlying tumor aggressiveness and treatment resistance. In this study, we evaluated the utility of RNA-based next-generation sequencing for the molecular characterization of STS and for elucidating transcriptomic mechanisms associated with aggressive tumor behavior. An observational cohort of 24 patients with histologically confirmed soft tissue sarcomas was analyzed, using adipose and skeletal muscle tissue as controls. RNA was extracted from tumor samples, libraries were prepared with a targeted pan-cancer panel, and sequencing was performed on the Illumina platform, followed by bioinformatic analysis using DRAGEN pipelines and DESeq2. RNA-NGS identified a predominance of single-nucleotide polymorphisms and significant differential gene expression, with overexpression of proliferation-related genes (, , ), extracellular matrix and microenvironment-associated genes (, ), and developmental regulators (, ). Subgroup analysis revealed a distinct transcriptomic profile in leiomyosarcoma, while gene fusion analysis detected clinically relevant alterations. These findings demonstrate that RNA-NGS provides biologically and clinically meaningful insights into the molecular landscape of soft tissue sarcomas and supports its integration into precision medicine-oriented diagnostic workflows. - Source: PubMed
Publication date: 2026/03/16
Serban BogdanCursaru AdrianIordache SergiuCretu BogdanNica MihaiIacobescu GeorgianPopa MihneaRadu EugenCirnu MadalinaCirstoiu Catalin