Ask about this productRelated genes to: HHEX antibody
- Gene:
- HHEX NIH gene
- Name:
- hematopoietically expressed homeobox
- Previous symbol:
- PRHX
- Synonyms:
- HEX, HOX11L-PEN
- Chromosome:
- 10q23.33
- Locus Type:
- gene with protein product
- Date approved:
- 1998-08-04
- Date modifiied:
- 2015-08-25
Related products to: HHEX antibody
Related articles to: HHEX antibody
- The thymus is vital for T cell development, yet avian thymocyte maturation remains poorly characterized. Here, we present a single-cell transcriptomic atlas of thymic development in Zhedong White geese across embryonic, gosling, juvenile, and adult stages. Morphological and histological analysis revealed a multilobulated, paired thymus with rapid post-hatch expansion and age-dependent involution. Single-cell RNA sequencing identified all major thymic cell types, with T cells predominant and γδ T cells unusually abundant compared to mammals. High-resolution profiling defined key T cell subsets and reconstructed sequential differentiation, showing DN cells transition from pre-commitment states marked by BCL11A, SPI1, and HHEX to committed states (BCL11B, TCF7) and β-selection gene activation. Thymic epithelial cells functioned as central signaling hubs, mediating microenvironmental regulation. Comparative analysis with human and mouse thymus revealed a conserved developmental framework, yet pronounced species-specific differences at the DP stage and in γδ T cell enrichment. These findings contribute foundational insights for avian immunology and poultry breeding. - Source: PubMed
Publication date: 2026/04/17
Wang CuiZhu ZuoyinLiu YiYang YongpingChen ShufangHe Daqian - Naringenin (NGN), a flavonoid widely utilized in agricultural and pharmaceutical applications, has increasingly become a source of environmental concern. This study systematically evaluated the developmental toxicity of NGN in zebrafish embryos. Our results showed that NGN exposure caused dose-dependent increases in embryonic mortality and induced a range of developmental malformations, including reduced body length, impaired eye and ear development, and cardiac dysfunction. Behavioral analyses revealed significant deficits in locomotor activity and sensory responses at concentrations of 5 and 10 mg/L. Molecular assessments via RT-qPCR demonstrated that NGN disrupted the expression of multiple genes critical for cardiac (kcnh2a, kcnh2b, hand2, has2, myh7, tnnt2a), otic (col2a1a, sox9a, sox9b), liver (hhex, leg1.1), visual (gnat1, gnat2), apoptotic (bax, casp9, casp3), and neurodevelopmental (pomca, bdnf, gfap, mbpa, s100b) pathways. Notably, NGN at 10 mg/L inhibited apoptosis and altered liver function, whereas a concentration of 15 mg/L promoted apoptosis, and these results suggest that NGN may interfere with the developmental processes of zebrafish embryos through different mechanisms at low and high concentrations, exhibiting a non-monotonic dose-response relationship. These findings highlight the potential ecological hazards of NGN contamination in aquatic environments, emphasizing the need for stricter management and further research into its long-term and combined effects with other pollutants. Our research offers new perspectives into the molecular and phenotypic mechanisms of NGN toxicity and underscores the importance of comprehensive risk assessment for emerging environmental contaminants. - Source: PubMed
Publication date: 2026/04/13
Ji RongHu HaichengZhang YitianLiu KehuiDu JiyangMa YuanyuanSong BinbinHan Ying - Tetraploidy occurs infrequently in mammals but remains widespread in amphibians. Blastocyst complementation using xenogeneic transplantation of tetraploid embryonic stem cells (4 -ESCs) represents a promising approach to mitigate organ shortages, yet robust generation of fully reconstituted organs in mammalian hosts remains elusive. In this study, CRISPR/Cas9, the Cre-LoxP system, and blastocyst complementation were combined to generate tetraploid mouse liver, heart, and pancreatic tissues. 4 -ESCs (tdTomato-labeled) were established and shown to maintain stable pluripotency and tetraploidy, as confirmed by karyotyping and immunofluorescence analyses. Subsequently, these cells were microinjected into and deficient blastocysts and lineage-ablated blastocysts, which were engineered to lack relevant organ-forming lineages. Tetraploid pups exhibited significantly reduced body mass and organ mass (liver and heart) relative to diploid controls ( <0.05). Fluorescence-activated cell sorting demonstrated a significant 4 -ESC (tdTomato-labeled) contribution within tetraploid organs (4N population) at E18.5, with tdTomato-positive fractions reaching 84.3% of hepatic cells, 67.8% of cardiac cells, and 73.4% of pancreatic cells. Single-cell transcriptome sequencing further revealed that tetraploidy markedly altered developmental trajectories and differentiation programs in liver and heart tissues, and 4 -ESCs showed preferential integration into tetraploid liver and heart with a substantial contribution to pancreatic regeneration. Collectively, these findings support the feasibility of 4 -ESC-based blastocyst complementation for human organ regeneration and establish a framework for developing strategies to alleviate organ shortages in clinical settings. - Source: PubMed
Wei ShuZou Guo-WeiZhang Yan-YanLi Shuai-PengHu MeiDu JuanLiu Jia-WenRan LinZhou Chi-KaiLin Jiang-Wei - The dynamic assembly and regulation of the IκB kinase (IKK) complex in the NF-κB pathway are central to the pathogenesis and progression of inflammatory bowel disease (IBD). We recently reported that the transcription factor hematopoietically-expressed homeobox (HHEX) promotes colitis-associated colorectal cancer, but the potential role of HHEX in intestinal inflammation remains uncharacterized. Here, we found that HHEX is upregulated in inflamed colons in a colitis mouse model and in clinical IBD samples. HHEX overexpression increased inflammatory cytokine expression, and HHEX loss largely abrogated the inflammatory response in vitro and intestinal inflammation in vivo. Mechanistically, IKKα phosphorylates HHEX at S213 to stabilize HHEX in response to TNF-α by inhibiting the interaction of HHEX with the E3 ubiquitin ligase MID2 and subsequent K48-linked ubiquitination and protein degradation. Importantly, HHEX interacts with and stabilizes the IKKα/IKKβ complex via its N-terminal domain, thereby activating the NF-κB pathway and establishing a positive feedback loop that exacerbates intestinal inflammation. Our study reveals a transcription-independent function of HHEX in promoting IKK complex assembly and colitis, identifying HHEX as an IBD susceptibility gene and a potential target for IBD treatment. - Source: PubMed
Publication date: 2026/03/17
Hua ZhebinXu WeiminDing WenjunFu ZhuoyueWang YaoshengYang YiqingLiu FangyuanDai ZhujiangTang WenboOu WeijunGe WensongChen YingWeiWang ZhongchuanLiu Chen-YingDu Peng - By virtue of its function as a key metabolic regulator, malignant transformation in the pancreas not only confers high aggressiveness but also disrupts systemic metabolism. However, the causal relationship between metabolic reprogramming and the progression of pancreatic ductal adenocarcinoma (PDAC) remains incompletely understood. This study identifies aberrant protein kinase A (PKA) activation in PDAC, correlating with poor prognosis. Mechanistically, downregulation of the transcription factor hematopoietically expressed homeobox (HHEX) represses protein kinase cAMP-dependent type II regulatory subunit beta (PRKAR2B), relieving inhibition on PKA catalytic activity. A high-glucose microenvironment promotes cAMP production, further activating PKA, which then enhances glycolysis via specific upregulation of hexokinase 2 (HK2). , high glucose synergized with PKA activation to promote metastasis, whereas glycolysis inhibition blocked new metastases. Thus, HHEX-PRKAR2B-mediated PKA activation is a critical hub for PDAC progression, modulated by glucose and reinforcing glycolysis via HK2, revealing novel therapeutic targets for metabolic intervention. - Source: PubMed
Publication date: 2026/01/14
Wen JunxiangLi QiuchenXu ShuxiangLu WenjunWu FeiLou JiataoWang Lin