Ask about this productRelated genes to: HOPX antibody
- Gene:
- HOPX NIH gene
- Name:
- HOP homeobox
- Previous symbol:
- -
- Synonyms:
- LAGY, HOP, OB1, NECC1, SMAP31
- Chromosome:
- 4q12
- Locus Type:
- gene with protein product
- Date approved:
- 2007-08-20
- Date modifiied:
- 2014-11-19
Related products to: HOPX antibody
Related articles to: HOPX antibody
- Hypoxia poses a serious threat to aquatic organisms, yet the regulatory roles of non-coding RNAs, particularly the competing endogenous RNA (ceRNA) network, in fish under hypoxic stress remain poorly understood. In this study, we conducted whole-transcriptome sequencing of yellow catfish (Pelteobagrus fulvidraco) liver tissue under hypoxic conditions to systematically identify hypoxia-responsive lncRNAs and miRNAs and construct a comprehensive ceRNA network. A total of 14 differentially expressed lncRNAs (DElncs) and 112 miRNAs (DEmiRs) were identified. Functional enrichment analysis revealed that the target genes of DElncs were significantly involved in mitochondrial membrane permeability, energy metabolism, and the HIF-1 and mTOR signaling pathways, while those of DEmiRs were enriched in MAPK, calcium, and ErbB signaling pathways. Furthermore, we identified 22 DEmiRs commonly regulated under both hypoxic and hypoxic-bacterial dual stresses, representing core regulators of environmental adaptation. By integrating expression correlation and target prediction, we constructed the first lncRNA-miRNA-mRNA ceRNA network in hypoxic yellow catfish, comprising 5 DElncs, 11 DEmiRs, and 17 ceDETGs. Within this network, lnc162 (significantly down-regulated) and lnc1375 (markedly up-regulated) may act to regulate key apoptotic and metabolic genes such as fosb, sgk1, pkm, and hopx by sponging specific miRNAs, as predicted by our ceRNA analysis. These results reveal that lncRNAs mediate hypoxic adaptation by coordinating apoptosis and metabolic reprogramming via ceRNA mechanisms. Our study provides novel insights into the molecular basis of hypoxia tolerance in teleosts and offers potential genetic targets for breeding hypoxia-resistant fish strains. - Source: PubMed
Publication date: 2026/04/26
Han BingShi YaxuanLiu XinsheTao YifanQiang JunYin ShaowuNing Xianhui - The intestinal mucosa is crucial for nutrient absorption and barrier function. In this study, a newly identified strain of Ligilactobacillus salivarius (L. sa. 8-2) exhibited a mucosal protective effect in chick intestinal injury models. However, the underlying mechanisms need to be clarified. In vivo, chicks were pre-fed with L. sa. 8-2 supernatant or its precipitate and then challenged with lipopolysaccharide (LPS) or Salmonella Typhimurium (STm). The results showed that L. sa. 8-2 and its supernatant significantly reduced intestinal epithelial apoptosis, increased goblet cell density and Muc2 mRNA abundance, and upregulated Claudin1 protein levels. Specifically, compared with the LPS-challenged group, L. sa. 8-2 supernatant accelerated epithelial renewal, as shown by elevated protein levels of proliferating cell nuclear antigen (PCNA) and increased mRNA abundance of cell cycle regulators Ccnd1 and Cdk2. Moreover, the L. sa. 8-2 supernatant markedly increased protein levels of both the active intestinal stem cell (aISC) marker LGR5 and the reserve ISC (rISC) marker HOPX in the intestinal crypt. In vitro, the enteroids were pre-treated with L. sa. 8-2 supernatant and then challenged with LPS. It was shown that the L. sa. 8-2 supernatant elevated the protein levels of LGR5 and HOPX compared with the injured group. Moreover, co-staining of LGR5 and HOPX revealed that more HOPX cells were co-localized with LGR5 cells in the L. sa. 8-2 supernatant pretreatment group, suggesting the activation of rISCs. Additionally, compared with the injured groups, L. sa. 8-2 supernatant preserved mitochondrial morphology and upregulated the fission-related protein FIS1. At both the mRNA and protein levels, L. sa. 8-2 supernatant upregulated the pyruvate metabolism-related enzyme LDHA and LDHB, while decreasing mRNA levels of Sdha (an oxidative phosphorylation-related enzyme), suggesting a metabolic shift from oxidative phosphorylation toward glycolysis and an enhancement of pyruvate utilization. Taken together, L. sa. 8-2 alleviates intestinal mucosal injury and promotes epithelial renewal by activating ISCs, which is mediated by promoting mitochondrial fission and subsequent enhancement of pyruvate utilization in the intestinal crypt. - Source: PubMed
Publication date: 2026/04/17
Hua YupingZou MinyaoZhang LingzhiChen LeixiaoRao XiWei GuozhenWei JiaxinWei MingpingWei YihangLi Jian - Retinal ganglion cell (RGC) axons form the optic nerve (ON). Numerous age-related ON diseases, including glaucoma, the second most common cause of worldwide blindness, result from multiple RGC stressors. Nearly all ON astrocytes in the optic nerve head (ONH): the junctional region between the ON and the retina in young-adult rodents expresses the homeodomain only (Hopx) protein. Hopx(+) ONH astrocytes are depleted during aging. ONH primary cultures which include Hopx(+) astrocytes secrete extracellular vesicles (ONH-EVs) which selectively enhance RGC survival and neurite extension in culture, while extracellular vesicles (EVs) secreted from distal ON cultures lacking Hopx(+) astrocytes do not. ONH-EVs also enhance RGC survival in vivo in a rodent model of glaucoma. Combining rat ONH single-cell (scRNA-seq) sequencing with EV proteomic analysis, we identified ONH-Hopx(+) astrocyte secreted factors. We interrogated the online Broad institute scRNA-seq database for rat RGC gene expression in control animals and following rodent ON crush, an RGC stress model, to correlate ONH-astrocyte secreted factors with RGC gene expression changes. Following stress, RGCs upregulate the complementary pathways involving Hopx(+) astrocytic-associated factors, suggesting reciprocal communication. Using a highly selective transgenic Hopx-cre ONH knockdown strategy, we demonstrate that eliminating Hopx(+) astrocytes also results in upregulation of RGC stress responses. Our results implicate age-related loss of young ONH-astrocytes as a crucial factor in the development of age-related optic nerve diseases, and discuss replacing ONH associated factors as a paradigm shift for ON disease treatment. - Source: PubMed
Publication date: 2026/04/27
Bernstein Steven LMehrabian ZaraGuo YanJouffroy JeanMead BenTomarev StanislavDurmaz EsmahanEpstein Jonathan AKronk AdamBlackshaw SethHoang Thanh - Mutations in BMP4 have been associated with malformations of the urinary tract in human patients. Genetic studies in mice have shown that these defects are linked to the expression of Bmp4 in the mesenchymal primordium of the ureter, where it acts as a critical signal for coordinated cytodifferentiation of the mesenchymal and epithelial tissues. Here, we used unbiased transcriptional profiling of ureters with genetic depletion of Bmp4 and pharmacological inhibition of BMP4 signaling to decipher the gene regulatory network controlled by BMP4 in the early ureter, focusing on transcription factors as possible drivers of cytodifferentiation. We show that in Bmp4-deficient ureters, expression of Grhl3, Msx2, Pparg, Trp63 and Foxa1 in the epithelial compartment, and of Gata6, Hopx, Id2, Id4, Myocd, Snai1 and Tbx18 in the mesenchymal primordium is reduced. Expression of Msx2, Pparg, Gata6, Id genes, Tbx18 and Snai1 requires direct BMP4 signaling input, whereas reduced expression of the other genes is likely due to secondary changes, including increased retinoic acid signaling. Conditional gene targeting of Smad4 revealed that BMP4-dependent activation of transcription factor genes is mediated in part by SMAD effectors in both ureteral tissues. Thus, our work links BMP4 (signaling) to known transcriptional regulators of ureteral cytodifferentiation and uncovers additional factors that may be relevant to this program. - Source: PubMed
Publication date: 2026/04/22
Deuper LenaHense NicolasBeckers AnjaThiesler HaukeMamo Tamrat MBergmann FlorianHildebrandt HerbertTrowe Mark-OliverKispert Andreas - The gut microbiota plays a crucial role in maintaining intestinal stem cell (ISC) homeostasis and epithelial barrier integrity. Here, we report that Blautia coccoides (B. coccoides) is significantly reduced in inflammatory bowel disease (IBD) patients and dextran sulfate sodium (DSS)-induced colitis mice. Through an integrated approach combining RNA sequencing, metabolomic profiling, and ISC lineage tracing across multiple mucosal injury models, we demonstrate that B. coccoides colonization enhances β-hydroxybutyrate (BHB) production in intestinal epithelial cells (IECs), which activates HOPX⁺ reserve ISCs and promotes regeneration of the LGR5⁺ ISC pool, thereby accelerating epithelial repair. We further show that B. coccoides-derived indole-3-lactic acid (ILA), a tryptophan (Trp) metabolite, is converted into indole-3-propionic acid (IPA) by commensal bacteria such as P. russellii or C. sporogenes, stimulating IEC BHB synthesis. Using an engineered Escherichia coli strain expressing BC-derived phenyllactate dehydrogenase (fldH), we establish that both dietary Trp and bacterial fldH activity are essential for ILA/IPA generation and subsequent mucosal healing. Our findings reveal a microbiota-metabolite-ISC regulatory axis critical for epithelial regeneration and propose novel metabolite-based therapeutic strategies for IBD and other intestinal disorders associated with barrier dysfunction. - Source: PubMed
Publication date: 2026/02/25
Zhang YananMeng JinxinTu ShuyuMa LinlinZhao XinyaGao JinsongWu JiananXu WeilvChen ShuxianCheng HairongZhang LiZhu Shu Jeffrey