Anti-Human LMO4, Rabbit Polyclonal
- Known as:
- Antibody toHuman LMO4, Rabbit Polyclonal
- Catalog number:
- kb3107gnp
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Sceti
- Gene target:
- Anti-Human LMO4 Rabbit Polyclonal
Related genes to: Anti-Human LMO4, Rabbit Polyclonal
- Gene:
- LMO4 NIH gene
- Name:
- LIM domain only 4
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 1p22.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-10-30
- Date modifiied:
- 2014-11-19
Related products to: Anti-Human LMO4, Rabbit Polyclonal
Related articles to: Anti-Human LMO4, Rabbit Polyclonal
- Genome-wide DNA methylation patterns in across host environments and developmental stages have not been systematically characterized. We performed whole-genome bisulfite sequencing (WGBS) on worms recovered from permissive C57BL/6 mice and non-permissive Sprague-Dawley rats at 24 and 42 days post infection (dpi). . exhibited globally low methylation levels (2.10%-2.86%). Hierarchical clustering indicated that sampling time explained the largest methylome differences, followed by sex- and host-associated variation. Worms from permissive hosts showed a more pronounced methylation decrease from 24 to 42 dpi, whereas worms from non-permissive hosts displayed attenuated changes alongside stunted growth. Sex-associated patterns shifted with maturation. Differentially methylated genes were enriched for phosphorylation-related terms and included , , , and . We identified 242 host/sex hotspot differentially methylated genes (e.g., ) enriched for transmembrane ion transport. Together, these results delineate host- and sex-associated signatures and nominate candidates for functional validation. - Source: PubMed
Publication date: 2026/04/17
Peng WeixuanCheng ShuangshuangWang YuepengLiu QiXu ShuhuaWang JipengHu WeiLu Yan - Bacterial diarrheal diseases continue to constitute a major burden on global public health, particularly within pediatric populations in low-resource settings. While clinically unified by the symptomology of diarrhea, the primary causative agents; Enterotoxigenic Escherichia coli (ETEC), Shigella species, Salmonella enterica, and Clostridioides difficile employ fundamentally distinct molecular strategies to subvert intestinal homeostasis. This review presents a comparative analysis of these ecosystem engineers, proposing that their pathogenicity is defined by their unique management of the host-microbiota metabolic and signaling conflict. We advance beyond the traditional host-pathogen dyad to explore a mechanistic triangle, integrating recent findings that the microbiota acts as a dynamic third player imposing colonization resistance via secondary bile acids and nutrient competition (proline), or conversely, providing metabolic fuel (formate, tetrathionate) for pathogen expansion. We synthesize advanced molecular insights from including the energetics of the Shigella T3SS sorting platform (Spa47); the multilayered "effector-immunity arms race" involving the Shigella effectors OspC1 and OspD3 in manipulating necroptosis; novel Salmonella T3SS-2 targets such as LMO4 and SteA-mediated ER contact sites; and the receptor diversity of C. difficile TcdB variants. Finally, we map these mechanisms to next-generation therapeutic vulnerabilities, highlighting the transition from broad-spectrum antibiotics to precision bacteriophage biocontrol (LPEK22, LPST94) and AI-discovered lysins (DeepLysin) as the future of intervention. - Source: PubMed
Publication date: 2026/04/20
Bayode Michael TosinOlawale Oluwatoyosi EzekielOlusola-Makinde Olubukola Olayemi - Immune responses to parasite infection involve the increased production of basophils and eosinophils. These two myeloid cell types have key roles in type 2 anti-parasite immunity and rely on GATA family transcription factors for their specification. The first committed step in basophil and eosinophil production is generation of basophil-eosinophil-mast cell progenitors (BEMPs) from oligopotent erythroid-primed multipotent progenitors (EMPPs). However, it is not well established how immune responses act on progenitors to initiate type 2 myelopoiesis. Here we show that infection with the helminth Heligmosomoides polygyrus increases EMPP commitment to myeloid fate at the expense of erythropoiesis. Upon infection with H. polygyrus, the IL-33 alarmin accumulated in the bone marrow, causing EMPPs to upregulate the GATA co-factor LMO4 and preferentially differentiate into myeloid cells. LMO4 was sufficient to instruct myeloid fate in EMPPs by interacting with GATA2, displacing the FOG1 co-factor and redistributing GATA binding from megakaryocyte-erythroid-specific to basophil, eosinophil and mast cell (BEM)-specific chromatin. Accordingly, mice carrying a GATA2 mutation that selectively impairs the LMO4-GATA2 interaction were deficient in GATA factor allocation to BEM chromatin, myeloid lineage commitment, basophil and eosinophil production, and parasite control. This identifies LMO4 as an IL-33-regulated master regulator of type 2 myelopoiesis, and transcription factor reallocation as a mechanism of lineage commitment. - Source: PubMed
Publication date: 2026/03/11
Fagnan AlexandreDi Genua CristinaMeng YiranDrissen RoyZhang ZishanZhang BowenFallon Padraic GPachnis VassilisMancini Erika JProgatzky FränzeNerlov Claus - Ménière's disease (MD) is a chronic inner ear disorder characterized by recurrent vertigo, fluctuating sensorineural hearing loss, and tinnitus. Despite these distinctive symptoms, its etiology remains poorly understood. We performed a genome-wide meta-analysis of 8,969 cases and 1,962,542 controls across five large biobanks, identifying five independent genome-wide significant loci and estimating an observed-scale SNP heritability of 7% (SE 0.8%), consistent with a modest but significant genetic contribution to MD risk. Fine-mapping and integrative functional analyses implicate two convergent biological processes - developmental regulation of the inner ear, involving , , and - and retinoic acid metabolism, with loci near and suggesting disrupted RA signaling in sensory and fluid-pressure homeostasis. These developmental regulator genes are robustly expressed in fetal and adult human inner ear cell types, supporting a model in which altered developmental programs predispose to adult vestibular and auditory dysfunction. Phenome-wide and genetic correlation analyses further reveal shared genetic architecture between MD and related traits, including vertigo, tinnitus, hearing loss, migraine, and sleep apnea, situating MD within a broader spectrum of sensory and neurological disorders. Collectively, these findings establish a genetic framework for Ménière's disease risk and implicate developmental regulators and retinoic acid signaling as key contributing pathways. - Source: PubMed
Publication date: 2026/02/11
Shi ZhuozhengMandla RaviLi JingjingLi XinzheZhang Zixuan EleanorChen SixingLapinska SandraFlynn-Carroll Alexander OPasaniuc BogdanEpstein Douglas JMathieson Iain - Mercuric chloride (HgCl), a common environmental neurotoxin, induces neuronal injury through incompletely characterized mechanisms. Recent findings suggest a regulatory role for microRNAs (miRNAs) in mercury-induced neurotoxicity, with miR-143-3p significantly enriched in the brain and implicated in neuronal viability. This study investigated the functional role and underlying mechanisms of miR-143-3p in HgCl-induced neurotoxicity using PC12 cells as a model system. Cells were treated with HgCl for 48 h, followed by evaluation of cell viability and apoptosis via MTT assay and flow cytometry, respectively. Neuronal morphology was assessed using inverted phase-contrast microscopy, while reactive oxygen species (ROS) levels were quantified using DCFH-DA staining. The expression levels of miR-143-3p and its downstream targets were determined by RT-qPCR, and protein expression was analyzed through western blotting. A luciferase reporter assay was employed to confirm the interaction between miR-143-3p and LMO4. Results revealed that silencing miR-143-3p alleviated HgCl₂-induced neurotoxicity in PC12 cells. Mechanistically, miR-143-3p was found to directly bind the 3' untranslated region (3'UTR) of LMO4. Overexpression of LMO4 conferred protection against HgCl₂-induced neuronal damage. Further analysis showed that miR-143-3p suppresses the Akt/GSK3β/mTOR signaling cascade by targeting LMO4. Either silencing LMO4 or pharmacologically inhibiting Akt diminished the neuroprotective effects observed upon miR-143-3p knockdown. These findings suggest that miR-143-3p exacerbates HgCl-induced neurotoxicity eby downregulating LMO4 and suppressing the Akt/GSK3β/mTOR pathway. - Source: PubMed
Publication date: 2025/09/01
Wang DileLiao YongguiHe Tao