LMO4 Antibody (OAAF06580)
- Known as:
- LMO4 Antibody (OAAF06580)
- Catalog number:
- oaaf06580
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- LMO4 Antibody (OAAF06580)
Related genes to: LMO4 Antibody (OAAF06580)
- 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: LMO4 Antibody (OAAF06580)
Related articles to: LMO4 Antibody (OAAF06580)
- To develop and validate a machine learning(ML)-based integrated predictive model combining genetic, epigenetic, and clinical factors for predicting leflunomide (LEF) treatment response in rheumatoid arthritis (RA) patients. - Source: PubMed
Publication date: 2026/06/24
Chen MengLiu HainaJin LeiFeng XinDai BingbingWang FangWang QiaoChen YulanYi ManJia BowenDong KangyiZhang JintaoFan ZhijunLi JiahuiZhao FengJia YuanyuanWang JianpengLiu MiaoXu JiayiFu Lingyu - Ménière disease (MD) is a chronic inner ear disorder characterized by recurrent vertigo, fluctuating sensorineural hearing loss, and tinnitus, but its etiology remains poorly understood. We performed a genome-wide meta-analysis of 8,969 MD case subjects and 1,962,542 control subjects across five biobanks, identifying five independent genome-wide significant loci and estimating an observed-scale SNP heritability of 7% (SE 0.8%), indicating a modest but significant contribution of common genetic variation to MD risk. The genome-wide significant signals comprise two independent variants at EYA4, two at EYA1, and one near CYP26A1, with odds ratios between 1.1 and 1.25. Associations at two additional loci, LMO4 and ALDH1A2, fell just below the genome-wide significance threshold (5 × 10 Publication date: 2026/06/16
Shi ZhuozhengMandla RaviLi JingjingLi XinzheZhang Zixuan EleanorChen SixingLapinska SandraFlynn-Carroll Alexander OPasaniuc BogdanEpstein Douglas JMathieson Iain - 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