SLC11A1 antibody - center region (OAAB05107)
- Known as:
- SLC11A1 (anti-) - central region (OAAB05107)
- Catalog number:
- oaab05107
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SLC11A1 antibody - center region (OAAB05107)
Related genes to: SLC11A1 antibody - center region (OAAB05107)
- Gene:
- SLC11A1 NIH gene
- Name:
- solute carrier family 11 member 1
- Previous symbol:
- LSH, NRAMP, NRAMP1
- Synonyms:
- -
- Chromosome:
- 2q35
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-21
- Date modifiied:
- 2016-02-17
Related products to: SLC11A1 antibody - center region (OAAB05107)
Related articles to: SLC11A1 antibody - center region (OAAB05107)
- Given its high mortality and broad societal impact, the COVID-19 pandemic is arguably one of the most consequential public health crises of the twenty-first century. Although previous studies have identified several genes associated with COVID-19 susceptibility, relatively little is known about the genes contributing to severe COVID-19, including their evolutionary histories. In the current study, we analyzed IL-4, TLR2, CCL2, and SLC11A1-immunity genes that have previously been implicated in severe COVID-19 and other immune-related diseases-in globally diverse populations from the 1000 Genomes Project. We also tested for associations between genetic variation at these genes and clinical COVID-19 phenotypes in nearly 4000 laboratory-confirmed COVID-19-positive individuals across two datasets from the GEN-COVID Multicenter Study in Italy. - Source: PubMed
Publication date: 2026/05/29
Cross Christopher NLisi AlessandroSimmonds Faith CFlores Marisol FerminWashington KareemHeinbockel ThomasCampbell Michael C - Pleural tuberculosis is one of the most frequent extrapulmonary manifestations of infection and is characterized by a pronounced immune-mediated response with a low bacillary burden. Host genetic factors appear to play a central role in its immunopathogenesis. - Source: PubMed
Publication date: 2026/05/02
Neto André AmateOlivo Taylor Endrigo ToscanoMastroianni Patríciade Nadai Mariane NunesForgerini Marcelade Nadai Tales Rubens - Mucinous colorectal adenocarcinoma (MAC) is characterized by poor prognosis and therapy resistance, yet its molecular and tumor microenvironment (TME) features remain inadequately understood, limiting the identification of effective therapeutic targets. Here, we performed a comprehensive analysis of MAC tumor characteristics and the TME using large-scale genetic and transcriptomic sequencing datasets. Our findings reveal that MAC tumor cells harbor a higher frequency of canonical mutations yet exhibit lower chromosomal instability. Additionally, we observed an increased infiltration of natural killer (NK) cells and highly expressed macrophages (Mac-SPP1) within the TME, along with heightened fibroblastic and myeloid inflammatory signals. Mac-SPP1, characterized by M2 macrophages, was associated with poor prognosis. Furthermore, we identified key prognosis-related genes, including , , and , and proposed potential therapeutic agents for overcoming treatment resistance. Our findings offer valuable insights into the molecular mechanisms underlying MAC and highlight the critical need for novel therapeutic strategies. - Source: PubMed
Publication date: 2026/03/30
Li JianxiaFu YangBai FanWu ZehuaQin GeDeng Yanhong - Spinocerebellar Ataxia type 2 (SCA2) and Amyotrophic Lateral Sclerosis type 13 (ALS13) are triggered by polyglutamine expansion in Ataxin-2 (ATXN2). To understand these neurodegenerative disorders at the molecular level, the brains of 10-month-old -CAG100-knockin mice were analyzed as microglial, astroglial and neuronal fractions via global RNA sequencing. Data were validated by comparison with the spinal cord oligonucleotide microarray profile or filtered by RNA-seq consistency. Here, we show that the mutation causes a massive inflammatory response in microglia and a reciprocal loss of neuronal transcripts in glial fractions, suggesting severe synapse loss. Beyond these general neurodegenerative signs, we identify pathognomonic changes in the machinery for protein translation and RNA splicing. Glial fractions showed upregulation of (to 2082%), , , , , , , , and as an unspecific neuroinflammatory signature, versus downregulation of axonal (to <19%), and synaptic , , , and mRNAs correlating with circuit disconnection. In all fractions, reductions in , , and were noted versus disease-specific inductions of ribosomal subunits, presumably mirroring the partial loss-of-function of ATXN2 as RNA translation modulator. Selective accumulations of embryonic factors and versus downregulation of adult specify the mutation impact on splicing and translation elongation. As a potential underpinning of toxic gain-of-function, the proteostasis transcript appeared increased in astroglial and microglial fractions. These transcriptome data suggest altered ribosomal and spliceosome machinery, with massive microgliosis versus mild astrogliosis, at the core of SCA2 and ALS13. - Source: PubMed
Publication date: 2026/04/15
Auburger GeorgKandi Arvind ReddyVutukuri RajkumarAlmaguer-Mederos Luis-EnriqueGispert SuzanaSen Nesli-EceKey Jana - While typhoid fever affects both sexes at an equal rate, males are at a higher risk for intestinal perforation, which increases mortality. The mechanisms behind the increased morbidity of typhoid fever in human males remain an important but understudied question. Using a 129X1/SvJ (NRAMP []) murine model of typhoid chronic infection, we determined that males in this model exhibit increased bacterial burden and mortality in comparison to females (median survival 7 vs 11 days post-infection, respectively). This decreased survival in males was influenced by the diet preceding infection as male mice fed a lithogenic diet, to induce gallstones important to chronic infection, or a normal diet had a lower median survival time, although no difference in the overall probability of survival was observed. We also explored how the systemic immune response may contribute to increased mortality by comparing serum cytokine levels between males and females. Males had higher overall levels of pro-inflammatory cytokines and IL-10 and lower levels of IL-27, which are known to inhibit the protective responses to infection. Together, we present the first report that the 129X1/SvJ murine model of infection responds to infection in a sex-dependent manner, characterized by maladjusted systemic cytokine production and increased bacterial burden in males. - Source: PubMed
Publication date: 2026/03/11
Bennett Aliyah NCole Allysa LGunn John S