[Gln22] _ 25359 _ Amyloid (6 _ 40)
- Known as:
- [Gln22] _ 25359 _ Amyloid (6 _ 40)
- Catalog number:
- SP-87936-1
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Alpha Dia
- Gene target:
- [Gln22] _ 25359 Amyloid (6 40)
Related genes to: [Gln22] _ 25359 _ Amyloid (6 _ 40)
- Gene:
- BTBD16 NIH gene
- Name:
- BTB domain containing 16
- Previous symbol:
- C10orf87
- Synonyms:
- FLJ25359, Em:AC061711.1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2016-02-12
Related products to: [Gln22] _ 25359 _ Amyloid (6 _ 40)
Related articles to: [Gln22] _ 25359 _ Amyloid (6 _ 40)
- Migraine is a common, disabling neurological disorder. Genome-wide association studies have mapped numerous migraine risk loci, but the causal genes and their cell-type context remain unclear. Prior work linked migraine GWAS to bulk brain eQTLs; however, tissue-average signals obscure cell-specific regulation. - Source: PubMed
Publication date: 2025/12/05
Ye HongHuang YajingWang ChengJin JianchengJiang ChaoyaFang JunjieXu Qiuhan - A high-salt diet (HSD) induces cognitive impairment and anxiety, with gut microbiota alterations serving as a potential underlying mechanism. Six-month-old male C57BL/6J mice were randomly assigned to the high-salt diet group (HS, n = 10, 8% NaCl) and the control group (ND, n = 10, 0.4% NaCl), and maintained on their respective diets for 180 days. Behavioral tests were conducted to assess the impact of chronic HSD on cognition and anxiety-like behaviors in mice. Hippocampal neuroinflammation was evaluated by RT-qPCR analysis, while neuronal damage was quantified using Nissl and NeuN staining. Correlation analysis was conducted to explore associations between differential gut microbiota and differentially expressed genes (DEGs) in the hippocampus. Our results demonstrated that HSD impaired cognition and emotion in mice through gut microbiota changes and hippocampal gene alterations, which subsequently promoted neuroinflammation and neuronal damage. Our study revealed that HSD increased Dubosiella and Anaeroplasma while decreasing Prevotellaceae_UCG_001 in the gut microbiota, upregulated Btbd16, Il1b, Prlr, Cd24a, Ak7, while downregulating Casp4 in hippocampal gene expression. Correlation analysis revealed significant correlations between Dubosiella and Il1b/Cd24a, Anaeroplasma and Ak7/Prlr/Casp4, Prevotellaceae_UCG_001 and Btbd16/Ak7. In summary, chronic HSD triggers gut microbiota dysbiosis and hippocampal gene expression changes, ultimately driving neuroinflammation and neuronal damage in the hippocampus, which culminates in cognitive deficits and anxiety. These findings provide new insights into the potential mechanisms of HSD-induced cognitive impairment. - Source: PubMed
Publication date: 2025/11/07
Xu WentingZhang ChenglinBai YudanZhang HanyueWei YuyangGe QianGuo YuyanLi MaiAn ChanyuanChen XinlinMa Kaige - Severe burns are a major global health concern, and are associated with long-term physical and psychological impairments, multi-organ dysfunction, and substantial morbidity and mortality. While burn injuries in adults trigger systemic immuno-metabolic alterations-characterized by white adipose tissue browning, elevated resting energy expenditure, widespread catabolism, and inflammation-these adaptive responses are considerably impaired in older adults, with molecular mechanisms behind these differences remaining largely unclear. As a key regulator of systemic metabolism, investigating the pathological role of adipose tissue (AT) postburn may reveal novel targets that could potentially improve patient outcomes. In this study, we conducted bulk mRNA sequencing and analysis of AT from adult and aged mice to elucidate the transcriptomic changes underlying the distinct postburn responses in these populations. After examining differentially expressed genes in the adult and aged burn mice, the top six upregulated genes in adults (Ucp1, Lgr6, Dio2, Lncbate10, Fabp3, Kng2) were primarily associated with thermogenesis, whereas those in the aged mice (Car6, Spata25, Gm128, Btbd16, Lipm, Abca13) were linked to inflammation, tissue repair, and lipid metabolism. Furthermore, our gene co-expression and enrichment map analysis identified burn-associated modules related to fatty acid oxidation, acetyl thioester CoA, and thermogenesis in adults, whereas leukocyte migration, tumor necrosis factor production, and sister chromatids were in aged mice. Notably, Ppara and Sfpi1 emerged as potential master regulators of co-expressed genes in burn AT of adult and aged mice, respectively. Our findings highlight age-specific differences in burn-induced AT responses and uncover potential molecular regulators that may inform targeted therapeutic strategies to mitigate the post-burn stress response. - Source: PubMed
Bhattachan PunitVlavcheski FilipWojtowicz-Piotrowski StephanieJeschke Marc G - There is a link between type 2 diabetes mellitus (T2DM) and bone mineral density (BMD), but the genetic reasons behind it are not yet clear. Our study found shared genetic markers and key genes connecting T2DM and BMD. This finding helps us understand their co-occurrence and may lead to new therapeutic strategies. - Source: PubMed
Publication date: 2025/06/23
Feng XinranXu HongbinGuo QianWang ZeyingBa RuikaiXuan KunBan Jinghao - Alzheimer's disease (AD) is one of the most common neurodegenerative diseases. However, the AD mechanism has not yet been fully elucidated to date, hindering the development of effective therapies. In our work, we perform a brain imaging genomics study to link genetics, single-cell gene expression data, tissue-specific gene expression data, brain imaging-derived volumetric endophenotypes, and disease diagnosis to discover potential underlying neurobiological pathways for AD. To do so, we perform brain-wide genome-wide colocalization analyses to integrate multidimensional imaging genomic biobank data. Specifically, we use (1) the individual-level imputed genotyping data and magnetic resonance imaging (MRI) data from the UK Biobank, (2) the summary statistics of the genome-wide association study (GWAS) from multiple European ancestry cohorts, and (3) the tissue-specific cis-expression quantitative trait loci (cis-eQTL) summary statistics from the GTEx project. We apply a Bayes factor colocalization framework and mediation analysis to these multi-modal imaging genomic data. As a result, we derive the brain regional level GWAS summary statistics for 145 brain regions with 482,831 single nucleotide polymorphisms (SNPs) followed by posthoc functional annotations. Our analysis yields the discovery of a potential AD causal pathway from a systems biology perspective: the SNP chr10:124165615:G>A (rs6585827) mutation upregulates the expression of BTBD16 gene in oligodendrocytes, a specialized glial cells, in the brain cortex, leading to a reduced risk of volumetric loss in the entorhinal cortex, resulting in the protective effect on AD. We substantiate our findings with multiple evidence from existing imaging, genetic and genomic studies in AD literature. Our study connects genetics, molecular and cellular signatures, regional brain morphologic endophenotypes, and AD diagnosis, providing new insights into the mechanistic understanding of the disease. Our findings can provide valuable guidance for subsequent therapeutic target identification and drug discovery in AD. - Source: PubMed
Publication date: 2023/08/25
Bao JingxuanWen JunhaoWen ZixuanYang ShuCui YuhanYang ZhijianErus GuraySaykin Andrew JLong QiDavatzikos ChristosShen Li