Briefcase incl pipets
- Known as:
- Briefcase incl pipets
- Catalog number:
- DBC-06
- Product Quantity:
- 1x
- Category:
- -
- Supplier:
- Capp
- Gene target:
- Briefcase incl pipets
Related genes to: Briefcase incl pipets
- Gene:
- CLEC4E NIH gene
- Name:
- C-type lectin domain family 4 member E
- Previous symbol:
- CLECSF9
- Synonyms:
- mincle
- Chromosome:
- 12p13.31
- Locus Type:
- gene with protein product
- Date approved:
- 2001-02-01
- Date modifiied:
- 2015-12-16
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1.0ml Serological Pipets, Bu Non_Sterile, Standard Tip1.0ml Serological Pipets, In Sterile, Open_Ended Tip10 point calibration, multi pipets10 point calibration, single pipets10ml Serological Pipets, Bul Non_Sterile, Standard Tip10mL Serologicsl Pipets, Sho Sterile, Standard Tip14-3-3 protein gamma (incl. pos. control) antibody Ab host: Mouse14-3-3 protein gamma (incl. pos. control) antibody Ab host: Mouse14-3-3 protein sigma SFN (incl. pos. control) IgG1 antibody Ab host: Mouse14-3-3 protein sigma / SFN (incl. pos. control) IgG1 antibody Ab host: Mouse1ml Pasteur Pipette,Individually Wrapped B5,Pasteur Pipets1ml Pasteur Pipette,individually wrapped, B5,Pasteur Pipets1ml Pasteur Pipette,Non-Sterile B5,Pasteur Pipets1_Butyne (incl. cylinder) 95%1_Butyne (incl. cylinder) 95% Related articles to: Briefcase incl pipets
- One of the key hallmarks of aging is the age-related decline in immune system function, accompanied by a chronic low-grade inflammation, or "inflammaging". Simultaneously, a reduced capacity of immune cells to recognize and eliminate pathogens, along with immune exhaustion, is also defined as a sign of aging. Cynomolgus macaques () belong to a group of non-human primates evolutionarily close to humans and are often used for preclinical research. - Source: PubMed
Publication date: 2026/08/13
Petrova Viktoria MBulgin Dmitry VRadomskaya Elena YuShevelov Vsevolod AZhukova Darya SChzhu Olga PManakhov Andrey DPopov Alexander VRybtsov Stanislav A - Although flavonoids have been shown to have various health benefits, their association with abdominal aortic aneurysm (AAA) and the underlying mechanisms remain unclear. This study included 188 101 UK Biobank participants who were free of AAA at baseline dietary assessment. Multivariable Cox proportional hazards models were used to analyze the association between flavonoid intake and AAA risk, and elastic net regression was applied to construct a metabolite signature to evaluate potential mediation effects. Additionally, network pharmacology integrated with single-cell RNA sequencing (scRNA-seq) was used to further explore the mechanism of flavonoids against AAA development. Compared with the lowest quartile, the highest quartile of proanthocyanidin intake was associated with a 29% lower risk of AAA. If proanthocyanidin intake in the population was increased from the lowest to the highest quartile, approximately 17.24% of new AAA cases could be prevented. We further identified a metabolic signature consisting of 28 metabolites that was associated with proanthocyanidin intake. Mediation analysis showed that this metabolic signature explained 14.57% of the association between proanthocyanidins intake and AAA risk, with inflammation-related metabolites playing a major role. Network pharmacology combined with scRNA-seq analysis revealed that the preventive effect of proanthocyanidins on AAA may result from their regulation of the C-type lectin receptor signaling pathway in macrophages, with CLEC4E being the most differentially expressed member of the C-type lectin family. These findings support a protective role of proanthocyanidins in AAA and indicate that CLEC4E may be an important potential target for its protective action. - Source: PubMed
Publication date: 2026/08/17
Sun XiaoyaRen JingyiZhang ZhenaoPei HuantingZhang ChongyueZhang XiaolongYin BowenWang ZiyiMa YuxiaLing Wenhua - Helicobacter pylori extracts cholesterol from the host epithelial cells during infection for nutrition and lipid raft formation. However, the presence of cholesterol in invading bacteria facilitates phagocytosis and subsequent immune responses by the host. To evade immune surveillance, H. pylori immediately converts cholesterol to cholesteryl 6'-O-acyl α-glucosides (αCAGs) to prevent phagocytosis by the host. In addition, a part of αCAGs translocate to phagosome membranes where they retard the phagosome maturation and the fusion with lysosomes, thereby prolonging survival in phagocytes. On the other hand, H. pylori αCAGs are possible targets of the host immune system because they are recognized by both invariant Vα14 TCR-bearing NKT (iNKT) cells and the C-type lectin receptor Mincle or Clec4e. iNKT cells produce proinflammatory cytokines when activated by the cytokines secreted by antigen-presenting cells (APCs) recognizing αCAGs via Mincle, while iNKT cells directly recognizing αCAGs with CD1d using invariant Vα14 TCR in a Mincle-independent manner produce both pro- and anti-inflammatory cytokines, suggesting their involvement in the regulation of the immune responses against H. pylori infection. This review classifies and discusses the interactions of H. pylori and the host mediated by cholesterol and its glycoside, αCAG, during infection, focusing on the possible ambivalent roles of iNKT cells in the control of the immune responses to the pathogen producing αCAG. - Source: PubMed
Publication date: 2026/06/16
Shimamura Michio - Clonal haematopoiesis (CH) activates inflammation and increases the risk of atherosclerosis. Whether lifestyle alters CH clone expansion or the phenotypic programming of CH mutant cells, thereby affecting atherosclerosis, is unknown. Here, in humans and mice and across mutations in Jak2, Tet2, Trp53 and Dnmt3a, we demonstrate mutation-dependent responses to sleep and exercise in CH and show that mutant cells are uniquely sensitive to lifestyle. In two human datasets, moderate-to-vigorous physical activity was associated with lower prevalence of non-DNMT3A-driven CH. In atherogenic mice with Jak2 or Tet2 loss of function (LOF), but not Trp53 LOF or Dnmt3a CH, uninterrupted sleep or exercise curtails clone expansion. In CH with the Jak2 mutation, sleep and exercise reduces clone expansion by selectively reprogramming mutant, but not cohabitant wild type, haematopoietic progenitor cells towards antiproliferative and metabolically healthy phenotypes by tempering bone marrow macrophage-haematopoietic progenitor cell IL-1β signalling. Sleep or exercise also lessens Jak2-driven, Tet2 LOF-driven and Trp53 LOF-driven, but not Dnmt3a-driven, atherosclerosis by locally reprogramming mutant vascular macrophages, independent of peripheral clone dynamics. In Jak2, but not adjacent wild type, aortic macrophages, uninterrupted sleep blunts CLEC4E-dependent inflammasome activation, consequently diminishing lesions. Exercise, meanwhile, activates PAC1 neurons in the locus coeruleus, raising the levels of peripheral noradrenaline, which signals through adrenergic receptor β2 (ADRβ2) whose expression is preserved by exercise in Jak2, but not cohabitant wild type, aortic macrophages, selectively repressing their inflammatory programming and atherosclerosis. Our findings establish that healthy lifestyles gene-specifically diminish CH and selectively reprogram mutant haematopoietic progenitor cells and macrophages to maintain cardiovascular health. - Source: PubMed
Publication date: 2026/06/10
Gerhardt TeresaJacob WalterGaebel LenaHeiser MerlinWolfram ChristopherHuynh PacificNakao TetsushiGindri Dos Santos BernardoToh PamelaDouglas AaronBrisnovali Niki FRadkevich EmirUddin Md MesbahYates Abi GKhamhoung AnnieYatim NaderGianeselli MatteoKiss Máté GGoswami SukanyaNelson DaniellaChen RachelD'Souza DarwinChen ZhihongKim-Schulze SeungheeFidler TrevorEzzat DanielKhurshid ShaanBick Alexander GNatarajan PradeepEllinor Patrick TRajbhandari Abha KMerad MiriamSwirski Filip KCohen OrenGoedeke LeighHonigberg Michael CMcAlpine Cameron S - Ischemic stroke (IS) remains a devastating condition with limited neuroprotective options. This study investigated the role of the transcription factor inhibitor of DNA binding 3 (ID3) in acute IS through an integrated approach. Combining bioinformatic analysis of Gene Expression Omnibus (GEO) datasets with machine learning (ML) algorithms, we identified ID3 as a consistently downregulated key gene, and its expression level correlated with neurological severity. Functional analysis suggested ID3 modulates neuroinflammation. Furthermore, ID3 and C-type lectin domain family 4 member E (CLEC4E) showed potential as diagnostic biomarkers. Using network pharmacology, pantothenic acid (PA) was predicted as a potential ID3-targeting drug. This was preliminarily tested in an oxygen-glucose deprivation/reperfusion (OGD/R) model, where PA treatment specifically upregulated ID3, ameliorated neuronal electrophysiological dysfunction, and restored action potential amplitude. Our work provides the first integrative evidence suggesting ID3 as a pivotal protective factor in acute IS and nominates PA as a candidate for further development as a neuroprotective agent. - Source: PubMed
Chen HongqiaoChen MingliMeng LianWei XingQin YanBi Zhumei