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
Related products to: Briefcase incl pipets
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
- 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 - - Source: PubMed
Publication date: 2026/04/23
Luo JinqinOu SiyangWang XinmiaoWang Yin-YingYang LuoJiang JingwenXu JueZhu GuanghuiChen Sujun - Activation of the NLRP3 inflammasome can be triggered by components of fungi, bacteria and viruses, as well as cellular stress and environmental irritants. The NLRP3 inflammasome has been well characterised in mouse and humans but limited information is available from other mammalian species. To gain a better understanding of the evolution of genes involved in the NLRP3 inflammasome pathway, we examined them in mammalian species representing the three major lineages (eutheria, metatheria and prototheria) and in chicken as an outgroup. Our results show that the inflammasome pathway machinery is generally well conserved in the species examined. We identified four NLRP members in echidna and seven in platypus as well as confirming Nlrp3 is present in marsupials and monotremes. Monotremes feature eleven Dectin family genes that are split across two chromosomes. Only three family members were found in opossum, Tasmanian devil and koala. Of the four Dectin family members known to be involved in the NLRP3 inflammasome pathway only Clec4e (Mincle) was identified in all species examined. Echidna possesses a single copy of Caspase-1 which, alongside previous results reported in the platypus, supports the conclusion that this is the only proinflammatory caspase in the monotremes. Our analysis suggests that Caspase-1 moved to a new chromosomal region in early mammalian evolution. This was followed by expansion of the cluster and accumulation of additional genes. The expansion of key gene families flanking Caspase-1 may have led to an expansion of inflammasome pathways and a more regulated immune system through the CARD genes. - Source: PubMed
Publication date: 2026/03/12
Stevens DavidDaish TasmanGrützner Frank - Reactive oxygen species (ROS) are critically implicated in ischemic stroke (IS), yet the transcriptional networks and predictive biomarkers underlying ROS dysregulation remain incompletely understood. - Source: PubMed
Publication date: 2026/03/10
Yang LifangLiang TianyuDing Xiaodi - Malassezia is the most prevalent fungus on human skin and it acts as both a skin commensal and an opportunistic pathogen. It is involved in many inflammatory skin diseases. Here we report transcriptome analyses of skin tissues from murine models colonized by Malassezia globosa. The results showed that differentially expressed genes (DEGs) of both intact-skin group and barrier-impaired group were enriched in pathways including C-type lectin receptor signaling pathway, Toll-like receptor signaling pathway, NOD-like receptor signaling pathway, Fc epsilon RI signaling pathway, Fc gamma R-mediated phagocytosis, neutrophil extracellular trap formation, and IL-17 signaling pathway. Quantitative real-time PCR confirmed that genes encoding pattern recognition receptors (PRRs) such as Clec7a, Clec4n, Clec4e, Tlr1, Tlr2, Tlr4, Nlrp3, Nlrc4, and Nod2; genes related to neutrophil extracellular trap formation such as Padi4 and Camp; and genes involved in IL-17 signaling pathway such as Il17a, Il17f, and Il23a, were all upregulated both in intact murine skin and barrier-impaired murine skin. This study provides a transcriptional perspective on the mechanisms of host-Malassezia interactions. The genes related to the host responses caused by Malassezia are similar in intact and barrier-impaired skin, with host responses in barrier-impaired skin being more intense. - Source: PubMed
Publication date: 2026/02/19
Hu JianJia QiuyuZhong LingzhiZhang JianzhongLi Houmin