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- Safety Data Sheet
Catalog #: Product Name: 10985 ImmunoCultâ„¢ Dendritic Cell Culture Kit 10989 ImmunoCultâ„¢ Dendritic Cell Maturation Supplement Catalog #: 10985 Product Name: ImmunoCultâ„¢ Dendritic Cell Culture Kit Catalog #: 10989 Product Name: ImmunoCultâ„¢ Dendritic Cell Maturation Supplement - Product Information Sheet
Catalog #: Lot #: Language: Product Name: Catalog #:100-1399Lot #:AllLanguage:EnglishProduct Name:JCV (LT) Peptide PoolCatalog #: 100-1399 Lot #: All Language: English Product Name: JCV (LT) Peptide Pool - Reference(Apr 2024) Molecular Neurodegeneration 19 10
Regulation of human microglial gene expression and function via RNAase-H active antisense oligonucleotides in vivo in Alzheimer’s disease
BackgroundMicroglia play important roles in maintaining brain homeostasis and neurodegeneration. The discovery of genetic variants in genes predominately or exclusively expressed in myeloid cells, such as Apolipoprotein E (APOE) and triggering receptor expressed on myeloid cells 2 (TREM2), as the strongest risk factors for Alzheimer’s disease (AD) highlights the importance of microglial biology in the brain. The sequence, structure and function of several microglial proteins are poorly conserved across species, which has hampered the development of strategies aiming to modulate the expression of specific microglial genes. One way to target APOE and TREM2 is to modulate their expression using antisense oligonucleotides (ASOs).MethodsIn this study, we identified, produced, and tested novel, selective and potent ASOs for human APOE and TREM2. We used a combination of in vitro iPSC-microglia models, as well as microglial xenotransplanted mice to provide proof of activity in human microglial in vivo.ResultsWe proved their efficacy in human iPSC microglia in vitro, as well as their pharmacological activity in vivo in a xenografted microglia model. We demonstrate ASOs targeting human microglia can modify their transcriptional profile and their response to amyloid-? plaques in vivo in a model of AD.ConclusionsThis study is the first proof-of-concept that human microglial can be modulated using ASOs in a dose-dependent manner to manipulate microglia phenotypes and response to neurodegeneration in vivo.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13024-024-00725-9.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 34811 ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢800 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 34811 Product Name: ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢800 Safety Data SheetCatalog #: Product Name: 05965 MyoCultâ„¢ Differentiation Kit (Human) Catalog #: 05965 Product Name: MyoCultâ„¢ Differentiation Kit (Human) Product Information SheetCatalog #: Lot #: Language: Product Name: Catalog #:100-1398Lot #:AllLanguage:EnglishProduct Name:BKV (LT) Peptide PoolCatalog #: 100-1398 Lot #: All Language: English Product Name: BKV (LT) Peptide Pool Reference(May 2024) Nature Communications 15High-speed optical imaging with sCMOS pixel reassignment
Fluorescence microscopy has undergone rapid advancements, offering unprecedented visualization of biological events and shedding light on the intricate mechanisms governing living organisms. However, the exploration of rapid biological dynamics still poses a significant challenge due to the limitations of current digital camera architectures and the inherent compromise between imaging speed and other capabilities. Here, we introduce sHAPR, a high-speed acquisition technique that leverages the operating principles of sCMOS cameras to capture fast cellular and subcellular processes. sHAPR harnesses custom fiber optics to convert microscopy images into one-dimensional recordings, enabling acquisition at the maximum camera readout rate, typically between 25 and 250 kHz. We have demonstrated the utility of sHAPR with a variety of phantom and dynamic systems, including high-throughput flow cytometry, cardiomyocyte contraction, and neuronal calcium waves, using a standard epi-fluorescence microscope. sHAPR is highly adaptable and can be integrated into existing microscopy systems without requiring extensive platform modifications. This method pushes the boundaries of current fluorescence imaging capabilities, opening up new avenues for investigating high-speed biological phenomena. The authors introduce a highspeed acquisition technique, sHAPR, for rapid exploration of biodynamics using fluorescence microscopy. The method leverages sCMOS cameras and custom fibre optics to convert microscopy images into 1D recordings, enabling acquisition at the maximum camera readout rate.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 34411 ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 34411 Product Name: ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 Safety Data SheetCatalog #: Product Name: 05833 STEMdiffâ„¢ Neural Progenitor Medium Catalog #: 05833 Product Name: STEMdiffâ„¢ Neural Progenitor Medium Safety Data SheetCatalog #: Product Name: 60150 Anti-Mouse Ly-49A Antibody, Clone YE1/32.8.5 Catalog #: 60150 Product Name: Anti-Mouse Ly-49A Antibody, Clone YE1/32.8.5 Product Information SheetCatalog #: Lot #: Language: Product Name: Catalog #:100-1397Lot #:AllLanguage:EnglishProduct Name:HPV18 (L2) Peptide PoolCatalog #: 100-1397 Lot #: All Language: English Product Name: HPV18 (L2) Peptide Pool Reference(Jun 2024) American Journal of Human Genetics 111 7Truncated variants of MAGEL2 are involved in the etiologies of the Schaaf-Yang and Prader-Willi syndromes
SummaryThe neurodevelopmental disorders Prader-Willi syndrome (PWS) and Schaaf-Yang syndrome (SYS) both arise from genomic alterations within human chromosome 15q11–q13. A deletion of the SNORD116 cluster, encoding small nucleolar RNAs, or frameshift mutations within MAGEL2 result in closely related phenotypes in individuals with PWS or SYS, respectively. By investigation of their subcellular localization, we observed that in contrast to a predominant cytoplasmic localization of wild-type (WT) MAGEL2, a truncated MAGEL2 mutant was evenly distributed between the cytoplasm and the nucleus. To elucidate regulatory pathways that may underlie both diseases, we identified protein interaction partners for WT or mutant MAGEL2, in particular the survival motor neuron protein (SMN), involved in spinal muscular atrophy, and the fragile-X-messenger ribonucleoprotein (FMRP), involved in autism spectrum disorders. The interactome of the non-coding RNA SNORD116 was also investigated by RNA-CoIP. We show that WT and truncated MAGEL2 were both involved in RNA metabolism, while regulation of transcription was mainly observed for WT MAGEL2. Hence, we investigated the influence of MAGEL2 mutations on the expression of genes from the PWS locus, including the SNORD116 cluster. Thereby, we provide evidence for MAGEL2 mutants decreasing the expression of SNORD116, SNORD115, and SNORD109A, as well as protein-coding genes MKRN3 and SNRPN, thus bridging the gap between PWS and SYS. Graphical abstract Mutations within MAGEL2 from chromosomal region 15q11–q13 cause Schaaf-Yang syndrome, which is phenotypically related to Prader-Willi syndrome, caused by deletion of the SNORD116 cluster within the same locus. We correlate mutations within MAGEL2 to spinal muscular atrophy and autism and also demonstrate its influence on the abundance of SNORD116.Catalog #: Product Name: 05230 STEMdiffâ„¢ Trilineage Differentiation Kit 05990 °Õ±ð³§¸éâ„¢-·¡8â„¢ Catalog #: 05230 Product Name: STEMdiffâ„¢ Trilineage Differentiation Kit Catalog #: 05990 Product Name: °Õ±ð³§¸éâ„¢-·¡8â„¢ Safety Data SheetCatalog #: Product Name: 60149 Anti-Human CD10 Antibody, Clone FR4D11 Catalog #: 60149 Product Name: Anti-Human CD10 Antibody, Clone FR4D11 Product Information SheetCatalog #: Lot #: Language: Product Name: Catalog #:100-1396Lot #:AllLanguage:EnglishProduct Name:HPV18 (L1) Peptide PoolCatalog #: 100-1396 Lot #: All Language: English Product Name: HPV18 (L1) Peptide Pool Items 2401 to 2412 of 13914 total
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