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- Safety Data Sheet
Catalog #: Product Name: 100-1614 Anti-Mouse TCR Beta Antibody, Clone H57-597, PerCP-Cy5.5 Catalog #: 100-1614 Product Name: Anti-Mouse TCR Beta Antibody, Clone H57-597, PerCP-Cy5.5 - Safety Data Sheet
Catalog #: Product Name: 100-1613 Anti-Mouse TCR Beta Antibody, Clone H57-597, FITC Catalog #: 100-1613 Product Name: Anti-Mouse TCR Beta Antibody, Clone H57-597, FITC - ReferenceA. Becerra-Calixto et al. (Oct 2025) Journal of Neuroinflammation 22
A neuroimmune cerebral assembloid model to study the pathophysiology of familial Alzheimer’s disease
Alzheimer’s disease (AD) is the leading cause of dementia globally. The accumulation of amyloid and tau proteins, neuronal cell death and neuroinflammation are seen with AD progression, resulting in memory and cognitive impairment. Microglia are crucial for AD progression as they engage with neural cells and protein aggregates to regulate amyloid pathology and neuroinflammation. Recent studies indicate that microglia contribute to the propagation of amyloid beta (Aβ) via their immunomodulatory functions including Aβ phagocytosis and inflammatory cytokine production. Three-dimensional cell culture techniques provide the opportunity to study pathophysiological changes in AD in human-derived samples that are difficult to recapitulate in animal models (e.g., transgenic mice). However, these models often lack immune cells such as microglia, which play a critical role in AD pathophysiology. In this study, we developed a neuroimmune assembloid model by integrating cerebral organoids (COs) with induced microglia-like cells (iMGs) derived from human induced pluripotent stem cells from familial AD patient with PSEN2 mutation. After 120 days in culture, we found that iMGs were successfully integrated within the COs. Interestingly, our assembloids displayed histological, functional and transcriptional features of the pro-inflammatory environment seen in AD, including amyloid plaque-like and neurofibrillary tangle-like structures, reduced microglial phagocytic capability, and enhanced neuroinflammatory and apoptotic gene expression. In conclusion, our neuroimmune assembloid model effectively replicates the inflammatory phenotype and amyloid pathology seen in AD. The online version contains supplementary material available at 10.1186/s12974-025-03544-x.Catalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ 05310 STEMdiffâ„¢ Hematopoietic Kit 100-0019 STEMdiffâ„¢ Microglia Differentiation Kit 100-0020 STEMdiffâ„¢ Microglia Maturation Kit 08570 STEMdiffâ„¢ Cerebral Organoid Kit Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 05310 Product Name: STEMdiffâ„¢ Hematopoietic Kit Catalog #: 100-0019 Product Name: STEMdiffâ„¢ Microglia Differentiation Kit Catalog #: 100-0020 Product Name: STEMdiffâ„¢ Microglia Maturation Kit Catalog #: 08570 Product Name: STEMdiffâ„¢ Cerebral Organoid Kit Safety Data SheetCatalog #: Product Name: 100-1612 Anti-Mouse TCR Beta Antibody, Clone H57-597, PE Catalog #: 100-1612 Product Name: Anti-Mouse TCR Beta Antibody, Clone H57-597, PE ReferenceR. B. Kang et al. (Oct 2025) Nature Communications 16Human pancreatic α-cell heterogeneity and trajectory inference analyses reveal SMOC1 as a β-cell dedifferentiation gene
β-cell dysfunction and dedifferentiation towards an α-cell-like phenotype are hallmarks of type 2 diabetes. However, the cell subtypes involved in β-to-α-cell transition are unknown. Using single-cell and single-nucleus RNA-seq, RNA velocity, PAGA/cell trajectory inference, and gene commonality, we interrogated α-β-cell fate switching in human islets. We found five α-cell subclusters with distinct transcriptomes. PAGA analysis showed bifurcating cell trajectories in non-diabetic while unidirectional cell trajectories from β-to-α-cells in type 2 diabetes islets suggesting dedifferentiation towards α-cells. Ten genes comprised the common signature genes in trajectories towards α-cells. Among these, the α-cell gene SMOC1 was expressed in β-cells in type 2 diabetes. Enhanced SMOC1 expression in β-cells decreased insulin expression and secretion and increased β-cell dedifferentiation markers. Collectively, these studies reveal differences in α-β-cell trajectories in non-diabetes and type 2 diabetes human islets, identify signature genes for β-to-α-cell trajectories, and discover SMOC1 as an inducer of β-cell dysfunction and dedifferentiation. Subject terms: Cell signalling, Diabetes, DifferentiationCatalog #: Product Name: 34411 ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 Catalog #: 34411 Product Name: ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢400 ReferenceB. Vanderperre et al. (Oct 2025) Communications Biology 8Novel regulators of heparan sulfate proteoglycans modulate cellular uptake of α-synuclein fibrils
Synucleinopathies are characterized by the accumulation and propagation of α-synuclein (α-syn) aggregates throughout the brain, leading to neuronal dysfunction and death. In this study, we used an unbiased FACS-based genome-wide CRISPR/Cas9 knockout screening to identify genes that regulate the entry and accumulation of α-syn preformed fibrils (PFFs) in cells. We identified key genes and pathways specifically implicated in α-syn PFFs intracellular accumulation, including heparan sulfate proteoglycans (HSPG) biosynthesis and Golgi trafficking. All confirmed hits affected heparan sulfate (HS), a post-translational modification known to act as a receptor for proteinaceous aggregates including α-syn and tau. Intriguingly, deletion of SLC39A9 and C3orf58 genes, encoding respectively a Golgi-localized exporter of Zn 2+ , and the Golgi-localized putative kinase DIPK2A, specifically impaired the uptake of α-syn PFFs, by preventing the binding of PFFs to the cell surface. Mass spectrometry-based analysis of HS chains in SLC39A9 -/- and C3orf58 -/- cells indicated major defects in HS homeostasis. Additionally, Golgi accumulation of NDST1, a prime HSPG biosynthetic enzyme, was detected in C3orf58 -/- cells. Interestingly, C3orf58 -/- human iPSC-derived microglia and dopaminergic neurons exhibited a strong reduction in their ability to internalize α-syn PFFs. Altogether, our data identifies new modulators of HSPGs that regulate α-syn PFFs cell surface binding and uptake. Subject terms: Cellular neuroscience, GlycobiologyCatalog #: Product Name: 05310 STEMdiff™ Hematopoietic Kit Catalog #: 05310 Product Name: STEMdiff™ Hematopoietic Kit Safety Data SheetCatalog #: Product Name: 100-1611 Anti-Mouse TCR Beta Antibody, Clone H57-597, APC Catalog #: 100-1611 Product Name: Anti-Mouse TCR Beta Antibody, Clone H57-597, APC ReferenceKim et al. (Oct 2025) Scientific Reports 15Attenuation of natural killer cell cytotoxicity by interaction between NKp30 of NK cells and dipeptidase 1 of colon cancer cells
Natural killer (NK) cells play a crucial role in immune surveillance by recognizing and eliminating tumor cells. However, tumors employ various mechanisms to evade NK cell-mediated immunity. NKp30 is a potent activating receptor on NK cells, but its function can be inhibited by specific ligands secreted by cancer cells. Here, we identified dipeptidase 1 (DPEP1) as a novel ligand for NKp30 in KM12C colon cancer cells, using co-immunoprecipitation, confocal microscopy, and flow cytometry. We examined how the DPEP1–NKp30 interaction affects NK cell activity and found that NK cytotoxicity increased in KM12C cells with DPEP1 knockdown but was significantly reduced in HCT116 cells overexpressing DPEP1. We further demonstrated that DPEP1 is secreted via extracellular vesicles and that its interaction with NKp30 suppressed the expression and secretion of perforin 1, granzyme B, CD107a, and interferon-γ in NK92 cells. In a xenograft mouse model treated with NK92 cells, tumors derived from HCT116/DPEP1 cells were significantly larger than those from HCT116/mock cells. Using peripheral blood-derived human NK cells, we confirmed that DPEP1 inhibited both cytotoxicity and granzyme B secretion. These findings suggest that disrupting the DPEP1–NKp30 interaction may enhance NK cell-mediated cytotoxicity and represent a novel therapeutic strategy for cancer immunotherapy. The online version contains supplementary material available at 10.1038/s41598-025-18475-z.Catalog #: Product Name: 100-0711 ImmunoCult™ NK Cell Expansion Kit Catalog #: 100-0711 Product Name: ImmunoCult™ NK Cell Expansion Kit ReferenceM. Amouzgar et al. (Oct 2025) Nature Communications 16A deep single cell mass cytometry approach to capture canonical and noncanonical cell cycle states
The cell cycle (CC) underpins diverse cell processes like cell differentiation, cell expansion, and tumorigenesis but current single-cell (sc) strategies study CC as: coarse phases, rely on transcriptomic signatures, use imaging modalities limited to adherent cells, or lack high-throughput multiplexing. To solve this, we develop an expanded, Mass Cytometry (MC) approach with 48 CC-related molecules that deeply phenotypes the diversity of scCC states. Using Cytometry by Time of Flight, we quantify scCC states across suspension and adherent cell lines, and stimulated primary human T cells. Our approach captures the diversity of scCC states, including atypical CC states beyond canonical definitions. Pharmacologically-induced CC arrest reveals that perturbations exacerbate noncanonical states and induce previously unobserved states. Notably, primary cells escaping CC inhibition demonstrated aberrant CC states compared to untreated cells. Our approach enables deeper phenotyping of CC biology that generalizes to diverse cell systems with simultaneous multiplexing and integration with MC platforms. Subject terms: Assay systems, Proteomics, Cell biology, Immunology, Systems biologyCatalog #: Product Name: 15021 RosetteSepâ„¢ Human T Cell Enrichment Cocktail 10981 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium 100-0956 ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Catalog #: 15021 Product Name: RosetteSepâ„¢ Human T Cell Enrichment Cocktail Catalog #: 10981 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó T Cell Expansion Medium Catalog #: 100-0956 Product Name: ±õ³¾³¾³Ü²Ô´Ç°ä³Ü±ô³Ùâ„¢-³Ý¹ó Safety Data SheetCatalog #: Product Name: 100-1610 Anti-Mouse TCR Beta Antibody, Clone H57-597 Catalog #: 100-1610 Product Name: Anti-Mouse TCR Beta Antibody, Clone H57-597 ReferenceL. Truszkowski et al. (Sep 2025) Open Research Europe 4 2Refined and benchmarked homemade media for cost-effective, weekend-free human pluripotent stem cell culture
Cost-effective, practical, and reproducible culture of human pluripotent stem cells (hPSCs) is required for basic and translational research. Basal 8 (B8) has emerged as a cost-effective solution for weekend-free and chemically-defined hPSC culture. However, the requirement to home-produce some recombinant growth factors for B8 can hinder access and reproducibility. Moreover, we found the published B8 formulation suboptimal in widely-used normoxic hPSC culture. Lastly, the performance of B8 in functional applications such as genome editing or organoid differentiation required systematic evaluation. We formulated B8 with commercially available, growth factors and adjusted its composition to support normoxic culture of WTC11 human induced pluripotent stem cell line. We compared this formulation (B8+) with commercial Essential 8 (cE8) and a home-made, weekend-free E8 formulation (hE8). We measured pluripotency marker expression and cell cycle by flow cytometry, and investigated the transcriptional profiles by bulk and single-cell RNA sequencing. We further assessed genomic stability, genome editing efficiency, single-cell cloning, and differentiation in both monolayer and organoids. Finally, we validated key findings using male (H1) and female (H9) human embryonic stem cells. hE8 performed comparably to cE8 across most functional assays and cell lines. In contrast, cells in B8+ displayed higher NANOG expression and improved genome editing efficiency. At the same time, B8+ led to gene expression changes indicative of marked lineage priming, reflected in altered morphology and differential response to some differentiation protocols. Both weekend-free media resulted in a modest transcriptional shift towards a less metabolically active state, consistent with intermittent media starvation. Homemade weekend-free media can provide a cost-effective alternative to commercial formulations. hE8, integrating some features of B8 while resembling cE8, emerges as a robust and practical option with limited compromises. B8+, though advantageous in some contexts, warrants caution due to lineage priming effects that may impact differentiation outcomes.Catalog #: Product Name: 05230 STEMdiffâ„¢ Trilineage Differentiation Kit Catalog #: 05230 Product Name: STEMdiffâ„¢ Trilineage Differentiation Kit Safety Data SheetCatalog #: Product Name: 100-1609 Anti-Mouse CD3 Antibody, Clone 17A2, FITC Catalog #: 100-1609 Product Name: Anti-Mouse CD3 Antibody, Clone 17A2, FITC Items 253 to 264 of 13914 total
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