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Items 265 to 276 of 14067 total
- ReferenceM. Shameem et al. (Dec 2025) Journal of Cardiovascular Development and Disease 12 12
Early Cytoskeletal Remodeling Drives Hypertrophic Cardiomyopathy Pathogenesis in MYH6/7 Mutant hiPSC-Derived Cardiomyocytes
Hypertrophic cardiomyopathy (HCM) is a common and deadly cardiac disease characterized by enlarged myocytes, increased myocardial wall thickening, and fibrosis. A majority of HCM cases are associated with mutations in the β-myosin heavy chain (MYH7) converter domain locus, which leads to varied pathophysiological and clinical manifestations. Using base-editing technology, we generated mutant human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) harboring HCM-causing myosin converter domain mutations (MYH7 c.2167C>T [R723C]; MYH6 c.2173C>T [R725C]) to define HCM pathogenesis in vitro. In this study, we integrated transcriptomic analysis with phenotypic and molecular analyses to dissect the HCM disease mechanisms using MYH6/7 myosin mutants. Our KEGG analysis of bulk RNA-sequencing data revealed significant upregulation of transcripts associated with HCM in the mutant hiPSC-CMs. Further, in-depth transcriptomic analysis using Gene-Ontology (GO-term) analysis for biological process showed upregulation of several transcripts associated with heart development and disease. Notably, our analysis showed robust upregulation of cytoskeletal transcripts, including actin-cytoskeleton networks, sarcomere components, and other structural proteins in the mutant CMs. Furthermore, cellular and nuclear morphological analysis showed that the MYH6/7 mutation induced cellular hypertrophy and increased aspect ratio compared to the isogenic control. Immunostaining experiments showed marked sarcomere disorganization with lower sarcomeric order and higher dispersion in the mutant hiPSC-CMs, highlighting the remodeling of the myofibril arrangement. Notably, the MYH6/7 mutant showed reduced cortical F-actin expression and increased central F-actin expression compared to the isogenic control, confirming the cytoskeletal remodeling and sarcomeric organization during HCM pathogenesis. These pathological changes accumulated progressively over time, underscoring the chronic and evolving nature of HCM driven by the MYH6/7 mutations. Together, our findings provide critical insights into the cellular and molecular underpinnings of MYH6/7-mutation-associated disease. These findings offer valuable insights into HCM pathogenesis, aiding in future therapies.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 ReferenceM. Gil et al. (Dec 2025) Glia 74 2A Human Model of Oligodendrocyte Development Shows MCLâ€1 Influences Oligodendrocyte Morphogenesis
Oligodendrocytes are the myelinating cells of the central nervous system. Regulation of the early stages of oligodendrocyte development is critical to the function of the cell. Specifically, myelin sheath formation is an energetically demanding event that requires precision, as alterations may lead to dysmyelination. Fatty acid βâ€oxidation has been shown to be critical for the function of oligodendrocytes. We previously showed that myeloid cell leukemiaâ€1 (MCLâ€1), a wellâ€characterized antiâ€apoptotic protein, is required for the development of murine oligodendrocytes in vivo. Further, MCLâ€1 regulates longâ€chain fatty acid βâ€oxidation in cancer cells through its interaction with Acylâ€CoA synthetase longâ€chain family member 1 (ACSL1), an enzyme responsible for the conversion of free longâ€chain fatty acids into fatty acylâ€CoA esters. Here, we introduce an in vitro system to isolate human stem cellâ€derived oligodendrocyte progenitor cells (OPCs) and investigate the involvement of MCLâ€1 during human oligodendrocyte development. Using this system, we pharmacologically inhibited MCLâ€1 in OPCs to investigate its nonâ€apoptotic function at this developmental stage. We also used a motor neuronâ€oligodendrocyte coâ€culture system to examine the downstream effects of MCLâ€1 at later developmental stages when oligodendrocytes begin to contact axons and generate myelin. We demonstrate that the mitochondrial network changes in human oligodendrocyte development resemble those reported in mouse tissue. Our findings point to MCLâ€1 as a critical factor essential for proper oligodendrocyte morphogenesis. A unified model of oligodendrocyte differentiation from human embryonic stem cells revealed that MCLâ€1 is critical for regulating the expression of oligodendrocyteâ€related genes and the morphogenesis of myelinating oligodendrocytes.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 ReferenceC. Arasa et al. (Dec 2025) European Journal of Immunology 55 12Staphylococcal Enterotoxin A Shapes Monocyte Transcription and Macrophage Polarization: Implications for Immune Responses in Infection and Inflammation
Staphylococcal enterotoxins (SE) crosslink the MHCâ€II on antigenâ€presenting cells (APC) with the Tâ€cell receptor, inducing a polyclonal Tâ€cell response. Although APCs are the initial targets of SE and are critical in shaping subsequent Tâ€cell activation, the effects of SE on APC function remain poorly understood. This study investigates the immunomodulatory effects of staphylococcal enterotoxin A (SEA) on monocytes and their differentiation into monocyteâ€derived dendritic cells (moDC) or macrophages (MDM). Transcriptomic analyses of human monocytes via RNA sequencing revealed SEAâ€induced enrichment of gene pathways associated with inflammation, infection, and dermatitis, effects that were amplified in the presence of T cells. Phenotypic and functional characterization showed that SEAâ€primed monocytes differentiated into MDM with an altered polarization, deviating from classical M1/M2 pathways. SEAâ€primed MDM exhibited downregulation of key markers, including HLAâ€DR, CD80, CD86, and PDâ€L1. Functional assays demonstrated that SEAâ€primed MDM pushed hyperinflammatory Tâ€cell responses, with significantly enhanced proliferation and IFNâ€Î³ secretion. In contrast, following SEAâ€priming, moDC retained robust antigenâ€presenting capabilities and displayed enhanced expression of molecules involved in Tâ€cell interactions. These findings provide mechanistic insights into SEAâ€mediated immune modulation, illustrating how SEA reprograms MDM functions and amplifies proinflammatory Tâ€cell responses. This advances our understanding of superantigenâ€driven immune interactions, offering a foundation for developing therapeutic strategies to mitigate superantigenâ€mediated immune conditions. Staphylococcal enterotoxin A (SEA) alters monocyte differentiation and function, while preserving T cell stimulatory capacity. SEAâ€primed macrophages downregulate antigenâ€presenting markers yet drive heightened Tâ€cell proliferation and IFNâ€Î³ secretion. These findings reveal mechanisms of SEAâ€mediated immune modulation and superantigenâ€driven inflammation.Catalog #: Product Name: 17951 EasySepâ„¢ Human T Cell Isolation Kit 19059 EasySepâ„¢ Human Monocyte Enrichment Kit 18000 EasySepâ„¢ Magnet Catalog #: 17951 Product Name: EasySepâ„¢ Human T Cell Isolation Kit Catalog #: 19059 Product Name: EasySepâ„¢ Human Monocyte Enrichment Kit Catalog #: 18000 Product Name: EasySepâ„¢ Magnet ReferenceR. Bhave et al. (Dec 2025) Scientific Reports 15 2Serum-free differentiation platform for the generation of B lymphocytes and natural killer cells from human CD34+ cord blood progenitors
Pre-clinical research on B and NK cell development relies on murine stromal cell-based systems with reduced physiological relevance and clinical applicability. A serum-free, fully humanized co-culture system utilizing human bone marrow-derived mesenchymal stromal cells (BM-MSCs) was developed to differentiate CB-CD34+ cells towards B and NK cell lineages. Differentiation dynamics were monitored via flow cytometry, with immunophenotypic analysis tracking progression from progenitors to mature cells. The system generated CD19+ IgM+ immature B cells and CD56+ CD16+ NK cells, recapitulating fetal stages of human lymphopoiesis. Serum-free media conditions ensured reproducibility and high overall yield of CD19+ B (35 ± 5.32%) and CD56+ NK (28.46 ± 7.01%) cell progenitors. Flow cytometry identified distinct population peaks, confirming temporal control over differentiation. This clinically relevant platform addresses the limitations of traditional models by providing a more physiologically accurate human microenvironment. The serum-free system supports applications in disease modeling, genotoxic compound screening, and mutational studies of hematopoiesis. By enabling scalable production of B and NK cells it aims to accelerate translational research for immunodeficiencies, cancer immunotherapy, and hematopoietic disorders.Catalog #: Product Name: 09600 StemSpanâ„¢ SFEM 09605 StemSpanâ„¢ SFEM II Catalog #: 09600 Product Name: StemSpanâ„¢ SFEM Catalog #: 09605 Product Name: StemSpanâ„¢ SFEM II ReferenceC. P. Pacini et al. (Dec 2025) European Journal of Immunology 55 12Selection and Characterisation of Minor Histocompatibility Antigenâ€Specific Regulatory T Cells in Fully HLAâ€Matched Setting for GVHD Therapy
Graftâ€versusâ€host disease is mediated by donorâ€derived T cells reactive against the recipient's broadly expressed minor histocompatibility antigens (mHA). Regulatory T cells (Treg) have been explored as a therapeutic approach for chronic GVHD (cGVHD). The promising results from polyclonal Treg trials in this setting have led us to develop a Treg product specific for mismatched minor antigens between patient and donor (mTreg), circumventing broad immune suppression risks. HLAâ€matched siblings of opposite sexes were used to obtain the sister's CD4+CD25hiCD127low Treg for coâ€culture with the respective brother's dendritic cells as a source of mismatched mHA. We have established the optimal culture conditions resulting in the highest mTreg proliferation and viability. Comprehensive phenotyping during the ex vivo selection shows PDâ€1, CTLAâ€4, CD39 and HLAâ€DR expression. Transcriptomic analysis revealed a switch in metabolic process, and upâ€regulation of functional Treg genes. Furthermore, mTreg possess specific and potent suppressive activity, in which there is a dependency on cellâ€toâ€cell contact and a role for HLA class II expression on mTreg. This protocol would allow the generation of Treg specific to an array of mHA from the recipient's healthy tissues, likely providing a directed and strong suppression of cGVHD. We optimised a protocol for mHAâ€specific Treg (mTreg) selection in an HLAâ€matched context while defining its phenotype, transcriptional state and function. mTreg were highly activated and exerted specific, HLA class IIâ€, contactâ€dependent suppression. This protocol can be explored as a highly personalised antigenâ€specific Tregâ€based therapy in future clinical trials for cGVHD.Catalog #: Product Name: 10971 ImmunoCultâ„¢ Human CD3/CD28 T Cell Activator 17858 EasySepâ„¢ Human CD14 Positive Selection Kit II 100-0784 ImmunoCultâ„¢ Human CD3/CD28 T Cell Activator Catalog #: 10971 Product Name: ImmunoCultâ„¢ Human CD3/CD28 T Cell Activator Catalog #: 17858 Product Name: EasySepâ„¢ Human CD14 Positive Selection Kit II Catalog #: 100-0784 Product Name: ImmunoCultâ„¢ Human CD3/CD28 T Cell Activator ReferenceS. Sagie et al. (Dec 2025) Cell Reports Medicine 6 12Lymphodepleting chemotherapy potentiates neoantigen-directed T cell therapy by enhancing antigen presentation
Adoptive cell therapy (ACT) targeting tumor-specific antigens holds promise for solid tumors, but limited neoantigen presentation remains a key barrier to efficacy. Here, we identify and characterize a T cell receptor (TCR), T104, for the KRAS.G12V mutation, a prevalent neoantigen in colorectal, lung, and pancreatic cancers. TCR-T104 selectively recognizes and kills KRAS.G12V-expressing tumor cells. Combining T cell therapy with lymphodepleting chemotherapy significantly enhances tumor cell killing, particularly by TCR-T cells, tumor-infiltrating lymphocytes (TILs), and T cell engager antibodies across multiple cancer types and target antigens. Mechanistically, chemotherapy upregulates immunoproteasome activity and human leukocyte antigen (HLA)-I surface expression. HLA-immunopeptidome analyses reveal that chemotherapy remodels the antigenic landscape across tumor cell lines and in vivo models, increasing peptide abundance and hydrophobicity while altering proteasomal cleavage preferences. These findings establish a synergistic role for chemotherapy in enhancing neoantigen presentation and T cell-mediated tumor recognition and suggest that fine-tuning these regimens could improve ACT efficacy, particularly in tumors with low-abundance neoantigens.Catalog #: Product Name: 19051 EasySep™ Human T Cell Enrichment Kit Catalog #: 19051 Product Name: EasySep™ Human T Cell Enrichment Kit ReferenceN. S. Wetzel et al. (Dec 2025) Neurology® Neuroimmunology & Neuroinflammation 13 1Patient-Derived Monoclonal Myelin Oligodendrocyte Glycoprotein Autoantibodies Mediate Cytotoxicity
Background and Objectives: Serum myelin oligodendrocyte glycoprotein (MOG) antibodies are a hallmark of the newly defined neuroinflammatory disease entity MOG antibody–associated disease (MOGAD). Yet, the lack of patient-derived recombinant human MOG (hMOG)–reactive autoantibodies limits investigations into the molecular mechanisms by which these autoantibodies mediate CNS pathology, thereby hindering rational therapeutic approaches. To understand the origins and disease-relevant mechanisms of autoantibodies in MOGAD, we generated and characterized monoclonal anti-hMOG antibodies (MOG-mAbs) from circulating B cells of patients with MOGAD.Methods: We isolated MOG-specific B-cell receptor (BCR) sequences from unique circulating B-cell clones of 6 patients with MOGAD using an antigen selection approach. BCR sequences were expressed as immunoglobulin (Ig)G1 antibodies, and their molecular features, epitope specificity, and binding to MOG isoforms were investigated. The MOG-mAbs’ ability to mediate antibody-dependent cellular phagocytosis (ADCP), natural killer (NK) cell–mediated antibody-dependent cellular cytotoxicity (ADCC), and complement-dependent cytotoxicity (CDC) toward MOG-expressing cells was assessed by live cell-based assays.Results: Of the 15 MOG-mAbs generated, 4 revealed evidence of affinity maturation, whereas the remaining 11 were germline encoded. Binding capacities to hMOG varied considerably, with the most frequent putative epitope mapping to a region that includes residue P42. The efficacy of these antibodies in mediating ADCP, ADCC, and CDC of MOG-expressing cells was heterogeneous and associated with their binding characteristics to MOG and its isoforms.Discussion: Taken together, the molecular characteristics and binding patterns of these patient-derived MOG-mAbs reveal a diverse repertoire of MOG-binding autoantibodies with pathogenic capacity in vitro. Consequently, these well-characterized patient autoantibodies offer a foundation for developing in vivo models of MOGAD, serve as tools to standardize diagnostic assays, and guide development of therapeutic strategies targeting either B cells or autoantibodies and their effector functions.Catalog #: Product Name: 17955 EasySep™ Human NK Cell Isolation Kit Catalog #: 17955 Product Name: EasySep™ Human NK Cell Isolation Kit ReferenceG. Melo et al. (Dec 2025) PLOS Pathogens 21 12Activation of B1 B cells by F. tularensis atypical LPS depends on classical complement and C3a
Francisella tularensis (Ft), a Gram-negative bacterium that causes tularemia, possesses a non-inflammatory atypical LPS (LPSFt) that is highly immunogenic through unknown mechanism. We previously showed that immunization with LPSFt, a type 2 T-independent (TI) antigen, elicits protective LPSFt-specific IgM (IgMFt) and IgG3Ft by B1 cells in a mechanism dependent on the IL-5 produced by innate lymphoid cells type 2 (ILC2). Here, we examined the role of complement in the B1 cells’ response against LPSFt. C3-/-, C1q-/- and C4-/- mice immunized with LPSFt failed to produce IgMFt and IgG3Ft. In contrast, the response of Cfb-/- and Mbl1/Mbl2-/- mice was comparable to that of WT mice. Thus, activation of the classical complement cascade, but not the alternative or the Mannose Binding Lectin pathway, is required for activation of B1 cells and production of LPSFt-specific antibodies. Complement activation generates the C3d fragment, which opsonizes antigens for recognition by complement receptor-2 (CR2), and the C3a and C5a anaphylatoxins. Our results show that C3d opsonized LPSFt and that the response to immunization was dependent on CR2 expression by B1 cells. Importantly, the response to LPSFt immunization was also drastically decreased in C3ar1-/-, but not in C5ar1-/- mice. C3a induced IL-5 in ILC2, which supported B1 cells activation. Decreased antibody production in C3ar1-/- and Cr2-/- mice correlated with increased susceptibility to tularemia. Together, these results demonstrate that the high immunogenicity of LPSFt depends on two effector mechanisms triggered by activation of the classical complement pathway: 1) tagging of LPSFt with C3d fragment, leading to its interaction with CR2 expressed by B1 cells; 2) production of the anaphylatoxin C3a that stimulated IL-5 secretion by ILC2. Our study increases our understanding of the B1 cells’ response to TI-2 antigens and identifies two complement effector mechanisms that can be harnessed for therapeutic interventions. Author summaryThe lipopolysaccharide (LPS) of the bacterium Francisella tularensis strongly stimulates B cells for antibody production independently of T cell help through unknown mechanism. In the present study we examined the role of the complement cascade in this process. We found that production of antibodies against this LPS depends on activation of the classical complement pathway but not the MBL-dependent lectin or the alternative pathways. Following complement activation, LPS became tagged with the C3d complement fragment leading to its interaction with the complement receptor CR2 expressed by B cells. Complement activation also resulted in production of the anaphylatoxin C3a that was required for B cells activation, possibly through induction of IL-5 by innate lymphoid cells 2. Our study increases our understanding of the B cells’ response to T-independent antigens and identifies two complement effector mechanisms that can be harnessed for therapeutic interventions.Catalog #: Product Name: 19842 EasySep™ Mouse ILC2 Enrichment Kit Catalog #: 19842 Product Name: EasySep™ Mouse ILC2 Enrichment Kit ReferenceM. Dastpak et al. (Dec 2025) PLOS One 20 12SF3B1K700E mutation in human embryonic stem cells causes aberrant expression of immune-related genes
SF3B1, a component of the U2 snRNP pre-mRNA splicing factor, plays a critical role in splicing and is frequently mutated in cancer, particularly hematologic malignancies. We investigated the effects of the most common SF3B1 mutation, heterozygous substitution of Lysine 700 to Glutamate (K700E), in human embryonic stem cells (hESC), using CRISPR-Cas9 to generate heterozygous SF3B1K700E clones. Interestingly, we observed the upregulation of several key transcription regulators associated with hematopoiesis and a broad range of immune genes in SF3B1K700E hESCs. Despite differences in the transcriptional and splicing profiles between hESC and myelodysplastic syndrome (MDS) cells harboring the SF3B1K700E mutation, several common immune gene programs were identified in both cell types. To elucidate the molecular mechanisms underlying dysregulated gene expression in SF3B1K700E hESCs, we mapped actively engaged RNA polymerase II (RNA Pol II) using Precision Run-On sequencing (PRO-seq). These analyses revealed that the SF3B1K700E mutation alters RNA Pol II elongation properties. Specifically, we observed a general increase in pause release in SF3B1K700E hESCs, consistent with recent work in leukemia cells suggesting that the SF3B1K700E mutation affects early transcription elongation. Taken together, our study identifies several candidate genes that could contribute to the SF3B1 mutated phenotype and clarifies the role for the U2 snRNP and pre-spliceosome assembly on transcription by RNA Pol II. Further, our data suggest that mutations of SF3B1 impact immune gene expression independent of cell type, providing new insights into the role of SF3B1K700E in hematologic malignancies.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 ReferenceJ. Ma et al. (Dec 2025) Communications Biology 8In vivo imaging reveals exosome-mediated intercellular communication in lens development
Lens transparency relies on proper intercellular communication. Exosomes are crucial mediators of intercellular communication and play a key role in organ homeostasis and development. However, their presence and dynamics in the lens remain unclear. Here, we report endogenous exosomes in the zebrafish lens using cryaa-driven Cd63-AcGFP labeling. Live imaging revealed dynamic exosome movement within lens cells and their potential transfer to adjacent tissues. Additionally, we found that the biogenesis of Cd63+ exosomes in the lens is regulated by the Syntenin-a pathway. And Syntenin-a knockdown delayed lens development by impairing lens cell differentiation, highlighting the potential role of lens cell–derived exosomes. Furthermore, ROR1+ lens progenitor cell-derived extracellular vesicles promoted lentoid differentiation in vitro, with proteomic analysis suggesting underlying mechanisms. Overall, our study addresses the gap in direct observation of endogenous lens exosomes, providing foundational insights into lens pathophysiology and a potential strategy for modulating the lens microenvironment. Visualization of endogenous exosomes in the zebrafish lens reveals their dynamic roles in intercellular communication and development, with Syntenin-a–regulated exosome biogenesis influencing lens cell differentiation.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 ReferenceR. Q. Notti et al. (Dec 2025) Nature Communications 16The resting and ligand-bound states of the membrane-embedded human T-cell receptor–CD3 complex
The T-cell receptor (TCR) initiates T-lymphocyte activation, but the mechanism of TCR activation remains uncertain. Here, we present cryogenic electron microscopy structures for the unliganded and human leukocyte antigen (HLA)-bound human TCR–CD3 complex in nanodiscs that provide a native-like lipid environment. Distinct from the open and extended conformation seen in detergent, the unliganded TCR–CD3 in nanodiscs adopts two related closed and compacted conformations that represent its physiologic resting state in vivo. By contrast, the HLA-bound complex adopts the open and extended conformation, and conformation-locking disulfide mutants show that ectodomain opening is necessary for maximal ligand-dependent T-cell activation. These structures also reveal conformation-dependent protein–lipid and glycan–glycan interactions within the TCR. Together, these results establish allosteric conformational change during TCR activation, reveal avenues for immunotherapeutic engineering, and highlight the importance of native-like lipid environments for membrane protein structure determination. The T-cell receptor (TCR) activation mechanism has remained uncertain. Here, the authors present molecular structures for the apo and ligand-bound human TCR–CD3 complex in lipid nanodiscs, revealing large conformational changes during activation.Catalog #: Product Name: 17661 EasySep™ Human APC Positive Selection Kit II Catalog #: 17661 Product Name: EasySep™ Human APC Positive Selection Kit II ReferenceD. Wang et al. (Dec 2025) Nature Communications 16Transcriptional regulation of protein synthesis by mediator kinase represents a therapeutic vulnerability in MYC-driven medulloblastoma
MYC-driven medulloblastoma (MB) is a highly aggressive brain tumor with poor prognosis and limited treatment options. Through CRISPR-Cas9 screening, we identify the Mediator-associated kinase CDK8 as a critical regulator of MYC-driven MB. Both genetic loss and pharmacological inhibition of CDK8 impair MB tumor growth. Moreover, we find that CDK8 cooperates with MYC to sustain the MYC-mediated translational program, as CDK8 depletion induces pronounced transcriptional changes in translation-associated gene sets, reduces ribosome biogenesis, and impairs protein synthesis. Mechanistically, CDK8 regulates the occupancy of RNA polymerase II at specific chromatin loci, facilitating epigenetic alterations that promote the transcription of ribosomal genes. Furthermore, combined inhibition of CDK8 and mTOR synergistically enhances therapeutic efficacy in vivo, leading to more pronounced tumor growth suppression. Overall, our findings establish a functional link between CDK8-mediated transcriptional regulation and mRNA translation, suggesting a promising therapeutic approach targeting protein synthesis for MYC-driven MB. MYC-driven medulloblastoma is an aggressive pediatric tumor with limited treatment options. Here, the authors show that CDK8 regulates ribosome biogenesis and that combined inhibition of CDK8 and mTOR demonstrates therapeutic efficacy in mouse models of this cancer.Catalog #: Product Name: 01700 ALDEFLUORâ„¢ Kit Catalog #: 01700 Product Name: ALDEFLUORâ„¢ Kit Items 265 to 276 of 14067 total
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