Product Information
Items 2077 to 2088 of 13914 total
- Reference(Dec 2024) Stem Cell Research & Therapy 15
Generation of vascularized pancreatic progenitors through co-differentiation of endoderm and mesoderm from human pluripotent stem cells
BackgroundThe simultaneous differentiation of human pluripotent stem cells (hPSCs) into both endodermal and mesodermal lineages is crucial for developing complex, vascularized tissues, yet poses significant challenges. This study explores a method for co-differentiation of mesoderm and endoderm, and their subsequent differentiation into pancreatic progenitors (PP) with endothelial cells (EC).MethodsTwo hPSC lines were utilized. By manipulating WNT signaling, we optimized co-differentiation protocols of mesoderm and endoderm through adjusting the concentrations of CHIR99021 and mTeSR1. Subsequently, mesoderm and endoderm were differentiated into vascularized pancreatic progenitors (vPP) by adding VEGFA. The differentiation characteristics and potential of vPPs were analyzed via transcriptome sequencing and functional assays.ResultsA low-dose CHIR99021 in combination with mTeSR1 yielded approximately 30% mesodermal and 70% endodermal cells. Introduction of VEGFA significantly enhanced EC differentiation without compromising PP formation, increasing the EC proportion to 13.9%. Transcriptomic analyses confirmed the effectiveness of our protocol, showing up-regulation of mesodermal and endothelial markers, alongside enhanced metabolic pathways. Functional assays demonstrated that vPPs could efficiently differentiate into insulin-producing ?-cells, as evidenced by increased expression of ?-cell markers and insulin secretion.ConclusionOur findings provide a robust method for generating vPPs, which holds significant promise for regenerative medicine applications, particularly in diabetes treatment.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13287-024-04120-5.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 Reference(Sep 2024) International Journal of Molecular Sciences 25 19Mesenchymal Stem Cells Derived from Human Urine-Derived iPSCs Exhibit Low Immunogenicity and Reduced Immunomodulatory Profile
Human-induced pluripotent stem cell (iPSC)-derived mesenchymal stem cells (iMSCs) represent a promising and renewable cell source for therapeutic applications. A systematic evaluation of the immunological properties and engraftment potential of iMSCs generated from urine-derived iPSCs is lacking, which has impeded their broader application. In this study, we differentiated urine-derived iPSCs into iMSCs and assessed their fundamental MSC characteristics, immunogenicity, immunomodulatory capacity and in vivo engraftment. Compared to umbilical cord-derived MSCs (UCMSCs), iMSCs demonstrated an enhanced proliferative capacity, a higher level of regenerative gene expression, and lower immunogenicity, strengthening resistance to apoptosis induced by allogeneic peripheral blood mononuclear cells (PBMCs) and the NK-92 cell line. In addition, iMSCs exhibited a diminished ability to inhibit T cell proliferation and activation compared with UCMSCs. Transcriptomic analyses further revealed the decreased expression of immune regulatory factors in iMSCs. After transfusion into mouse models, iMSCs engrafted in the lungs, liver, and spleen and exhibited the ability to migrate to tumor tissues. Our results indicated that iMSCs generated from urine-derived iPSCs have a significant replicative capacity, low immunogenicity and unique immunomodulatory properties, and hence offer obvious advantages in immune privilege and allogenic therapeutic application prospects.Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 05240 STEMdiffâ„¢ Mesenchymal Progenitor Kit Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 05240 Product Name: STEMdiffâ„¢ Mesenchymal Progenitor Kit Reference(Jun 2025) Nature Communications 16AAV-based delivery of RNAi targeting ataxin-2 improves survival and pathology in TDP-43 mice
Amyotrophic lateral sclerosis (ALS) involves motor neuron death due to mislocalized TDP-43. Pathologic TDP-43 associates with stress granules (SGs), and lowering the SG-associated protein ataxin-2 (ATXN2) using Atxn2-targeting antisense oligonucleotides prolongs survival in TAR4/4 sporadic ALS mice but failed in clinical trials likely due to poor target engagement. Here we show that an AAV with potent motor neuron transduction delivering Atxn2-targeting miRNAs reduces Atxn2 throughout the central nervous system at doses 40x lower than published work. In TAR4/4 mice, miAtxn2 increased survival (50%) and strength, and reduced motor neuron death, inflammation, and phosphorylated TDP-43. TAR4/4 transcriptomic dysregulation recapitulated ALS gene signatures that were rescued by miAtxn2, identifying potential therapeutic mechanisms and biomarkers. In slow progressing hemizygous mice, miAtxn2 slowed disease progression, and in ALS patient-derived lower motor neurons, our AAV vector transduced >95% of cells and potently reduced ATXN2 at MOI 4 logs lower than previously reported. These data support AAV-RNAi targeting ATXN2 as a translatable therapy for sporadic ALS. Amado et al. develop a gene therapy for sporadic ALS using motor neuron-targeting AAVs to deliver RNAi targeting ataxin-2. In a mouse model, survival, strength, and disease-related pathology are improved; and human motor neurons are strongly transduced.Catalog #: Product Name: 100-0276 mTeSRâ„¢ Plus Catalog #: 100-0276 Product Name: mTeSRâ„¢ Plus Reference(Jun 2025) Molecular Therapy. Methods & Clinical Development 33 3Ubiquitination-targeted therapies improve BMD iPSC myogenic cell engraftment and dystrophin expression in vivo
Becker muscular dystrophy (BMD) is caused by in-frame mutations in dystrophin gene, leading to progressive muscle weakness, and cardiac and respiratory complications. Currently, there is no cure. We have recently identified the importance of poly-ubiquitination in regulating dystrophin stability through the binding of lncRNA H19 to the dystrophin C-terminal zinc-finger domain (ZNF), inhibiting TRIM63-mediated poly-ubiquitination. We also demonstrated that BMD mutations lead to conformational changes in ZNF domain, reduced lncRNA H19 binding and increased dystrophin ubiquitination. Here we used BMD iPSCs to investigate the in vitro myogenic potential of BMD myogenic cells, as well as in vitro and in vivo studies to evaluate the therapeutic efficacy of three candidate molecules targeting dystrophin ubiquitination pathway. In vitro assays indicated significant deficiencies in myogenic cell differentiation of BMD iPSCs, including reduced proliferation, cell-cycle arrest, increased apoptosis, senescence, and membrane damage, and impaired myotube formation. In vivo engraftment demonstrated significant improvement in BMD iPSC myogenic cell survival and dystrophin expression in the animals treated with two molecules: a TRIM63 inhibitor and an ?-synuclein aggregation inhibitor. These findings provide promising evidence for the potential therapeutic efficacy of these ubiquitination pathway inhibitors to improve muscle progenitor cell survival and dystrophin expression in BMD patients. Graphical abstract Regulation of dystrophin stability via poly-ubiquitination is crucial in Becker muscular dystrophy (BMD). BMD mutations impair lncRNA H19 binding, increasing dystrophin ubiquitination. Darabi and colleagues’ studies, using BMD iPSCs and in vivo models, demonstrate that inhibiting TRIM63 or ?-synuclein aggregation improves myogenic cell survival and dystrophin expression, suggesting promising therapeutic avenues for BMD.Catalog #: Product Name: 100-0276 mTeSR™ Plus Catalog #: 100-0276 Product Name: mTeSR™ Plus Reference(Sep 2024) eBioMedicine 108 3Global and single-cell proteomics view of the co-evolution between neural progenitors and breast cancer cells in a co-culture model
SummaryBackgroundPresence of nerves in tumours, by axonogenesis and neurogenesis, is gaining increased attention for its impact on cancer initiation and development, and the new field of cancer neuroscience is emerging. A recent study in prostate cancer suggested that the tumour microenvironment may influence cancer progression by recruitment of Doublecortin (DCX)-expressing neural progenitor cells (NPCs). However, the presence of such cells in human breast tumours has not been comprehensively explored.MethodsHere, we investigate the presence of DCX-expressing cells in breast cancer stromal tissue from patients using Imaging Mass Cytometry. Single-cell analysis of 372,468 cells across histopathological images of 107 breast cancers enabled spatial resolution of neural elements in the stromal compartment in correlation with clinicopathological features of these tumours. In parallel, we established a 3D in vitro model mimicking breast cancer neural progenitor-innervation and examined the two cell types as they co-evolved in co-culture by using mass spectrometry-based global proteomics.FindingsStromal presence of DCX + cells is associated with tumours of higher histological grade, a basal-like phenotype, and shorter patient survival in tumour tissue from patients with breast cancer. Global proteomics analysis revealed significant changes in the proteomic landscape of both breast cancer cells and neural progenitors in co-culture.InterpretationThese results support that neural involvement plays an active role in breast cancer and warrants further studies on the relevance of nerve elements for tumour progression.FundingThis work was supported by the 10.13039/501100005416Research Council of Norway through its Centre of Excellence funding scheme, project number 223250 (to L.A.A), the 10.13039/100008730Norwegian Cancer Society (to L.A.A. and H.V.), the Regional Health Trust Western Norway (Helse Vest) (to L.A.A.), the 10.13039/501100008728Meltzer Research Fund (to H.V.) and the 10.13039/100000002National Institutes of Health (NIH)/10.13039/100000057NIGMS grant R01 GM132129 (to J.A.P.).Catalog #: Product Name: 85850 ³¾°Õ±ð³§¸éâ„¢1 Catalog #: 85850 Product Name: ³¾°Õ±ð³§¸éâ„¢1 Product Information SheetCatalog #: Lot #: Language: Product Name: Catalog #:100-1600Lot #:AllLanguage:EnglishProduct Name:Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, APCCatalog #: 100-1600 Lot #: All Language: English Product Name: Anti-Human CD80 (B7-1) Antibody, Clone 2D10.4, APC Reference(Jun 2025) APL Bioengineering 9 2Development of large-scale gastruloid array to identify aberrant developmental phenotypes
Adherent two-dimensional human gastruloids have provided insights into early human embryogenesis. Even though the model system is highly reproducible, no available automated technology can screen and sort large numbers of these near-millimeter-sized complex structures for large-scale assays. Here, we developed a microraft array-based technology to perform image-based assays of large numbers of fixed or living gastruloids and sort individual gastruloids for downstream assays, such as gene expression analysis. Arrays of 529 indexed magnetic microrafts each (789?µm side length) possessing flat surfaces were photopatterned with a central circular region (500?µm diameter) of extracellular matrix with an accuracy of 93?±?1% to form a single gastruloid on each raft. An image analysis pipeline extracted features from transmitted light and fluorescence images of the gastruloids. The large microrafts were released and collected by an automated sorting system with efficiencies of 98?±?4% and 99?±?2%, respectively. The microraft array platform was used to assay individual euploid and aneuploid (possessing abnormal numbers of chromosomes) gastruloids with clear phenotypic differences. Aneuploid gastruloids displayed significantly less DNA/area than euploid gastruloids. However, even gastruloids with the same condition displayed significant heterogeneity. Both noggin (NOG) and keratin 7 (KRT7), two genes involved in spatial patterning within gastruloids, were upregulated in aneuploid relative to that in the euploid gastruloids. Moreover, relative NOG and KRT7 expressions were negatively correlated with DNA/area. The microraft arrays will empower novel screens of single gastruloids for a better understanding of key mechanisms underlying phenotypic differences between gastruloids.Catalog #: Product Name: 100-0276 mTeSR™ Plus Catalog #: 100-0276 Product Name: mTeSR™ Plus Product Information SheetCatalog #: Lot #: Language: Product Name: Catalog #:100-1638Lot #:AllLanguage:EnglishProduct Name:Anti-Mouse Ly-6C Antibody, Clone HK1.4, PerCP-Cy5.5Catalog #: 100-1638 Lot #: All Language: English Product Name: Anti-Mouse Ly-6C Antibody, Clone HK1.4, PerCP-Cy5.5 Reference(Sep 2024) Stem Cell Research & Therapy 15 3Influence of mesenchymal and biophysical components on distal lung organoid differentiation
BackgroundChronic lung disease of prematurity, called bronchopulmonary dysplasia (BPD), lacks effective therapies, stressing the need for preclinical testing systems that reflect human pathology for identifying causal pathways and testing novel compounds. Alveolar organoids derived from human pluripotent stem cells (hPSC) are promising test platforms for studying distal airway diseases like BPD, but current protocols do not accurately replicate the distal niche environment of the native lung. Herein, we investigated the contributions of cellular constituents of the alveolus and fetal respiratory movements on hPSC-derived alveolar organoid formation.MethodsHuman PSCs were differentiated in 2D culture into lung progenitor cells (LPC) which were then further differentiated into alveolar organoids before and after removal of co-developing mesodermal cells. LPCs were also differentiated in Transwell® co-cultures with and without human fetal lung fibroblast. Forming organoids were subjected to phasic mechanical strain using a Flexcell® system. Differentiation within organoids and Transwell® cultures was assessed by flow cytometry, immunofluorescence, and qPCR for lung epithelial and alveolar markers of differentiation including GATA binding protein 6 (GATA 6), E-cadherin (CDH1), NK2 Homeobox 1 (NKX2-1), HT2-280, surfactant proteins B (SFTPB) and C (SFTPC).ResultsWe observed that co-developing mesenchymal progenitors promote alveolar epithelial type 2 cell (AEC2) differentiation within hPSC-derived lung organoids. This mesenchymal effect on AEC2 differentiation was corroborated by co-culturing hPSC-NKX2-1+ lung progenitors with human embryonic lung fibroblasts. The stimulatory effect did not require direct contact between fibroblasts and NKX2-1+ lung progenitors. Additionally, we demonstrate that episodic mechanical deformation of hPSC-derived lung organoids, mimicking in situ fetal respiratory movements, increased AEC2 differentiation without affecting proximal epithelial differentiation.ConclusionOur data suggest that biophysical and mesenchymal components promote AEC2 differentiation within hPSC-derived distal organoids in vitro.Supplementary InformationThe online version contains supplementary material available at 10.1186/s13287-024-03890-2.Catalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ 100-0276 mTeSRâ„¢ Plus Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 100-0276 Product Name: mTeSRâ„¢ Plus Product Information SheetCatalog #: Lot #: Language: Product Name: Catalog #:100-1637Lot #:AllLanguage:EnglishProduct Name:Anti-Mouse Ly-6C Antibody, Clone HK1.4, APCCatalog #: 100-1637 Lot #: All Language: English Product Name: Anti-Mouse Ly-6C Antibody, Clone HK1.4, APC Reference(Dec 2024) Bio-protocol 14 24CRISPR/Cas9-Based Protocol for Precise Genome Editing in Induced Pluripotent Stem Cells
The advent of clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-based genome editing has marked a significant advancement in genetic engineering technology. However, the editing of induced pluripotent stem cells (iPSCs) with CRISPR presents notable challenges in ensuring cell survival and achieving high editing efficiency. These challenges become even more complex when considering the specific target site. P53 activation as a result of traditional CRISPR editing can lead to apoptosis, potentially worsening cell health or even resulting in cell death. Mitigating this apoptotic response can enhance cell survival post-CRISPR editing, which will ultimately increase editing efficiency. In our study, we observed that combining p53 inhibition with pro-survival small molecules yields a homologous recombination rate of over 90% when using CRISPR in human iPSCs. This protocol significantly streamlines the editing process and reduces the time and resources necessary for creating isogenic lines. Key features • The combination of p53 inhibition and pro-survival small molecules promotes cell survival and increases the efficiency of genome editing.• Genome editing can be completed in as little as 8 weeks for iPSCs, significantly reducing the total time required.• Achieves a homologous recombination rate of over 90% in human iPSCs.Catalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ 100-0276 mTeSRâ„¢ Plus Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 100-0276 Product Name: mTeSRâ„¢ Plus Product Information SheetCatalog #: Lot #: Language: Product Name: Catalog #:100-1636Lot #:AllLanguage:EnglishProduct Name:Anti-Mouse Ly-6C Antibody, Clone HK1.4, PECatalog #: 100-1636 Lot #: All Language: English Product Name: Anti-Mouse Ly-6C Antibody, Clone HK1.4, PE Items 2077 to 2088 of 13914 total
Shop ByFilter Results- Resource Type
-
- Product Information Sheet 2907 items
- Reference 7892 items
- Safety Data Sheet 3052 items
- Technical Manual 63 items
- Product Type
-
- 35 items
- Cell Culture Media and Supplements 27 items
- Cell Engineering and Molecular Tools 3 items
- Cell Isolation Products 5 items
- Instruments and Software 4 items
- Tissue and Cell Culture Dissociation Reagents 2 items
- Training and Education 1 item
- Area of Interest
-
- 29 items
- Angiogenic Cell Research 49 items
- Antibody Development 1 item
- Cancer 601 items
- Cell Line Development 137 items
- Cell Therapy Development 1 item
- Chimerism 5 items
- Cord Blood Banking 25 items
- Disease Modeling 4 items
- Drug Discovery and Toxicity Testing 182 items
- Endothelial Cell Biology 2 items
- Epithelial Cell Biology 158 items
- HIV 52 items
- HLA 8 items
- Hybridoma Generation 1 item
- Immunology 743 items
- Infectious Diseases 4 items
- Neuroscience 491 items
- Organoids 1 item
- Respiratory Research 1 item
- Stem Cell Biology 2493 items
- Transplantation Research 54 items
- Brand
-
- 0 20 items
- ALDECOUNT 7 items
- ALDEFLUOR 216 items
- AggreWell 55 items
- ArciTect 1 item
- BrainPhys 45 items
- CellPore 1 item
- ClonaCell 84 items
- CryoStor 65 items
- ES-Cult 77 items
- EasyPick 1 item
- EasySep 752 items
- EpiCult 12 items
- HepatiCult 1 item
- ImmunoCult 7 items
- IntestiCult 142 items
- Lymphoprep 9 items
- MammoCult 45 items
- MegaCult 34 items
- MesenCult 133 items
- MethoCult 444 items
- MyeloCult 64 items
- MyoCult 2 items
- NeuroCult 353 items
- NeuroFluor 1 item
- PancreaCult 3 items
- PneumaCult 78 items
- RSeT 7 items
- ReLeSR 1 item
- RoboSep 23 items
- RosetteSep 253 items
- STEMdiff 54 items
- STEMvision 3 items
- SepMate 29 items
- StemSpan 219 items
- TeSR 1456 items
- ThawSTAR 1 item
- mFreSR 3 items
- Cell and Tissue Source
-
- 24 items
- Cell Line
-
- 24 items
- Cell Type
-
- 27 items
- Airway Cells 41 items
- B Cells 134 items
- Brain Tumor Stem Cells 81 items
- Cancer Cells and Cell Lines 116 items
- Cardiomyocytes, PSC-Derived 8 items
- Dendritic Cells 59 items
- Dermal Cells 1 item
- Endoderm, PSC-Derived 1 item
- Endothelial Cells 1 item
- Endothelial Cells, PSC-Derived 1 item
- Epithelial Cells 49 items
- Granulocytes and Subsets 61 items
- Hematopoietic Stem and Progenitor Cells 777 items
- Hepatic Cells 2 items
- Hybridomas 75 items
- Innate Lymphoid Cells 3 items
- Intestinal Cells 13 items
- Kidney Cells 1 item
- Leukemia/Lymphoma Cells 8 items
- Leukopaks 1 item
- Mammary Cells 68 items
- Mesenchymal Stem and Progenitor Cells 132 items
- Monocytes 105 items
- Mononuclear Cells 33 items
- Myeloid Cells 99 items
- NK Cells 80 items
- Neural Cells, PSC-Derived 17 items
- Neural Stem and Progenitor Cells 381 items
- Neurons 135 items
- Plasma 3 items
- Pluripotent Stem Cells 1689 items
- Prostate Cells 7 items
- Renal Cells 2 items
- T Cells 179 items
- T Cells, CD4+ 85 items
- T Cells, CD8+ 49 items
- T Cells, Regulatory 18 items
- Species
-
- 41 items
Loading...Copyright © 2025 º£½ÇÆÆ½â°æ. All rights reserved.