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Items 817 to 828 of 13914 total
- Safety Data Sheet
Catalog #: Product Name: 100-1399 JCV (LT) Peptide Pool Catalog #: 100-1399 Product Name: JCV (LT) Peptide Pool - ReferenceJ. Schröter et al. (May 2024) Scientific Data 11
A large and diverse brain organoid dataset of 1,400 cross-laboratory images of 64 trackable brain organoids
Brain organoids represent a useful tool for modeling of neurodevelopmental disorders and can recapitulate brain volume alterations such as microcephaly. To monitor organoid growth, brightfield microscopy images are frequently used and evaluated manually which is time-consuming and prone to observer-bias. Recent software applications for organoid evaluation address this issue using classical or AI-based methods. These pipelines have distinct strengths and weaknesses that are not evident to external observers. We provide a dataset of more than 1,400 images of 64 trackable brain organoids from four clones differentiated from healthy and diseased patients. This dataset is especially powerful to test and compare organoid analysis pipelines because of (1) trackable organoids (2) frequent imaging during development (3) clone diversity (4) distinct clone development (5) cross sample imaging by two different labs (6) common imaging distractors, and (6) pixel-level ground truth organoid annotations. Therefore, this dataset allows to perform differentiated analyses to delineate strengths, weaknesses, and generalizability of automated organoid analysis pipelines as well as analysis of clone diversity and similarity. Subject terms: Disease model, Machine learningCatalog #: Product Name: 05872 ¸é±ð³¢±ð³§¸éâ„¢ Catalog #: 05872 Product Name: ¸é±ð³¢±ð³§¸éâ„¢ Safety Data SheetCatalog #: Product Name: 100-1398 BKV (LT) Peptide Pool Catalog #: 100-1398 Product Name: BKV (LT) Peptide Pool ReferenceG. Yang et al. (May 2024) ACS Omega 9 19Preclinical Evaluation of JAB-2485, a Potent AURKA Inhibitor with High Selectivity and Favorable Pharmacokinetic Properties
As a critical mitotic regulator, Aurora kinase A (AURKA) is aberrantly activated in a wide range of cancers. Therapeutic targeting of AUKRA is a promising strategy for the treatment of solid tumors. In this study, we evaluated the preclinical characteristics of JAB-2485, a small-molecule inhibitor of AURKA currently in Phase I/IIa clinical trial in the US ( NCT05490472 ). Biochemical studies demonstrated that JAB-2485 is potent and highly selective on AURKA, with subnanomolar IC 50 and around 1500-fold selectivity over AURKB or AURKC. In addition, JAB-2485 exhibited favorable pharmacokinetic properties featured by low clearance and good bioavailability, strong dose–response relationship, as well as low risk for hematotoxicity and off-target liability. As a single agent, JAB-2485 effectively induced G2/M cell cycle arrest and apoptosis and inhibited the proliferation of small cell lung cancer, triple-negative breast cancer, and neuroblastoma cells. Furthermore, JAB-2485 exhibited robust in vivo antitumor activity both as monotherapy and in combination with chemotherapies or the bromodomain inhibitor JAB-8263 in xenograft models of various cancer types. Together, these encouraging preclinical data provide a strong basis for safety and efficacy evaluations of JAB-2485 in the clinical setting.Catalog #: Product Name: 84534 MethoCult™ GF H84534 Catalog #: 84534 Product Name: MethoCult™ GF H84534 Safety Data SheetCatalog #: Product Name: 100-1397 HPV18 (L2) Peptide Pool Catalog #: 100-1397 Product Name: HPV18 (L2) Peptide Pool ReferenceR. Drexler et al. (May 2024) Nature Medicine 30 6A prognostic neural epigenetic signature in high-grade glioma
Neural–tumor interactions drive glioma growth as evidenced in preclinical models, but clinical validation is limited. We present an epigenetically defined neural signature of glioblastoma that independently predicts patients’ survival. We use reference signatures of neural cells to deconvolve tumor DNA and classify samples into low- or high-neural tumors. High-neural glioblastomas exhibit hypomethylated CpG sites and upregulation of genes associated with synaptic integration. Single-cell transcriptomic analysis reveals a high abundance of malignant stemcell-like cells in high-neural glioblastoma, primarily of the neural lineage. These cells are further classified as neural-progenitor-cell-like, astrocyte-like and oligodendrocyte-progenitor-like, alongside oligodendrocytes and excitatory neurons. In line with these findings, high-neural glioblastoma cells engender neuron-to-glioma synapse formation in vitro and in vivo and show an unfavorable survival after xenografting. In patients, a high-neural signature is associated with decreased overall and progression-free survival. High-neural tumors also exhibit increased functional connectivity in magnetencephalography and resting-state magnet resonance imaging and can be detected via DNA analytes and brain-derived neurotrophic factor in patients’ plasma. The prognostic importance of the neural signature was further validated in patients diagnosed with diffuse midline glioma. Our study presents an epigenetically defined malignant neural signature in high-grade gliomas that is prognostically relevant. High-neural gliomas likely require a maximized surgical resection approach for improved outcomes. Subject terms: Translational research, CNS cancer, DNA methylationCatalog #: Product Name: 05790 BrainPhys™ Neuronal Medium Catalog #: 05790 Product Name: BrainPhys™ Neuronal Medium Safety Data SheetCatalog #: Product Name: 100-1396 HPV18 (L1) Peptide Pool Catalog #: 100-1396 Product Name: HPV18 (L1) Peptide Pool ReferenceY. Abe et al. (May 2024) Communications Biology 7PRMT5-mediated methylation of STAT3 is required for lung cancer stem cell maintenance and tumour growth
STAT3 is constitutively activated in many cancer types, including lung cancer, and can induce cancer cell proliferation and cancer stem cell (CSC) maintenance. STAT3 is activated by tyrosine kinases, such as JAK and SRC, but the mechanism by which STAT3 maintains its activated state in cancer cells remains unclear. Here, we show that PRMT5 directly methylates STAT3 and enhances its activated tyrosine phosphorylation in non-small cell lung cancer (NSCLC) cells. PRMT5 expression is also induced by STAT3, suggesting the presence of a positive feedback loop in cancer cells. Furthermore, methylation of STAT3 at arginine 609 by PRMT5 is important for its transcriptional activity and support of tumour growth and CSC maintenance. Indeed, NSCLC cells expressing the STAT3 mutant which R609 was replaced to alanine (R609K) show significantly impaired tumour growth in nude mice. Overall, our study reveals a mechanism by which STAT3 remains activated in NSCLC and provides a new target for cancer therapeutic approaches. Subject terms: Oncogenes, Non-small-cell lung cancer, Growth factor signallingCatalog #: Product Name: 01700 ALDEFLUOR™ Kit Catalog #: 01700 Product Name: ALDEFLUOR™ Kit Safety Data SheetCatalog #: Product Name: 100-1395 HPV16 (E6) Peptide Pool Catalog #: 100-1395 Product Name: HPV16 (E6) Peptide Pool ReferenceJ. H. Kim et al. (Jun 2024) Cancer Research Communications 4 6Hemangiosarcoma Cells Promote Conserved Host-derived Hematopoietic Expansion
Hemangiosarcoma and angiosarcoma are soft-tissue sarcomas of blood vessel–forming cells in dogs and humans, respectively. These vasoformative sarcomas are aggressive and highly metastatic, with disorganized, irregular blood-filled vascular spaces. Our objective was to define molecular programs which support the niche that enables progression of canine hemangiosarcoma and human angiosarcoma. Dog-in-mouse hemangiosarcoma xenografts recapitulated the vasoformative and highly angiogenic morphology and molecular characteristics of primary tumors. Blood vessels in the tumors were complex and disorganized, and they were lined by both donor and host cells. In a series of xenografts, we observed that the transplanted hemangiosarcoma cells created exuberant myeloid hyperplasia and gave rise to lymphoproliferative tumors of mouse origin. Our functional analyses indicate that hemangiosarcoma cells generate a microenvironment that supports expansion and differentiation of hematopoietic progenitor populations. Furthermore, gene expression profiling data revealed hemangiosarcoma cells expressed a repertoire of hematopoietic cytokines capable of regulating the surrounding stromal cells. We conclude that canine hemangiosarcomas, and possibly human angiosarcomas, maintain molecular properties that provide hematopoietic support and facilitate stromal reactions, suggesting their potential involvement in promoting the growth of hematopoietic tumors. We demonstrate that hemangiosarcomas regulate molecular programs supporting hematopoietic expansion and differentiation, providing insights into their potential roles in creating a permissive stromal-immune environment for tumor progression.Catalog #: Product Name: 05100 MyeloCult™ H5100 04435 MethoCult™ H4435 Enriched Catalog #: 05100 Product Name: MyeloCult™ H5100 Catalog #: 04435 Product Name: MethoCult™ H4435 Enriched Safety Data SheetCatalog #: Product Name: 100-1394 HPV16 (E7) Peptide Pool Catalog #: 100-1394 Product Name: HPV16 (E7) Peptide Pool ReferenceS. Luanpitpong et al. (May 2024) Frontiers in Cell and Developmental Biology 12 7OGT and OGA gene-edited human induced pluripotent stem cells for dissecting the functional roles of O -GlcNAcylation in hematopoiesis
Hematopoiesis continues throughout life to produce all types of blood cells from hematopoietic stem cells (HSCs). Metabolic state is a known regulator of HSC self-renewal and differentiation, but whether and how metabolic sensor O -GlcNAcylation, which can be modulated via an inhibition of its cycling enzymes O -GlcNAcase (OGA) and O -GlcNAc transferase (OGT), contributes to hematopoiesis remains largely unknown. Herein, isogenic, single-cell clones of OGA -depleted (OGAi) and OGT -depleted (OGTi) human induced pluripotent stem cells (hiPSCs) were successfully generated from the master hiPSC line MUSIi012-A, which were reprogrammed from CD34 + hematopoietic stem/progenitor cells (HSPCs) containing epigenetic memory. The established OGAi and OGTi hiPSCs exhibiting an increase or decrease in cellular O -GlcNAcylation concomitant with their loss of OGA and OGT, respectively, appeared normal in phenotype and karyotype, and retained pluripotency, although they may favor differentiation toward certain germ lineages. Upon hematopoietic differentiation through mesoderm induction and endothelial-to-hematopoietic transition, we found that OGA inhibition accelerates hiPSC commitment toward HSPCs and that disruption of O -GlcNAc homeostasis affects their commitment toward erythroid lineage. The differentiated HSPCs from all groups were capable of giving rise to all hematopoietic progenitors, thus confirming their functional characteristics. Altogether, the established single-cell clones of OGTi and OGAi hiPSCs represent a valuable platform for further dissecting the roles of O -GlcNAcylation in blood cell development at various stages and lineages of blood cells. The incomplete knockout of OGA and OGT in these hiPSCs makes them susceptible to additional manipulation, i.e., by small molecules, allowing the molecular dynamics studies of O -GlcNAcylation.Catalog #: Product Name: 04435 MethoCultâ„¢ H4435 Enriched 34811 ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢800 Catalog #: 04435 Product Name: MethoCultâ„¢ H4435 Enriched Catalog #: 34811 Product Name: ´¡²µ²µ°ù±ð°Â±ð±ô±ôâ„¢800 Items 817 to 828 of 13914 total
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