Creative Bioarray provides liver fibrosis animal models for preclinical drug discovery, efficacy evaluation, and translational liver disease research. Our platform includes chemical-induced, and surgery-induced models for anti-fibrotic drug development. https://t.co/FHB52K8KlH
Creative Bioarray offers a well-established and widely validated High-Fat Diet-Induced Obesity (DIO) model for translational research and innovative therapeutic drug development. https://t.co/IY2t1w7pQS
OncoSelect™ Tumor Efficacy Screening Panel integrates well-characterized tumor cell lines, drug-resistant derivatives, and tumor microenvironment components to bridge the gap between in vitro pharmacology and clinical translation. https://t.co/YzFMig4LK5
Primary cells covering 60+ cell types from 80+ tissue sources across 20+ species, low-passage and high-purity for human and animal biomedical research. https://t.co/V3QZ7dyMKq
Curated portfolio of 2,000+ tumor cell lines spanning 100+ tissues and 200+ cancer diseases, STR-authenticated and mycoplasma-tested for oncology research. https://t.co/tJg8igapEx
Short (<6 h) and long (>8 h) sleep duration, compared with a normal sleep duration (6–8 h), are associated with increased risk of systemic diseases with evidence from genetic correlations and time-to-incident survival predictions. https://t.co/M6vVkkvjMK
With years of expertise, Creative Bioarray serves as a trusted partner in safety evaluation, specializing in preclinical toxicology testing. Our comprehensive testing platform supports applications throughout all stages of product development. https://t.co/qjSNYwveIc
Immunoglobulin E (IgE)-sensitized mast cells (IgE-MCs) for targeted drug delivery and augmented cancer immunotherapy
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https://t.co/V3QZ7dyMKq
A 100% Healing Rate: Stem Cell Exosomes Make Diabetic Foot Ulcers Vanish, With Zero Recurrence in 24 Months.
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The ciPSC medium supplemented with activin and IWR1 stabilizes ciPSCs and reduces heterogeneity. It enables ciPSC differentiation into cardiomyocytes with functional traits. https://t.co/FlN9bKVBgw
Kuthethur et al. demonstrated that depletion of the AAA+ ATPase FIGNL1 in BRCA2-deficient cells restored RAD51 loading and rescued HR defects, suggesting that recombination failure in BRCA2-deficient cells is primarily due to excessive removal of RAD51 by FIGNL1.