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Hematopoiesis News
A Single Nanobody Neutralizes Multiple Epochally Evolving Human Noroviruses by Modulating Capsid Plasticity
[Nature Communications] Researchers showed that a llama-derived nanobody M4 neutralized multiple GII.4 variants with high potency in human intestinal enteroids.
Newsletters
A Human Lung Alveolus-on-a-Chip Model of Acute Radiation-Induced Lung Injury
[Nature Communications] A microfluidic organ-on-a-chip lined by human lung alveolar epithelium interfaced with pulmonary endothelium was used to model acute radiation-induced lung injury in vitro.
Newsletters
D-Mannose Induces TFE3-Dependent Lysosomal Degradation of EGFR and Inhibits the Progression of NSCLC
[Oncogene] Scientists reported that D-mannose up-regulated lysosomal activity by enhancing TFE3-mediated lysosomal biogenesis, thereby increasing the degradation of epidermal growth factor receptor (EGFR) and significantly down-regulating its protein level.
Intestinal Cell News
Sleeping Beauty Transposon Mutagenesis Identified Genes and Pathways Involved in Inflammation-Associated Colon Tumor Development
[Nature Communications] Investigators found that TNFα could induce stemness and activate senescence signaling by enhancing cell plasticity in colonic epithelial cells, which could act as a selective pressure to mutate senescence-related genes in inflammation-associated colonic tumors.
Dermal Cell News
Glycyl-tRNA Synthetase Induces Psoriasis-Like Skin by Facilitating Skin Inflammation and Vascular Endothelial Cell Angiogenesis
[Journal Of Investigative Dermatology] Glycyl-tRNA synthetase (GARS) was highly expressed in human skin keratinocytes, and GARS knockdown in keratinocytes suppressed cell proliferation and promoted apoptosis via the nuclear factor kappa-B/mitogen-activated protein kinase signaling pathway.
Dermal Cell News
Carnitine Acetyltransferase Deficiency Mediates Mitochondrial Dysfunction-Induced Cellular Senescence in Dermal Fibroblasts
[Aging Cell] Carnitine acetyltransferase knockdown caused mitochondrial dysfunction, as indicated by increased oxidative stress, disruption of mitochondrial morphology, and a metabolic shift from oxidative phosphorylation to glycolysis.