
Key PointsmDia1 deficiency led to a cell-autonomous overexpression of CD14 on granulocytes and a hypersensitive innate immune response. mDia1 heterozygous and knockout mice developed age-dependent MDS that was accelerated by chronic stimulation of the innate immunity.
Lipopolysaccharides, Male, Mice, Knockout, Heterozygote, Lipopolysaccharide Receptors, Formins, Bone Marrow Cells, Immunity, Innate, Mice, Gene Expression Regulation, Myelodysplastic Syndromes, Animals, Chromosomes, Human, Pair 5, Humans, Female, RNA, Messenger, Chromosome Deletion, Carrier Proteins, Adaptor Proteins, Signal Transducing, Granulocytes
Lipopolysaccharides, Male, Mice, Knockout, Heterozygote, Lipopolysaccharide Receptors, Formins, Bone Marrow Cells, Immunity, Innate, Mice, Gene Expression Regulation, Myelodysplastic Syndromes, Animals, Chromosomes, Human, Pair 5, Humans, Female, RNA, Messenger, Chromosome Deletion, Carrier Proteins, Adaptor Proteins, Signal Transducing, Granulocytes
| citations This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 47 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
