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1. Truncating NFKB1 variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis

3. Autoimmunity, hypogammaglobulinemia, lymphoproliferation, and mycobacterial disease in patients with activating mutations in STAT3

4. Loss-of-function mutation in IKZF2 leads to immunodeficiency with dysregulated germinal center reactions and reduction of MAIT cells

5. Loss of DIAPH1 causes SCBMS, combined immunodeficiency, and mitochondrial dysfunction

6. Identification of novel regulators of STAT3 activity

8. Truncating NFKB1variants cause combined NLRP3 inflammasome activation and type I interferon signaling and predispose to necrotizing fasciitis

9. Enrichment of rare variants in population isolates

10. Enrichment of rare variants in population isolates: single AICDA mutation responsible for hyper-IgM syndrome type 2 in Finland

11. Dominant NFKB1 Mutations Cause Antibody Deficiency and Autoinflammatory Episodes

12. In vivo characterization of two novel regulators of the JAK/STAT pathway in Drosophila melanogaster

13. Functional Characterization of the Infection-Inducible Peptide Edin in Drosophila melanogaster

14. Not4 enhances JAK/STAT pathway-dependent gene expression in Drosophila and in human cells

15. Genome-wide RNA interference in Drosophila cells identifies G protein-coupled receptor kinase 2 as a conserved regulator of NF-κB signaling

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