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

4. 49 Early-Onset Common Variable Immunodeficiency in a Patient with Heterozygous Variants in Interferon Response-Associated Genes TRAF3 and IRF4

5. Long-term follow up of families with pathogenic NFKB1 variants reveals incomplete penetrance and frequent inflammatory sequelae

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

7. Damaging heterozygous mutations in NFKB1 lead to diverse immunologic phenotypes

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

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

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

15. ADA2 deficiency: Clonal lymphoproliferation in a subset of patients

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

18. Dominant NFKB1 Mutations Cause Antibody Deficiency and Autoinflammatory Episodes

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

22. Genome-Wide RNA Interference in Drosophila Cells Identifies G Protein-Coupled Receptor Kinase 2 as a Conserved Regulator of NF-κB Signaling

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

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

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