Filter your results
- 1
- 1
- 2
- 2
- 1
- 1
- 2
- 2
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 2
- 2
- 2
- 2
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
- 1
|
|
sorted by
|
|
A recessive form of hyper-IgE syndrome by disruption of ZNF341-dependent STAT3 transcription and activityScience Immunology, 2018, 3 (24), pp.eaat4956. ⟨10.1126/sciimmunol.aat4956⟩
Journal articles
hal-02392068v1
|
||
|
Human HOIP and LUBAC deficiency underlies autoinflammation, immunodeficiency, amylopectinosis, and lymphangiectasia.Journal of Experimental Medicine, 2015, ⟨10.1084/jem.20141130⟩
Journal articles
pasteur-01158038v1
|