Excess type I interferon signaling in the mouse seminiferous tubules leads to germ cell loss and sterility.


Type I (α and β) interferons (IFNs) elicit antiproliferative and antiviral activities via the surface receptor IFNAR. Serendipitous observations in transgenic mice in 1988 strongly suggested that IFNα/β overexpression in the testis disrupts spermatogenesis. Here, we compare a new mouse strain transgenic for IFNβ (Tg10) and a sister strain lacking the IFNAR1… (More)
DOI: 10.1074/jbc.M111.229120


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