
Science Translational Medicine
- Volume 14
- Issue 665
- 05 Oct 2022

ONLINE COVER NO Change in the NOSe. This image of transient axonal glycoprotein 1 (TAG-1) staining reveals normal olfactory bulb morphogenesis and olfactory fiber projections in a mouse lacking expression of the gene encoding nitric oxide synthase 1 (NOS1). Chachlaki et al. studied the role of NOS1 in congenital hypogonadotropic hypogonadism (CHH), finding that NOS1 activity affected the number of gonadotropin-releasing hormone-producing neurons and their migration in the developing mouse brain, whereas olfactory bulb morphogenesis was maintained. Nos1 deficiency in mice resulted in defects in sexual maturation, olfaction, hearing, and cognition, mirroring the findings in six humans with CHH caused by NOS1 mutations. Administration of sildenafil or inhaled nitric oxide during minipuberty could ameliorate these symptoms in Nos1 mutant mice, suggesting a potential treatment for humans with NOS1 mutations.
Credit: Chachlaki et al./Science Translational Medicine- Konstantina Chachlaki
- Andrea Messina
- et al.
NOS1 mutations cause hypogonadotropic hypogonadism with sensory and cognitive deficits that can be reversed in infantile mice
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A germline SNP in BRMS1 predisposes patients with lung adenocarcinoma to metastasis and can be ameliorated by targeting c-fos
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Science Translational Medicine is the leading weekly online journal publishing research at the intersection of science, engineering and medicine. The goal of Science Translational Medicine is to promote human health by providing a forum for communicating the latest research advances from biomedical, translational, and clinical researchers from all established and emerging disciplines relevant to medicine.
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