Associated Papers
Human germline biallelic loss-of-function OSMR variants cause severe allergic disease.
Sharma M et al.
Medrxiv : the Preprint Server for Health Sciences, 2025
Clinical and genetic features of Chinese patients with lichen and macular primary localized cutaneous amyloidosis.
Lu P et al.
Clinical and Experimental Dermatology, 2019
A novel missense mutation in oncostatin M receptor beta causing primary localized cutaneous amyloidosis.
Saeedi M et al.
Biomed Research International, 2014
MCP-1 as an effector of IL-31 signaling in familial primary cutaneous amyloidosis.
Shiao YM et al.
The Journal of Investigative Dermatology, 2013
Association of the oncostatin m receptor gene polymorphisms with papillary thyroid cancer in the korean population.
Hong IK et al.
Clinical and Experimental Otorhinolaryngology, 2011
New insight into mechanisms of pruritus from molecular studies on familial primary localized cutaneous amyloidosis.
Tanaka A et al.
The British Journal of Dermatology, 2009
Identification of an oncostatin M receptor mutation associated with familial primary cutaneous amyloidosis.
Babilas P et al.
The British Journal of Dermatology, 2009
A novel OSMR mutation in familial primary localized cutaneous amyloidosis in a Japanese family.
Arita K et al.
Journal of Dermatological Science, 2009
Familial primary localized cutaneous amyloidosis in Brazil.
Sakuma TH et al.
Archives of Dermatology, 2009
Oncostatin M receptor-beta mutations underlie familial primary localized cutaneous amyloidosis.
Arita K et al.
American Journal of Human Genetics, 2008
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