期刊
JOURNAL OF INVESTIGATIVE DERMATOLOGY
卷 137, 期 4, 页码 801-804出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jid.2016.12.013
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资金
- NIH [DE018549, UL1TR001117, P30AR066527, F33DE024668, K12DE022793, 5K08AR063729-04]
- DoD [W81XWH-13-1-0299]
- Harrington Discovery Institute (Cleveland, OH) Scholar-Innovator Award
Mascarenhas et al. report that TRPV4 expression is upregulated in mast cells in response to the proteolytic cathelicidin fragment LL37 in a murine rosacea model and that TRPV4 loss of function attenuates mast cell degranulation. These findings render TRPV4 a translational-medical target in rosacea. However, signaling mechanisms causing increased expression of TRPV4 await elucidation. Moreover, we ask whether TRPV4-mediated Ca++-influx evokes mast cell degranulation.
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