Sugar Fix Keeps RIPK3 at Bay.

Giogha, Cristina; Lawlor, Kate E

Giogha, Cristina; Lawlor, Kate E.

Affiliation

Giogha C; Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC 3168, Australia. Electronic address: cristina.giogha@hudson.org.au.
Lawlor KE; Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC 3168, Australia; Department of Molecular and Translational Science, Monash University, Clayton, VIC 3168, Australia. Electronic address: kate.lawlor@hudson.org.au.

Immunity ; 50(3): 539-541, 2019 03 19.

Article in En | MEDLINE | ID: mdl-30893581

ABSTRACT

ABSTRACT

Immunometabolism is emerging as an important modulator of immune responses. In this issue of Immunity, Li et al. (2019) examine the link between lipopolysaccharide (LPS)-induced glucose metabolism and innate immune signaling and identify how ß-N-acetylglucosamine (O-GlcNAc) modification of the RIPK3 RHIM domain limits inflammation and necroptosis.

Subject(s)

Inflammation; Sugars; Humans; N-Acetylglucosaminyltransferases; Receptor-Interacting Protein Serine-Threonine Kinases; Serine; Threonine

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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Sugars / Inflammation Limits: Humans Language: En Journal: Immunity Journal subject: ALERGIA E IMUNOLOGIA Year: 2019 Type: Article

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