Qingcai Meng

ORCID: 0000-0003-4710-4846
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About
Contact & Profiles
Research Areas
  • interferon and immune responses
  • Inflammasome and immune disorders
  • Immune Response and Inflammation
  • NF-κB Signaling Pathways
  • Cell death mechanisms and regulation
  • Immune Cell Function and Interaction
  • Calcium signaling and nucleotide metabolism
  • HIV Research and Treatment
  • Plant-Microbe Interactions and Immunity

Yale University
2019

Howard Hughes Medical Institute
2019

Sun Yat-sen University
2015-2019

Beijing Ditan Hospital
2014

Capital Medical University
2014

NLRC5 is an important regulator in innate immune responses. However, the ability of to inhibit NF-κB activation controversial different cell types. How dynamic modification shapes signaling remains unknown. We demonstrated that undergoes robust ubiquitination by TRAF2/6 after lipopolysaccharide treatment, which leads dissociation NLRC5–IκB kinase complex. Experimental and mathematical analyses revealed K63-linked at lysine 1,178 generates a coherent feedforward loop further sensitize...

10.1083/jcb.201505091 article EN cc-by-nc-sa The Journal of Cell Biology 2015-11-30

Abstract The noncanonical NF‐κB signaling pathway plays a critical role in variety of biological functions including chronic inflammation and tumorigenesis. Activation largely relies on the abundance as well processing family member p100/p52. Here, TRIM14 is identified novel positive regulator pathway. promotes activation by targeting p100/p52 vitro vivo. Furthermore, mechanistic study shows that recruits deubiquitinase USP14 to cleave K63‐linked ubiquitin chains at multiple sites, thereby...

10.1002/advs.201901261 article EN cc-by Advanced Science 2019-11-11

Interleukin‐1β (IL‐1β) secretion downstream of Toll‐like receptor (TLR) activation is tightly controlled at the transcriptional and post‐translational levels. NLRP3 inflammasome involved in maturation pro‐IL‐1β, with expression identified as limiting factor for activation. Previously, we had demonstrated that zinc‐finger protein GFI1 inhibits pro‐IL‐1β transcription. Here, show IL‐1β macrophages. suppressed Nlrp3 transcription via two mechanisms: (1) by binding to Gli‐responsive element 1...

10.1016/j.febslet.2014.10.025 article EN FEBS Letters 2014-11-04
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