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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

TRAF-type zinc finger domain containing 1

The innate immune system confers host defense against viral and microbial infection, and TRAFD1 is a negative feedback regulator that controls excessive immune responses (Sanada et al., 2008 [PubMed 18849341]).[supplied by OMIM, Dec 2009] (from NCBI)
Top mentioned proteins: TLR4, TRAF6, TRAM, AGE, Interleukin-6
Papers on FLN29
TRAFD1 (FLN29) Interacts with Plekhm1 and Regulates Osteoclast Acidification and Resorption.
Odgren et al., Worcester, United States. In Plos One, 2014
Investigations of potential Plekhm1 interaction partners by mass spectrometry identified TRAFD1 (FLN29), a protein previously shown to suppress toll-like receptor signaling in monocytes/macrophages, thereby dampening inflammatory responses to innate immunity.
[Changes of immune function in patients with 2009 influenza A (H1N1)].
Fu et al., Shenzhen, China. In Zhonghua Er Ke Za Zhi, 2010
(5) The expression levels of negative regulator of SOCS1, SOCS3, IRAK-M, TRAF4 and FLN29 were significantly increased in the patients with influenza A, especially in severe cases than those in NC group (P < 0.05).
FLN29 deficiency reveals its negative regulatory role in the Toll-like receptor (TLR) and retinoic acid-inducible gene I (RIG-I)-like helicase signaling pathway.
Yoshimura et al., Fukuoka, Japan. In J Biol Chem, 2009
FLN29, in addition to playing a negative regulatory role in the TLR4 signaling pathway, negatively regulates the RIG-I-like helicase signaling pathway at the level of IPS-1/TRAF6 and IPS-1/TRAF3 complexes
NMR assignment of the N-terminal TRAF-like RING zinc finger domain of human FLN29.
Aubin et al., Ottawa, Canada. In Biomol Nmr Assign, 2008
The human FLN29 protein may play a role in this process via protein-protein interactions.
[Changes and significance for regulatory factors for signal pathways of Toll-like receptors in immunological pathogenesis of Kawasaki disease].
Yang et al., Shenzhen, China. In Zhonghua Er Ke Za Zhi, 2008
Transcription levels of regulatory factors such as FLN29, RP105 and MD-1 were up-regulated to some extents and expression level of DAP12 mRNA in KD patients were found to be lower than that in normal controls (P < 0.05), while all of the four regulatory factors were found to be lower than those in ID patients (P < 0.05).
[Progress of the study on endotoxin tolerance mechanisms].
Zhou et al., Chongqing, China. In Sheng Li Ke Xue Jin Zhan, 2006
Quantitative, structural and functional changes of receptors, adaptor proteins and transcription factors in TLR4 signaling pathways might have effects on the decrease in proinflammatory cytokines, increase in anti-inflammatory cytokines and activation of special signaling pathways (such as PI3K pathways) as well as some negative regulation factors (SHIP1,SOCS, FLN29, et al) during the development of endotoxin tolerance.
FLN29, a novel interferon- and LPS-inducible gene acting as a negative regulator of toll-like receptor signaling.
Yoshimura et al., Fukuoka, Japan. In J Biol Chem, 2006
FLN29 is a new negative feedback regulator of TLR signaling
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