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Abbreviation : ECSIT
Long Form : evolutionarily conserved signaling intermediate in Toll pathways
No. Year Title Co-occurring Abbreviation
2019 CRBN Is a Negative Regulator of Bactericidal Activity and Autophagy Activation Through Inhibiting the Ubiquitination of ECSIT and BECN1. BECN1, CRBN, CRBNKD, CRBNKO, mROS, TLR4
2019 p62 Negatively Regulates TLR4 Signaling via Functional Regulation of the TRAF6-ECSIT Complex. MEF, TRAF6
2018 ECSIT links TLR and BMP signaling in FOP connective tissue progenitor cells. BMP, CTPCs, FOP, TLR
2018 Inhibition of TRAF6 ubiquitin-ligase activity by PRDX1 leads to inhibition of NFKB activation and autophagy activation. BECN1, PRDX1, PRDX1KD, TLR4, TRAF6
2018 Recurrent ECSIT mutation encoding V140A triggers hyperinflammation and promotes hemophagocytic syndrome in extranodal NK/T cell lymphoma. ENKTL, HPS, IFN, TNF
2017 [Amphioxus ortholog of ECSIT, an evolutionarily conserved adaptor in the Toll and BMP signaling pathways]. TLR, TRAF6
2015 Hepatitis B virus X protein increases the IL-1beta-induced NF-kappaB activation via interaction with evolutionarily conserved signaling intermediate in Toll pathways (ECSIT). HBx, IL-1beta, NF-kappaB, TLR
2015 Identification and function of an evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) from Crassostrea hongkongensis. BMP, ORF, OXPHOS, TLR
2015 Ubiquitination of ECSIT is crucial for the activation of p65/p50 NF-kappaBs in Toll-like receptor 4 signaling. TLR, TRAF6
10  2014 Role of evolutionarily conserved signaling intermediate in Toll pathways (ECSIT) in the antibacterial immunity of Marsupenaeus japonicus. TLR
11  2012 Towards Alzheimer's root cause: ECSIT as an integrating hub between oxidative stress, inflammation and mitochondrial dysfunction. Hypothetical role of the adapter protein ECSIT in familial and sporadic Alzheimer's disease pathogenesis. AD
12  2012 [Effect of lipopolysaccharide and transforming growth factor-beta 1 on expression and signal pathway of Toll like receptor 4 in dental pulp cells]. ELISA, FCM, IL-6, LPS, NF-kappaB, TGF-beta1, TLR4