Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion.
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The TWEAK receptor Fn14 is a potential cell surface portal for targeted delivery of glioblastoma therapeuticsCrystal Structure of Human TWEAK in Complex with the Fab Fragment of a Neutralizing Antibody Reveals Insights into Receptor BindingIRS1 is highly expressed in localized breast tumors and regulates the sensitivity of breast cancer cells to chemotherapy, while IRS2 is highly expressed in invasive breast tumorsCRL4A-FBXW5-mediated degradation of DLC1 Rho GTPase-activating protein tumor suppressor promotes non-small cell lung cancer cell growthTWEAK-independent Fn14 self-association and NF-κB activation is mediated by the C-terminal region of the Fn14 cytoplasmic domainMinimizing the non-specific binding of nanoparticles to the brain enables active targeting of Fn14-positive glioblastoma cells.Structural basis and targeting of the interaction between fibroblast growth factor-inducible 14 and tumor necrosis factor-like weak inducer of apoptosisFn14 receptor promotes invasive potential and metastatic capacity of non-small lung adenocarcinoma cells through the up-regulation of integrin α6Blocking TWEAK-Fn14 interaction inhibits hematopoietic stem cell transplantation-induced intestinal cell death and reduces GVHD.Identification of aurintricarboxylic acid as a selective inhibitor of the TWEAK-Fn14 signaling pathway in glioblastoma cellsThe HER2- and heregulin β1 (HRG)-inducible TNFR superfamily member Fn14 promotes HRG-driven breast cancer cell migration, invasion, and MMP9 expression.Antitumor activity of a humanized, bivalent immunotoxin targeting fn14-positive solid tumorsTumor necrosis factor-like weak inducer of apoptosis (TWEAK) promotes glioblastoma cell chemotaxis via Lyn activation.Mcl-1 mediates TWEAK/Fn14-induced non-small cell lung cancer survival and therapeutic response.The TWEAK-Fn14 system as a potential drug target.TWEAK/Fn14 signaling in tumors.The TWEAK Receptor Fn14 Is an Src-Inducible Protein and a Positive Regulator of Src-Driven Cell Invasion.TWEAK/Fn14 Axis-Targeted Therapeutics: Moving Basic Science Discoveries to the Clinic.Enavatuzumab, a Humanized Anti-TWEAK Receptor Monoclonal Antibody, Exerts Antitumor Activity through Attracting and Activating Innate Immune Effector CellsFN14 expression correlates with MET in NSCLC and promotes MET-driven cell invasion.
P2860
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P2860
Elevated expression of Fn14 in non-small cell lung cancer correlates with activated EGFR and promotes tumor cell migration and invasion.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
Elevated expression of Fn14 in ...... r cell migration and invasion.
@en
type
label
Elevated expression of Fn14 in ...... r cell migration and invasion.
@en
prefLabel
Elevated expression of Fn14 in ...... r cell migration and invasion.
@en
P2093
P2860
P1476
Elevated expression of Fn14 in ...... r cell migration and invasion.
@en
P2093
Christopher B Kingsley
Emily Cheng
Galen Hostetter
Glen J Weiss
Jeffrey A Winkles
Joseph C Loftus
Kaushal Asrani
Landon Inge
Nathan M Jameson
Nhan L Tran
P2860
P304
P356
10.1016/J.AJPATH.2012.03.026
P407
P577
2012-05-23T00:00:00Z