Pages that link to "Q28571207"

The following pages link to The death receptor antagonist FAIM promotes neurite outgrowth by a mechanism that depends on ERK and NF-kapp B signaling (Q28571207):

Displaying 46 items.

• Fas Apoptosis Inhibitory Molecule Contains a Novel β-Sandwich in Contact with a Partially Ordered Domain (Q27653514) (← links)
• Fas apoptotic inhibitory molecule (Q28562265) (← links)
• TNFα induces survival through the FLIP-L-dependent activation of the MAPK/ERK pathway (Q28580836) (← links)
• The death receptor antagonist FLIP-L interacts with Trk and is necessary for neurite outgrowth induced by neurotrophins (Q28580900) (← links)
• Bex1, a novel interactor of the p75 neurotrophin receptor, links neurotrophin signaling to the cell cycle (Q28583606) (← links)
• Nuclear factor-kappaB activation via tyrosine phosphorylation of inhibitor kappaB-alpha is crucial for ciliary neurotrophic factor-promoted neurite growth from developing neurons (Q30460154) (← links)
• Crystallization and preliminary X-ray crystallographic studies of human FAIM protein (Q34049181) (← links)
• MiR-133b targets antiapoptotic genes and enhances death receptor-induced apoptosis (Q34245074) (← links)
• Multiple transcription factor families regulate axon growth and regeneration (Q35539750) (← links)
• TNFα sensitizes neuroblastoma cells to FasL-, cisplatin- and etoposide-induced cell death by NF-κB-mediated expression of Fas. (Q35609210) (← links)
• IL-10 Protects Neurites in Oxygen-Glucose-Deprived Cortical Neurons through the PI3K/Akt Pathway (Q35772509) (← links)
• The MAPK and PI3K pathways mediate CNTF-induced neuronal survival and process outgrowth in hypothalamic organotypic cultures (Q36087417) (← links)
• NF-kappaB in the survival and plasticity of neurons (Q36269312) (← links)
• Fas apoptosis inhibitory molecule expression in B cells is regulated through IRF4 in a feed-forward mechanism (Q36653424) (← links)
• Axonal transport of neural membrane protein 35 mRNA increases axon growth (Q36702557) (← links)
• Loss of Fas apoptosis inhibitory molecule leads to spontaneous obesity and hepatosteatosis (Q36847534) (← links)
• Soluble epoxide inhibition is protective against cerebral ischemia via vascular and neural protection. (Q37197332) (← links)
• Fas apoptosis inhibitory molecule enhances CD40 signaling in B cells and augments the plasma cell compartment (Q37408346) (← links)
• Mitochondrial proteomics as a selective tool for unraveling Parkinson's disease pathogenesis (Q37727186) (← links)
• NF-κΒ Signaling in Neurite Growth and Neuronal Survival (Q37810565) (← links)
• Regulation of neural process growth, elaboration and structural plasticity by NF-κB. (Q37860703) (← links)
• Role of transcription factors in peripheral nerve regeneration (Q37987916) (← links)
• NF-κB signaling pathways: role in nervous system physiology and pathology (Q38025541) (← links)
• Role of p75 neurotrophin receptor in stem cell biology: more than just a marker (Q38183736) (← links)
• Effect of lipopolysaccharide on global gene expression in the immature rat brain (Q38518025) (← links)
• Fas apoptosis inhibitory molecules: more than death-receptor antagonists in the nervous system (Q38888419) (← links)
• Fas apoptosis inhibitory molecule is upregulated by IGF-1 signaling and modulates Akt activation and IRF4 expression in multiple myeloma. (Q39247614) (← links)
• Virally delivered, constitutively active NFκB improves survival of injured retinal ganglion cells. (Q39450768) (← links)
• Fas apoptosis inhibitory molecule regulates T cell receptor-mediated apoptosis of thymocytes by modulating Akt activation and Nur77 expression. (Q39982673) (← links)
• The long form of Fas apoptotic inhibitory molecule is expressed specifically in neurons and protects them against death receptor-triggered apoptosis. (Q40066489) (← links)
• Analysis of CD95 threshold signaling: triggering of CD95 (FAS/APO-1) at low concentrations primarily results in survival signaling (Q40161643) (← links)
• Cytotoxicity and apoptotic gene expression in an in vitro model of the blood-brain barrier following exposure to poly(butylcyanoacrylate) nanoparticles. (Q40167936) (← links)
• Nuclear factor kappa B signaling either stimulates or inhibits neurite growth depending on the phosphorylation status of p65/RelA (Q41887851) (← links)
• X-linked inhibitor of apoptosis protein negatively regulates neuronal differentiation through interaction with cRAF and Trk. (Q41984256) (← links)
• FAIM-L is an IAP-binding protein that inhibits XIAP ubiquitinylation and protects from Fas-induced apoptosis. (Q42251118) (← links)
• Identification and characterization of new isoforms of human fas apoptotic inhibitory molecule (FAIM). (Q42370702) (← links)
• Developmental switch in NF-kappaB signalling required for neurite growth (Q42567149) (← links)
• Amyloid-β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNFα from neuronal protection to death. (Q42642136) (← links)
• Expression analysis, single nucleotide polymorphisms and combined genotypes in candidate genes and their associations with growth and carcass traits in Qinchuan cattle (Q43931464) (← links)
• BCL-XL regulates TNF-alpha-mediated cell death independently of NF-kappaB, FLIP and IAPs (Q46508943) (← links)
• Neuroprotection by neurotrophic factors and membrane depolarization is regulated by calmodulin kinase IV. (Q46851049) (← links)
• Inhibition of Apoptosis by Expression of Antiapoptotic Proteins in Recombinant Human Keratinocytes (Q47951325) (← links)
• Genetic deletion of faim reveals its role in modulating c-FLIP expression during CD95-mediated apoptosis of lymphocytes and hepatocytes. (Q51758301) (← links)
• FAIM Opposes Aggregation of Mutant SOD1 That Typifies Some Forms of Familial Amyotrophic Lateral Sclerosis (Q90175831) (← links)
• FAIM Is a Non-redundant Defender of Cellular Viability in the Face of Heat and Oxidative Stress and Interferes With Accumulation of Stress-Induced Protein Aggregates (Q90347873) (← links)
• FAIM: An Antagonist of Fas-Killing and Beyond (Q92544543) (← links)