TRAF-mediated modulation of NF-kB AND JNK Activation by TNFR2

Cabal-Hierro, Lucía; Rodríguez, Montserrat; Artime, Noelia; Iglesias, J. M.; Ugarte, L De; Prado, Miguel A.; Lazo, Pedro S.

doi:10.1016/j.cellsig.2014.08.011

Cited by 56 publications

(45 citation statements)

References 51 publications

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“…XIAP transcription is regulated by nuclear factor (NF)-κB (20) which is more strongly activated by particle than by photon radiation via IκB phosphorylation and degradation (21-23), a process modulated by TNF receptor-associated factor (TRAF)2 (24,25). DNA microarray analysis revealed the increase in TRAF2 levels in C-ion-but not in X-ray-irradiated MIAPaCa-2 cells (data not shown).…”

Section: Discussionmentioning

confidence: 75%

Carbon-Ion Irradiation Suppresses Migration and Invasiveness of Human Pancreatic Carcinoma Cells MIAPaCa-2 via Rac1 and RhoA Degradation

Fujita¹,

Imadome²,

Shoji³

et al. 2015

International Journal of Radiation Oncology*Biology*Physics

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Section: Discussionmentioning

confidence: 75%

Carbon-Ion Irradiation Suppresses Migration and Invasiveness of Human Pancreatic Carcinoma Cells MIAPaCa-2 via Rac1 and RhoA Degradation

Fujita¹,

Imadome²,

Shoji³

et al. 2015

International Journal of Radiation Oncology*Biology*Physics

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“…Trimerization of TNFR2 is induced upon binding of mTNF-α, leading to the recruitment of TRAF2 to the intracellular TRAF binding motif, which subsequently causes the recruitments of TRAF1, cIAP1, and cIAP2 [54] (Figure 2). TRAF2 is a key mediator in this signaling pathway that triggers the subsequent signaling cascades leading to activation of NF-κB [55]. The activation TRAF2-cIAP1/2 complex is recruited to NF-κB-inducing kinase (NIK) by TRAF3, resulting in proteosomal degradation of NIK [56].…”

Section: Tnf-α Receptor 2 Signalingmentioning

confidence: 99%

“…TNF-α-mediated JNK activation depends at least in part on MEKK1 [62,65]. As opposed to TRAF1 and TRAF3, TRAF2 positively regulates JNK activation [55]. It has been suggested that TNFR2 harbors two sequences that are adaptors specific for JNK signaling [69].…”

Section: Tnf-α Receptor 2 Signalingmentioning

confidence: 99%

Targeting of Tumor Necrosis Factor Alpha Receptors as a Therapeutic Strategy for Neurodegenerative Disorders

et al. 2015

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Numerous studies have revealed the pleiotropic functions of tumor necrosis factor alpha (TNF-α), and have linked it with several neurodegenerative disorders. This review describes the signaling pathways induced by TNF-α via its two receptors (TNFR1 and TNFR2), and their functions in neurodegenerative processes as in Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), and ischemic stroke. It has become clear that TNF-α may exert divergent actions in neurodegenerative disorders, including neurodegenerative and neuroprotective effects, which appear to depend on its signaling via either TNFR1 or TNFR2. Specific targeting of these receptors is a promising therapeutic strategy for many disorders.

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“…TRAF2 is one of the most extensively expressed TRAF family members and plays an important role in TNF signal transduction of almost all branching pathways as an adaptor protein and regulatory factor [24]. TRAF2 can interact with anti-apoptotic factors to inhibit cell apoptosis [25,26].…”

Section: Discussionmentioning

confidence: 99%

Screening for the protective effect target of deproteinized extract of calf blood and its mechanisms in mice with CCl4-induced acute liver injury

Han

Gao

et al. 2017

PLoS ONE

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Liver injury is a common pathological basis of various liver diseases, and long-term liver injury is often an important initiation factor leading to liver fibrosis and even liver cirrhosis and hepatocellular carcinoma (HCC). It has been reported that deproteinized extract of calf blood (DECB) can inhibit the replication of hepatitis B virus and confers a protective effect on the liver after traumatic liver injury. However, few studies on the regulatory factors and mechanisms of DECB have been reported. In this current study, an acute mouse liver injury model was established with carbon tetrachloride (CCl4). The differentially expressed genes and related cell signal transduction pathways were screened using mRNA expression microarray. STEM software V1.3.6 was used for clustering gene functions, and the DAVID and KEGG databases were applied for the analysis. A total of 1355 differentially expressed genes were selected, among which nine were validated by RT-qPCR. The results showed that the Fas, IL1b, Pik3r1, Pik3r5, Traf2, Traf2, Csf2rb2, Map3k14, Pik3cd and Ppp3cc genes were involved in the regulation of DECB in an acute mouse liver injury model. Targets of the protective effects of DECB and its related mechanisms were found in mice with acute liver injury induced by carbon tetrachloride, which may provide an important theoretical basis for further DECB research.

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TRAF-mediated modulation of NF-kB AND JNK Activation by TNFR2

Cited by 56 publications

References 51 publications

Carbon-Ion Irradiation Suppresses Migration and Invasiveness of Human Pancreatic Carcinoma Cells MIAPaCa-2 via Rac1 and RhoA Degradation

Carbon-Ion Irradiation Suppresses Migration and Invasiveness of Human Pancreatic Carcinoma Cells MIAPaCa-2 via Rac1 and RhoA Degradation

Targeting of Tumor Necrosis Factor Alpha Receptors as a Therapeutic Strategy for Neurodegenerative Disorders

Screening for the protective effect target of deproteinized extract of calf blood and its mechanisms in mice with CCl4-induced acute liver injury

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