CD40-mediated cell death requires TRAF6 recruitment

Jundi, Malek; Nadiri, Amal; Al-Zoobi, Loubna; Hassan, Ghada S.; Mourad, Walid

doi:10.1016/j.imbio.2011.07.007

Cited by 14 publications

(10 citation statements)

References 39 publications

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“…On the other hand, an important role for reactiveoxygen species, lysosomal membrane permeabilization and cathepsin B release has been reported for CD40-induced death of Burkitt lymphoma cells. This study also demonstrated the implication of TRAF6 [69]. It is worth noting at this point that in some normal cells such as liver epithelial ones, CD40 was capable of inducing apoptotic events by activating JNK, ERK1/2, and their downstream signaling effector, AP-1 as well as the Jak2/STAT3 signaling pathway [75].…”

Section: Mechanisms Underlying Cd40-mediated Apoptosis In Tumor Cellssupporting

confidence: 63%

“…Low level of CD40 engagement was shown to promote cell proliferation and differentiation, whereas at high levels, it has been shown that CD40 induces cell cycle arrest and cell death (Fig. 1) [68,69]. Crosslinking CD40 on surface of normal B cells and those derived from low grade malignancies, such as CLL, hairy cell leukemia and follicular lymphoma induced cell proliferation.…”

Section: Cd40-mediated Growth Control Of Tumor Cellsmentioning

confidence: 96%

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Role of CD154 in cancer pathogenesis and immunotherapy

Hassan¹,

Stagg²,

Mourad³

2015

Cancer Treatment Reviews

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Section: Mechanisms Underlying Cd40-mediated Apoptosis In Tumor Cellssupporting

confidence: 63%

Section: Cd40-mediated Growth Control Of Tumor Cellsmentioning

confidence: 96%

Role of CD154 in cancer pathogenesis and immunotherapy

Hassan¹,

Stagg²,

Mourad³

2015

Cancer Treatment Reviews

Self Cite

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“…However, its expression has been observed in a wide variety of cells including platelets, mast cells, macrophages, basophils, NK cells, B lymphocytes as well as non-haematopoietic cells [26]. As a member of the TNF-α receptor family, CD40 relies on interaction with TRAF proteins to mediate an intracellular signal in response to CD40L binding [27,28]. The downstream protein of TRAF2/3 can activate consecutive initiation of MEK4 and MEK7, resulting in the activation of stress-activated protein kinases JNK1/2 [29].…”

Section: Discussionmentioning

confidence: 99%

Differential apoptosis gene expressions of rhabdomyosarcoma cells in response to enterovirus 71 infection

Shi¹,

Li²,

Hou³

et al. 2012

BMC Infect Dis

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BackgroundEnterovirus 71 (EV71) infection can induce the apoptosis of infected cells. The aim of this study is to explore the effect of EV71 infection on apoptosis mechanisms in virus-infected human rhabdomyosarcoma (RD) cells.MethodsThe apoptosis of RD cells was examined using annexin V-FITC/PI by flow cytometry and cytokines were detected by ELISA. Cellular RNA was extracted and transcribed to cDNA. PCR array was employed to analyze the expressions of 84 apoptotic genes from EV71-infected RD cells at 8 and 20 h postinfection, respectively. In addition, the expressions of FasL, caspase, AKT2, JNK1/2, c-Jun and NF-κB proteins were detected by western blotting.ResultsFlow cytometry demonstrated that the apoptosis or death of EV71-infected RD cells was increased by 37.1% with a multiplicity of infection (MOI) of 5 at 20 h postinfection. The production of IL-4, IL-10 and TNF-α was enhanced by the subsequent EV71 infection. PCR array revealed significant changes in the expressions of apoptotic genes. Among 84 genes, 42 genes were down-regulated after EV71 infection at 8 h, whereas 32 genes were up-regulated at 20 h postinfection. Moreover, the ligands of TNF superfamily such as FasL, CD40L and TNF-α were significantly up-regulated and enhanced the expressions of apoptosis-related cysteine peptidases, including caspase-10, -8, -7 and -3. In addition, EV71 infection induces the phosphorylation of AKT2, JNK1/2, c-Jun and NF-κB at 20 h postinfection.ConclusionPCR array for the determination of apoptosis gene expressions is an informative assay in elucidating biological pathways. During the early stage of EV71 infection, the apoptotic process of RD cells is significantly delayed. EV71 infection can also induce the expressions of FasL, TNF-α and CD40L, which contribute to the apoptosis of RD cells.

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“…Unlike other TRAFs, it is also involved in IL-1 signaling, leading to the activation of NF-kB (nuclear factor kappaB) (Ishida et al, 1996;Lee and Lee, 2002). TRAF6 and TRAF3 maintain the balance of apoptosis and anti-apoptosis in RAdncCD40L-infected carcinoma cells (Elmetwali et al, 2010;Jundi et al, 2012). The most abundant amounts of the TRAF1, TRAF2 and TRAF6 protein can be detected in thymus, testis and epidermis, while in other tissues the expression is low or even absent, which reveals a tissue-specific difference of TRAF protein expression in normal human tissues (Zapata et al, 2000).…”

Section: Introductionmentioning

confidence: 99%