Signaling Activated by the Death Receptors of the TNFR Family

Anděra, Ladislav

doi:10.5507/bp.2009.029

Cited by 40 publications

(28 citation statements)

References 100 publications

(103 reference statements)

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“…FAS (also known as Apo-1 or CD95), a cell-surface receptor, plays a key role in apoptotic signaling in many cell types (5). FAS ligand (FASL) (also known as CD95L), a member of the tumor necrosis factor super family, can trigger an apoptotic cascade by cross-linking with its receptor, FAS (6,7).…”

Section: Introductionmentioning

confidence: 99%

Lack of association between the FAS/FASL polymorphisms and cervical cancer risk: A meta-analysis

Pan

2013

Biomedical Reports

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Abstract. FAS/FASL gene promoter polymorphisms are associated with cervical cancer risk, however, results from previous studies have been conflicting. To obtain a more precise estimation of the association between these polymorphisms and cancer risk, a meta-analysis was performed. All eligible studies up to November 1st, 2012, concerning FAS-670 A/G, FAS-1377 G/A and FASL-844 T/C polymorphisms and cervical cancer risk, were collected from the following electronic databases: PubMed, Excerpta Medica Database and Chinese Biomedical Literature Database. The odds ratio (OR) and 95% confidence interval (95% CI) were used to assess the strength of the association via the additive, codominant, dominant and recessive models. In total, 10 publications with 11 case-control studies (10 on FAS-670 A/G, 5 on FAS-1377 G/A and 6 on FASL-844 T/C polymorphisms) were included in this meta-analysis. No association between FAS-670 A/G, FAS-1377 G/A and FASL-844 T/C polymorphisms and cervical cancer susceptibility for all the genetic models was identified. Following stratification of the studies by ethnicity or source of controls, similar results were obtained. In conclusion, our findings showed that the FAS-670 A/G, FAS-1377 G/A and FASL-844 T/C polymorphisms are not associated with cervical cancer risk. Future studies with larger sample sizes are required to further evaluate these associations.

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Section: Introductionmentioning

confidence: 99%

Lack of association between the FAS/FASL polymorphisms and cervical cancer risk: A meta-analysis

Pan

2013

Biomedical Reports

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“…Under special conditions TNF-R1, TNF-R2, Fas-and Apo-2L receptors TRAIL-R1 and TRAIL-R2 can initiate necrotic-like cell death [10,21,22]. The most extensively studied pathway leading to necroptosis is triggered by binding of TNFα to TNF-R1 (see review [23]). TNFα generally induces prosurvival signal through NFkB but is also able to induce apoptosis or necrotic-like cell death.…”

Section: Biochemical Aspectsmentioning

confidence: 99%

“…In parallel, a negative feedback loop of NFkB is proven by A20 a dual E3 ligase and ubiquitin hydrolase that cleaves off the K63-linked polyubiquitin chain from RIPK1 and subsequently marks RIPK1 for proteasomal degradation. This contributes to limit the proinflammatory activation of NFkB [23].…”

Section: Biochemical Aspectsmentioning

confidence: 99%

Necroptosis: Biochemical, Physiological and Pathological Aspects

Dunai

Bauer

Rudolf

2011

Pathol. Oncol. Res.

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Programmed cell death is a key component of tissue homeostasis, normal development and wide variety of diseases. Conventional view refers to programmed cell death form as caspase-mediated apoptosis while necrosis is considered as an accidental and unwanted cell demise, carried out in a non-regulated manner and caused by extreme conditions. However, accumulating evidences indicate that necrotic cell death can also be a regulated process. The term necroptosis has been introduced to describe a cell death receptor-induced, caspase-independent, highly regulated type of programmed cell death process with morphological resemblance of necrosis. Necroptosis recently has been found to contribute to a wide range of pathologic cell death forms including ischemic brain injury, neurodegenerative diseases and viral infection, therefore a better understanding of the necroptotic signaling machinery has clinical relevance.

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“…While TNFR2 does not have a death domain, TNFR1 plays a principal role in TNF-α-mediated activation and triggers a series of intracellular events (Wu et al, 2012). Initially, TNF-α binds to the extracellular portion of TNFR1 to induce allosteric changes and lead to the recruitment of multiple proteins including TNFR-associated death domain (TRADD), RIP1, Fas-associated death domain (FADD), cellular inhibitor of apoptosis proteins (cIAPs), TNFR-associated factor-2 (TRAF2) and TRAF5 which together constitute the so-called complex I (Andera, 2009). At complex I, cIAPs mediate the K63-linked polyubiquitination of RIP1 triggering the canonical pathway activation of the transcription factor NF-κB.…”

Section: Tnfrmentioning

confidence: 99%

Connections Between Various Trigger Factors and the RIP1/RIP3 Signaling Pathway Involved in Necroptosis

Zhang¹,

Líu²

2013

Asian Pacific Journal of Cancer Prevention

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Programmed cell death is a basic cellular process that is critical to maintaining tissue homeostasis. In contrast to apoptosis, necrosis was previously regarded as an unregulated and uncontrollable process. However, as research has progressed, necrosis, also known as necroptosis or programmed necrosis, is drawing increasing attention, not least becasu of its possible impications for cancer research. Necroptosis exhibits a unique signaling pathway that requires the involvement of receptor interaction protein kinases 1 and 3 (RIP1 and RIP3), mixed lineage kinase domain-like (MLKL), and phosphoglycerate mutase 5 (PGAM5) and can be specifically inhibited by necrostatins. Not only does necroptosis serve as a backup cell death program when apoptosis is inhibited, but it is now recognized to play a pivotal role in regulating various physiological processes and the pathogenesis of a variety of human diseases such as ischemic brain injury, immune system disorders and cancer. The control of necroptosis by various defined trigger factors and signaling pathways now offers the opportunity to target this cellular process for therapeutic purposes. The purpose of this paper is to review current findings concerning the connections between various trigger factors and the RIP1/RIP3 signaling pathway as it relates to necroptosis.

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Signaling Activated by the Death Receptors of the TNFR Family

Cited by 40 publications

References 100 publications

Lack of association between the FAS/FASL polymorphisms and cervical cancer risk: A meta-analysis

Lack of association between the FAS/FASL polymorphisms and cervical cancer risk: A meta-analysis

Necroptosis: Biochemical, Physiological and Pathological Aspects

Connections Between Various Trigger Factors and the RIP1/RIP3 Signaling Pathway Involved in Necroptosis

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