Cell Death Signaling

Green, Douglas R.; Llambi, Fabien

doi:10.1101/cshperspect.a006080

Cited by 879 publications

(750 citation statements)

References 284 publications

(212 reference statements)

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“…72 The cell-surface death receptors (DRs), belonging to the TNFR superfamily and featuring the presence of a cytosolic DD, can be divided into two categories: TNFR1, DR3 and possibly DR6-binding TNFR1-associated death domain-containing protein and exerting pro-inflammatory and pro-survival functions, or Fas/CD-95, DR4 and DR5 engaging FADD (Fas-associated protein with DD) and exerting primarily pro-apoptotic functions. Furthermore, crosstalk might occur between these two opposing processes.…”

Section: Apoptosis Regulation By the Ubiquitin Systemmentioning

confidence: 99%

The ubiquitin system: a critical regulator of innate immunity and pathogen–host interactions

Chai

Liu

2016

Cell Mol Immunol

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The ubiquitin system comprises enzymes that are responsible for ubiquitination and deubiquitination, as well as ubiquitin receptors that are capable of recognizing and deciphering the ubiquitin code, which act in coordination to regulate almost all host cellular processes, including host-pathogen interactions. In response to pathogen infection, the host innate immune system launches an array of distinct antimicrobial activities encompassing inflammatory signaling, phagosomal maturation, autophagy and apoptosis, all of which are fine-tuned by the ubiquitin system to eradicate the invading pathogens and to reduce concomitant host damage. By contrast, pathogens have evolved a cohort of exquisite strategies to evade host innate immunity by usurping the ubiquitin system for their own benefits. Here, we present recent advances regarding the ubiquitin system-mediated modulation of host-pathogen interplay, with a specific focus on host innate immune defenses and bacterial pathogen immune evasion.

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Section: Apoptosis Regulation By the Ubiquitin Systemmentioning

confidence: 99%

The ubiquitin system: a critical regulator of innate immunity and pathogen–host interactions

Chai

Liu

2016

Cell Mol Immunol

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“…The most common mutation of JAK2 consists of a substitution of valine with phenylalanine at position 617 in the JH2 domain (JAK2 V617F) in exon 14, which affects the inhibitory function of the pseudokinase JH2 domain, inducing an increased activity in myeloid progenitor cells, leading to proliferation and excessive production of mature cells (27,29,(31)(32)(33). JAK2 V617F and exon 12 mutations signal through the same C-terminal tyrosine kinase of JAK2, but result in very different phenotypic readouts.…”

Section: Introductionmentioning

confidence: 99%

Prevalence of the Janus kinase 2 V617F mutation in Philadelphia-negative myeloproliferative neoplasms in a Portuguese population

et al. 2017

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Abstract. Myeloproliferative neoplasms (MPNs) result from the malignant transformation of a hematopoietic stem-cell (HSC), leading to abnormal amplification and proliferation of myeloid lineages. Identification of the Janus kinase 2 (JAK2) V617F mutation developed the knowledge of Philadelphia-negative (PN)-MPNs, contributing to and influencing the definition of the phenotype and prognostic impact. Considering the lack of Portuguese epidemiological data, the present study intends to characterize the prevalence of the JAK2 mutation in a PN-MPN versus a control Portuguese population. Caucasian Portuguese PN-MPN patients (n=133) and 281 matched control subjects were investigated. No significant differences were identified between the case and control groups concerning age distribution or smoking habits. Pathology distribution was as follows: 60.2% with essential thrombocythemia (ET), 29.3% with polycythemia vera (PV) and 10.5% with primary myelofibrosis (PMF). A total of 75.0% of patients were positive for the presence of the JAK2 V617F mutation. In addition, the prevalence of PV was 87.2%, ET was 73.4% and PMF was 50.0%. The JAK2 V617F mutation is observed in various MPN phenotypes, and has an increased incidence in ET patients and a decreased incidence in PV patients. These data may contribute to improving the knowledge of the pathophysiology of these disorders, and to a more rational and efficient selection of therapeutic strategies to be adopted, notably because most of the patients are JAK2 V617F negative.

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“…Calcium ions can activate calpain proteases in the cytoplasm, which subsequently destroy the integrity of lysosomes and unleash hydrolytic enzymes such as cathepsin proteases. These events synergistically induce cell swelling, cell lysis, and eventually cell death (Green & Llambi, 2015; Troulinaki & Tavernarakis, 2012). Recent studies have identified an additional type of programmed cell death that could be regulated and controlled at the same time sharing the pathological hallmarks of necrosis, which is regulated necrosis or necroptosis (Weinlich, Oberst, Beere, & Green, 2017).…”

Section: Necrosis: Autophagy‐related Cell Death That Contributes To Tmentioning

confidence: 99%

The emerging roles of protein homeostasis‐governing pathways in Alzheimer's disease

et al. 2018

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Pathways governing protein homeostasis are involved in maintaining the structural, quantitative, and functional stability of intracellular proteins and involve the ubiquitin–proteasome system, autophagy, endoplasmic reticulum, and mTOR pathway. Due to the broad physiological implications of protein homeostasis pathways, dysregulation of proteostasis is often involved in the development of multiple pathological conditions, including Alzheimer's disease (AD). Similar to other neurodegenerative diseases that feature pathogenic accumulation of misfolded proteins, Alzheimer's disease is characterized by two pathological hallmarks, amyloid‐β (Aβ) plaques and tau aggregates. Knockout or transgenic overexpression of various proteostatic components in mice results in AD‐like phenotypes. While both Aβ plaques and tau aggregates could in turn enhance the dysfunction of these proteostatic pathways, eventually leading to apoptotic or necrotic neuronal death and pathogenesis of Alzheimer's disease. Therefore, targeting the components of proteostasis pathways may be a promising therapeutic strategy against Alzheimer's disease.

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Cell Death Signaling

Cited by 879 publications

References 284 publications

The ubiquitin system: a critical regulator of innate immunity and pathogen–host interactions

The ubiquitin system: a critical regulator of innate immunity and pathogen–host interactions

Prevalence of the Janus kinase 2 V617F mutation in Philadelphia-negative myeloproliferative neoplasms in a Portuguese population

The emerging roles of protein homeostasis‐governing pathways in Alzheimer's disease

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