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

Zhang, Yuanyuan; Líu, Hao

doi:10.7314/apjcp.2013.14.12.7069

Cited by 17 publications

(10 citation statements)

References 63 publications

(43 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This is triggered by multiple stimulators, and interacts with death receptors (TNFR1, TRAIL-R or Fas), T-cell receptors (TCR), Toll-like receptors (TLRs), cellular metabolic and genotoxic stress, and a number of anti-cancer agents [127–129]. In TNF-α induced necroptosis, three complexes are essential and are key regulators that trigger this response, including complex I, complex IIa and complex IIb [130, 131].…”

Section: Programmed Cell Death In the Treatment Of Osteosarcomamentioning

confidence: 99%

“…Both RIP1 and RIP3 necrosome recruits and activates MLKL and phosphoglycerate mutase 5(PGAM5). MLKL is phosphorylated and multimerized, is inserted into the plasma membrane, and forms channels that increases Na+ influx, osmotic pressure and membrane rupture; ending with necroptosis induced-cell death [129, 136]. PGAM5 recruits and activates mitochondrial fission factor dynamin-related protein 1 (Drp1), leading to mitochondrial fission; which is a key factor for necrosis execution [137, 140] (Figure 3).…”

Section: Programmed Cell Death In the Treatment Of Osteosarcomamentioning

confidence: 99%

See 1 more Smart Citation

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Yang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

Osteosarcoma is the most common primary bone tumor in children and adolescents. Although combined therapy including surgery and multi-agent chemotherapy have resulted in great improvements in the overall survival of patients, chemoresistance remains an obstacle for the treatment of osteosarcoma. Molecular targets or effective agents that are actively involved in cell death including apoptosis, autophagy and necroptosis have been studied. We summarized how these agents (novel compounds, miRNAs, or proteins) regulate apoptotic, autophagic and necroptotic pathways; and discussed the current knowledge on the role of these new agents in chemotherapy resistance in osteosarcoma.

show abstract

Section: Programmed Cell Death In the Treatment Of Osteosarcomamentioning

confidence: 99%

Section: Programmed Cell Death In the Treatment Of Osteosarcomamentioning

confidence: 99%

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Yang

et al. 2016

Oncotarget

View full text Add to dashboard Cite

show abstract

“…141 Necroptosis shares characteristics of both necrosis and apoptosis. 142, 143 A study on mice model has showing that a bolus dose of necroptosis inhibitor, necrostatin-1, in mice at the time of coronary reperfusion dramatically reduced infarct size after I/R njury.…”

Section: Mirnas In Cardiovascular Necrosismentioning

confidence: 99%

Small molecules, big effects: the role of microRNAs in regulation of cardiomyocyte death

et al. 2014

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are a class of small non-coding RNAs involved in posttranscriptional regulation of gene expression, and exerting regulatory roles in plethora of biological processes. In recent years, miRNAs have received increased attention for their crucial role in health and disease, including in cardiovascular disease. This review summarizes the role of miRNAs in regulation of cardiac cell death/cell survival pathways, including apoptosis, autophagy and necrosis. It is envisaged that these miRNAs may explain the mechanisms behind the pathogenesis of many cardiac diseases, and, most importantly, may provide new avenues for therapeutic intervention that will limit cardiomyocyte cell death before it irreversibly affects cardiac function. Through an in-depth literature analysis coupled with integrative bioinformatics (pathway and synergy analysis), we dissect here the landscape of complex relationships between the apoptosis-regulating miRNAs in the context of cardiomyocyte cell death (including regulation of autophagy–apoptosis cross talk), and examine the gaps in our current understanding that will guide future investigations.

show abstract

“…1 The various membrane proteins can be recruited to aggregate within the membrane to form little islands of proteins with their support molecules to initiate or "trigger" numerous cellular responses. [4][5][6][7][8][9][10][11] "Chemical Triggers"…”

Section: "Triggers" Of Cell Life and Programmed Cell Deathmentioning

confidence: 99%

Coupling of physical characteristics of non-ionizing irradiation to specific mechanisms of cell death: are we there yet?

Thomsen¹

2015

Energy-Based Treatment of Tissue and Assessment VIII

View full text Add to dashboard Cite

The recent discovery of the various specific" triggers" and mechanisms of cell life and death responses suggests that certain non-ionizing irradiation spectra and other physical signals could be coupled with specific cellular "triggers" to improve diagnostic or treatment effects. Genetic, chemical and/or physical modifications of specific extrinsic cellular "triggers" have centered on chemical binding of specific molecules to specific receptors, i.e. chemical " triggers" thus allowing development of specific drugs to counteract the initiating function of the "triggers" in single cells. Investigations of non-ionizing irradiation effects on cells and tissues indicate that their "triggers" involve intimate interactions of linked components of the extracellular matrix and the cytoskeleton in tissues. Therefore, the search for single "triggers" that may work well for chemical "triggers" in single cells in culture may not be effective for discovery of the mechanisms that initiate sensing of the stimulations of non-ionizing irradiation and mechanical force.In cell biology, the mechanisms of life and death usually involve a series of complex, chemical, mechanical and/or electrical events that are highly interactive with many other physiological and pathological mechanisms within and outside the cell. To distinguish one event from any of the others the following things have to be established:1. Precise description of the ultimate cellular response to be studied i.e. cell death, cell movement, energy production, protein synthesis, cell division, etc. The definitions of these responses could and should be refined as an investigator finds out more information about the events in his studies. For example, cell death could be due to apoptosis (identified by production of apoptotic bodies) therefore future studies could be focused on finding markers of the extrinsic or intrinsic apoptotic pathways.2. Identification of a specific act or " triggered" reaction that initiates a series of events which produces the cellular response to be studied. For example, apoptosis can be "triggered" by ligand binding of tumor necrosis factor (TNF) to the "death receptor" found on the surfaces of certain cells.3. "Markers" are the key substance(s) or reaction(s) that distinguish a specific series of events. The series can produce several markers along the way. For instance, a key marker of apoptosis is the production of caspase 8.4. Identification of "end points", the results or cellular responses of the series of events or a subset of events. These are frequently are measureable thus useful for mathematical modeling. Ultimate cell responses such as cell death are "endpoints" but other well-defined products or reactions found within the series of events, such as caspase 8 production which occurs early in apoptosis also can be designated as desired endpoints of study. Keynote Paper Energy-based Treatment of Tissue and Assessment VIII, edited by Thomas P. Ryan Proc. of SPIE Vol. 9326, 932603 · © 2015 SPIE · CCC code: 1605-7422/15/$18

show abstract

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

Cited by 17 publications

References 63 publications

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Cell apoptosis, autophagy and necroptosis in osteosarcoma treatment

Small molecules, big effects: the role of microRNAs in regulation of cardiomyocyte death

Coupling of physical characteristics of non-ionizing irradiation to specific mechanisms of cell death: are we there yet?

Contact Info

Product

Resources

About