So-Jin Kim added an answer:Are there tools to visualize necroptosis?
Recently, I received the comments of referee that I should detect the TEM to confirm the necroptosis.
However, I wonder there is a tool for this.
Is there any histological and/or TEM analysis for necroptosis?
How about for necrosis?
Thank you for your answer and kindly message :)
It will be helpful to me !!Following
Closed account added an answer:What are some off targets of Necrostatin 1 other than IDO?
Are there any off targets of Necrostatin 1 beyond IDO (and the obvious target, RIP1)?
We have observed prevention of cell death using a compound we study in combination with Nec1 but have used siRNA to demonstrate that RIP1 is not responsible for our compound's induction of cell death.
DEAR RESEARCHERS,THE QUESTION IS VERY INTERESTING ,HERE I AM AGAIN GIVING FURTHER COMMENTS
Name giving is part of human nature as an attempt to classify objects and structure the world around us. In a scientific context such name giving is ideally organized according to strict rules of nomenclature that form a system of terms and principles allowing accurate communication between specialists in particular disciplines. However, for reasons of convenience or eloquence, such strict conventions are often disregarded, sometimes to the extent that a name no longer evokes a clear idea of the object. A good example is the ‘CD' naming system in immunology, where many casual users would be hard pressed to recall the molecules corresponding to any but the most frequently used CD denominators. Nevertheless, as Shakespeare reminds us in Romeo and Juliette, ‘What's in a name? That what we call a rose by any other name would smell as sweet.' Indeed, what matters is the object rather than its name. However, when it comes to naming compounds, a question arises: To what extent can we yield to the pressures of convenience, eloquence or discovery history rather than follow the agreed-upon nomenclature rules? What is more important, a molecule's chemical composition or its intended use? Very often, compounds are named after the biological target against which they were discovered. This provides an easy and attractive way of naming molecules, but it risks causing a bias in research aims and the way in which results are interpreted. Indeed, names can clarify, but they can also blur or confuse. Two papers ‘Activity and specificity of Necrostatin-1, small molecule inhibitor of RIP1 kinase' in Cell Death and Differentiation1 and ‘Necrostatin-1 analogs: Critical issues on the specificity, activity and in vivo use in experimental disease models' in Cell Death and Disease2 raise important considerations on the use of necrostatin-1 (Nec-1) and its analogs to study the implication of RIPK1 kinase activity in experimental disease models.Following
Anne von Koschembahr added an answer:If in addition to activation of a TNFa pathway another pathway that induces apoptosis is active, how does the cell decide to die?
When the cell undergoes ATP depletion, apoptosis cannot occur and the cell dies by necroptosis (programmed necrosis). In TNFa -induced necroptosis, activation of Complex IIb ( Ripk1 / Ripk3 ) kills the cell without ATP depletion (I think). If in addition to activation of TNFa pathway another pathway that induces apoptosis is active, how does the cell decide to die?
Wouldn't it then be important to determine the various populations of cell death, in order to determine if TNF-alpha causes an apoptotic response versus necrosis? Could one say that this response may be a cell-type specific response?Following
Dorothy C Bennett added an answer:Does G2/M arrest necessarily lead to cell death? How so?
Is there a signaling pathway or a particular signal induced by arrest between S phase and mitosis (cells don't divide after synthesizing new DNA) that initiates cell death? Is this death necessarily mediated by caspases?
DNA damage signalling can also lead to cell senescence (at least partly through CHK2-p53-p21) rather than cell death. It is not entirely clear how cells choose one or the other, but probably with lower levels of damage signalling you would get more senescence (permanent arrest) and less death. So cells that fail to complete S phase or mitosis can end up in a kind of G1 phase with tetraploid or subtetraploid DNA, as several groups have shown.Following
Lei Shang added an answer:How can I identify the cell with the staining of Annexin V (-)/PI (+) using flow cytometry?Annexin V (+)/PI (+) represent necrosis and later apoptosis, Annexin V (-)/PI (-) represent normal, Annexin V (+)/PI (-) represent early apoptosis. So what about Annexin V (-)/PI (+), please help me and attach your related references.Maybe someone give me the answer about primary necrosis, but how to understand this kind of cell death, what the relationship between primary necrosis and necrosis??Following
Demba Sarr added an answer:Does anyone know the best way to induce Necroptosis in cells? TNF, TRAIL...?I would like to induce necroptosis in trophoblast cell line.Thank you Scott. I will keep you posted and sorry for the delay.Following
Lei Shang added an answer:How to knockdown the expression of RIP3?I cannot find a inhibitor of RIP3 to make the deletion. Can somebody give me some information to attenuate protein level?Thanks Linkermann!! I agree with your comment.Following
Dominique Vanhecke added an answer:Is there a natural situation (in vivo) where intact endosomes could be released from cells?What happens to endosomes following cell death (apoptosis, necrosis etc).Thank you very much for your input.
But I was wondering whether in addition to these microvesicles there can also be intact organelles, in this case intact endosomes be released under some circumstances. A big difference is that in contrast to microvesicles the endosomes would be so-called "inside-out" with respect to the orientation of membrane bound proteins.Following