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-/- means both copies of the gene (both alleles) are knocked out


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There is actually no preference for apoptosis or necrosis in cells of the human body - both types can occur in all cells and they have different triggers. The main differences can be seen in this figure (from here): Apoptosis (also called programmed cell death) has three different triggers (intrinsic, extrinsic and Perforin/Granzyme pathways), see the image ...


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Although both involve DNA fragmentation, the pattern produced is very different. During apoptosis, DNA fragmentation is done in a regular, controlled pattern, which if run on a gel produces a characteristic "ladder" pattern. Necrosis, on the other hand, is a more stochastic process, and will produce a smear. This details the difference rather nicely, ...


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Apoptosis is very tightly controlled for obvious reasons. Setting it off without proper control would result in the uncontrolled loss of cells. Apoptosis is one of the major pathways which are either mutated or shut-off in cancers, preventing the body from eliminating malingnant cells. These two papers are interesting in this context: Apoptosis: A Review of ...


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Usually the cell death mechanisms are overridden and therefore oncogenesis. The pathway components themselves are not mutated. One classical case I can cite is that of Ras-oncogene. See this article for details. Usually the survival/growth signals (MAP-kinase) are activated with simultaneous inactivation of apoptotic regulators (Akt-pathway). A mutation of ...


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According to Google Scholar, there were ~40000 hits for "apoptose" and ~120k hits for "undergo apoptosis" in published literature, both of which had significant numbers of high-impact articles. Therefore, it is clear that both expressions are sufficiently used in literature for either to be used. Personally, I would say "undergo apoptosis" being both ...


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The answer given above by Chris is correct, but does leave out one relatively recently discovered method of cell death, somewhere between the two responses of apoptosis and necrosis. It's called pyroptosis. It's a form of programmed cell death (in immune cells, e.g. macrophages), so it is similar to apoptosis. However, instead of a neat and tidy non-...


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Not at all. In order to self destruct, you don't need to disable all necessary functions, you just need to disable one. That's why the functions are called "essential". To take a very simple example, in every movie you've seen where the self destruct has been activated, that self destruct mechanism was almost certainly a bomb that blew the ship/installation/...


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This is pretty unlikely, since one of the most important steps for cancer cells is to shut off apoptosis and proteins which control it (like p53, BCL2 and so on). Cancer cells (especially when they are genetically unstable) acquire so much mutations and misregulations, that these would otherwise trigger apoptosis which would result in the removal of the cell....


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Yes, tons of things induce apoptosis. Here is a good list that you can get for research grade Sigma-Aldrich Even your immune system can tell cells to "commit suicide." Now the trick is, getting drugs, proteins, pathways, and your immune system to selectively target cancer cells.


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Necrosis can be described as accidental cell death or damage, triggered possibly from external environmental factors such as exposure to radiation, toxins, excessive heat and etc...whereas, Apoptosis is a programmed form of a cell death mechanism. This process may be used to recycle unwanted cells in the body. Therefore, the particular stimulus that the cell ...


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In both pathways 'the cell does itself' the difference is in the reason. In short: Intrinsic apoptosis is a response to 'internal damage' eg. damaged DNA, chromosom rearrangement, hang ups in division, hypoxia, etc. that the cell senses itself and 'decides to commit suicide'. This is done by the mitochondrial pathway - release of cytochrome C from the ...


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Apoptosis can occur without cell cycle already being arrested. For instance, in the case of extrinsic apoptosis, which could be induced by T lymphocytes, for example, a trimeric receptor such as TNF-R or TRAIL-R's containing a DD can be bound at any time by the death ligand secreted by (TNF, TRAIL) or bound to the immune cell membrane (FasL, TRAIL). The DD ...


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Your question is quite well-formed, however all I can say so far is: I don't know. Maybe it is known, however I could not find any information on this in the literature. In general, little is known about the crosstalk between circadian rhythms and apoptosis. It is known that circadian rhythms regulate DNA damage repair, so I would assume that the same is ...


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Benign tumors can absolutely have mechanisms available to them to commit to and carry out apoptosis. An example of this would be benign prostatic hyperplasia, in which the balance of apoptotic and proliferating cells is offset, but apoptosis is still occurring, simply at a lower comparative rate than the proliferation. Benign tumors can therefore be caused ...


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From my readings, it seems that when procaspases 8 or 10 are unavailable, the cell will shift to necroptosis. What makes these procaspases unavailable and why does a cell second the necropotosis? This seems to be right. Mice with a conditional deletion of caspase-8 in the intestinal epithelium (Casp8ΔIEC) spontaneously developed inflammatory lesions ...


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'Eutely' is the term used for organisms with a fixed number of somatic cells. I'm not aware of any term for sub-organismic structures.


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Here some resources, Cell harvesting effects on Annexin V staining. Protocol for apoptotic analysis using Annexin V. Quite a long discussion about this issue. Another protocol. Cheers, Pedro


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The cell you've marked "B" is dead, as is common in cells in a saliva sample. The particular path to cell death is very hard to say with an unstained light micrograph, but the fact that you have a dead blebby cell in a saliva sample is not diagnostic or indicative of anything.


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There are lots and lots of specific single mutations that cause problems with apoptosis. Some of the most common are in P53, PTEN, MYC, APC, and KRAS. If you want a specific amino acid change, KRAS G12D is particularly potent. It works by disabling a regulatory domain and causing KRAS to be constitutively active. These aren't "reversible" in a strict sense ...


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The answer is no. There is no method currently known whereby we could get a stem cell to transfer its genome to a cancerous cell and thus get its apoptosis mechanism functioning again. It's just not that easy to get a genome transfered - destroying the defective copy of the genome which is stored in the nucleus and getting a new copy of the entire genome ...


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The answer is, in part, it depends. Let's think of the PI3K/AKT pathway. Akt actively phosphorylates BAD which abrogates the Bax/Bak apoptosis pathway. RTK's at the plasma membrane activate this pathway when bound with survival factors. In the absence of survival factors, Akt would become dephosphorylated and you'd have a net movement toward apoptosis. In a ...


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There is indeed a positive correlation between gastric reflux disease and esophageal cancer, and also between stomach ulcerations and stomach cancer. There are more than one possible mechanisms for these correlations to arise, but what you are proposing is definitely a prime suspect. http://www.webmd.com/heartburn-gerd/news/20130523/chronic-heartburn-may-...


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The processes of apoptosis is not so simple, there is a lot of genes and proteins that participate in it. In cancer cells some of them mutate and not working properly. Lack of apoptosis is the main problem in cancer. If cell not working properly, it dies. But not in cancer. So theoretically, yes. If we will fix the apoptosis, the cell probably will die. It'...


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In some cases yes — when there is a mutation in apoptotic regulators such as Bcl2 family of proteins. In other cases it is difficult to identify and only identification is that those cells are growing rapidly; in other words failure to undergo apoptosis is not the cause but the effect of the cancerous transformation (as in case of p53, Ras, Myc mutations etc)...


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Pan is referring to all. So a pan-caspase inhibitor is a molecule that inhibits all caspases indiscriminately. Note that pan means all in Greek.


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The term pan, in my opinion, is perhaps one of the most vague that exists in science! I can partley answer this question (ironically as vague as the term pan) by referring you to the term pan-neuronal. A pan neuronally expressed genes has features, which include the expression of many "generic" genes required non-specifically for neuronal function, such as ...


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I found this reference: "Inhibition of fatty acid synthase (FAS) suppresses HER2/neu (erbB-2) oncogene overexpression in cancer cells". Cerulenin is not a magic bullet, but in some cases it may help.


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The definition of a tumor is a population of cells that: Divides out-of-control 2.. Does not exhibit apoptosis 3.. Does not differentiate Additionally the two-hit hypothesis states that at least two genes need to be involved. There are many genes, predominantly involved in the regulation of the cell cycle, that when their function is disrupted the cell ...


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