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MeSH Review

Cell Death

 
 
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Disease relevance of Cell Death

 

Psychiatry related information on Cell Death

 

High impact information on Cell Death

  • The Fas/FasL system is responsible for activation-induced cell death but also plays an important role in lymphocyte-mediated killing under certain circumstances [11].
  • TNF and TNFR family proteins play important roles in the control of cell death, proliferation, autoimmunity, the function of immune cells, or the organogenesis of lymphoid organs [12].
  • Recent evidence has indicated that the caspase family of cysteine proteases is a central effector in apoptotic cell death and is absolutely responsible for many of the morphological features of apoptosis [13].
  • In contrast, healthy cells require caspase activation to undergo cell death induced by surface receptors [13].
  • Although much has been learned regarding how these cytosolic tyrosine kinases are activated and recruited to the TCR complex, relatively little is understood about how these initial events are translated into transcriptional activation of genes that regulate cytokine production, cell proliferation, and cell death [14].
 

Chemical compound and disease context of Cell Death

 

Biological context of Cell Death

 

Anatomical context of Cell Death

 

Associations of Cell Death with chemical compounds

  • Although it is not fully established for all cases, the major driving force for the necrotic cell death process, and very possibly the other processes, appears to be the generation of free radicals and peroxynitrite [29].
  • Calcium ions are ubiquitous and versatile signaling molecules, capable of decoding a variety of extracellular stimuli (hormones, neurotransmitters, growth factors, etc.) into markedly different intracellular actions, ranging from contraction to secretion, from proliferation to cell death [30].
  • Excitotoxicity is a process in which glutamate or other excitatory amino acids induce neuronal cell death [31].
  • Increased de novo ceramide synthesis triggers apoptosis and is associated with massive cell death during neural tube closure, raising the possibility that neural degeneration in HSN1 is due to ceramide-induced apoptotic cell death [32].
  • H2B S10A mutants are resistant to cell death elicited by H(2)O(2) while H2B S10E phospho-site mimics promote cell death and induce the "constitutive" formation of condensed chromatin [33].
 

Gene context of Cell Death

 

Analytical, diagnostic and therapeutic context of Cell Death

References

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