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We conclude that the novel 465* gene causes cell death by apoptosis.
Finally, the PKR gene is a candidate "death gene" since overexpression of this gene could bring about apoptosis in U937 cells.
Therefore, the products of this gene may be multi-functional, regulating apoptosis, tumor development, and neuronal regeneration.
The anti-apoptosis gene surviving promotes cell transformation.
In this study we were able to demonstrate the role of this gene in chemotherapy‐induced apoptosis.
Gene expression analysis demonstrated apoptosis as a possible cell killing mechanism.
Apoptosis is a gene‐driven mode of cell death that may be identified by distinct morphological features, endonuclease‐initiated DNA degradation, and by the involvement of specific apoptosis‐regulating proteins.
The induction of apoptosis appears to be associated with down‐regulation of the anti‐apoptotic Buffy gene and up‐regulation of the pro‐apoptotic Debcl gene.
This is the first report known to us of a functional polymorphism in a gene involved in DNA damage-induced apoptosis.
Inhibitors of RNA or protein synthesis block this death, suggesting that gene expression is important for apoptosis in this system.

Related Questions

What are the mechanisms of cancer apoptosis?5 answersApoptosis, or regulated cell death, is a critical process in cancer treatment. It involves several pathways, including the intrinsic and extrinsic pathways, which converge at the executioner caspases. The Bcl-2 gene family plays a crucial role in regulating the intrinsic apoptotic pathway, controlling signals for cell survival and death. Anti-cancer therapies often target the apoptotic signaling pathways to trigger cancer cell death and prevent chemoresistance. BH3-mimetic drugs, which mimic the function of pro-apoptotic BH3-only proteins, have been developed to induce apoptosis in cancer cells by inhibiting apoptosis inhibitory proteins. Dysregulation of apoptosis is a key hallmark of cancer, and understanding the apoptotic signaling pathways is important for developing effective anti-cancer therapeutics. Pro-apoptotic and anti-apoptotic proteins, such as Bax and Bcl-2 family proteins, act as regulators in cell division and growth and are potential targets for developing therapeutics. Inactivation of apoptosis is a dysregulatory process in many cancer types, and research is focused on developing apoptosis-targeted therapeutics.
What genes are directly related to apoptosis in synovial degeneration in knee osteoarthritis?5 answersHTR2B and SLC5A3 genes are directly related to apoptosis in synovial degeneration in knee osteoarthritis. miR-155-5p and CASP3 genes also play a role in macrophage apoptosis in knee osteoarthritis. LncRNA MEG3 and PTEN genes are involved in the regulation of synovial cell apoptosis in knee osteoarthritis. Fas-1377 G>A polymorphism in the Fas gene is associated with susceptibility to knee osteoarthritis and apoptosis. miR-27a and PLK2 genes are involved in chondrocyte apoptosis in knee osteoarthritis.
What is the role of caspases in apoptosis?5 answersCaspases play a critical role in apoptosis, which is a form of programmed cell death. They are cysteine proteases that act as initiators and executioners of apoptosis. Apoptosis is a necessary event in tissue homeostasis and occurs during developmental processes. Caspases are also involved in other neurodevelopmental processes such as axon guidance, synapse formation, axon pruning, and synaptic functions in the central nervous system. The activation of caspases is regulated by the mitochondrial pathway of cell death. In multicellular organisms, caspases are activated through macromolecular signaling and play key roles in programmed cell death and inflammation. Overall, caspases are crucial for the regulation and execution of apoptosis, as well as other cellular processes in the central nervous system.
Can apoptosis promote inflamamtion?4 answersApoptosis can actually suppress inflammation. When cells undergo apoptosis, they remain intact and actively suppress inflammation, unlike cells undergoing necrotic death which release factors that stimulate inflammation. Apoptotic cells release adenosine monophosphate (AMP), which is converted to adenosine by macrophages. Adenosine then activates the A2a adenosine receptor, leading to the suppression of the inflammatory response in macrophages. Neutrophils, a type of white blood cell, are programmed to undergo apoptosis, limiting their pro-inflammatory potential and promoting the resolution of the acute inflammatory response. Therefore, apoptosis can play a role in promoting the resolution of inflammation rather than promoting inflammation itself.
How traumatic brain injury triggers apoptosis?4 answersTraumatic brain injury (TBI) triggers apoptosis, or programmed cell death, in neurons and glial cells. Apoptosis has been observed in both acute and chronic stages of TBI, with apoptotic cells found in contusions and regions remote from the site of impact. The occurrence and location of apoptosis differ from necrosis, another form of cell death observed in TBI. The timing and area of apoptosis in TBI are distinct, indicating specific mechanisms at play. Multiple pathways can lead to neural cell apoptosis following TBI, including those involving excitatory amino acids, intracellular calcium increases, and free radicals. The balance between pro- and anti-apoptotic factors is disrupted in TBI, leading to an increase in apoptotic cell death.
What enzymes trigger apoptosis?10 answers