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Apoptosis is a multi-step, multi-pathway cell-death programme that is inherent in every cell of the body. In cancer, the apoptosis cell-division ratio is altered. Cancer treatment by chemotherapy and irradiation kills target cells primarily by inducing apoptosis. [98]
PUMA has been shown to be active in inducing apoptosis in hematopoietic and intestinal tissue following γ-irradiation. [12] [55] Since inhibition of PUMA does not directly cause spontaneous malignancies, therapeutics to inhibit PUMA function in healthy tissue could lessen or eliminate the side effects of traditional cancer therapies. [7]
Unfortunately, regenerative potential of the adult heart is limited. The Hippo pathway is a recently identified signaling cascade that plays an evolutionarily conserved role in organ size control by inhibiting cell proliferation, promoting apoptosis, regulating fates of stem/progenitor cells, and in some circumstances, limiting cell size.
Neurodegenerative diseases such as Alzheimer's, Parkinson's, and Huntington's are all age-related diseases and involve increased apoptosis where cells die that are still able to function or that contribute to support function of tissue. Apaf-1-ALT is an Apaf-1 mutant found in prostate cancer, which does not have residues 339-1248.
In the average adult between 50 and 70 billion cells die each day due to apoptosis. Inhibition of apoptosis can result in a number of cancers, autoimmune diseases, inflammatory diseases, and viral infections. Hyperactive apoptosis can lead to neurodegenerative diseases, hematologic diseases, and tissue damage.
Necrosis is caused by factors external to the cell or tissue, such as infection, or trauma which result in the unregulated digestion of cell components. In contrast, apoptosis is a naturally occurring programmed and targeted cause of cellular death. While apoptosis often provides beneficial effects to the organism, necrosis is almost always ...
In glioma cells, the effects of TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) have been shown to induce DISC-mediated apoptosis. Specifically, TRAIL works by activating two death receptors, DR4 and DR5 ; these bind to FADD, which then interacts with caspase-8 to assemble the DISC.
During apoptosis (programmed cell death), the cell's cytoskeleton breaks up and causes the membrane to bulge outward. [13] These bulges may separate from the cell, taking a portion of cytoplasm with them, to become known as apoptotic blebs. [14] Phagocytic cells eventually consume these fragments and the components are recycled. [citation needed]