Apoptosis modulation

MaUk AA, Radhakiishnan N, Reddy K, Smith AD, Singhal PC (2002) Morphine-induced macrophage apoptosis modulates migration of macrophages use of in vitro model of urinary tract infection. J Endourol 16 605-610... 

Jilka RL, Weinstein RS, Bellido T, Parfitt AM, Manolagas SC (1998) Osteoblast programmed cell death (apoptosis) modulation by growth factors and cytokines. J Bone Miner Res 13 793-802... 

The positive influence of the Grinization on thrombocyte number is caused by the immune-modulating, cytoprotecting, antioxidant and apoptosis-modulating action of the biologically active components of the Grinization multi-nutrient complex. 

Trichothecenes inhibit synthesis of protein, RNA and DNA as well as mitochondrial and electron transport chain function stimulate lipid peroxidation alter cell membrane function induce apoptosis modulate immune responses activate mitogen-activated protein kinases (MAPKs) and induce gene expression of numerous chemokines and cytokines and alter neurotransmitter levels. 

The biochemical mechanisms responsible for the cancer-preventive effects of green tea have not been clearly defined. Laboratory studies have shown that green tea possesses antioxidant and free radical scavenger activities, inhibits cell proliferation," induces apoptosis, modulates carcinogen-metabolizing enzymes, " - and suppresses inflammatory responses, - all of which could contribute to the observed preventive effects. 

Lowe, S., Ruley, H., Jacks, T. andHousman, D. (1993) p53-dependent apoptosis modulates the cytotoxicity of anticancer agents. Cell 74, 957-967. 

These mechanisms are commonly viewed as separate pathways and are capable of functioning independently, but cross-talk can occur between them at multiple levels, depending on the apoptosis-modulating proteins expressed. 

Enantiospecific synthesis of heterocycles linked to purines Different apoptosis modulation of enantiomers in breast cancer cells 13CMD 4924. 

Isolated rat type II lung cells were more sensitive than Clara cells to cadmium-induced apoptosis and cell viability (LIg et al. 2002). On exposure to 10 jUmol/1 cadmium acetate, the levels of the apoptosis-modulating proteins p53 and Bax were increased at 2 h and 5-12 h, respectively. The expression of p53 preceded the expression of Bax and the apoptotic process. The exposure to 10/ nol/l cadmium acetate did not significantly increase the formation of cellular reactive oxygen species. However, after the exposure to a high concentration of cadmium acetate (100/anol/1), a 30% increase of the reactive oxygen species level was observed. Catalase, superoxide dismutase, dimethyl sulphoxide, or tetramethylthiourea did not protect against cadmium-induced apoptosis. 

Alterations to the P53 gene are the most common genetic defects known in cancer [5]. The protein product of P53 is involved in a number of pathways that directly and indirectly lead to apoptosis. Many genes that are involved in apoptosis can be induced by this protein, which is a transcriptional transactivator. The emerging hypothesis is that p53 is a central node of a complex apoptotic network that may function differ ently in diver se cell types and tissues. For example, Bax, the prototype proapoptotic member of the Bcl2 family, can be transcriptionally induced by p53 in certain, but not all, cell types. Like p53, Bax can modulate the extent to which cells are sensitive to apoptosis caused by therapeutic agents. 

Other, more general effects of insulin on cellular function include stimulation of cell growth (increase in DNA and protein synthesis), inhibition of apoptosis, and modulation of ion-channel activity. 

Mitogen activated protein kinase (MARK) cascades are three kinase modules activated by phosphorylation. The three kinase modules are composed of a MAPK, a MAPKK, and a MAPKKK. There are multiple members of each component of the MAPK cascade that are conserved from yeast to human. Activation of selective MAPK modules by specific stimuli regulates cell functions such as gene expression, adhesion, migration, differ entiation, and apoptosis. 

Family of transcription factors that modulate the expression of genes which control immune, inflammatory, and acute-phase responses, as well as cell growth, responses to stress, apoptosis, and oncogenesis. All members of this family have a Rel-homology domain that contains sequences responsible for dimerization and DNA binding. In vertebrates, this family includes NF-kB1 (also known as p50), NF-kB2 (also known as p52), Rel (also known as cRel), Rel-A (also known as p65), and Rel-B. 

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