Caspase

Some experiments were aimed at finding how SOD1 becomes pro-apoptotic (promoting programmed cell death) due to the fact that healthy SOD1 are against programmed cell death (Pasinelli et al. 2004). The pro-apoptotic characteristic of mutant SOD1 is demonstrated in vivo and in vitro. The mitochondria inside cells firmly control apoptosis, and the mutant SOD1 that aggregates inside mitochondria triggers the programmed cell death of motor neurons (Pasinelli et al. 2004). One experiment studied proteins that interact with mutant SOD1, specifically Bcl-2 which is anti-apoptotic, in order to explain the apoptotic nature of mutant SOD1 (Pasinelli et al. 2004). The methods that were used involve in vitro approaches and Western blot analysis. The outcomes were that mutant SOD1 and Bcl-2 interact with each other in vivo in the spinal cord, and they both together are pro-apoptotic (Pasinelli et al. 2004). In other words, Bcl-2 was an anti-apoptotic protein when standing alone, and when it directly interacted with mutant SOD1, the protein and the gene convert to pro-apoptosis, or in support of cell death; this could be due to a conformational change in Bcl-2.…

Mitochondria and caspases are essential elements of the controlling mechanism of apoptosis 1. Caspases, a family of enzymes that are key effectors of apoptosis, are cysteine proteases that cut after aspartic acid residues. Several of these enzymes, like caspase 3 and caspase 7, are responsible for many of the effects of apoptosis. These effects include cell shrinkage, PS externalization, and membrane microvesiculation 2-5. Cytochrome C, a component of the electron transport chain, is normally…

increased neurodegeneration is not known. Our results suggest that the circadian kinase, Casein kinase I, inhibits the activation of caspases to prevent Tau cleavage, and that the defects in the circadian clock confer sensitivity to expression of active caspase in response to prolonged light. We establish a link between the circadian clock factors, light, cell death pathways, and Tau toxicity. I continued my work on neurodegenerative processes as a Senior Research Scientist using mammalian…

been associated with gut homeostasis and determining the severity of inflammation in IBD. Inflammasomes are a set of intracellular protein complexes that enable activation of inflammatory caspases that are responsible for the processing of the pro-inflammatory cytokines that help with the initiation of an adaptive immunity response. Inflammasomes are key regulators in the innate system. Inflammasomes complexes have been divided in the NLR family or PYHIN family. There are 22 NLR genes in the…

way to treat inflammatory diseases such as rheumatoid arthritis (15). The use of Yp protein, YopM has been suggested as one effector to be tested as a therapeutic (15). Blocking of host inflammatory signaling is important for pathogen survival. The inflammasome is a multi-protein complex that activates caspases, which cleave precursor forms of interleukin-1β (IL-1β) and interleukin-18 (IL-18) into their active forms (16). Activation of the inflammasome subsequently leads to pyroptotic cell…

pathways which include a death receptor-associated extrinsic pathway and a mitochondria- dependent intrinsic pathway. Caspases regulate the final execution of apoptosis in both pathways. In the extrinsic pathway, Caspase-8 initiates the cascade ultimately activating the final executioner caspase-3 (Earnshaw, 1999). In the intrinsic pathway, Caspase-8 can cleave Bid to generate truncated Bid to interact then with pro-apoptotic Bax for translocation and accumulation in mitochondria to initiate the…

Intrinsic apoptotic marker caspase 9 and extrinsic apoptotic marker caspase 8 were cleaved and activated to be analyzed. Members of the Bcl-2 family, caspase 3, and Apad-1 were also analyzed. The results showed that in the infected cells, pro-caspase 8 degradation remained minimal after infection and was barely more apparent than the mock cells. 12 hours post infection Caspase 9 activated cleaved fragments were notable, and at 24 hours post infection were considerably greater. These results…

The human body is made up of thousands of cells, each with a defined genetic program that allows them to work synchronically to regulate the metabolic and physiological processes required by the organism. All cells die (not accidentally), because in old age or because they are Cell death by apoptosis plays a crucial role in tissue development and homeostasis. This process is carried out through mitochondrial permeabilization and the activation of caspases. The condensation of chromatin and the…

outer membrane and transition pore formation. So, any injury caused to the mitochondrial membrane leads to release of pro-apoptotic proteins (bax and bad), or the survival proteins (bcl-2 and bcl-x) or both (Graham et al., 2000). Expression Studies of brain tissue of neocortex and hippocampus of epilepsy patients with Temporal Lobe Epilepsy (TLE) have confirmed the elevated levels of bcl-2 protein (Henshall et al., 2000, Xu et al., 2007; Dirnagel et al., 1999). A diverse response of bcl-2 was…

evaluate the pathogenesis of pancreatic toxicity induced by patulin exposure and the role of goji extract to eliminate its toxicity. It has been reported that the relationship of the endocrine–exocrine parts of the pancreas is a complex one because of the close anatomical and functional links. The impairment of the endocrine part of the pancreas has a marked effect upon its exocrine component. It was stated that islet hormones regulate acinar cell functions as they reach to them with portal…