Bài thuyết trình "Apoptosis" giới thiệu đến các bạn những nội dung về khái niệm, lịch sử nghiên cứu Apoptosis, kích hoạt Caspase Apoptosis, bất hoạt Apoptosis, ứng dụng của Apoptosis. Mời các bạn cùng tham khảo nội dung bài thuyết trình để nắm bắt nội dung chi tiết.

The spermine analogue N1,N11-diethylnorspermine (DENSPM) efficiently depletes the cellular pools of putrescine, spermidine and spermine by down-regulating the activity of the polyamine biosynthetic enzymes and up-regulating the activity of the catabolic enzyme spermidine/ spermine N1-acetyltransferase (SSAT). In the breast cancer cell line L56Br-C1, treatment with 10 lM DENSPM induced SSAT activity 60 and 240-fold at 24 and 48 h after seeding, respectively, which resulted in polyamine depletion. ...

Zinc (Zn), an endogenous regulator of apoptosis, and has abilitiesboth to induceapoptosis and inhibit the inductionof apoptosis via the modulation of caspase activity. Due to the multifunctions of Zn, the intracellular Zn level is strictly regulated by a complex system in physiological and patho-logical conditions. The commitment of Zn to the regulation of apoptosis is not fully understood. In the present study, we investigated the role of intracellular Zn level in the induction of apoptosis in human leukemia cells (HL-60 cells) using a Zn ionophore [pyrithione (Py)]....

Previous results have shown that theoncoembryonicmarker a-fetoprotein (AFP) is able to induce apoptosis in tumor cells through activation of caspase 3, bypassing Fas-dependent and tumor necrosis factor receptor-dependent signaling. In this study we further investigate the molecular interactions involvedin the AFP-mediatedsignaling of apoptosis. We show that AFP treatment of tumor cells is accompaniedby cytosolic translocation of mitochondrial cytochromec. In a cell-free system, AFP mediates process-ing andactivation of caspases 3 and9 by synergistic enhancement of the low-dose cytochromec-mediated sig-nals....

Here, we show that recombinant bovine PDE5A1 is pro-teolysedby recombinant caspase-3 inin vitroand transfected Cos-7 cells. In addition, the treatment of PDE5A1-trans-fectedCos-7andPC12cellswithstaurosporine, anapoptotic agent that activates endogenous caspase-3, also induced proteolysis and inactivation of PDE5A1. These findings suggest that there is specificity in the interaction between caspase-3 and PDE5A1 that requires application of an apoptotic stimulus.

Viral subversion of apoptosis regulation plays an important role in the outcome of host⁄virus interactions. Although human cytomegalovirus (HCMV) encodes several immediate early (IE) antiapoptotic proteins (IE1, IE2, vMIA and vICA), no proapoptotic HCMV protein has yet been iden-tified. Here we show that US28, a functional IE HCMV-encoded chemo-kine receptor, which may be involved in both viral dissemination and immune evasion, constitutively induces apoptosis in several cell types.

Caspases are a family of cysteine proteases with roles in cytokine matur-ation or apoptosis. Caspase-2 was the first pro-apoptotic caspase identified, but its functions in apoptotic signal transduction are still being elucidated. This study examined the regulation of the activity of caspase-2 using recombinant proteins and a yeast-based system. Our data suggest that for human caspase-2 to be active its large and small subunits must be separ-ated. For maximal activity its prodomain must also be removed....

Anovel caspase-like activity, which is directly regulatedwith cell proliferation is a candidate to regulate the abundance of the cyclin-dependent kinase inhibitor, p27 KIP1 , in human lymphoid cells.This activity, whichwe termKIPase activity, can also cleave a subset of caspase substrates.Here we demonstrate thatKIPase is anovel enzymedistinct fromany of the previously characterized human caspases.We show thatKIPase is active in a variety of cell lineages, its activity is associated with the proliferation of the human T-cell line, Jurkat, and is not inhibited by the broad spectrum caspase inhibitor z-VAD-fmk....

PTP-S2⁄TC45 is a nuclear protein tyrosine phosphatase that activates p53 and induces caspase 1-dependent apoptosis. We analyzed the role of ICE protease-activating factor (Ipaf), an activator of caspase 1 in p53-depend-ent apoptosis. We also determined the sequence of events that lead to apoptosis upon caspase 1 activation by Ipaf.

Previous results have shown that the human oncoembryonic proteina-feto-protein (AFP) induces dose-dependent targeting apoptosis in tumor cells, accompanied by cytochromecrelease and caspase 3 activation. AFP posi-tively regulates cytochrome c⁄dATP-mediated apoptosome complex forma-tion in a cell-free system, stimulates release of the active caspases 9 and 3 and displaces cIAP-2 from the apoptosome and from its complex with recombinant caspases 3 and 9 [Semenkova et al. (2003) Eur. J. Biochem.

To investigate the mechanism of increased expression of caspase-1 caused by exogenousHippi, observed earlier in HeLa and Neuro2A cells, in this work we identified a specific motif AAAGACATG ()101 to)93) at the caspase-1 gene upstream sequence where HIPPI could bind. Various muta-tions in this specific sequence compromised the interaction, showing the specificity of the interactions.

Despite a dogma that apoptosis does not induce inflammation, Fas ligand (FasL), a well-known death factor, possesses pro-inflammatory activity. For example, FasL induces nuclear factorjB (NF-jB) activity and interleukin 8 (IL-8) production by engagement of Fas in human cells.

Caspase-3 is a cysteine protease that plays a central role in the execution of apoptosis induced by a wide variety of stimuli. However, little is known about the mechanisms involved in the regulation of caspase-3 gene tran-scription.

Tumour necrosis factor-a(TNF-a) is a cytokine that is involved in many functions, including the inflammatory response, immunity and apoptosis. Some of the responses of TNF-a are mediated by caspase-1, which is involved in the production of the pro-inflammatory cytokines interleukin-1b, interleukin-18 and interleukin-33.

Many protein substrates of caspases are cleaved at noncanonical sites in comparison to the recognition motifs reported for the three caspase sub-groups. To provide insight into the specificity and aid in the design of drugs to control cell death, crystal structures of caspase-7 were determined in complexes with six peptide analogs (Ac-DMQD-Cho, Ac-DQMD-Cho, Ac-DNLD-Cho, Ac-IEPD-Cho, Ac-ESMD-Cho, Ac-WEHD-Cho) that span the major recognition motifs of the three subgroups.

DYRK1A is a member of the dual-specificity tyrosine-phosphorylation-reg-ulated protein kinase family and is implicated in Down’s syndrome. Here, we identify the cysteine aspartyl protease caspase9, a critical component of the intrinsic apoptotic pathway, as a substrate of DYRK1A. Depletion of DYRK1A from human cells by short interfering RNA inhibits the basal phosphorylation of caspase9 at an inhibitory site, Thr125.

Dinucleoside polyphosphates (NpnN¢s; where N and N¢ are nucleosides andn= 3–6 phosphate residues) are naturally occurring compounds that may act as signaling molecules. One of the most successful approaches to understand their biological functions has been through the use of NpnN¢ analogs.

Hydrogen peroxide (H2O2) is a well known oxidative stress inducer causing apoptosis of many cells. Previously, we have shown that heat shock pre-treatment blocked the release of the second mitochondria-derived activator of caspase (Smac) to the cytosol and inhibited apoptosis of C2C12 myo-blast cells in response to H2O2.

Cell death by the process of apoptosis plays important roles in development, tissue homeostasis, diseases and drug responses. The cysteine aspartyl prote-ase caspase-9 plays a central role in the mitochondrial or intrinsic apoptotic pathway that is engaged in response to many apoptotic stimuli.

DNA fragmentation is a hallmark of apoptosis that occurs in a variety of cell types; however, it remains unclear whether caspase-3 is required for its induction. To investigate this, we produced caspase-3 knockout Chinese hamster ovary (CHO)-K1 cells and examined the effects of gene knockout and treatment with caspase-3 inhibitors.