zVAD-fmk, unlike BocD-fmk, does not inhibit caspase-6 acting on 14-3-3/Bad pathway in apoptosis of p815 mastocytoma cells

Yee, Su-Bog; Baek, Soo Jin; Park, Hwan Tae; Jeong, Sang Hoon; Jeong, Jin Hee; Kim, Tae Hyun; Kim, Jong Min; Jeong, Byung Kap; Park, Bong Soo; Kwon, Taeg Kyu; Yoon, Ina; Yoo, Young Hyun

doi:10.1038/emm.2006.75

Cited by 11 publications

(6 citation statements)

References 24 publications

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“…5C). This finding is also compatible with other studies (33)(34)(35). Caspases are roughly divided into initiator caspases and effector caspases (e.g., caspase-3, -6 and -7).…”

Section: Discussionsupporting

confidence: 81%

“…Caspases are roughly divided into initiator caspases and effector caspases (e.g., caspase-3, -6 and -7). Although caspase-3 and -7 are structurally similar and can be inhibited by Z-VAD-FMK, caspase-6 shows very different characteristics and cannot be inhibited by Z-VAD-FMK (33). In addition, caspase-6 is activated by both caspase-3-dependent and -independent cascades (36).…”

Section: Discussionmentioning

confidence: 99%

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Activation of caspases and apoptosis in response to low-voltage electric pulses

Matsuki

Takeda²,

Ishikawa³

et al. 2010

Oncol Rep

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Abstract. Few studies have examined apoptosis induced by low-voltage electric pulses (LVEPs). LVEP-induce changes in membrane potential that are below the membrane breakdown threshold and increase membrane permeability without electroporation (pore formation) through the transport of extracellular substances via phagocytosis. We demonstrated that propidium iodide uptake and apoptosis increased in accordance with the duration and number of LVEPs in B16 cells, which showed relatively good viability under mild electric field conditions. We showed that LVEP-induced apoptosis was achieved through caspase-8 and -9 activation and subsequent caspase-3 activation. Long-duration LVEPs caused only mild cell damage, such that the apoptosis ratio (apoptosis/total cell death) in electric pulse-treated cells was similar to that in non-treated control cells. To assess the relative degree of caspase dependency in LVEP-induced apoptosis, the apoptosis rate and caspase-3 activity were analyzed using a pan-caspase inhibitor (Z-VAD-FMK). Z-VAD-FMK treatment inhibited, but did not abolish, LVEP-induced apoptosis, indicating that caspases other than caspase-3 participate in this pathway. Moreover, LVEP treatment inhibited cell growth, suggesting that LVEP treatment may be a valuable anticancer therapy. Although the mechanism of LVEP-induced apoptosis remains unclear, it may be related to dysfunctional membrane transport of Ca 2+ and other extracellular substances involved in caspase activation.

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“…5C). This finding is also compatible with other studies (33)(34)(35). Caspases are roughly divided into initiator caspases and effector caspases (e.g., caspase-3, -6 and -7).…”

Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Activation of caspases and apoptosis in response to low-voltage electric pulses

Matsuki

Takeda²,

Ishikawa³

et al. 2010

Oncol Rep

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“…The affinity of 14-3-3s for client proteins is known to be regulated by phosphorylation of the ligands or by phosphorylation of 14-3-3 protein itself (e.g., for Bax or c-Abl binding). However, the release of client proteins from the complexes with 14-3-3 proteins can also result from a decrease of 14-3-3 protein amount which was recently demonstrated by proteomic analysis in several apoptotic experimental systems [Park et al, 2005;Rahmani et al, 2005;Choi et al, 2006;Yee et al, 2006]. Downregulation of an unspecified 14-3-3 isoform on both mRNA and protein levels was also observed during CD43-mediated apoptosis in TF-1 cells [Č ermák et al, 2002].…”

Section: Discussionmentioning

confidence: 93%

Isoform‐specific cleavage of 14‐3‐3 proteins in apoptotic JURL‐MK1 cells

Kuželová

Grebeňová

Pluskalová

et al. 2009

J of Cellular Biochemistry

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The proteins of 14-3-3 family are substantially involved in the regulation of many biological processes including the apoptosis. We studied the changes in the expression of five 14-3-3 isoforms (beta, gamma, epsilon, tau, and zeta) during the apoptosis of JURL-MK1 and K562 cells. The expression level of all these proteins markedly decreased in relation with the apoptosis progression and all isoforms underwent truncation, which probably corresponds to the removal of several C-terminal amino acids. The observed 14-3-3 modifications were partially blocked by caspase-3 inhibition. In addition to caspases, a non-caspase protease is likely to contribute to 14-3-3's cleavage in an isoform-specific manner. While 14-3-3 gamma seems to be cleaved mainly by caspase-3, the alternative mechanism is essentially involved in the case of 14-3-3 tau, and a combined effect was observed for the isoforms epsilon, beta, and zeta. We suggest that the processing of 14-3-3 proteins could form an integral part of the programmed cell death or at least of some apoptotic pathways.

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“…To test the necessity of caspase activity for generation of cleaved neoepitopes, we performed NGF-deprivation in the presence of a pan-caspase inhibitor (ZVAD). Of note, there is data to suggest that ZVAD does not effectively inhibit caspase-6 [24]. We quantified the fluorescence intensity of staining within axons.…”

Section: Resultsmentioning

confidence: 99%

Caspase-mediated cleavage of actin and tubulin is a common feature and sensitive marker of axonal degeneration in neural development and injury

Sokolowski

Gamage

Heffron

et al. 2014

acta neuropathol commun

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BackgroundAxon degeneration is a characteristic feature of multiple neuropathologic states and is also a mechanism of physiological neurodevelopmental pruning. The vast majority of in vivo studies looking at axon degeneration have relied on the use of classical silver degeneration stains, which have many limitations including lack of molecular specificity and incompatibility with immunolabeling methods. Because Wallerian degeneration is well known to involve cytoskeletal disassembly and because caspases are recently implicated in aspects of this process, we asked whether antibodies directed at caspase-generated neoepitopes of beta-actin and alpha-tubulin would be useful immunohistochemical markers of pathological and developmental axon degeneration.ResultsHere we demonstrate that several forms of axon degeneration involve caspase-mediated cleavage of these cytoskeletal elements and are well-visualized using this approach. We demonstrate the generation of caspase-induced neoepitopes in a) an in vitro neuronal culture model using nerve growth factor-deprivation-induced degeneration and b) an in vivo model using ethanol-induced neuronal apoptosis, and c) during normal developmental pruning and physiological turnover of neurons.ConclusionsOur findings support recent experimental data that suggests caspase-3 and caspase-6 have specific non-redundant roles in developmental pruning. Finally, these findings may have clinical utility, as these markers highlight degenerating neurites in human hypoxic-ischemic injury. Our work not only confirms a common downstream mechanism involved in axon degeneration, but also illuminates the potential utility of caspase-cleavage-neoepitope antibodies as markers of neurodegeneration.

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zVAD-fmk, unlike BocD-fmk, does not inhibit caspase-6 acting on 14-3-3/Bad pathway in apoptosis of p815 mastocytoma cells

Cited by 11 publications

References 24 publications

Activation of caspases and apoptosis in response to low-voltage electric pulses

Activation of caspases and apoptosis in response to low-voltage electric pulses

Isoform‐specific cleavage of 14‐3‐3 proteins in apoptotic JURL‐MK1 cells

Caspase-mediated cleavage of actin and tubulin is a common feature and sensitive marker of axonal degeneration in neural development and injury

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