Differential cleavage of Mst1 by caspase-7/-3 is responsible for TRAIL-induced activation of the MAPK superfamily

Song, Jae J.

doi:10.1016/j.cellsig.2008.01.001

Cited by 62 publications

(57 citation statements)

References 33 publications

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“…In addition, MST1 may be differentially targeted by different caspases to activate distinct MAPK pathways. [18][19][20][21][22][23] MST1 has been implicated in T-cell biology, as mice lacking MST1 exhibit a variety of T-cell abnormalities. 24 Cross-talk between MST1 and Akt appears able to antagonize Akt1 activity, 25 which is involved in T-cell costimulation and the regulation of NF-kB-dependent gene transcription.…”

Section: Gck-ii Kinases Regulate Lymphocyte Adhesion Migration Prolmentioning

confidence: 99%

Germinal center kinases in immune regulation

Yin

Shi

et al. 2012

Cell Mol Immunol

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Section: Gck-ii Kinases Regulate Lymphocyte Adhesion Migration Prolmentioning

confidence: 99%

Germinal center kinases in immune regulation

Yin

Shi

et al. 2012

Cell Mol Immunol

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“…For this reason, TRAIL has been an anti-cancer therapy target since the mid-1990s; however, no significant survival benefits have been found. Previous studies have reported that TRAIL can bind to and therefore activate NF-κB, leading to the transcription of genes known to antagonize the death signaling pathway (19).…”

Section: Introductionmentioning

confidence: 99%

Geldanamycin induces apoptosis in human gastric carcinomas by affecting multiple oncogenic kinases that have synergic effects with TNF-related apoptosis-inducing ligand

Chen

Pan

2015

Oncology Letters

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Abstract. The aim of the present study was to evaluate the effect of geldanamycin (GA) on the treatment of human gastric carcinomas and to investigate the molecular mechanism that provides the basis for the combination of GA with the tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) induction strategy. The expression of target proteins at the mRNA level was determined using reverse transcription-polymerase chain reaction (RT-PCR), and apoptosis was evaluated with the terminal deoxynucleotidyl transferase mediated digoxigenin-dUTP nick-end labeling and Annexin V/propidium iodide (PI) staining methods. Phosphorylation of targeted kinases was studied using immunocytochemistry methods, and malignant phenotypes were studied using in vitro assays. GA treatment inhibits proliferation, migration and invasion, and induces apoptosis in human gastric cancer SGC-7901 cells, most likely by decreasing the expression of B-RAF and by phosphorylation of protein kinase B (AKT) and ERK. The inhibitory role of AKT in TRAIL regulation holds considerable potential for achieving a synergic effect in clinical therapy, using a combination of GA treatment and TRAIL induction. The present study provides a basis for the future application of heat shock protein 90 (Hsp90) inhibitors, such as GA, in the clinical treatment of gastric cancer, particularly in combination therapies with TRAIL inducers.

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“…As STK4 is differentially cleaved by CASP3, 6 and 7 producing fragments with specific functions, we assessed the cleavage of STK3 by these caspases (Song and Lee 2008). Murine brain lysate was incubated with active-site titrated recombinant CASP3, 6 or 7, and STK3 cleavage was assessed.…”

Section: Differential Cleavage Of Stk3 By Casp3 6 Andmentioning

confidence: 99%

“…It is possible that these two fragments of STK3, as described earlier for two fragments of STK4, may not have the same function in vivo. Indeed, the 40 kDa fragment of STK4 produced by CASP7 cleavage has been identified to selectively phosphorylate JNK and p38 while the 36 kDa fragment of STK4, produced by CASP3 cleavage, has been identified to selectively phosphorylate ERK (Song and Lee 2008).…”

Section: Caspase-dependent Processing Of Stk3mentioning

confidence: 99%

Organ-specific alteration in caspase expression and STK3 proteolysis during the aging process

Lessard‐Beaudoin

Laroche

Loudghi

et al. 2016

Neurobiology of Aging

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Caspases and their substrates are key mediators of apoptosis and strongly implicated in various physiological processes. As the STK family is involved in apoptosis, and STK3 is a recently identified caspase-6 substrate, we assessed the expression and cleavage of STK3 in murine peripheral organs and brain regions during the aging process. We also assessed caspase-3, -6, -7 and -8 expression and activity in order to delineate potential mechanism(s) underlying the generation of the STK3 fragments observed, and their relation to the apoptotic pathway. We demonstrate for the first time the cleavage of STK3 by caspase-7 and show that STK3 protein levels globally increase throughout the organism with age. In contrast, caspase-3, -6, -7 and -8 expression and activity vary significantly amongst the different organs analyzed suggesting differential effects of aging on the apoptotic mechanism and/or non-apoptotic functions of caspases throughout the organism. These results further our understanding of the role of caspases and their substrates in the normal aging process and highlight a potential role for STK3 in neurodegeneration.3

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Differential cleavage of Mst1 by caspase-7/-3 is responsible for TRAIL-induced activation of the MAPK superfamily

Cited by 62 publications

References 33 publications

Germinal center kinases in immune regulation

Germinal center kinases in immune regulation

Geldanamycin induces apoptosis in human gastric carcinomas by affecting multiple oncogenic kinases that have synergic effects with TNF-related apoptosis-inducing ligand

Organ-specific alteration in caspase expression and STK3 proteolysis during the aging process

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