The IAP family: endogenous caspase inhibitors with multiple biological activities

Yang, Yee Hwa; Li, Xiao Ming

doi:10.1038/sj.cr.7290046

Cited by 267 publications

(180 citation statements)

References 49 publications

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“…BMPR2 supports survival by stabilizing XIAP ), a potent inhibitor of apoptosis through caspase-3/7 inhibition (Yang and Li, 2000). Ca 2 þ channel TRPC1, whose disruption can reduce glioma proliferation (Bomben and Sontheimer, 2010), seems to be required by glioma.…”

Section: Mir-135a Selectively Induces Apoptosis Of Glioma S Wu Et Almentioning

confidence: 99%

MiR-135a functions as a selective killer of malignant glioma

Lin

et al. 2011

Oncogene

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Glioma is the most common and fatal primary brain tumor. Thus far, therapeutic strategies to efficiently and specifically antagonize glioma are limited and poorly developed. Here we report that glia-enriched miR-135a, a microRNA that is dramatically downregulated in malignant glioma and correlated with the pathological grading, is capable of inducing mitochondria-dependent apoptosis of malignant glioma by regulating various genes including STAT6, SMAD5 and BMPR2, as well as affecting the signaling pathway downstream. Moreover, this lethal effect is selectively towards malignant glioma cells, but not neurons and glial cells, through a novel mechanism. Our findings suggest an important role of miR-135a in glioma etiology and provide a potential candidate for malignant glioma therapy.

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Section: Mir-135a Selectively Induces Apoptosis Of Glioma S Wu Et Almentioning

confidence: 99%

MiR-135a functions as a selective killer of malignant glioma

Lin

et al. 2011

Oncogene

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“…IAPs possess ubiquitinligase activity that leads to the degradation of mature caspase 3 and 9 (Yang and Li, 2000), thus blocking both apoptotic pathways. The inhibition of apoptosis via IAPs can be overridden by SMAC/diablo, a protein that inhibits the functions of IAPs (Du et al, 2000).…”

Section: Apoptotic Pathwaysmentioning

confidence: 99%

Multistep and multitask Bax activation

Ghibelli

Diederich

2010

Mitochondrion

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Bax is a pro-apoptotic protein allowing apoptosis to occur through the intrinsic, damage-induced pathway, and amplifying that one occurring via the extrinsic, receptor mediated pathway. Bax is present in viable cells and activated by pro-apoptotic stimuli. Activation implies structural changes, consisting of exposure of the N terminus and hydrophobic domains; changes in localization, consisting in migration from cytosol to mitochondria and endoplasmic reticulum membranes; changes in the aggregation status, from monomer to dimer and multimer. Bax has multiple critical domains, namely the N terminus exposed after activation; two hydrophobic stretches exposed for membrane anchorage; two reactive cysteines allowing multimerization; the BH3 domain for interactions with the Bcl-2 family members; alpha helix 1 for t-Bid interaction. Bax has also multiple functions: it releases different mitochondrial factors such as cytochrome c, SMAC/diablo; it regulates mitochondrial fission, the mitochondrial permeability transition pore; it promotes Ca 2+ leakage through ER membrane. Altogether, Bax activation is a complex multi-step phenomenon. Here, we analyze these events as logically separable or alternative steps, attempting to assess their role, timing and reciprocal relation.

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“…The first are the inhibitors of apoptosis (IAPs) [25], [26]. These proteins bind to caspases directly and thus block caspase function.…”

Section: Cell Death Genesmentioning

confidence: 99%

Thyroid hormone regulation of apoptotic tissue remodeling during anuran metamorphosis

Shi

Hsia

et al. 2001

Cell Res

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Anuran metamorphosis involves systematic transformations of individual organs in a thyroid hormone (TH)-dependent manner. Morphological and cellular studies have shown that the removal of larval organs/ tissues such the tail and the tadpole intestinal epithelium is through programmed cell death or apoptosis. Recent molecular investigations suggest that TH regulates metamorphosis by regulating target gene expression through thyroid hormone receptors (TRs), which are DNA-binding transcription factors. Cloning and characterization of TH response genes show that diverse groups of early response genes are induced by TH. The products of these TH response genes are believed to directly or indirectly affect the expression and/or functions of cell death genes, which are conserved at both sequence and function levels in different animal species. A major challenge for future research lies at determining the signaling pathways leading to the activation of apoptotic processes and whether different death genes are involved in the regulation of apoptosis in different tissues/organs to effect tissue-specific transformations.

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The IAP family: endogenous caspase inhibitors with multiple biological activities

Cited by 267 publications

References 49 publications

MiR-135a functions as a selective killer of malignant glioma

MiR-135a functions as a selective killer of malignant glioma

Multistep and multitask Bax activation

Thyroid hormone regulation of apoptotic tissue remodeling during anuran metamorphosis

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