Tankyrase function at telomeres, spindle poles, and beyond

Hsiao, Susan J.; Smith, Susan

doi:10.1016/j.biochi.2007.07.012

Cited by 222 publications

(246 citation statements)

References 77 publications

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“…TNKS1-mediated PARsylation of axin 1 and 2 (regulators of the Wnt signalling pathway) led to their degradation through the ubiquitin-proteasome pathway [18]. TNKS1 has a number of other binding partners that, though diverse, share a common RXXG/ PDG (or degenerate)-binding motif [15,19,20]. Here we identify CPAP as an RXXPDG-containing TNKS1 binding partner.…”

Section: Introductionmentioning

confidence: 81%

Tankyrase 1 regulates centrosome function by controlling CPAP stability

2012

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CPAP-a gene mutated in primary microcephaly-is required for procentriole formation. Here we show that CPAP degradation and function is controlled by the poly(ADP-ribose) polymerase tankyrase 1. CPAP is PARsylated by tankyrase 1 in vitro and in vivo. Overexpression of tankyrase 1 leads to CPAP proteasomal degradation, preventing centriole duplication, whereas depletion of tankyrase 1 stabilizes CPAP in G1, generating elongated procentrioles and multipolarity. Tankyrase 1 localizes to centrosomes exclusively in G1, coinciding with CPAP degradation. Hence, tankyrase 1-mediated PARsylation regulates CPAP levels during the cell cycle to limit centriole elongation and ensure normal centrosome function.

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Section: Introductionmentioning

confidence: 81%

Tankyrase 1 regulates centrosome function by controlling CPAP stability

2012

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“…For example, ADP-ribosylation enhances transcriptional activation by histones (45) and increases activity of the cation channel P2X7 (44,46) and of the transcriptional insulator CCCTCbinding factor (47) and decreases activity of glutamate dehydrogenase (48), glycogen synthase kinase 3␤ (49), and the circadian rhythm regulator CLOCK (50). ADP-ribosylation has also been reported to enhance protein ubiquitination and degradation (51,52). Our findings that PEPCK-C levels were lower when PEPCK was co-expressed with TiPARP than when expressed alone in HEK293 cells (Fig.…”

Section: Discussionmentioning

confidence: 99%

Aryl Hydrocarbon Receptor Activation by Dioxin Targets Phosphoenolpyruvate Carboxykinase (PEPCK) for ADP-ribosylation via 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-inducible Poly(ADP-ribose) Polymerase (TiPARP)

Diani-Moore

Zhang

Ram

et al. 2013

Journal of Biological Chemistry

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Background: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-activated aryl hydrocarbon receptor (AHR) decreases gluconeogenesis by suppressing phosphoenolpyruvate carboxykinase (PEPCK) transcription via TCDD-inducible poly(ADPribose)-polymerase (TiPARP). Results: AHR enhances PEPCK ADP-ribosylation through TiPARP, and AHR suppression increases ADP-ribosylation PARP-independently. Conclusion: ADP-ribosylation, a new PEPCK posttranslational modification, is subject to complex regulation by the AHR. Significance: AHR gene activation leads to ADP-ribosylation of PEPCK with implications for energy metabolism beyond TCDD toxicity.

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“…There are two Poly (ADP-ribose) polymerases (PARPs) that are implicated in Wnt/ -catenin signaling: Tankyrase 1 (PARP5a) and Tankyrase 2 (PARP5b) [140,141]. To a large extent, Tankyrases 1 and 2 appear to have redundant functions.…”

Section: Tankyrasesmentioning

confidence: 99%

“…In contrast to Tankyrase 1, Tankyrase 2 lacks the HPS domain [141]. The PARP domain catalyzes poly(ADP-ribosyl)ation, the SAM and Ankyrin domains participate in the formation of protein-protein complexes with substrates, while the functions of the HPS remain obscure.…”

Section: Tankyrasesmentioning

confidence: 99%

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Wnt/beta-Catenin Signaling and Small Molecule Inhibitors

Voronkov¹,

Krauß²

2012

CPD

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Wnt/ -catenin signaling is a branch of a functional network that dates back to the first metazoans and it is involved in a broad range of biological systems including stem cells, embryonic development and adult organs. Deregulation of components involved in Wnt/ -catenin signaling has been implicated in a wide spectrum of diseases including a number of cancers and degenerative diseases. The key mediator of Wnt signaling, -catenin, serves several cellular functions. It functions in a dynamic mode at multiple cellular locations, including the plasma membrane, where -catenin contributes to the stabilization of intercellular adhesive complexes, the cytoplasm where -catenin levels are regulated and the nucleus where -catenin is involved in transcriptional regulation and chromatin interactions. Central effectors of -catenin levels are a family of cysteine-rich secreted glycoproteins, known as Wnt morphogens. Through the LRP5/6-Frizzled receptor complex, Wnts regulate the location and activity of the destruction complex and consequently intracellularcatenin levels. However, -catenin levels and their effects on transcriptional programs are also influenced by multiple other factors including hypoxia, inflammation, hepatocyte growth factor-mediated signaling, and the cell adhesion molecule E-cadherin. The broad implications of Wnt/ -catenin signaling in development, in the adult body and in disease render the pathway a prime target for pharmacological research and development. The intricate regulation of -catenin at its various locations provides alternative points for therapeutic interventions.

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Tankyrase function at telomeres, spindle poles, and beyond

Cited by 222 publications

References 77 publications

Tankyrase 1 regulates centrosome function by controlling CPAP stability

Tankyrase 1 regulates centrosome function by controlling CPAP stability

Aryl Hydrocarbon Receptor Activation by Dioxin Targets Phosphoenolpyruvate Carboxykinase (PEPCK) for ADP-ribosylation via 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD)-inducible Poly(ADP-ribose) Polymerase (TiPARP)

Wnt/beta-Catenin Signaling and Small Molecule Inhibitors

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