A novel mitochondrial septin-like protein, ARTS, mediates apoptosis dependent on its P-loop motif

Larisch, Sarit; Yi, Young-Su; Lotan, Rachel; Kerner, Hedviga; Eimerl, Sarah; Parks, W. Tony; Gottfried, Yossi; Reffey, Stephanie Birkey; Caestecker, Mark P. de; Danielpour, David; Book-Melamed, Naomi; Timberg, Rina; Duckett, Colin S.; Lechleider, Robert J.; Steller, Hermann; Orly, Joseph; Kim, Seong‐Jin; Roberts, Anita B.

doi:10.1038/35046566

Cited by 231 publications

(246 citation statements)

References 37 publications

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“…The signature motifs (G-boxes) of the GTPase superfamily are present in all septin family members except ARTS, a splice variant of Sept4 that lacks the G4 box [56]. Many septins bind and hydrolyze GTP [7,28,45,55].…”

Section: Regulation Of Septin Polymerizationmentioning

confidence: 99%

Some assembly required: yeast septins provide the instruction manual

Versele

Thorner

2005

Trends in Cell Biology

200

205

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Septins are a family of conserved proteins that form hetero-oligomeric complexes that assemble into filaments. The filaments can be organized into linear arrays, coils, rings and gauzes. They serve as membrane-associated scaffolds and as barriers to demarcate local compartments, especially for the establishment of the septation site for cytokinesis. Studies in budding and fission yeast have revealed many of the protein-protein interactions that govern the formation of multi-septin complexes. GTP binding and phosphorylation direct the polymerization of filaments that is required for septin-collar assembly in budding yeast, whereas a homolog of anillin instructs timely formation of the ring of septin filaments at the medial cortex in fission yeast. These insights should aid understanding of the organization and function of the diverse septin structures in animal cells.

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Section: Regulation Of Septin Polymerizationmentioning

confidence: 99%

Some assembly required: yeast septins provide the instruction manual

Versele

Thorner

2005

Trends in Cell Biology

200

205

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“…The upstream activator of TAK1, TAB1 (Shibuya et al, 1996), may be linked to receptor activation via HPK1 or Xlinked inhibitor of apoptosis (XIAP) in case of TGF-b or BMP, respectively (Wang et al, 1997;Yamaguchi et al, 1999). Recently, ARTS, apoptosis-related protein in the TGF-b signaling pathway (Larisch et al, 2000), a protein belonging to the septin family, was found to enhance cell death by TGF-b. ARTS is localized to mitochondria and translocates to nucleus when apoptosis occurs (Fig.…”

Section: Regulation Of Apoptosis By Smadsmentioning

confidence: 99%

Regulation of cell proliferation by Smad proteins

Dijke

Goumans

Itoh

2002

Journal Cellular Physiology

398

278

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Transforming growth factor-b (TGF-b) family members which include TGF-bs, activins, and bone morphogenetic proteins (BMPs) regulate a broad spectrum of biological responses on a large variety of cell types. TGF-b family members initiate their cellular responses by binding to distinct receptors with intrinsic serine/ threonine kinase activity and activation of speci®c downstream intracellular effectors termed Smad proteins. Smads relay the signal from the cell membrane to the nucleus, where they affect the transcription of target genes. Smad activation, subcellular distribution, and stability have been found to be intricately regulated and a broad array of transcription factors have been identi®ed as Smad partners. Important activities of TGF-b are its potent anti-mitogenic and pro-apoptotic effects that, at least in part, are mediated via Smad proteins. Escape from TGF-b/ Smad-induced growth inhibition and apoptosis is frequently observed in tumors. Certain Smads have been found to be mutated in speci®c types of cancer and gene ablation of particular Smads in mice has revealed increased rate of tumorigenesis. In late stage tumors, TGF-b has been shown to function as a tumor promoter. TGFb can stimulate the de-differentiation of epithelial cells to malignant invasive and metastatic ®broblastic cells. Interestingly, TGF-b may mediate these effects directly on tumor cells via subverted Smad-dependent and/or Smad-independent pathways.

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“…potentiates transforming growth factor-b/Smad2 pathway Transforming growth factor-b is a potent inducer of growth inhibition and apoptosis of NRP-154 cells (Larisch-Bloch et al, 2000). Using retroviral cDNA expression libraries, we identified an antisense transcript of ELAC2 as a possible mediator for conferring a TGFb resistant phenotype to NRP-154 prostate cells.…”

Section: Elac2mentioning

confidence: 99%

ELAC2, a putative prostate cancer susceptibility gene product, potentiates TGF-β/Smad-induced growth arrest of prostate cells

et al. 2006

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Transforming growth factor-b (TGF-b) elicits a potent growth inhibitory effect on many normal cells by binding to specific serine/threonine kinase receptors and activating specific Smad proteins, which regulate the expression of cell cycle genes, including the p21 cyclin-dependent kinase (CDK) inhibitor gene. Interestingly, cancer cells are often insensitive to the anti-mitogenic effects of TGF-b for which the molecular mechanisms are not well understood. In this study, we found that the candidate prostate cancer susceptibility gene ELAC2 potentiates TGF-b/Smadinduced transcriptional responses. ELAC2 associates with activated Smad2; the C-terminal MH2 domain of Smad2 interacts with the N-terminal region of ELAC2. Small interfering siRNA-mediated knock-down of ELAC2 in prostate cells suppressed TGF-b-induced growth arrest. Moreover, ELAC2 was shown to specifically associate with the nuclear Smad2 partner, FAST-1 and to potentiate the interaction of activated Smad2 with transcription factor Sp1. Furthermore, activation of the p21 CDK inhibitor promoter by TGF-b is potentiated by ELAC2. Taken together our data indicate an important transcriptional scaffold function for ELAC2 in TGF-b/ Smad signaling mediated growth arrest.

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A novel mitochondrial septin-like protein, ARTS, mediates apoptosis dependent on its P-loop motif

Cited by 231 publications

References 37 publications

Some assembly required: yeast septins provide the instruction manual

Some assembly required: yeast septins provide the instruction manual

Regulation of cell proliferation by Smad proteins

ELAC2, a putative prostate cancer susceptibility gene product, potentiates TGF-β/Smad-induced growth arrest of prostate cells

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