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New Thermoplastic Elastomers based on Ethylene-Butadiene-Rubber (EBR) by Switching from Anionic to Coordinative Chain Transfer Polymerization.
Angew Chem Int Ed Engl
December 2024
CNRS - UMR5128 - University of Lyon, 43 av du 11 nov 1918, Villeurbanne, FRANCE.
Article Synopsis
- - The research developed a new type of olefin triblock copolymer using an innovative process that combines anionic and coordinative chain transfer polymerization to create polymers made of polystyrene (PS), ethylene butadiene rubber (EBR), and crystalline polyethylene (PE).
- - The preparation involved transmetalating PS chains to create macro chain transfer agents, allowing for the effective copolymerization of ethylene and butadiene, followed by further extension with pure ethylene to form well-defined triblock structures.
- - The resulting materials exhibit a balance of good mechanical and rheological properties, showing low viscosity and high performance as thermoplastic elastomers, particularly effective at temperatures above 150 °C.
CISD2 counteracts the inhibition of ER-mitochondrial calcium transfer by anti-apoptotic BCL-2.
Biochim Biophys Acta Mol Cell Res
January 2025
KU Leuven, Laboratory for Molecular and Cellular Signaling, Department of Cellular and Molecular Medicine, Leuven Kanker Instituut, Campus Gasthuisberg O/N-1 B-802, Herestraat 49, BE-3000 Leuven, Belgium. Electronic address:
CISD2, a 2Fe2S cluster domain-containing protein, is implicated in Wolfram syndrome type 2, longevity and cancer. CISD2 is part of a ternary complex with IP receptors (IPRs) and anti-apoptotic BCL-2 proteins and enhances BCL-2's anti-autophagic function. Here, we examined how CISD2 impacted the function of BCL-2 in apoptosis and in controlling IPR-mediated Ca signaling.
View Article and Find Full Text PDFDissecting the neuroprotective interaction between the BH4 domain of BCL-w and the IP3 receptor.
Cell Chem Biol
October 2024
Departments of Cancer Biology and Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Linde Program in Cancer Chemical Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA. Electronic address:
BCL-w is a BCL-2 family protein that promotes cell survival in tissue- and disease-specific contexts. The canonical anti-apoptotic functionality of BCL-w is mediated by a surface groove that traps the BCL-2 homology 3 (BH3) α-helices of pro-apoptotic members, blocking cell death. A distinct N-terminal portion of BCL-w, termed the BCL-2 homology 4 (BH4) domain, selectively protects axons from paclitaxel-induced degeneration by modulating IP3 receptors, a noncanonical BCL-2 family target.
View Article and Find Full Text PDFRecent advances in canonical versus non-canonical Ca-signaling-related anti-apoptotic Bcl-2 functions and prospects for cancer treatment.
Biochim Biophys Acta Mol Cell Res
June 2024
KU Leuven, Lab. Molecular & Cellular Signaling, Dep. Cellular & Molecular Medicine, Campus Gasthuisberg O/N-I bus 802, Herestraat 49, BE-3000 Leuven, Belgium. Electronic address:
Cell fate is tightly controlled by a continuous balance between cell survival and cell death inducing mechanisms. B-cell lymphoma 2 (Bcl-2)-family members, composed of effectors and regulators, not only control apoptosis at the level of the mitochondria but also by impacting the intracellular Ca homeostasis and dynamics. On the one hand, anti-apoptotic protein Bcl-2, prevents mitochondrial outer membrane permeabilization (MOMP) by scaffolding and neutralizing proapoptotic Bcl-2-family members via its hydrophobic cleft (region composed of BH-domain 1-3).
View Article and Find Full Text PDFBik promotes proteasomal degradation to control low-grade inflammation.
J Clin Invest
December 2023
Brigham and Women's Hospital, Division of Pulmonary and Critical Medicine, Harvard Medical School, Boston, Massachusetts, USA.
Although chronic low-grade inflammation does not cause immediate clinical symptoms, over the longer term, it can enhance other insults or age-dependent damage to organ systems and thereby contribute to age-related disorders, such as respiratory disorders, heart disease, metabolic disorders, autoimmunity, and cancer. However, the molecular mechanisms governing low-level inflammation are largely unknown. We discovered that Bcl-2-interacting killer (Bik) deficiency causes low-level inflammation even at baseline and the development of spontaneous emphysema in female but not male mice.
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