Tex264 is an endoplasmic reticulum (ER) membrane protein that was recently demonstrated to act as an ER-phagy receptor under starvation conditions to mediate endoplasmic reticulum autophagy. However, how Tex264 functions in the central nervous system (CNS) and tumors is unclear. Here, we identified 89 proteins from the rat brain that may specifically interact with Tex264 and confirmed the interaction between sorting nexin 27 (SNX27) and Tex264 by coimmunoprecipitation and immunofluorescence. Our results indicated that Tex264 may promote recycling of membrane proteins from endosomes to the cell plasma membrane by recruiting SNX27 retromer vesicles. siRNA-mediated knockdown of TEX264 in HeLa cells did not affect cell proliferation but did significantly inhibit cell migration through a mechanism that may involve a reduction in SNX27-mediated Itg5 receptor membrane recycling. Results of this study helped identify potential binding Tex264 partners and provide insights into Tex264 functions in the CNS and in tumors.
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http://dx.doi.org/10.1155/2022/4304419 | DOI Listing |
Sci Rep
December 2024
Department of Cardiothoracic Surgery, the First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Plasma secretory proteins are associated with various diseases, including aortic dissection (AD). However, current research on the correlation between AD and plasma protein levels is scarce or lacks specificity. This study aimed to explore plasma secretory proteins as potential biomarkers for AD.
View Article and Find Full Text PDFAutophagy
December 2024
Life Sciences Institute and Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, USA.
Type I topoisomerases (TOP1) are critical to remove the topological stress when DNA double strands are unwound. The TOP1 cleavage complexes (TOP1cc) are normally transient, and the stabilization of TOP1cc by its inhibitors, such as camptothecin (CPT), may lead to DNA damage and become cytotoxic. The proteasome pathway degrades trapped TOP1, which is necessary for the repair machinery to gain access to the DNA; however, this process is mainly described when the CPT concentration is high, at levels which are clinically unachievable.
View Article and Find Full Text PDFPancreatic ductal adenocarcinoma (PDA) evades immune detection partly via autophagic capture and lysosomal degradation of major histocompatibility complex class I (MHC-I). Why MHC-I is susceptible to capture via autophagy remains unclear. By synchronizing exit of proteins from the endoplasmic reticulum (ER), we show that PDAC cells display prolonged retention of MHC-I in the ER and fail to efficiently route it to the plasma membrane.
View Article and Find Full Text PDFTrends Biochem Sci
January 2025
School of Biological Sciences, Nanyang Technological University, Singapore. Electronic address:
DNA is constantly subject to damage from endogenous and exogenous factors, leading to mutations and disease. While DNA is traditionally repaired in the nucleus, Lascaux et al. reveal a novel role for the lysosome in DNA repair, demonstrating that topoisomerase 1 (TOP1) cleavage complex (TOP1cc) DNA lesions are degraded via TEX264-mediated selective autophagy.
View Article and Find Full Text PDFMol Cell
October 2024
Department of Cancer Biology, Penn Center for Genome Integrity, Basser Center for BRCA, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104-6160, USA. Electronic address:
In a recent study in Cell, Lascaux et al. implicate TEX264 in the autophagy-driven resolution of nuclear topoisomerase 1 cleavage complexes (TOP1cc) in lysosomes, altering current concepts on the mechanism of action for clinically relevant doses of TOP1 inhibitors.
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