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Showing 1-30 of 56 results for "HPA001204" within Papers
Anya Wernersson et al.
Diabetologia, 63(11), 2372-2384 (2020-07-18)
Human enteroviral infections are suggested to be associated with type 1 diabetes. However, the mechanism by which enteroviruses can trigger disease remains unknown. The present study aims to investigate the impact of enterovirus on autophagy, a cellular process that regulates
Wenxian Wu et al.
Autophagy, 17(12), 3992-4009 (2021-03-30)
Macroautophagy/autophagy and necroptosis represent two opposing cellular s tress responses. Whereas autophagy primarily fulfills a cyto-protective function, necroptosis is a form of regulated cell death induced via death receptors. Here, we aimed at investigating the molecular crosstalk between these two
Huan Yang et al.
Autophagy, 15(9), 1539-1557 (2019-03-16)
Autophagosome-lysosome fusion is a common critical step in various forms of macroautophagy/autophagy including mitophagy, the selective degradation of mitochondria. Regulations of this fusion process remain poorly defined. Here we have determined the role of SIGMAR1, a unique endoplasmic reticulum membrane
Hongxu Xian et al.
Nature communications, 10(1), 2059-2059 (2019-05-06)
Mitophagy is the selective autophagic targeting and removal of dysfunctional mitochondria. While PINK1/Parkin-dependent mitophagy is well-characterized, PINK1/Parkin-independent route is poorly understood. Using structure illumination microscopy (SR-SIM), we demonstrate that the SNARE protein Syntaxin 17 (STX17) initiates mitophagy upon depletion of
Manuela Moriggi et al.
International journal of molecular sciences, 22(6) (2021-04-04)
Mutations in the acidic alpha-glucosidase (GAA) coding gene cause Pompe disease. Late-onset Pompe disease (LOPD) is characterized by progressive proximal and axial muscle weakness and atrophy, causing respiratory failure. Enzyme replacement therapy (ERT), based on recombinant human GAA infusions, is
Hong Huang et al.
Autophagy, 19(1), 189-203 (2022-04-26)
SCFD1 (sec1 family domain containing 1) was recently shown to function in autophagosome-lysosome fusion, and multiple studies have demonstrated the regulatory impacts of acetylation (a post-translational modification) on macroautophagy/autophagy. Here, we demonstrate that both acetylation- and phosphorylation-dependent mechanisms control SCFD1's
Hiroki Tanaka et al.
Journal of inherited metabolic disease, 45(6), 1191-1202 (2022-09-15)
Lysosomal storage disorders (LSDs) are inherited metabolic diseases caused by genetic defects in lysosomal enzymes or related factors. LSDs are associated with excessive accumulation of natural substrates in lysosomes leading to central nervous system and peripheral tissue damage. Abnormal autophagy
Rachel J Carter et al.
Cell death & disease, 13(5), 436-436 (2022-05-05)
The recruitment of DRP1 to mitochondrial membranes prior to fission is facilitated by the wrapping of endoplasmic reticulum (ER) membranes around the mitochondria. To investigate the complex interplay between the ER membranes and DRP1 in the context of mitochondrial structure
Pazit Beckerman et al.
Nature medicine, 23(4), 429-438 (2017-02-22)
African Americans have a heightened risk of developing chronic and end-stage kidney disease, an association that is largely attributed to two common genetic variants, termed G1 and G2, in the APOL1 gene. Direct evidence demonstrating that these APOL1 risk alleles
Yingxin Shi et al.
The Journal of biological chemistry, 298(9), 102341-102341 (2022-08-06)
Human papillomaviruses (HPVs) cause a subset of head and neck squamous cell carcinomas (HNSCCs). Previously, we demonstrated that HPV16 oncogene E6 or E6/E7 transduction increases the abundance of O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT), but OGT substrates affected by this increase
Rongrong Hua et al.
Journal of cellular biochemistry, 120(9), 15915-15923 (2019-05-14)
The sequential reactivation of mechanistic target of rapamycin (mTOR) inhibited autophagic flux in neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R), which was characterized by reduction of autophagosome formation and restriction of autolysosome degradation. However, its detailed molecular mechanism was still unknown.
Suzan Schwertheim et al.
Journal of personalized medicine, 13(7) (2023-07-29)
Non-alcoholic fatty liver disease (NAFLD) embraces simple steatosis in non-alcoholic fatty liver (NAFL) to advanced non-alcoholic steatohepatitis (NASH) associated with inflammation, fibrosis, and cirrhosis. NAFLD patients often have metabolic syndrome and high risks of cardiovascular and liver-related mortality. Our aim
The autophagosomal SNARE protein syntaxin 17 is an essential factor for the hepatitis C virus life cycle
Ren H, et al.
Journal of Virology, 520(7548), JVI-00551 (2016)
The autophagosomal SNARE protein syntaxin 17 is an essential factor for the hepatitis C virus life cycle
Ren H, et al.
Journal of virology, JVI-00551 (2016)
Christina G Towers et al.
Developmental cell, 50(6), 690-703 (2019-08-06)
While autophagy is thought to be an essential process in some cancer cells, it is unknown if or how such cancer cells can circumvent autophagy inhibition. To address this, we developed a CRISPR/Cas9 assay with dynamic live-cell imaging to measure
Eleonora Turco et al.
Molecular cell, 74(2), 330-346 (2019-03-12)
The autophagy cargo receptor p62 facilitates the condensation of misfolded, ubiquitin-positive proteins and their degradation by autophagy, but the molecular mechanism of p62 signaling to the core autophagy machinery is unclear. Here, we show that disordered residues 326-380 of p62
Polymorphisms in the syntaxin 17 gene are not associated with human cutaneous malignant melanoma
Zhao Z Z, et al.
Melanoma Research, 19(2), 80-80 (2009)
Yukako Oe et al.
PLoS genetics, 18(6), e1010264-e1010264 (2022-07-01)
Autophagy is an indispensable process that degrades cytoplasmic materials to maintain cellular homeostasis. During autophagy, double-membrane autophagosomes surround cytoplasmic materials and either fuse with endosomes (called amphisomes) and then lysosomes, or directly fuse with lysosomes, in both cases generating autolysosomes
Suresh Kumar et al.
Cell, 184(24), 5950-5969 (2021-11-07)
The biogenesis of mammalian autophagosomes remains to be fully defined. Here, we used cellular and in vitro membrane fusion analyses to show that autophagosomes are formed from a hitherto unappreciated hybrid membrane compartment. The autophagic precursors emerge through fusion of FIP200
Suresh Kumar et al.
Nature cell biology, 22(8), 973-985 (2020-08-06)
Autophagy is a homeostatic process with multiple functions in mammalian cells. Here, we show that mammalian Atg8 proteins (mAtg8s) and the autophagy regulator IRGM control TFEB, a transcriptional activator of the lysosomal system. IRGM directly interacted with TFEB and promoted
Lara Cantarero et al.
Human molecular genetics, 29(22), 3589-3605 (2020-12-30)
Mutations in the GDAP1 gene cause Charcot-Marie-Tooth (CMT) neuropathy. GDAP1 is an atypical glutathione S-transferase (GST) of the outer mitochondrial membrane and the mitochondrial membrane contacts with the endoplasmic reticulum (MAMs). Here, we investigate the role of this GST in
Zhiyuan An et al.
Virulence, 12(1), 1965-1979 (2021-07-27)
Acinetobacter baumanniitriggers autophagy, affects the degradation of autophagy, and causes severe inflammatory injury. LncRNA growth arrest-specific transcript 5 (LncRNA-GAS5) and Yin and Yang 1 (YY1) are known to play an important role in the regulation of autophagy, however, the precise
Qiuhong Shen et al.
Autophagy, 17(5), 1157-1169 (2020-04-09)
The fusion of autophagosomes and endosomes/lysosomes, also called autophagosome maturation, ensures the degradation of autophagic cargoes. It is an important regulatory step of the macroautophagy/autophagy process. STX17 is the key autophagosomal SNARE protein that mediates autophagosome maturation. Here, we report
Tomonori Kimura et al.
The EMBO journal, 36(1), 42-60 (2016-12-10)
Autophagy is a process delivering cytoplasmic components to lysosomes for degradation. Autophagy may, however, play a role in unconventional secretion of leaderless cytosolic proteins. How secretory autophagy diverges from degradative autophagy remains unclear. Here we show that in response to
Yuanli Zhen et al.
Autophagy, 11(9), 1608-1622 (2015-08-12)
The HOPS (homotypic fusion and protein sorting) complex functions in endocytic and autophagic pathways in both lower eukaryotes and mammalian cells through its involvement in fusion events between endosomes and lysosomes or autophagosomes and lysosomes. However, the differential molecular mechanisms
Yuexi Gu et al.
The EMBO journal, 38(22), e101994-e101994 (2019-10-19)
Mammalian homologs of yeast Atg8 protein (mAtg8s) are important in autophagy, but their exact mode of action remains ill-defined. Syntaxin 17 (Stx17), a SNARE with major roles in autophagy, was recently shown to bind mAtg8s. Here, we identified LC3-interacting regions
Hana Kimura et al.
Journal of lipid research, 59(5), 805-819 (2018-03-20)
Lipid droplets (LDs) are ubiquitous organelles that contain neutral lipids and are surrounded by a phospholipid monolayer. How proteins specifically localize to the phospholipid monolayer of the LD surface has been a matter of extensive investigations. In the present study
Yueguang Rong et al.
The Journal of cell biology, 221(7) (2022-05-06)
The stimulator of interferon genes (STING) plays a critical role in innate immunity. Emerging evidence suggests that STING is important for DNA or cGAMP-induced non-canonical autophagy, which is independent of a large part of canonical autophagy machineries. Here, we report
Masaaki Uematsu et al.
Autophagy, 13(8), 1452-1464 (2017-06-10)
Macroautophagy/autophagy, which is one of the main degradation systems in the cell, is mediated by a specialized organelle, the autophagosome. Purification of autophagosomes before fusion with lysosomes is important for both mechanistic and physiological studies of the autophagosome. Here, we
Ryuji Nomura et al.
Histochemistry and cell biology, 135(6), 531-538 (2011-05-19)
Calreticulin (CRT)-1 is a major Ca(2+)-buffering protein in the lumen of the endoplasmic reticulum. Human and murine CRT-2 was isolated in 2002, but the subcellular localization and function is still unclear. Here, we studied the intracellular localization and function of
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