Results 111 to 120 of about 2,496,873 (280)

The Cancer Cell Metabolic Reprogramming Remodels the Tumor Microenvironment: Molecular Mechanisms and Therapeutic Strategies

Advanced Science, EarlyView.
This review elucidates how cancer cell metabolic reprogramming—across glucose, lipid, amino acid, and nucleotide pathways—remodels the tumor microenvironment to suppress anti‐tumor immunity and promote immune escape. Targeting these metabolic axes offers promising strategies to overcome immunotherapy resistance and enhance cancer treatment.
Guoqing Xiang, Zhicheng Zhou, Xue Jiang, Zhenguang Du, Yangyang Zhan, Xinli Liu   +5 more
wiley   +1 more source

Hunter syndrome (mucopolysaccharidosis type II): Molecular mechanisms, CNS biomarkers, and emerging therapeutic strategies

Experimental and Molecular Pathology
Hunter syndrome (mucopolysaccharidosis type II, MPS II) is an X-linked lysosomal storage disorder caused by deficiency of iduronate-2-sulfatase (IDS), leading to lysosomal accumulation of glycosaminoglycans (GAGs), dermatan sulfate and heparan sulfate ...
Amelia Michelle Sojung Moon, Hyung-Goo Kim, Sang Hoon Lee, Sang Hoon Kim, Euiyeon Lee, Mohammad Abdur Rashid, Yongkyu Park, Chong Kun Cheon, Mi-Hyeon Jang   +8 more
doaj   +1 more source

Multiplexing Iduronate-2-Sulphatase (MPS-II) into a 7-Plex Lysosomal Storage Disorder MS/MS Assay Using Cold-Induced Phase Separation. [PDF]

Int J Neonatal Screen, 2023
Courtney E, Pickens CA, Cuthbert C, Petritis K.   +3 more
europepmc   +1 more source

Impaired Chaperone‐Mediated Autophagy Accelerates Intervertebral Disc Degeneration by Inducing MIDN Accumulation to Target TSC2 for Proteasomal Degradation

Advanced Science, EarlyView.
This graphical abstract illustrates how chaperone‐mediated autophagy (CMA) regulates intervertebral disc degeneration (IDD). Under normal homeostasis (B), CMA degrades cytoplasmic Midnolin (MIDN) to maintain proteostasis. Under inflammatory stress (A), impaired CMA leads to cytoplasmic MIDN accumulation.
Xianglong Chen, Haiyang Gao, Wang Wu, Pengzhi Shi, Yuhang Chen, Anran Zhang, Zhangrong Cheng, Wenbo Wu, Zimu Yu, Yukun Zhang   +9 more
wiley   +1 more source

Extracellular Vesicles Released by Genetically Modified Macrophages Activate Autophagy and Produce Potent Neuroprotection in Mouse Model of Lysosomal Storage Disorder, Batten Disease. [PDF]

Cells, 2023
El-Hage N, Haney MJ, Zhao Y, Rodriguez M, Wu Z, Liu M, Swain CJ, Yuan H, Batrakova EV.   +8 more
europepmc   +1 more source

OAF Blocks SIAH1‐Mediated Degradation of SCPX, a Therapeutic Strategy for MASLD

Advanced Science, EarlyView.
This study shows OAF directly binds to SCPX and inhibits its interaction with the E3 ligase SIAH1, thereby protecting SCPX from ubiquitin‐dependent degradation and stabilizing its levels. This OAF‐SCPX axis represents a novel pathway in lipid homeostasis, highlighting OAF as a promising therapeutic candidate for MASLD.
Zongxi Li, Jingyue Song, Kaili Ma, Shunan Tang, Shuqian Wang, Wenya Ji, Chen Lu, Ting Zhang, Huaping Zheng, Xiaowei Zheng, Shanshan Lai, Cheng Deng   +11 more
wiley   +1 more source

The Association Between Lysosomal Storage Disorder Genes and Parkinson's Disease: A Large Cohort Study in Chinese Mainland Population. [PDF]

Front Aging Neurosci, 2021
Zhao YW, Pan HX, Liu Z, Wang Y, Zeng Q, Fang ZH, Luo TF, Xu K, Wang Z, Zhou X, He R, Li B, Zhao G, Xu Q, Sun QY, Yan XX, Tan JQ, Li JC, Guo JF, Tang BS.   +19 more
europepmc   +1 more source

Altered cerebellar granule cell differentiation and synapse maturation in a mouse model of a lysosomal lipid storage disease.

, 2020
The rare Niemann-Pick type C1 (NPC1) disease is a lysosomal lipid storage disorder, caused by mutations in the Npc1 gene. Since the encoded protein mediates the outflow of cholesterol from endosomal-lysosomal compartments, these mutations cause ...
Sonia Canterini, Serena Camuso, Micaela Lucarelli, Alessandro Rava, Lucy Babicola, Fiorenza Maria Teresa   +5 more
core  

Quantitative Visualization of Intracellular Nanometabolism Using Peak‐Shifted Dual‐State Emissive FRET Nanoprobes

Advanced Science, EarlyView.
This study reveals the long‐elusive intracellular dissolution mechanism of carrier‐free nanomedicines. By utilizing peak‐shifted dual‐state emissive FRET nanoprobes (PDFNPs) that undergo a distinct ratiometric fluorescence peak shift upon disassembly, we achieve real‐time, quantitative tracking of dissolution kinetics in live cells.
Farsai Taemaitree, Jinwoo Sung, Yutaro Miki, Ryuju Suzuki, Yoshitaka Koseki, Kunikazu Ishii, Minsang Kim, Keita Tanita, Kota Sato, Toru Nakazawa, Satoshi Katsube, Daisuke Unabara, Tasuku Hamaguchi, Keisuke Kawakami, Koji Yonekura, Akihide Hibara, Atsushi Wakamiya, Hiroshi Uji‐I, Hitoshi Kasai   +18 more
wiley   +1 more source

Deficiency in NPC2 results in disruption of mitochondria-late endosome/lysosomes contact sites and endo-lysosomal lipid dyshomeostasis

Scientific Reports
Dysfunction of the endo-lysosomal intracellular Cholesterol transporter 2 protein (NPC2) leads to the onset of Niemann–Pick Disease Type C (NPC), a lysosomal storage disorder.
Raffaele Pastore, Lihang Yao, Nathan Hatcher, Martin Helley, Janet Brownlees, Radha Desai   +5 more
doaj   +1 more source