Results 1 to 10 of about 3,136 (126)

BRET‐Based Approaches for Ion Channels: Emerging Applications and Future Directions [PDF]

open access: yesArchiv der Pharmazie, Volume 359, Issue 9, September 2026.
Bioluminescence resonance energy transfer (BRET) is a versatile method for studying ligand–protein interactions. Its compatibility with high‐throughput screening and real‐time kinetics has made it widely used in drug discovery. Here, we summarize recent applications of BRET‐based methods for studying ligand binding to ion channels, highlighting key ...
Nadine Kock   +6 more
wiley   +2 more sources

A High‐Loading Zn Single‐Atom Nanozyme Targets the Zn/HIF‐1α/GLUT1 Axis to Disrupt Glucose Metabolic Reprogramming and Remodel the Tumor Immune Microenvironment [PDF]

open access: yesAdvanced Science, EarlyView.
A high‐loading Zn single‐atom nanozyme (ZMG@CS) delivers ML‐SA5 and GOx to lysosomes. ML‐SA5 activates TRPML1 to release endogenous Zn2+, while the nanozyme provides exogenous Zn2+ and GOx‐driven acidification amplifies ROS production. Together, these effects suppress the HIF‐1α/GLUT1 axis, disrupt glucose and redox homeostasis, induce disulfidptosis ...
Zhenxin Wang   +12 more
wiley   +2 more sources

HIV-1 gp120-induced lysosomal stress responses are controlled by TRPML1 redox sensors [PDF]

open access: yesRedox Report
Background Increased lysosomal stress responses (LSR) are commonly implicated in the pathogenesis of neurodegenerative disorders including HIV-1-associated neurocognitive disorders (HAND).
Nirmal Kumar   +2 more
doaj   +2 more sources

TRPML1—Emerging Roles in Cancer

open access: yesCells, 2020
The mucolipin-1 (TRPML1) channel maintains lysosomal ionic homeostasis and regulates autophagic flux. Defects of TRPML1 lead to lysosomal storage diseases and neurodegeneration.
Yassine El Hiani
exaly   +3 more sources

TRPML1 Promotes Protein Homeostasis in Melanoma Cells by Negatively Regulating MAPK and mTORC1 Signaling

open access: yesCell Reports, 2019
Summary: We screen ion channels and transporters throughout the genome to identify those required by human melanoma cells but not by normal human melanocytes.
Zhiyu Zhao   +2 more
exaly   +3 more sources

TRPML1 as a potential therapeutic target for triple-negative breast cancer: a review

open access: yesFrontiers in Oncology, 2023
Triple-negative breast cancer (TNBC) is the most refractory subtype of breast cancer, and effective treatments are urgently needed owing to its poor prognosis.
Ying Pan   +6 more
exaly   +3 more sources

TRPML1 suppresses pulmonary fibrosis by limiting collagen and elastin deposition [PDF]

open access: yesThe EMBO Journal
In pulmonary fibrosis lung tissue is thickened and scarred, and the lungs become progressively stiffer and smaller, leading to low levels of blood oxygen and shortness of breath. Lung fibrosis is not curable and life expectancy is reduced.
Eva-Maria Weiden   +29 more
doaj   +2 more sources

Unraveling Lysosomal Exocytosis: From Molecular Mechanisms to Physiological Functions [PDF]

open access: yesTraffic, Volume 27, Issue 1, March 2026.
Lysosomal exocytosis is propelled by specific molecular mechanisms that direct its microtubule‐dependent transport and subsequent fusion with the plasma membrane. This process fulfills essential physiological functions such as plasma membrane repair, maintenance of cellular homeostasis, and participation in signal transduction.
Shanshan Jiang   +7 more
wiley   +2 more sources

PRELID1 and VDAC3 Coordinate a Senescence‐Like State in Germinal Center B Cells to Promote IL‐7–Driven Antitumor Immunity in Colorectal Cancer [PDF]

open access: yesAdvanced Science, Volume 13, Issue 23, 23 April 2026.
Colorectal cancer is characterized by an immunosuppressive microenvironment that limits immunotherapy efficacy. We identify a senescence‐like state in germinal center B cells driven by the PRELID1–VDAC3 axis, which promotes IL‐7 secretion, alleviates CD8+ T‐cell exhaustion, and enhances antitumor immunity. Targeting this pathway improves responsiveness
Yuhan Liao   +8 more
wiley   +2 more sources

TRPML1 agonists synergize with enzyme replacement therapy in fibroblasts from Pompe disease patients [PDF]

open access: yesJournal of Translational Medicine
Objective Pompe disease is a severe and progressive metabolic myopathy caused by pathogenic variants of the GAA gene, deficiency of acid alpha-glucosidase (GAA), and lysosomal glycogen storage.
Carla Damiano   +10 more
doaj   +2 more sources

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