Results 101 to 110 of about 51,687 (291)

Emerging fluorescence tools for the study of proteostasis in cells

open access: yes, 2022
Understanding how cells maintain the functional proteome and respond to stress conditions is critical for deciphering molecular pathogenesis and developing treatments for conditions such as neurodegenerative diseases. Efforts towards finer quantification
Tze Cin Owyong (13127181)   +1 more
core   +1 more source

Nuclear Translocation of PFKFB3 Promotes Disuse‐Induced Muscle Atrophy via Scaffolding Nedd4‐Mediated JunB Ubiquitination

open access: yesAdvanced Science, EarlyView.
Disuse‐induced muscle atrophy is driven by a non‐metabolic, nuclear function of the enzyme PFKFB3. Acting as a scaffold, PFKFB3 facilitates Nedd4‐mediated ubiquitination and degradation of the anti‐atrophy transcription factor JunB. Inhibiting this novel PFKFB3–Nedd4–JunB signaling axis stabilizes JunB and alleviates muscle wasting, revealing a highly ...
Mengjun Ma   +12 more
wiley   +1 more source

Restores Aβ Clearance by Overcoming PCSK9–LRP1 Dysregulation and TRIB3‐Mediated Autophagy Blockade in Alzheimer's Disease

open access: yesAdvanced Science, EarlyView.
PCSK9 upregulation in cerebrovascular endothelial cells and microglia destabilizes the Aβ transporter LRP1, while TRIB3‐associated autophagy blockade further limits intracellular Aβ degradation. A RAP‐modified tea‐polyphenol nanoparticle co‐delivers siPCSK9 and siTRIB3 to restore LRP1‐mediated Aβ efflux and autophagy‐dependent degradation, reducing Aβ ...
Jie Miao   +8 more
wiley   +1 more source

Polymer Concepts in Cellular Function

open access: yes
Advanced Science, EarlyView.
Miao Yu   +7 more
wiley   +1 more source

Molecular Landscapes of Tumor Dormancy in Gynecologic Malignancies: From Survival Mechanisms to Precision Interception

open access: yesAdvanced Science, EarlyView.
This Review outlines the biological framework of entry, maintenance, and awakening in dormant minimal residual disease across gynecologic cancers. By mapping critical biological dependencies—from metabolic plasticity to microenvironment interactions—it evaluates novel interception concepts and presents a translational framework combining single‐cell ...
Shih‐Hsuan Cheng   +7 more
wiley   +1 more source

Huntingtin Aggregate‐Responsive Autophagy Gene Circuit Mitigates Disease Pathology in R6/2 Mice

open access: yesAdvanced Science, EarlyView.
CD98‐mediated receptor‐mediated transcytosis enables LIP‐CD98 nanocarriers to cross the blood–brain barrier and deliver ARAA to neurons. mHTT aggregates activate the 11G–NarX sensor, initiating Auto‐P and Trans‐P signaling through the VP48–NarL relay.
Jie Zhu   +8 more
wiley   +1 more source

Impairment of lipid homeostasis causes lysosomal accumulation of endogenous protein aggregates through ESCRT disruption

open access: yeseLife
Protein aggregation increases during aging and is a pathological hallmark of many age-related diseases. Protein homeostasis (proteostasis) depends on a core network of factors directly influencing protein production, folding, trafficking, and degradation.
John Yong   +10 more
doaj   +1 more source

Enhanced ER proteostasis and temperature differentially impact the mutational tolerance of influenza hemagglutinin

open access: yeseLife, 2018
We systematically and quantitatively evaluate whether endoplasmic reticulum (ER) proteostasis factors impact the mutational tolerance of secretory pathway proteins.
Angela M Phillips   +6 more
doaj   +1 more source

USP4‐Dependent CHAF1B Stabilization Regulates Distinct SETDB1 Ubiquitin States Linked to AKT T308 Signaling and Lipogenic Remodeling in HCC

open access: yesAdvanced Science, EarlyView.
USP4 stabilizes CHAF1B by limiting K48‐linked ubiquitination. Stabilized CHAF1B supports UHRF1‐associated K63‐linked SETDB1 ubiquitination and cytoplasmic redistribution, whereas CHAF1B loss favors VHL‐dependent K11‐associated degradative ubiquitination and proteasomal loss of SETDB1.
Saiyan Bian   +9 more
wiley   +1 more source

Lipid Metabolic Dysregulation Driven by OSMR Mutations Underlies Amyloidogenesis in Primary Localized Cutaneous Amyloidosis

open access: yesAdvanced Science, EarlyView.
OSMR mutations disrupt STAT5 signaling and AKR1B10‐mediated lipid metabolism, leading to lipid accumulation and protein aggregation in keratinocytes. This metabolic reprogramming drives amyloid deposition in primary localized cutaneous amyloidosis, revealing a mechanistic link between lipid dysregulation and amyloidogenesis.
Huiting Liu   +8 more
wiley   +1 more source

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