Results 171 to 180 of about 9,562,225 (293)

Rab1A Promotes Hepatic Steatosis by Suppressing Mitophagy via the Raf‐1/ERK1/2/PINK1 Signaling Axis

open access: yesAdvanced Science, EarlyView.
Why does fat accumulate in the liver? Our study reveals Rab1A as the molecular switch that silences the cell's mitochondrial cleanup crew. Turning Rab1A off reactivates mitophagy, clears excess fat, and reverses fatty liver disease in mice—offering a promising new therapeutic target for MASLD, a growing global health challenge.
Li Zhang   +9 more
wiley   +1 more source

Diverse database and machine learning model to narrow the generalization gap in RNA structure prediction. [PDF]

open access: yesSci Adv
de Lajarte AA   +11 more
europepmc   +1 more source

Gonadotropin‐Inhibitory Hormone (GnIH) and Its Receptor GPR147 Mediates Acute Stress‐Induced Activation of the Locus Coeruleus‐SAM Axis

open access: yesAdvanced Science, EarlyView.
ABSTRACT Gonadotropin‐inhibitory hormone (GnIH, also known as RFamide‐related peptide‐3, RFRP‐3) is a hypothalamic neuropeptide that regulates vertebrate reproduction via its receptor GPR147. Although GnIH is known to mediate stress‐induced reproductive suppression, its role in broader stress responses remains unclear.
Jiani Zhang   +18 more
wiley   +1 more source

Prediction and modelling of RNA structure and interactions

open access: yes
BMC Bioinformatics is calling for submissions to our Collection on “Prediction and modelling of RNA structure and interactions”. This Collection welcomes submissions on novel algorithms, computational methods and tools on the topics of classification,
Letizia Chiodo   +2 more
core   +1 more source

Limits in accuracy and a strategy of RNA structure prediction using experimental information. [PDF]

open access: yesNucleic Acids Res, 2019
Wang J   +5 more
europepmc   +1 more source

Copper‐Driven Epithelial Barrier Disruption: A Novel Mechanism of COPD Acute Exacerbations Mediated by the TNF‐α/ATP7A Axis

open access: yesAdvanced Science, EarlyView.
This study reveals a copper‐driven mechanism of COPD acute exacerbations mediated by the TNF‐α/ATP7A axis. TNF‐α suppresses the copper transporter ATP7A via competitive NF‐κB/CREB1/CBP signaling, resulting in intracellular copper accumulation, mitochondrial oxidative stress, and epithelial barrier disruption.
Xinru Xiao   +7 more
wiley   +1 more source

A Method for RNA Structure Prediction Shows Evidence for Structure in lncRNAs. [PDF]

open access: yesFront Mol Biosci, 2018
Delli Ponti R   +3 more
europepmc   +1 more source

NeuroSuite for Long‐Term Functional and Structural Studies of Air‐Liquid Interface Cerebral Organoids

open access: yesAdvanced Science, EarlyView.
NeuroSuite provides a modular hardware‐software platform integrating Neuroweb and NeuroMaps to enable long‐term, in situ electrophysiological interrogation of air–liquid interface organoid slices while preserving tissue architecture. Its components can be used together or independently to capture real‐time activity, spatial network dynamics, and ...
Belquis Haider   +14 more
wiley   +1 more source

Applications of artificial intelligence in RNA 3D structure prediction and RNA interaction modeling

open access: yes四川大学学报. 自然科学版
RNA performs central roles in essential biological processes including gene regulation and immune responses by adopting specific three-dimensional (3D) architectures and mediating precise interactions with proteins, small molecules, and other ...
WEI Rui, ZHANG Le, XIAO Ming
doaj  

BAP31 Drives Cartilage Calcification through Disruption of Autophagosome–Lysosome Fusion in Osteoarthritis

open access: yesAdvanced Science, EarlyView.
Mechanical stress activates BAP31 in chondrocytes. BAP31 competes with ATG14 for binding to STX17, disrupting the STX17–ATG14 complex required for autophagosome–lysosome fusion. The resultant autophagic flux blockade drives the generation of autophagy‐derived exosomes, which mediate pathological cartilage calcification in OA. Chondrocyte‐targeted BAP31
Zhi‐hua Xu   +13 more
wiley   +1 more source

Home - About - Disclaimer - Privacy