Results 151 to 160 of about 1,905,470 (305)

The photoswitchable cannabinoid azo‐HU308 enables optical control of Ca2+ dynamics in INS‐1 β‐cells via off‐target effects on TRPC channels

open access: yesFEBS Open Bio, EarlyView.
Light activation of the photoswitchable cannabinoid ligand azo‐HU308 triggers Ca2+ influx in pancreatic β‐cells through TRPC channels, independent of CB2 cannabinoid receptors. This reveals a non‐GPCR pathway for cannabinoid modulation of β‐cell Ca2+ dynamics and establishes azo‐HU308 as an optical tool to study cannabinoid signaling through TRP ...
Alexander E. G. Viray, James A. Frank
wiley   +1 more source

Loss of popdc3 Impairs Mitochondrial Function and Causes Skeletal Muscle Atrophy and Reduced Swimming Ability in Zebrafish

open access: yesJournal of Cachexia, Sarcopenia and Muscle
Background The Popeye domain containing 3 (POPDC3) protein is essential for the maintenance of skeletal muscle homeostasis. POPDC3 is a pathogenic variant gene of limb‐girdle muscular dystrophy (LGMD), and its variants lead to LGMDR26.
Chen‐Chen Sun   +7 more
doaj   +1 more source

COP9 signalosome is required for adipose tissue maintenance and metabolic health

open access: yesJournal of Lipid Research
Constitutive photomorphogenesis mutant 9 (COP9) signalosome (CSN) is composed of eight subunits (CSN1 through CSN8). It acts as an essential regulator of Cullin-RING-ubiquitin ligases (CRLs), which target critical cellular regulators for degradation via ...
Hongyi Zhou   +5 more
doaj   +1 more source

Autophagosome marker, LC3, is released extracellularly via several distinct pathways

open access: yesFEBS Open Bio, EarlyView.
This study establishes a novel HiBiT‐tagging system for ultrasensitive detection of LC3, revealing multiple pathways for its extracellular secretion. It demonstrates that LC3 is released via both autophagy‐dependent and ‐independent mechanisms, including a novel route for nonlipidated LC3‐I.
Koki Saito   +3 more
wiley   +1 more source

Rescuing protein homeostasis [PDF]

open access: yesNature Reviews Drug Discovery, 2012
openaire   +1 more source

DDX3X induces mesenchymal transition of endothelial cells by disrupting BMPR2 signaling

open access: yesFEBS Open Bio, EarlyView.
Elevated DDX3X expression led to downregulation of BMPR2, a key regulator of endothelial homeostasis and function. Our co‐immunoprecipitation assays further demonstrated a molecular interaction between DDX3X and BMPR2. Notably, DDX3X promoted lysosomal degradation of BMPR2, thereby impairing its downstream signaling and facilitating endothelial‐to ...
Yu Zhang   +7 more
wiley   +1 more source

Disrupting protein homeostasis [PDF]

open access: yesNature Reviews Drug Discovery, 2015
openaire   +1 more source

Antibiofilm activity of a chionodracine‐derived peptide by NMR‐based metabolomics of cell‐free supernatant of Acinetobacter baumannii clinical strains

open access: yesFEBS Open Bio, EarlyView.
KHS‐Cnd peptide is able to impair biofilm formation and disaggregate mature biofilms in Acinetobacter baumannii clinical isolates. Differences in extracellular metabolites reflect changes in biofilm metabolism due to KHS‐Cnd treatment. Among the differentially represented extracellular metabolites upon KHS‐Cnd treatment, the significantly altered ...
Fernando Porcelli   +9 more
wiley   +1 more source

TMC4 localizes to multiple taste cell types in the mouse taste papillae

open access: yesFEBS Open Bio, EarlyView.
Transmembrane channel‐like 4 (TMC4), a voltage‐dependent chloride channel, plays a critical role in amiloride‐insensitive salty taste transduction. TMC4 is broadly expressed in all mature taste cell types, suggesting a possible involvement of multiple cell types in this pathway.
Momo Murata   +6 more
wiley   +1 more source

Exploring the origins of neurodevelopmental proteasomopathies associated with cardiac malformations: are neural crest cells central to certain pathological mechanisms?

open access: yesFrontiers in Cell and Developmental Biology
Neurodevelopmental proteasomopathies constitute a recently defined class of rare Mendelian disorders, arising from genomic alterations in proteasome-related genes.
Virginie Vignard   +18 more
doaj   +1 more source

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