Results 111 to 120 of about 65,433 (290)
Modulating extracellular matrix (ECM) elasticity with fibrillar collagen offers great potential for regenerative medicine, drug discovery, and disease modeling by replicating in vivo mechanical signals.
A. Hamraoui, O. Sénépart, L. Belliard
doaj +1 more source
Hyperosmotic stress triggers the relocation of the CFIm complex from the nucleus to the cytoplasm. This shift creates a nuclear ‘stoichiometric bottleneck’, limiting CFIm availability for mRNA processing. Consequently, specific mRNAs like NUDT21 and DICER1 undergo targeted 3′UTR shortening, demonstrating how spatial protein dynamics drive rapid ...
Hitomi Soumiya +2 more
wiley +1 more source
Loss of AMBRA1 activates MAPK and angiogenesis signaling pathways in melanoma cells
Loss of AMBRA1 in melanoma cells activates multiple oncogenic pathways associated with tumor progression. Transcriptomic and protein network analyses revealed that AMBRA1 depletion enhances MAPK/ERK signaling, angiogenesis, TGF‐β/EMT signaling, and Wnt/axon guidance pathways.
Milad Ibrahim +4 more
wiley +1 more source
IGFBP4 knockdown (KD) impairs preadipocyte proliferation and is associated with IGF1R protein downregulation and attenuated AKT phosphorylation. The mechanisms by which IGFBP4 KD influences the IGF1R/AKT signaling pathway involve newly synthesized proteins and lysosomal degradation pathways. Created in BioRender.
Yujia Guo +6 more
wiley +1 more source
The cytoskeleton‐mediated transport of mitochondria via tunnelling nanotubes restores respiration, increases ATP production, rescues cells from apoptosis, activates the AKT/mTOR signalling pathway, promotes cell migration and invasiveness, contributes to cancer progression and treatment resistance.
Stanislava Martínková, Jan Trnka
wiley +1 more source
Malformin A1–mediated cytotoxicity in ovarian cancer cells occurs through pyroptosis and autophagy
This study investigated the effects of the natural compound Malformin A1 (MA1) on the cytoskeleton that regulates cell proliferation and migration. Disruption of the cytoskeleton can impair these processes and promote cancer cell death. MA1 disrupted cytoskeletal organization, induced DNA damage, inflammation, activated autophagy, and pyroptosis ...
Nada Abdullah Hassan +11 more
wiley +1 more source
Ionomycin suppresses cancer cell growth by disrupting mitochondrial transcription
In this study, we identify a new function for the selective Ca2+ ionophore, ionomycin, as an inhibitor of mitochondrial transcription. Both total and nascent RNA analyses revealed that ionomycin treatment reduces the transcription of mitochondrial genes.
Lishen Wang +10 more
wiley +1 more source
ATZ‐1 promotes DNA replication efficiency to maintain normal meiotic function
Absence of ATZ‐1 interferes with meiotic DNA replication and cell cycle function via CHK‐1. This causes downstream defects associated with DNA damage and genomic integrity. Taken together, this study suggests that ATZ‐1 influences DNA replication efficiency and cell cycle function to maintain normal meiotic function.
Taylin E. Gourley +5 more
wiley +1 more source
In silico and in vitro exploration of a tyrosinase for biocatalytic production of catechols
Tyrosinase from Ralstonia pseudosolanacearum is a promising biocatalyst for producing valuable catechols from monophenol substrates. This tyrosinase is uniquely suited to this due to its high monophenolase : diphenolase ratio. We combined in silico docking and in vivo kinetic characterisation of this tyrosinase with 11 industrially relevant monophenols,
James Britton +6 more
wiley +1 more source
Adenosine triphosphate as a modulator of protein interactions and stability
ATP is best known as the cell's energy currency, but it also shapes how proteins fold, interact, aggregate and form biomolecular condensates. This review explains the emerging physical principles behind these effects, including weak binding to charged protein regions, magnesium‐dependent behaviour and concentration‐dependent control of protein ...
Shuyuan Tan, Robin Curtis
wiley +1 more source

