Results 101 to 110 of about 341,882 (288)
An activity‐dependent pathway links prefrontal circuit hypoactivity to cognitive impairment. Reduced PVA–mPFC activity upregulates NEPAS, which suppresses PTX3 secretion, leading to impaired angiogenesis, myelin deficits, and memory decline. Rescue is achieved by NEPAS knockdown or chemogenetic circuit activation.
Boya Hu +11 more
wiley +1 more source
While yeast Rap1 regulates telomere length and protects telomeres from non-homologous end joining, its role in higher eukaryotes is controversial.
Rekha Rai +3 more
doaj +1 more source
This study focused on concatemer formation and integration pattern of transgenes in zebrafish embryos. A reporter plasmid based on enhanced green fluorescent protein (eGFP) driven by Cytomegalovirus (CMV) promoter, pCMV-pax6in-eGFP, was constructed to ...
huwei@ihb.ac.cn +5 more
core
This study elucidates that β‐elemene promotes cellular uptake of L. gasseri‐derived lactate by enhancing the membrane translocation of MCT1 in a CD147‐dependent manner. Intracellular lactate, through the lactylation of RBBP4 at the K26 site, recruits EP300 to the promoter regions of downstream genes (POLD1/POLD3), catalyzing H3K27ac modification.
Jiancheng He +10 more
wiley +1 more source
Reprogramming and genome integrity: role of non-homologous end joining [PDF]
The study by Tilgner et al.1 investigates the role of non-homologous end joining (NHEJ) in reprogramming of human somatic cells to induced pluripotent stem cells and in regulation of their differentiation. NHEJ is the major double-strand break (DSB) repair pathway in mammalian cells.2 It is a highly coordinated process relying on a number of essential ...
openaire +2 more sources
MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining. Hung et al.
These are the original data files for the Molecular Cell manuscript titled "MRI is a DNA Damage Response Adaptor during Classical Non-Homologous End Joining" by Hung et al.
Sleckman, B (via Mendeley Data)
core +1 more source
DNA Replication Errors Drive Genome‐Wide Small Inverted Triplication Dynamics
This study provides insight into the dynamic equilibrium mechanism of a novel structural variant, small inverted triplication (SIT), which is generated by misalignment of the 3’ flap generated under DNA replication stress with palindromic sequence. Alternatively, the end sequence may fold back on itself to form an inverted fragment.
Yi Lei +12 more
wiley +1 more source
Targeting Supramolecular Active Complexes of Nav1.7/Nav1.8 to Relieve Chronic Neuropathic Pain
In mice and patients with severe chronic neuropathic pain (NP), Nav1.7, Nav1.8, TrkB, and five cytoskeletal proteins form supramolecular active complexes (SMACs) with polygonal lattice structures as noxious signal amplifiers in dorsal root ganglion (DRG) neurons.
Liting Sun +27 more
wiley +1 more source
This study identifies SNRPF as a critical oncogenic driver in ovarian cancer. By regulating a self‐sustaining SNRPF–DDX24–E2F4 feedback loop through intron retention and nonsense‐mediated decay, SNRPF couples RNA splicing with transcriptional regulation to promote tumor progression.
Yingwei Li +4 more
wiley +1 more source
Molecular, genetic, virological, and biochemical analysis in combination with global proteome and phosphoproteome profiling and functional assays were applied to study the role of PR130 in the context of HSV‐1 replication. The observations reveal that host‐intrinsic mechanisms regulate HSV‐1 replication and highlight PR130 as a susceptibility factor of
Johannes Jungwirth +10 more
wiley +1 more source

