Results 101 to 110 of about 1,037,544 (299)

DNA and RNA base editors can correct the majority of pathogenic single nucleotide variants

open access: yesnpj Genomic Medicine
The majority of human genetic diseases are caused by single nucleotide variants (SNVs) in the genome sequence. Excitingly, new genomic techniques known as base editing have opened efficient pathways to correct erroneous nucleotides.
Ariel Dadush   +8 more
doaj   +1 more source

Gut microbiome and aging—A dynamic interplay of microbes, metabolites, and the immune system

open access: yesFEBS Letters, EarlyView.
Age‐dependent shifts in microbial communities engender shifts in microbial metabolite profiles. These in turn drive shifts in barrier surface permeability of the gut and brain and induce immune activation. When paired with preexisting age‐related chronic inflammation this increases the risk of neuroinflammation and neurodegenerative diseases.
Aaron Mehl, Eran Blacher
wiley   +1 more source

Diversity and complexity in neural organoids

open access: yesFEBS Letters, EarlyView.
Neural organoid research aims to expand genetic diversity on one side and increase tissue complexity on the other. Chimeroids integrate multiple donor genomes within single organoids. Self‐organising multi‐identity organoids, exogenous cell seeding, or enforced assembly of region‐specific organoids contribute to tissue complexity.
Ilaria Chiaradia, Madeline A. Lancaster
wiley   +1 more source

Hyperosmotic stress induces PARP1‐mediated HPF1‐dependent mono(ADP‐ribosyl)ation

open access: yesFEBS Letters, EarlyView.
Sorbitol‐induced hyperosmotic stress rapidly induces reversible mono(ADP‐ribosyl)ation (MARylation) on PARP1 without the signs of genotoxic signaling. We show that PARP1 autoMARylation is HPF1 dependent and forms hydroxylamine‐resistant O‐glycosidic linkages.
Anna Georgina Kopasz   +11 more
wiley   +1 more source

Machine learning research 1989-90 [PDF]

open access: yes
Multifunctional knowledge bases offer a significant advance in artificial intelligence because they can support numerous expert tasks within a domain. As a result they amortize the costs of building a knowledge base over multiple expert systems and they ...
Porter, Bruce W., Souther, Arthur
core   +1 more source

An improved SNAP-ADAR tool enables efficient RNA base editing to interfere with post-translational protein modification

open access: yesNature Communications
RNA base editing relies on the introduction of adenosine-to-inosine changes into target RNAs in a highly programmable manner in order to repair disease-causing mutations.
Karthika Devi Kiran Kumar   +14 more
doaj   +1 more source

Linking neurogenesis, oligodendrogenesis, and myelination defects to neurodevelopmental disruption in primary mitochondrial disorders

open access: yesFEBS Letters, EarlyView.
Mitochondrial remodeling shapes neural and glial lineage progression by matching metabolic supply with demand. Elevated OXPHOS supports differentiation and myelin formation, while myelin compaction lowers mitochondrial dependence, revealing mitochondria as key drivers of developmental energy adaptation.
Sahitya Ranjan Biswas   +3 more
wiley   +1 more source

Targeted gene modification in Fragaria vesca mediated by CRISPR/Cas9 system [PDF]

open access: yes, 2016
Genome editing is becoming an important biotechnological tool for gene function analysis and crop improvement, being the CRISPR-Cas9 (Clustered Regularly Interspaced Short Palindromic Repeat-CRISPR associated protein 9) system the most widely used.
Martín-Pizarro, Carmen, Posé, David
core  

Breaking genetic shackles: The advance of base editing in genetic disorder treatment

open access: yesFrontiers in Pharmacology
The rapid evolution of gene editing technology has markedly improved the outlook for treating genetic diseases. Base editing, recognized as an exceptionally precise genetic modification tool, is emerging as a focus in the realm of genetic disease therapy.
Fang Xu   +13 more
doaj   +1 more source

An isoform of 14‐3‐3 protein regulates transbilayer lipid movement at the plasma membrane

open access: yesFEBS Letters, EarlyView.
Loss of 14‐3‐3ζ in CHO cells confers resistance to exogenous phosphatidylserine (PS) and impairs endocytosis‐independent inward flip‐flop of fluorescent PS at the plasma membrane. RNAi‐mediated knockdown reproduces this defect, while no additive effect is seen in ATP11C‐deficient cells.
Akiko Yamaji‐Hasegawa   +3 more
wiley   +1 more source

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