Results 191 to 200 of about 271,229 (377)

Genome-wide binding of the CRISPR endonuclease Cas9 in mammalian cells

open access: yesNature Biotechnology, 2014
Xuebing Wu   +12 more
semanticscholar   +1 more source

The Redox Activity of Protein Disulphide Isomerase Functions in Non‐Homologous End‐Joining Repair to Prevent DNA Damage

open access: yesAging Cell, EarlyView.
Schematic diagram illustrating the protective role of protein disulphide isomerase (PDI) against DNA damage via non‐homologous end‐joining (NHEJ), which repairs double stranded DNA breaks (DSBs). Induction of DNA damage results in the formation of γH2AX and p53‐binding protein 1 foci during NHEJ repair of DSBs.
Sina Shadfar   +12 more
wiley   +1 more source

Insights Into Cockayne Syndrome Type B: What Underlies Its Pathogenesis?

open access: yesAging Cell, EarlyView.
Cockayne Syndrome complementation group B (CS‐B) is a highly debilitating progeroid syndrome that often culminates in the death of patients before adulthood. This review explores the pathogenesis of CS‐B and proposes that a combination of DNA damage accumulation, transcriptional dysregulation, and mitochondrial dysfunction is its underlying cause ...
Ricardo Afonso‐Reis   +3 more
wiley   +1 more source

Stabilisation of PRCP by deubiquitinase‐targeting chimera (DUBTAC) to replenish autophagy for ameliorating pathological cardiac hypertrophy

open access: yesBritish Journal of Pharmacology, EarlyView.
Background and Purpose Autophagy is essential for cellular homeostasis, and its impairment contributes to cardiac hypertrophy. Modulating autophagy has shown potential in treating pathological hypertrophy. Prolylcarboxypeptidase (PRCP), a lysosomal enzyme that hydrolyzes angiotensin II to Ang1‐7, has an unclear role in cardiac autophagy and hypertrophy.
Fangchao Zhou   +16 more
wiley   +1 more source

Mitochondrial Mutation Leads to Cardiomyocyte Hypertrophy by Disruption of Mitochondria‐Associated ER Membrane

open access: yesCell Proliferation, EarlyView.
Cardiomyocytes with high m.3243A>G burden exhibited hypertrophic phenotype. Mitochondria dysfunction occurred and tended to become round in cardiomyocytes with high m.3243A>G burden. Mitochondria‐associated ER membrane (MAM) was disrupted in cardiomyocytes with high m.3243A>G burden.
Miao Yu   +10 more
wiley   +1 more source

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