Results 191 to 200 of about 271,229 (377)
The cleavage site of the restriction endonuclease Ava II [PDF]
J. Gregor Sutcliffe, George M. Church
openalex +1 more source
Genome-wide binding of the CRISPR endonuclease Cas9 in mammalian cells
Xuebing Wu+12 more
semanticscholar +1 more source
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
Analysis of Endonuclease R· Eco RI Fragments of DNA from Lambdoid Bacteriophages and Other Viruses by Agarose-Gel Electrophoresis [PDF]
Robert B. Helling+2 more
openalex +1 more source
Insights Into Cockayne Syndrome Type B: What Underlies Its Pathogenesis?
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
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
Properties of the Main Endonuclease Specific for Apurinic Sites of Escherichia coli (Endonuclease VI) [PDF]
Françis Gossard, Walter G. Verly
openalex +1 more source
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