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Brian Luke

Name	Brian Luke
Ort	Heidelberg (Wirkungsort) Deutschland
Akademischer Grad bzw. Titel	Dr.
Beziehung	Universität Heidelberg. Zentrum für Molekulare Biologie Johannes Gutenberg-Universität Mainz. Institut für Organismische und Molekulare Evolutionsbiologie
Weitere Angaben	Group Leader in the DKFZ-ZMBH Alliance, Luke Lab
Datensatztyp	Person
GND-Nummer	1043325530
Datensatz-ID	1043325530
Beteiligt an alle anzeigen Genetic requirements for repair of lesions caused by single genomic ribonucleotides in S phase Towards a mechanistic understanding of R-Loop regulation and function at telomeres Metabolic remodeling maintains a reducing environment for rapid activation of the yeast DNA replication checkpoint Molecular and physiological consequences of faulty eukaryotic ribonucleotide excision repair Npl3 stabilizes R‐loops at telomeres to prevent accelerated replicative senescence Molecular and physiological consequences of faulty eukaryotic ribonucleotide excision repair Npl3 stabilizes R-loops at telomeres to prevent accelerated replicative senescence A novel autosomal recessive TERT T1129P mutation in a dyskeratosis congenita family leads to cellular senescence and loss of CD34+ hematopoietic stem cells not reversible by mTOR-inhibition

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Brian Luke

Genetic requirements for repair of lesions caused by single genomic ribonucleotides in S phase

Towards a mechanistic understanding of R-Loop regulation and function at telomeres

Metabolic remodeling maintains a reducing environment for rapid activation of the yeast DNA replication checkpoint

Molecular and physiological consequences of faulty eukaryotic ribonucleotide excision repair

Npl3 stabilizes R‐loops at telomeres to prevent accelerated replicative senescence

Molecular and physiological consequences of faulty eukaryotic ribonucleotide excision repair

Npl3 stabilizes R-loops at telomeres to prevent accelerated replicative senescence

A novel autosomal recessive TERT T1129P mutation in a dyskeratosis congenita family leads to cellular senescence and loss of CD34+ hematopoietic stem cells not reversible by mTOR-inhibition