List of works - Rosine Onclercq-Delic

A balanced pyrimidine pool is required for optimal Chk1 activation to prevent ultrafine anaphase bridge formation.

scientific article published on 6 July 2016

A decrease in NAMPT activity impairs basal PARP-1 activity in cytidine deaminase deficient-cells, independently of NAD

scientific article published on 17 August 2020

A major role for mitotic CDC2 kinase inactivation in the establishment of the mitotic DNA damage checkpoint

scientific article

A role for Tau protein in maintaining ribosomal DNA stability and cytidine deaminase-deficient cell survival

scientific article published on 25 September 2017

BLM Deficiency Is Not Associated with Sensitivity toHydroxyurea‐Induced Replication Stress ⬇️

scientific article published on September 8, 2010

Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase

scientific article

Cytidine Deaminase Deficiency Reveals New Therapeutic Opportunities against Cancer

scientific article published on 6 September 2016

Cytidine deaminase deficiency impairs sister chromatid disjunction by decreasing PARP-1 activity

scientific article

Dephosphorylation and Subcellular Compartment Change of the Mitotic Bloom's Syndrome DNA Helicase in Response to Ionizing Radiation ⬇️

scientific article published on December 10, 2001

Possible anti-recombinogenic role of Bloom's syndrome helicase in double-strand break processing

scientific article

Predisposition to therapy-related acute leukemia with balanced chromosomal translocations does not result from a major constitutive defect in DNA double-strand break end joining

scientific article published on 4 August 2006

Pyrimidine Pool Disequilibrium Induced by a Cytidine Deaminase Deficiency Inhibits PARP-1 Activity, Leading to the Under Replication of DNA.

scientific article published on 16 July 2015

Pyrimidine pool imbalance induced by BLM helicase deficiency contributes to genetic instability in Bloom syndrome ⬇️

scientific article published on June 28, 2011

The Bloom Syndrome Protein Limits the Lethality Associated with RAD51 Deficiency

scientific article published on 09 March 2010

Three new BLM gene mutations associated with Bloom syndrome

scientific article

Topoisomerase IIα prevents ultrafine anaphase bridges by two mechanisms

scientific article published on 13 May 2020

List of works by Rosine Onclercq-Delic

A balanced pyrimidine pool is required for optimal Chk1 activation to prevent ultrafine anaphase bridge formation.

A decrease in NAMPT activity impairs basal PARP-1 activity in cytidine deaminase deficient-cells, independently of NAD

A major role for mitotic CDC2 kinase inactivation in the establishment of the mitotic DNA damage checkpoint

A role for Tau protein in maintaining ribosomal DNA stability and cytidine deaminase-deficient cell survival

BLM Deficiency Is Not Associated with Sensitivity toHydroxyurea‐Induced Replication Stress ⬇️

Bloom's syndrome and PICH helicases cooperate with topoisomerase IIα in centromere disjunction before anaphase

Cytidine Deaminase Deficiency Reveals New Therapeutic Opportunities against Cancer

Cytidine deaminase deficiency impairs sister chromatid disjunction by decreasing PARP-1 activity

Dephosphorylation and Subcellular Compartment Change of the Mitotic Bloom's Syndrome DNA Helicase in Response to Ionizing Radiation ⬇️

Possible anti-recombinogenic role of Bloom's syndrome helicase in double-strand break processing

Predisposition to therapy-related acute leukemia with balanced chromosomal translocations does not result from a major constitutive defect in DNA double-strand break end joining

Pyrimidine Pool Disequilibrium Induced by a Cytidine Deaminase Deficiency Inhibits PARP-1 Activity, Leading to the Under Replication of DNA.

Pyrimidine pool imbalance induced by BLM helicase deficiency contributes to genetic instability in Bloom syndrome ⬇️

The Bloom Syndrome Protein Limits the Lethality Associated with RAD51 Deficiency

Three new BLM gene mutations associated with Bloom syndrome

Topoisomerase IIα prevents ultrafine anaphase bridges by two mechanisms