about
A role for oxidized DNA precursors in Huntington's disease-like striatal neurodegenerationCancer Stem Cell-Based Models of Colorectal Cancer Reveal Molecular Determinants of Therapy Resistance.The Mutyh base excision repair gene influences the inflammatory response in a mouse model of ulcerative colitis.Proliferation of Multiple Cell Types in the Skeletal Muscle Tissue Elicited by Acute p21 Suppression.UCN-01 enhances cytotoxicity of irinotecan in colorectal cancer stem-like cells by impairing DNA damage response.Critical requirement for cell cycle inhibitors in sustaining nonproliferative states.CHK1-targeted therapy to deplete DNA replication-stressed, p53-deficient, hyperdiploid colorectal cancer stem cells.Different DNA repair strategies to combat the threat from 8-oxoguanine.hMTH1 expression protects mitochondria from Huntington's disease-like impairment.The fine tuning of metabolism, autophagy and differentiation during in vitro myogenesis.The MUTYH base excision repair gene protects against inflammation-associated colorectal carcinogenesisMUTYH mediates the toxicity of combined DNA 6-thioguanine and UVA radiation.Role of MUTYH and MSH2 in the control of oxidative DNA damage, genetic instability, and tumorigenesis.Platelet-derived growth factor receptor beta-subtype regulates proliferation and migration of gonocytes.Establishment of patient-derived renal cell carcinoma (RCC) models based on orthotopic xenografts (PDX) and cancer stem cell (CSC) isolation to provide prognostic and predictive informationMutT homolog-1 attenuates oxidative DNA damage and delays photoreceptor cell death in inherited retinal degeneration
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description
researcher ORCID ID = 0000-0003-2918-0124
@en
wetenschapper
@nl
name
Gabriele De Luca
@ast
Gabriele De Luca
@en
Gabriele De Luca
@nl
type
label
Gabriele De Luca
@ast
Gabriele De Luca
@en
Gabriele De Luca
@nl
prefLabel
Gabriele De Luca
@ast
Gabriele De Luca
@en
Gabriele De Luca
@nl
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P31
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0000-0003-2918-0124