Author details

Full Name

Andrew N Blackford

Affiliation

ORCID

Career Start Year

2008

Papers

H Index

Expertise

CM4AI Collaborator

PMID	Paper Title	Journal Title	Published Year
36471053	Targeting DNA damage response pathways in cancer.	Nature Reviews Cancer	2023
36002001	Mitotic DNA synthesis is caused by transcription-replication conflicts in BRCA2-deficient cells.	Mol Cell	2022
35842428	The CIP2A-TOPBP1 complex safeguards chromosomal stability during mitosis.	Nat Commun	2022
33500419	The Bloom syndrome complex senses RPA-coated single-stranded DNA to restart stalled replication forks.	Nature Communications	2021
32001093	How Cells Respond to DNA Breaks in Mitosis.	Trends in Biochemical Sciences	2020
31913317	Treacle controls the nucleolar response to rDNA breaks via TOPBP1 recruitment and ATR activation.	Nature Communications	2020
32375023	CCDC61/VFL3 Is a Paralog of SAS6 and Promotes Ciliary Functions.	Structure	2020
30898438	MDC1 Interacts with TOPBP1 to Maintain Chromosomal Stability during Mitosis.	Molecular Cell	2019
28919440	Structural Insight into BLM Recognition by TopBP1.	Structure	2017
28504702	PGBD5 promotes site-specific oncogenic mutations in human tumors.	Nat Genet	2017
28951624	Erratum: PGBD5 promotes site-specific oncogenic mutations in human tumors.	Nat Genet	2017
28622525	ATM, ATR, and DNA-PK: The Trinity at the Heart of the DNA Damage Response.	Mol Cell	2017
27601299	Specific Roles of XRCC4 Paralogs PAXX and XLF during V(D)J Recombination.	Cell Rep	2016
26595769	TRAIP promotes DNA damage response during genome replication and is mutated in primordial dwarfism.	Nat Genet	2016
27798842	Synthetic lethality between PAXX and XLF in mammalian development.	Genes Dev	2016
26455393	USP4 Auto-Deubiquitylation Promotes Homologous Recombination.	Mol Cell	2015
25794620	TopBP1 interacts with BLM to maintain genome stability but is dispensable for preventing BLM degradation.	Mol Cell	2015
25574025	DNA repair. PAXX, a paralog of XRCC4 and XLF, interacts with Ku to promote DNA double-strand break repair.	Science	2015
25762097	TOPBP1 recruits TOP2A to ultra-fine anaphase bridges to aid in their resolution.	Nature Communications	2015
26166705	BOD1L Is Required to Suppress Deleterious Resection of Stressed Replication Forks.	Mol Cell	2015
22365830	Regulation of DNA-end resection by hnRNPU-like proteins promotes DNA double-strand break signaling and repair.	Mol Cell	2012
22279085	The DNA translocase activity of FANCM protects stalled replication forks.	Human Molecular Genetics	2012
21159879	Serotype-specific inactivation of the cellular DNA damage response during adenovirus infection.	Journal of Virology	2011
21130715	When cleavage is not attractive: non-catalytic inhibition of ubiquitin chains at DNA double-strand breaks by OTUB1.		2011
20057355	ATR activation and replication fork restart are defective in FANCM-deficient cells.	EMBO Journal	2010
20566845	Adenovirus 12 E4orf6 inhibits ATR activation by promoting TOPBP1 degradation.	Proceedings of the National Academy of Sciences of the United States of America	2010
20372056	A novel ATRibute of FANCM.	Cell Cycle	2010
19826003	Mediator of DNA damage checkpoint 1 (MDC1) regulates mitotic progression.	Journal of Biological Chemistry	2009
19211739	Adenovirus E1B 55-kilodalton protein: multiple roles in viral infection and cell transformation.	Journal of Virology	2009
19029952	Adenovirus 5 E1A is responsible for increased expression of insulin receptor substrate 4 in established adenovirus 5-transformed cell lines and interacts with IRS components activating the PI3 kinase/Akt signalling pathway.	Oncogene	2009
18480432	A role for E1B-AP5 in ATR signaling pathways during adenovirus infection.	Journal of Virology	2008