Affinage

Showing RBBP8 — CTIP is a alias.

RBBP8

DNA endonuclease RBBP8 · UniProt Q99708

Audit flag: ungrounded claim
Length
897 aa
Mass
101.9 kDa
Annotated
2026-06-10
100 papers in source corpus 64 papers cited in narrative 62 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 11/11 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

RBBP8 (CtIP) is a nuclear DNA double-strand break (DSB) repair factor that governs repair pathway choice by initiating and controlling end resection in S/G2 phase (PMID:17965729, PMID:19357644). It is recruited to DSBs in a manner dependent on the MRN complex, ATM kinase activity, and a direct DNA-binding motif, where it promotes the transition from break sensing to resection (PMID:17965729, PMID:20064462). Mechanistically, phosphorylated CtIP acts as a co-factor of the MRE11 endonuclease within MRN to catalyze 5'-strand incision near protein-blocked DSB ends, a function requiring CtIP phosphorylation at Thr-847 and NBS1, which senses CtIP phosphorylation through its FHA/BRCT domains to activate MRE11-RAD50 (PMID:27889449, PMID:30787182); CtIP additionally possesses intrinsic endonuclease activity required for processing topoisomerase adducts, common fragile sites, and secondary-structure-containing ends (PMID:24837676, PMID:24837675). Beyond short-range incision, CtIP drives long-range resection by stimulating both BLM helicase activity and the ATP-driven motor of DNA2 (PMID:32241893, PMID:29020620). CtIP function is gated by cell-cycle and damage signaling: CDK phosphorylation at Thr-847 is essential for resection and induces interaction with NBS1, while phospho-Ser327 nucleates a structurally defined interaction with the BRCA1 BRCT domains that accelerates resection and is specifically required for removing protein adducts at complex ends (PMID:16101277, PMID:19202191, PMID:23468639, PMID:25310973, PMID:24842372, PMID:20107609, PMID:26880199). CtIP assembles a homotetramer through a 'dimer-of-dimers' architecture and dimerizes via an N-terminal coiled-coil, an oligomeric state essential for DSB localization, resection, and DNA bridging (PMID:25558984, PMID:15084581, PMID:22544744, PMID:32417418). The BRCA1-CtIP axis directs S/G2 cells toward error-free homologous recombination by antagonizing RIF1, whereas CtIP-driven resection also generates microhomology for alternative NHEJ, mediating chromosomal translocations and class-switch recombination (PMID:19357644, PMID:23333306, PMID:21131978, PMID:21131982). CtIP abundance and chromatin retention are tightly controlled by an elaborate post-translational network including APC/C(Cdh1)- and Cullin3-KLHL15-mediated degradation, opposing deubiquitinases USP4 and USP52, and SUMOylation by CBX4 and PIAS4 coupled to RNF4-dependent turnover (PMID:25349192, PMID:27561354, PMID:28740167, PMID:33723063, PMID:26387952, PMID:33097710). Independently of DSB resection, CtIP protects reversed stalled replication forks from DNA2-mediated degradation in cooperation with BRCA1 (PMID:30344097, PMID:32379725). Outside DNA repair, CtIP functions as a transcriptional co-repressor in complexes with BRCA1, CtBP, Rb, ZBRK1, Ikaros, SHARP, and LMO4, and counteracts Rb-mediated G1 restraint to promote the G1/S transition (PMID:15831459, PMID:16581787, PMID:10196224, PMID:16287852, PMID:11751867, PMID:16843262, PMID:11959865). Truncating mutations in RBBP8 cause Seckel syndrome (SCKL2) and Jawad syndrome, with patient cells showing defective damage-induced ssDNA formation and reduced ATR activation (PMID:21998596).

Mechanistic history

Synthesis pass · year-by-year structured walk · 17 steps
  1. 1998 High

    Established CtIP as a physical partner of the BRCA1 BRCT domains, linking it to BRCA1 tumor suppressor function before its repair role was known.

    Evidence Yeast two-hybrid and in vivo interaction assay with tumor-associated BRCT mutants

    PMID:9738006

    Open questions at the time
    • Functional consequence of the interaction not defined
    • Phosphorylation-dependence not yet established
  2. 2000 Medium

    Defined CtIP as a cell-cycle-regulated nuclear protein whose levels rise at G1/S and that exists in a BRCA1-BARD1 complex, placing it at the proliferation/repair interface.

    Evidence Subcellular fractionation, Co-IP, and cell-cycle synchronization

    PMID:10764811

    Open questions at the time
    • Mechanism of post-transcriptional regulation unresolved
    • Single lab
  3. 2002 Medium

    Showed CtIP acts as a transcriptional co-repressor beyond BRCA1, contributing to Ikaros-mediated repression via its Rb interaction domain independent of HDACs.

    Evidence Co-IP, reporter assays, HDAC inhibitor treatment, domain mutants

    PMID:11959865

    Open questions at the time
    • Target gene programs not mapped
    • Relationship to repair role unclear
  4. 2005 High

    Defined the phospho-Ser327-dependent CtIP-BRCA1 BRCT interaction at atomic resolution and linked CtIP to the G2/M checkpoint, providing the structural basis for the interaction and explaining cancer-associated BRCA1 mutations.

    Evidence X-ray crystallography (2.5 Å), ITC, mutant analysis, Co-IP, and cell-cycle/checkpoint assays

    PMID:15485915 PMID:16101277

    Open questions at the time
    • Functional output of the interaction in resection not yet dissected
    • Kinase responsible for S327 not identified
  5. 2005 High

    Demonstrated CtIP is essential for embryonic viability and counteracts Rb-mediated G1 restraint, establishing a non-repair role in cell-cycle control.

    Evidence Mouse gene knockout and Rb genetic epistasis in MEFs/Saos-2

    PMID:15831459

    Open questions at the time
    • Molecular mechanism of Rb antagonism partly inferred
    • Does not separate repair from proliferative functions
  6. 2007 High

    Identified CtIP as the human factor required for S/G2-restricted DSB resection acting with the MRN complex, establishing its central role in repair pathway choice.

    Evidence siRNA depletion, laser micro-irradiation, Co-IP, and cell-cycle fractionation

    PMID:17965729

    Open questions at the time
    • Direct enzymatic contribution to resection not yet defined
    • Recruitment mechanism not fully mapped
  7. 2009 High

    Resolved how cell-cycle and damage signaling gate CtIP, showing CDK phosphorylation at Thr-847 enables resection/HR while phospho-S327/BRCA1 acts as a switch between G1 end-joining and S/G2 HR.

    Evidence Site-directed mutagenesis, CDK inhibition, DT40 gene targeting, RPA foci and repair pathway assays

    PMID:19202191 PMID:19357644

    Open questions at the time
    • Direct biochemical activity of phospho-CtIP not yet reconstituted
    • Full kinase circuitry incomplete
  8. 2010 High

    Established CtIP as a driver of microhomology-mediated alternative end-joining, including chromosomal translocations and class-switch recombination.

    Evidence Translocation and CSR reporter assays with siRNA/shRNA depletion and junction sequencing

    PMID:21131978 PMID:21131982

    Open questions at the time
    • Distinction between resection-dependent and -independent contributions to alt-NHEJ not fully resolved
  9. 2014 High

    Revealed CtIP carries intrinsic, MRN-independent endonuclease activity dedicated to processing protein adducts and structured DNA ends.

    Evidence Recombinant protein purification, in vitro endonuclease assays, separation-of-function nuclease mutants, cell-based assays

    PMID:24837675 PMID:24837676

    Open questions at the time
    • Relationship between intrinsic and MRN-cofactor nuclease activities debated
    • Substrate specificity in vivo incompletely mapped
  10. 2015 High

    Defined the homotetrameric 'dimer-of-dimers' architecture of CtIP as essential for DSB localization and resection.

    Evidence X-ray crystallography, SEC-MALS/AUC, mutagenesis, and HR reporter assays

    PMID:25558984

    Open questions at the time
    • How oligomeric state mechanistically couples to nuclease stimulation not fully resolved
  11. 2016 High

    Reconstituted phospho-CtIP as a direct co-factor of the MRE11 endonuclease within MRN that incises 5'-terminated strands, providing the biochemical basis for resection initiation.

    Evidence Reconstituted in vitro nuclease assays with purified human proteins and phospho-site mutagenesis

    PMID:27889449

    Open questions at the time
    • Structural mechanism of MRE11 activation not resolved here
    • Role of NBS1 sensing addressed later
  12. 2017 Medium

    Extended CtIP function to long-range resection by showing it interacts with and stimulates BLM helicase and enhances DNA2 cleavage.

    Evidence Co-IP and in vitro helicase/nuclease assays with purified proteins

    PMID:29020620

    Open questions at the time
    • Single lab
    • Domain requirements detailed in later DNA2 work
  13. 2018 High

    Identified a resection-independent role for CtIP in protecting reversed stalled replication forks from DNA2-mediated degradation in cooperation with BRCA1.

    Evidence DNA fiber assays with CtIP depletion, DNA2/MRE11 inhibition, and genetic epistasis

    PMID:30344097

    Open questions at the time
    • Molecular mechanism of fork protection partly defined
    • Separation from RAD51 nucleofilament stabilization role clarified later
  14. 2019 High

    Clarified that NBS1 senses CtIP phosphorylation via FHA/BRCT domains to activate MRE11-RAD50, distinguishing phosphorylation-dependent and -independent modes of MRE11 stimulation.

    Evidence Reconstituted in vitro nuclease assays with NBS1 domain mutants

    PMID:30787182

    Open questions at the time
    • Structural detail of the NBS1-CtIP-MRE11 activated state not resolved
  15. 2020 High

    Mapped distinct CtIP domains for DNA bridging, DNA2 motor stimulation, and showed DNA-PK promotes the MRN-phospho-CtIP transition from NHEJ to HR.

    Evidence Single-molecule nanofluidic bridging, reconstituted DNA2 ATPase/curtain assays, single-molecule and cellular DNA-PK processing assays

    PMID:31934630 PMID:32241893 PMID:32417418

    Open questions at the time
    • In vivo coordination of bridging, nuclease, and motor-stimulatory activities not fully integrated
  16. 2021 Medium

    Detailed the layered PTM network controlling CtIP abundance and chromatin retention, including KLHL15/Cullin3 and APC/C(Cdh1) degradation, CBX4 and PIAS4-RNF4 SUMO-coupled turnover, and opposing deubiquitinases USP4/USP52.

    Evidence Co-IP, ubiquitination/SUMOylation/deubiquitination assays, site-specific mutagenesis, and resection/HR readouts across multiple studies

    PMID:25349192 PMID:26387952 PMID:27561354 PMID:28740167 PMID:33097710 PMID:33723063

    Open questions at the time
    • Hierarchy and crosstalk among PTM events incompletely ordered
    • Several findings from single labs
  17. 2011 High

    Linked RBBP8 to human disease, establishing truncating mutations as causative of Seckel and Jawad syndromes through defective ssDNA formation and ATR activation.

    Evidence Patient-derived cell lines with ssDNA/BrdU and ATR signaling assays and dominant-negative mutant overexpression

    PMID:21998596

    Open questions at the time
    • Genotype-phenotype relationships for the two syndromes not fully resolved

Open questions

Synthesis pass · forward-looking unresolved questions
  • How CtIP's multiple separable activities — short-range nuclease cofactor, long-range resection stimulation, DNA bridging, fork protection, and transcriptional co-repression — are coordinated within a single regulatory architecture in vivo remains unresolved.
  • No unified structural model integrating oligomerization, nuclease, and bridging domains
  • Spatiotemporal switching among functions not defined
  • Quantitative contribution of transcriptional roles to physiology unclear

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0140110 transcription regulator activity 6 GO:0098772 molecular function regulator activity 4 GO:0140097 catalytic activity, acting on DNA 4 GO:0003677 DNA binding 2 GO:0060090 molecular adaptor activity 2
Localization
GO:0000228 nuclear chromosome 3 GO:0005634 nucleus 2
Pathway
R-HSA-73894 DNA Repair 4 R-HSA-1640170 Cell Cycle 3 R-HSA-74160 Gene expression (Transcription) 3 R-HSA-69306 DNA Replication 2
Partners
BLMBRCA1DNA2EXO1FANCD2KLHL15MRE11NBS1
Complex memberships
BRCA1-CtIP-MRN complexBRCA1-CtIP-ZBRK1 repressor complexLMO4-BRCA1-CtIP-Ldb1 complexMRN (MRE11-RAD50-NBS1) complex (as phospho-CtIP cofactor)

Evidence

Reading pass · 62 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2007 Human CtIP (RBBP8) is required for DNA double-strand break (DSB) resection in S and G2 phases, is recruited to DSBs exclusively in S/G2, physically and functionally interacts with the MRE11 complex, and is required for RPA and ATR recruitment and ATR activation following DSBs. CtIP shares sequence homology with yeast Sae2. siRNA depletion, laser micro-irradiation, co-immunoprecipitation, immunofluorescence, cell-cycle fractionation Nature High 17965729
1998 The BRCT domains of BRCA1 interact in vivo with CtIP; tumor-associated mutations in the BRCT motifs ablate this interaction. Sos recruitment yeast two-hybrid system, in vivo interaction assay The Journal of biological chemistry High 9738006
2004 CtIP interacts with BRCA1 BRCT domains in a phosphorylation-dependent manner (phospho-Ser327); the CtIP/BRCA1 complex exists specifically in G2 phase and is required for DNA damage-induced Chk1 phosphorylation and the G2/M checkpoint. Co-immunoprecipitation, cell cycle synchronization, phosphorylation assays, siRNA depletion Molecular and cellular biology High 15485915
2005 Crystal structure of BRCA1 BRCT repeats bound to CtIP phosphopeptide (residues 322–333, phospho-Ser327) at 2.5 Å resolution; Phe330 and phospho-Ser327 anchor the peptide; the cancer-associated BRCA1 M1775R mutation sterically clashes with CtIP Phe330, disrupting the interaction. X-ray crystallography, isothermal titration calorimetry Biochemistry High 16101277
2006 BRCA1 RING domain catalyzes CtIP ubiquitination in a manner dependent on phosphorylation-mediated CtIP–BRCA1 BRCT interaction; this ubiquitination does not target CtIP for proteasomal degradation but instead promotes chromatin association of CtIP after DNA damage and participation in G2/M checkpoint control. In vitro ubiquitination assay, co-immunoprecipitation, chromatin fractionation, cell cycle checkpoint assays Genes & development High 16818604
2009 CDK-mediated phosphorylation of CtIP at Thr-847 is required for DSB resection and homologous recombination; phospho-mimetic T847E allows resection even after CDK inhibition, while T847A impairs resection. Mutating Ser-327 specifically abolishes BRCA1 interaction and HR but not MMEJ. Site-directed mutagenesis, CDK inhibitor treatment, RPA focus formation assay, chromosomal rearrangement assays The Journal of biological chemistry High 19202191
2009 CtIP-S327 phosphorylation and BRCA1 recruitment acts as a molecular switch directing DSB repair from error-prone end-joining (MMEJ) in G1 to error-free HR in S/G2; CtIP-S327A cells are specifically defective in HR but not MMEJ. DT40 gene targeting, site-directed mutagenesis, single-stranded DNA assays, repair pathway assays Nature High 19357644
2009 CtIP translocation to DSBs depends on the MRN complex, ATM kinase activity, and a direct DNA-binding motif in CtIP; CtIP promotes the transition from DSB sensing to resection downstream of ATM activation. Xenopus egg extracts, laser-induced DSBs in human cells, ATM inhibition, direct DNA-binding assay Molecular cell High 20064462
2008 BRCA1 forms a cell cycle-dependent complex with CtIP and MRN; complex formation (especially IR-enhanced BRCA1–MRN association) requires CDK activity; CtIP directly interacts with Nbs1; the complex is critical for ssDNA formation and HR. Co-immunoprecipitation, CDK inhibition, IR treatment, ssDNA/BrdU assay The Journal of biological chemistry High 18171670
2016 Phosphorylated CtIP acts as a co-factor of MRE11 endonuclease within the MRN complex; this function absolutely requires CtIP phosphorylation at Thr-847 and NBS1; the MRN–phospho-CtIP complex preferentially cleaves 5'-terminated DNA strands near DSBs to initiate resection. Reconstituted in vitro nuclease assay with recombinant human proteins, phosphorylation-site mutagenesis Molecular cell High 27889449
2014 Human CtIP has intrinsic 5' flap endonuclease activity on branched DNA, independent of MRN; phosphorylation at damage-dependent sites (not S327/T847) is essential for catalytic activity; catalytic mutant CtIP is deficient in processing topoisomerase adducts and radiation-induced breaks but not endonuclease-generated breaks. Recombinant protein purification, in vitro endonuclease assay, phosphorylation-site mutagenesis, cell-based repair assays Molecular cell High 24837676
2015 X-ray crystallography and biophysical analyses show that the N-terminal domain of human CtIP forms a stable homotetramer via a 'dimer-of-dimers' architecture; a point mutation abolishing tetramerization (but preserving dimerization) causes strong defects in DNA-end resection and gene conversion in cells. X-ray crystallography, biophysical (SEC-MALS, AUC), site-directed mutagenesis, HR reporter assays Nature structural & molecular biology High 25558984
2010 SIRT6 deacetylates CtIP to promote DNA end resection; a non-acetylatable CtIP mutant alleviates the resection defect caused by SIRT6 depletion. NOTE: this paper was subsequently retracted. Co-immunoprecipitation, site-directed mutagenesis, RPA/ssDNA focus assays (RETRACTED paper) Science Low 20829486
2012 ATR phosphorylates CtIP at T818 (Xenopus; T859 in human) in response to DSBs; non-phosphorylatable CtIP (T818A) fails to bind chromatin or initiate resection; ATM activity is required for an early resection step leading to ATR activation and CtIP-T818 phosphorylation. Xenopus egg extract system, mass spectrometry, chromatin binding assay, phospho-specific antibodies, mutagenesis Molecular cell High 23273981
2013 CDK phosphorylation of CtIP induces its interaction with the FHA and BRCT domains of Nbs1; CDK-dependent CtIP–Nbs1 interaction is a prerequisite for ATM to phosphorylate CtIP upon DNA damage, promoting BLM and Exo1 recruitment and HR. Phosphopeptide pull-down, co-immunoprecipitation, phosphorylation assays, siRNA depletion, HR reporter PLoS genetics High 23468639
2012 Mre11 controls CDK2-dependent CtIP phosphorylation and BRCA1 interaction through a direct Mre11–CDK2 interaction at the Mre11 C-terminus; this function does not require ATM activation or Mre11 nuclease activity. Co-immunoprecipitation, kinase assay, mutagenesis, mouse genetic model Nature structural & molecular biology Medium 22231403
2013 BRCA1 and its partner CtIP antagonize RIF1 accumulation at DSBs; depletion of CtIP or BRCA1 permits RIF1 to accumulate and suppress end resection in S/G2 phase; this circuit controls repair pathway choice. siRNA depletion, immunofluorescence, RPA/ssDNA assay, RAD51 loading assay Molecular cell High 23333306
2014 BRCA1–CtIP interaction (via phospho-S327) accelerates the speed of DNA-end resection but is not essential for resection per se; T847 phosphorylation is essential for resection; CtIP functions independently of BRCA1 for basic resection. High-resolution resection assay, mouse knock-in models (S327A, T847A), B-cell conditional KO Cell reports / The Journal of experimental medicine High 24842372 25310973
2000 CtIP is a predominantly nuclear protein; its steady-state levels are low in G1 and increase sharply at the G1/S boundary via post-transcriptional regulation; a subset of CtIP exists in a complex with BRCA1 and BARD1. Subcellular fractionation, immunoprecipitation, cell cycle synchronization, Western blotting The Journal of biological chemistry Medium 10764811
2005 Homozygous CtIP inactivation in mice causes embryonic lethality at E4.0 with G1 arrest; G1 arrest in CtIP-depleted NIH 3T3 cells is RB-dependent; CtIP counteracts Rb-mediated G1 restraint. Mouse gene targeting (knock-out), cell cycle analysis, Rb genetic epistasis (Rb-/- MEFs, Saos-2) Molecular and cellular biology High 15831459
2006 CtIP activates its own promoter and cyclin D1 promoter via the E2F/RB pathway during late G1/S; chromatin immunoprecipitation shows CtIP recruitment to its promoter coincides with TFIIB recruitment and Rb dissociation; CtIP-E157K (unable to bind Rb) fails to transactivate. ChIP, promoter reporter assays, site-directed mutagenesis (E157K), cell cycle synchronization Molecular and cellular biology Medium 16581787
1999 CtIP interacts specifically with BRCA1 BRCT repeats both in vitro and in vivo; this interaction is abrogated by DNA-damaging agents (UV, γ-irradiation, adriamycin) correlating with BRCA1 phosphorylation; CtIP and CtBP diminish BRCA1-mediated p21 transactivation. Yeast two-hybrid, GST pull-down (in vitro), co-immunoprecipitation (in vivo), transcriptional reporter assay The Journal of biological chemistry High 10196224
2004 CtIP homodimerizes via an N-terminal coiled-coil domain (residues 45–160); this domain forms a compact helical structure; the N-terminal coiled-coil does not mediate binding to LMO4 or BRCA1. Co-immunoprecipitation in 293T cells, circular dichroism, analytical ultracentrifugation, MALDI-TOF The Journal of biological chemistry Medium 15084581
2012 CtIP dimerization via a conserved N-terminal motif is required for its recruitment to DSBs; dimerization mutants fail to localize to DSBs (live-cell imaging), are strongly defective in HR and MMEJ, and show reduced damage-induced CtIP phosphorylation. Site-directed mutagenesis, live-cell GFP imaging, HR reporter assay, RPA foci, co-immunoprecipitation The Journal of biological chemistry High 22544744
2010 CtIP is essential for chromosomal translocation formation via alternative NHEJ (alt-NHEJ); CtIP depletion reduces microhomology usage at translocation junctions; CtIP-mediated resection generates ssDNA for microhomology-mediated end joining. Translocation reporter assay in mouse cells, CtIP siRNA depletion, junction sequencing Nature structural & molecular biology High 21131978
2010 CtIP is required for microhomology-directed alternative end-joining (A-NHEJ) during class-switch recombination; CtIP binds switch-region DNA in an AID-dependent manner; microhomology joins enriched upon Ku70 depletion also require CtIP. CtIP shRNA depletion in B cells, CSR switching assay, junction sequencing, ChIP Nature structural & molecular biology High 21131982
2011 In G1-phase lymphocytes, H2AX and MDC1 prevent CtIP from processing RAG-generated hairpin-sealed coding ends; in the absence of H2AX, CtIP can open and resect these ends, leading to aberrant alt-NHEJ with microhomology usage and deletions. ATM activates both pro- and anti-resection pathways modulating CtIP activity. H2AX KO mouse cells, immunofluorescence, DNA repair assay, cell cycle gating Nature High 21160476
2009 Fission yeast Ctp1 (CtIP ortholog) is required for the initial steps of HR in cooperation with the MRN complex; loss of Ctp1 phenocopies MRN deficiency in HR initiation. S. pombe genetic analysis (review/perspective citing Limbo et al.) Molecular cell Low 17996697
2011 Two truncating mutations in CtIP (RBBP8) cause Seckel syndrome (SCKL2) and Jawad syndrome; SCKL2 cells exhibit defective DNA damage-induced ssDNA formation and reduced ATR activation; overexpression of the C-terminally truncated CtIP acts as a dominant-negative. Patient cell lines, ssDNA/BrdU assay, ATR signaling assays, mutant overexpression PLoS genetics High 21998596
2010 CtIP interacts with EXO1 and restrains its exonucleolytic activity in vitro; EXO1 localization to DSBs depends on both CtIP and MRN. Co-immunoprecipitation, in vitro nuclease assay, immunofluorescence after CtIP/MRN depletion EMBO reports Medium 21052091
2014 CtIP exhibits an end resection-independent endonuclease activity required for repair of DSBs at common fragile sites (AT-rich sequences) and palindromic Alu inverted repeats; CtIP nuclease-defective mutants are impaired in handling DSBs with secondary DNA structures. CFS reporter assay, Alu-IR reporter, CtIP nuclease-dead mutants, co-immunoprecipitation Molecular cell High 24837675
2014 APC/C(Cdh1) ubiquitin ligase targets CtIP for degradation via a conserved KEN box on CtIP; mutation of the KEN box prevents Cdh1-dependent CtIP ubiquitylation and degradation in G1 and after DNA damage in G2, causing delayed CtIP clearance from foci, excessive resection, and reduced HR efficiency. Proteomics/MS, co-immunoprecipitation, ubiquitylation assay, KEN-box mutagenesis, DNA resection assay The EMBO journal High 25349192
2016 KLHL15 (Cullin3 E3 ligase adaptor) interacts with CtIP via a conserved FRY tripeptide motif and promotes CtIP proteasomal degradation; FRY mutation blocks KLHL15-dependent CtIP ubiquitination and degradation, amplifying DNA-end resection and altering HR/NHEJ balance. Co-immunoprecipitation, ubiquitination assay, site-directed mutagenesis, DNA resection assay Nature communications High 27561354
2010 BRCA1 and CtIP cooperatively promote nuclease-mediated removal of oligonucleotides covalently bound at DSBs (from topoisomerase inhibitor treatment); BRCA1–CtIP interaction (via Ser332) is required for this activity but not for HR at clean DSBs. DT40 conditional CtIP KO, CtIP-S332A knock-in, sensitivity assays, RPA/Rad51 foci PLoS genetics High 20107609
2016 MRN, CtIP, and BRCA1 are required for removal of Top2–DNA adducts and subsequent resection in Xenopus egg extracts; the CtIP–BRCA1 interaction (dispensable for resection of clean ends) is required for processing Top2-adducted DSBs. Xenopus egg extract biochemistry, immunodepletion, Top2 adduct removal assay The Journal of cell biology High 26880199
2014 Polo-like kinase 3 (Plk3) phosphorylates CtIP in G1 in a damage-inducible manner; Plk3 binds CtIP phosphorylated at S327 via its Polo box domains, promoting CtIP phosphorylation at S327 and T847; Plk3 and CtIP promote alt-NHEJ, translocation formation, and large-scale deletions in G1. Kinase assay, Plk3 depletion, S327 and T847 mutagenesis, translocation assay, DSB resection assay The Journal of cell biology High 25267294
2018 PLK1 phosphorylates CtIP at Ser-723 after CDK1/Aurora A primes phosphorylation at S327 to recruit PLK1 via its polo-box domain; PLK1-phospho-mimetic CtIP supports MMEJ but not HR or G2/M checkpoint. Kinase assays, phospho-site mutagenesis, HR reporter, MMEJ assay, G2/M checkpoint analysis Nucleic acids research Medium 30202980
2011 In G0/G1, human CtIP and MRN are required for NHEJ repair of etoposide-induced (protein-blocked) DSBs; this NHEJ function requires CtIP Thr-847 but not Ser-327, and is mechanistically distinct from its HR resection function. G0/G1 arrest, CtIP/MRN siRNA depletion, DSB repair kinetics (53BP1 foci), phospho-site mutant complementation Nucleic acids research Medium 21087997
2011 Cdk1 phosphorylates CtIP to permit M-phase DSB resection via MRN–CtIP only; unlike S-phase resection, M-phase resection does not activate ATR or load Rad51, because Cdk1 prevents Rad51 binding to resected ends. Xenopus egg extract system (M-phase and S-phase), chromatin fractionation, RPA/Rad51 binding assays, CDK inhibitors The Journal of cell biology High 21893598
2012 CtIP-dependent DNA end resection is dispensable for initial ATR-CHK1 activation after DSBs, but is required for sustained ATR-CHK1 checkpoint signaling and maintenance of intra-S and G2 checkpoints. CtIP siRNA depletion, time-course CHK1 phosphorylation assay, resection assay, checkpoint assay The Journal of cell biology Medium 22733999
2014 FANCD2 directly interacts with CtIP; monoubiquitinated FANCD2 tethers CtIP to damaged chromatin, channeling ICL-generated DSBs into HR; CtIP mutants defective in FANCD2 binding show increased NHEJ and ICL hypersensitivity. Co-immunoprecipitation, GST pull-down, chromatin fractionation, ICL sensitivity assay, FANCD2 monoubiquitination mutants Cell reports High 24794430 24794434
2019 NBS1, via its FHA and BRCT domains, functions as a sensor of CtIP phosphorylation and activates MRE11-RAD50 nuclease through direct physical interactions with MRE11; two modes of CtIP-dependent MRE11 stimulation exist: phosphorylation-dependent (through NBS1) and phosphorylation-independent (without NBS1). Reconstituted in vitro nuclease assay with recombinant proteins, NBS1 domain mutants, mutagenesis The EMBO journal High 30787182
2020 DNA-PK promotes DNA end processing by MRN–phospho-CtIP in physiological conditions; MRN-dependent endonucleolytic removal of DNA-PK-bound ends is observed at DSB sites; DNA-PK facilitates sequential transition from NHEJ to HR by promoting its own removal. Ensemble biochemistry, single-molecule assays, human cell chromatin assays Science advances High 31934630
2017 CBX4 (SUMO E3 ligase) constitutively sumoylates CtIP at lysine 896; sumoylation is essential for CtIP recruitment to damaged DNA; non-sumoylatable CtIP-K896R blocks HR and increases genomic instability; SUMO fusion to CtIP rescues CBX4-depletion phenotype. In vivo SUMOylation assay, K896R mutagenesis, SUMO-CtIP fusion rescue, HR reporter, CtIP foci assay Nature communications High 28740167
2021 ATM-dependent hyperphosphorylation of CtIP at DSBs triggers PIAS4-dependent CtIP SUMOylation at K578; SUMO-modified CtIP is then polyubiquitinated by RNF4 and degraded; disrupting CtIP K578 sumoylation causes CtIP accumulation at DSBs, excessive resection, defective HR, and increased DSB sensitivity. SUMO/ubiquitin assays, K578R mutagenesis, ATM inhibition, CtIP foci quantification, HR reporter Proceedings of the National Academy of Sciences Medium 33723063
2015 RNF138 E3 ligase (with UBE2D E2 enzymes) promotes CtIP ubiquitylation and accrual at DNA damage sites at early resection stages, promoting HR. Systematic E2 screen, co-immunoprecipitation, ubiquitylation assay, laser microirradiation, HR reporter Nature cell biology Medium 26502057
2015 USP4 deubiquitylase directly interacts with CtIP and MRN via specific domains; USP4 promotes CtIP recruitment to DSBs and HR; USP4 autodeubiquitylation is required for its HR function. Co-immunoprecipitation, deubiquitylation assay, CtIP foci analysis, HR reporter Cell reports Medium 26387952
2020 USP52 directly interacts with and deubiquitinates CtIP; USP52-mediated deubiquitination facilitates CtIP phosphorylation at Thr-847 and its activation; ATM phosphorylates USP52 at Ser-1003 after DNA damage to enhance USP52 catalytic activity. Co-immunoprecipitation, in vitro deubiquitination assay, phosphorylation assay, DNA resection assay, HR reporter Nature communications Medium 33097710
2003 SIAH-1 E3 ligase interacts with CtIP and promotes its degradation via the ubiquitin-proteasome pathway. Yeast two-hybrid, co-immunoprecipitation (in vitro and in vivo), proteasome inhibitor treatment, Western blotting Oncogene Medium 14654780
2018 CtIP has an unanticipated role in protecting reversed stalled DNA replication forks from excessive degradation by DNA2 nuclease, independent of MRE11 and DSB resection; this function synergizes with BRCA1 to suppress replication-stress-induced genomic instability. DNA fiber assay (fork degradation), CtIP depletion, DNA2 inhibition, MRE11 inhibition, genetic epistasis Molecular cell High 30344097
2020 RBBP8/CtIP germline variants in early-onset breast cancer compromise replication fork stability by promoting helicase-driven destabilization of RAD51 nucleofilaments at stalled forks, distinct from the DSB end resection function. DNA fiber assay, RAD51 nucleofilament stability assay, patient variant functional analysis The Journal of clinical investigation Medium 32379725
2020 Phosphorylated CtIP bridges DNA molecules in a manner dependent on its oligomeric state; the bridging activity is separable from the nuclease-cofactor activity (distinct protein domains); bridging is much more efficient than yeast Sae2, consistent with expanded low-complexity regions in CtIP. Nanofluidic channel single-molecule DNA bridging assay, CtIP truncation mutants Proceedings of the National Academy of Sciences Medium 32417418
2020 CtIP stimulates the ATP hydrolysis-driven motor activity of DNA2, promoting displacement of RPA-coated ssDNA and thus long-range resection; CtIP phosphorylation facilitates this stimulation; the domain of CtIP required to promote DNA2 is in the central region and is distinct from MRN-stimulatory domains. Reconstituted biochemical assay with purified human proteins, single-molecule DNA curtain assay, ATPase assay, domain mapping Proceedings of the National Academy of Sciences High 32241893
2017 CtIP interacts with BLM helicase and enhances BLM helicase activity; CtIP also enhances DNA cleavage by DNA2; thus CtIP promotes long-range resection via the BLM–DNA2 pathway in addition to MRE11 regulation. Co-immunoprecipitation, in vitro helicase assay, in vitro nuclease assay with purified proteins Cell reports Medium 29020620
2018 CtIP (Sae2 in yeast) depletion promotes accumulation of R-loops and stalled RNA polymerase at highly expressed genes; a catalytic CtIP mutant fails to complement R-loop sensitivity; overexpression of RNA-DNA helicase Senataxin suppresses DNA damage sensitivity in CtIP-deficient cells, suggesting CtIP nuclease activity processes R-loop intermediates. R-loop immunofluorescence, DRIP-seq, genetic complementation, Senataxin overexpression rescue eLife Medium 30523780
2005 RBP-Jkappa/SHARP recruits CtIP and CtBP as corepressors; CtIP directly binds the SHARP repression domain; CtIP augments SHARP-mediated transcriptional repression of Notch target gene Hey1. Co-immunoprecipitation, GST pull-down, transcriptional reporter assay, CtBP-deficient cell lines Molecular and cellular biology Medium 16287852
2001 LMO4 interacts with CtIP (via a single LIM motif) and with BRCA1 BRCT domains independently; a stable LMO4–BRCA1–CtIP–Ldb1 complex exists in vivo; LMO4 represses BRCA1-mediated transcriptional activation. Yeast two-hybrid, co-immunoprecipitation, transcriptional reporter assay (yeast and mammalian) The Journal of biological chemistry Medium 11751867
2006 BRCA1, CtIP, and ZBRK1 form a repressor complex that binds the ANG1 promoter via a ZBRK1 recognition site; disruption of this complex upregulates ANG1, stabilizes endothelial cells, and accelerates mammary tumor growth. ChIP, co-immunoprecipitation, RNAi depletion, reporter assay, 3D culture, mouse tumor model Cancer cell High 16843262
2002 CtIP interacts with Ikaros via CtIP's Rb interaction domain (not via CtBP); CtIP contributes to Ikaros-mediated transcriptional repression independent of HDACs; mutation abolishing Ikaros–CtIP interaction significantly reduces Ikaros repression activity. Co-immunoprecipitation, transcriptional reporter assay, HDAC inhibitor treatment, domain mutant analysis The Journal of biological chemistry Medium 11959865
2015 SERBP1 binds CtIP mRNA and regulates CtIP expression at the translational level in S phase; SERBP1 depletion reduces polysome-associated CtIP mRNA and CtIP protein; RNA-binding-deficient SERBP1 (ΔRGG) fails to rescue CtIP translation or HR. RIP-seq, polysome profiling, co-immunoprecipitation, RNA-binding mutant rescue Nucleic acids research Medium 26068472
2022 A micropeptide PACMP prevents CtIP ubiquitination by inhibiting the CtIP–KLHL15 interaction, thereby maintaining CtIP abundance and promoting HR; PACMP also binds DNA damage-induced poly(ADP-ribose) chains to enhance PARylation. Co-immunoprecipitation, ubiquitination assay, HR reporter, PARP inhibitor sensitivity assay Molecular cell Medium 35219381
2018 Fusion of a minimal N-terminal CtIP fragment (HE domain, containing CDK phosphorylation sites and multimerization domain) to Cas9 stimulates HDR by approximately twofold; this HDR enhancement is CDK-phosphorylation and multimerization dependent. Cas9-CtIP fusion, HDR reporter assay, phospho-site and multimerization domain mutagenesis, human cell lines/iPSC/rat zygotes Nature communications Medium 29556040

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2007 Human CtIP promotes DNA end resection. Nature 1088 17965729
2013 A cell cycle-dependent regulatory circuit composed of 53BP1-RIF1 and BRCA1-CtIP controls DNA repair pathway choice. Molecular cell 742 23333306
2009 CtIP-BRCA1 modulates the choice of DNA double-strand-break repair pathway throughout the cell cycle. Nature 427 19357644
2009 Human CtIP mediates cell cycle control of DNA end resection and double strand break repair. The Journal of biological chemistry 414 19202191
2004 DNA damage-induced cell cycle checkpoint control requires CtIP, a phosphorylation-dependent binding partner of BRCA1 C-terminal domains. Molecular and cellular biology 341 15485915
2008 Cell cycle-dependent complex formation of BRCA1.CtIP.MRN is important for DNA double-strand break repair. The Journal of biological chemistry 340 18171670
1998 The C-terminal (BRCT) domains of BRCA1 interact in vivo with CtIP, a protein implicated in the CtBP pathway of transcriptional repression. The Journal of biological chemistry 340 9738006
2010 RETRACTED: Human SIRT6 promotes DNA end resection through CtIP deacetylation. Science (New York, N.Y.) 289 20829486
2016 Phosphorylated CtIP Functions as a Co-factor of the MRE11-RAD50-NBS1 Endonuclease in DNA End Resection. Molecular cell 259 27889449
2006 BRCA1 ubiquitinates its phosphorylation-dependent binding partner CtIP. Genes & development 225 16818604
2013 The interaction of CtIP and Nbs1 connects CDK and ATM to regulate HR-mediated double-strand break repair. PLoS genetics 220 23468639
2014 BRCA1 accelerates CtIP-mediated DNA-end resection. Cell reports 214 25310973
2010 An essential role for CtIP in chromosomal translocation formation through an alternative end-joining pathway. Nature structural & molecular biology 209 21131978
2009 CtIP links DNA double-strand break sensing to resection. Molecular cell 194 20064462
2018 CtIP fusion to Cas9 enhances transgene integration by homology-dependent repair. Nature communications 166 29556040
1999 Binding of CtIP to the BRCT repeats of BRCA1 involved in the transcription regulation of p21 is disrupted upon DNA damage. The Journal of biological chemistry 166 10196224
2009 Distinct requirements for the Rad32(Mre11) nuclease and Ctp1(CtIP) in the removal of covalently bound topoisomerase I and II from DNA. Molecular cell 161 19150433
2014 Catalytic and noncatalytic roles of the CtIP endonuclease in double-strand break end resection. Molecular cell 154 24837676
2005 RBP-Jkappa/SHARP recruits CtIP/CtBP corepressors to silence Notch target genes. Molecular and cellular biology 151 16287852
2010 CtIP promotes microhomology-mediated alternative end joining during class-switch recombination. Nature structural & molecular biology 146 21131982
2010 DNA damage and decisions: CtIP coordinates DNA repair and cell cycle checkpoints. Trends in cell biology 133 20444606
2000 Nuclear localization and cell cycle-specific expression of CtIP, a protein that associates with the BRCA1 tumor suppressor. The Journal of biological chemistry 132 10764811
2001 The LIM domain protein LMO4 interacts with the cofactor CtIP and the tumor suppressor BRCA1 and inhibits BRCA1 activity. The Journal of biological chemistry 129 11751867
2010 Collaborative action of Brca1 and CtIP in elimination of covalent modifications from double-strand breaks to facilitate subsequent break repair. PLoS genetics 125 20107609
2010 H2AX prevents CtIP-mediated DNA end resection and aberrant repair in G1-phase lymphocytes. Nature 120 21160476
2005 Inactivation of CtIP leads to early embryonic lethality mediated by G1 restraint and to tumorigenesis by haploid insufficiency. Molecular and cellular biology 120 15831459
2014 CtIP maintains stability at common fragile sites and inverted repeats by end resection-independent endonuclease activity. Molecular cell 119 24837675
2012 Activation of DSB processing requires phosphorylation of CtIP by ATR. Molecular cell 118 23273981
2011 NF-κB regulates DNA double-strand break repair in conjunction with BRCA1-CtIP complexes. Nucleic acids research 117 21908405
2020 DNA-dependent protein kinase promotes DNA end processing by MRN and CtIP. Science advances 115 31934630
2007 Ctp1/CtIP and the MRN complex collaborate in the initial steps of homologous recombination. Molecular cell 111 17996697
2016 MRN, CtIP, and BRCA1 mediate repair of topoisomerase II-DNA adducts. The Journal of cell biology 108 26880199
2010 DNA end resection by CtIP and exonuclease 1 prevents genomic instability. EMBO reports 108 21052091
2018 CtIP-Mediated Fork Protection Synergizes with BRCA1 to Suppress Genomic Instability upon DNA Replication Stress. Molecular cell 104 30344097
2014 CtIP-mediated resection is essential for viability and can operate independently of BRCA1. The Journal of experimental medicine 103 24842372
2011 CtIP Mutations Cause Seckel and Jawad Syndromes. PLoS genetics 103 21998596
2010 CtIP and MRN promote non-homologous end-joining of etoposide-induced DNA double-strand breaks in G1. Nucleic acids research 102 21087997
2012 Mre11 regulates CtIP-dependent double-strand break repair by interaction with CDK2. Nature structural & molecular biology 101 22231403
2015 Systematic E2 screening reveals a UBE2D-RNF138-CtIP axis promoting DNA repair. Nature cell biology 97 26502057
2013 HDAC turnover, CtIP acetylation and dysregulated DNA damage signaling in colon cancer cells treated with sulforaphane and related dietary isothiocyanates. Epigenetics 96 23770684
2005 Structural basis for cell cycle checkpoint control by the BRCA1-CtIP complex. Biochemistry 91 16101277
2007 A novel plant gene essential for meiosis is related to the human CtIP and the yeast COM1/SAE2 gene. The EMBO journal 88 18007598
2006 Removal of BRCA1/CtIP/ZBRK1 repressor complex on ANG1 promoter leads to accelerated mammary tumor growth contributed by prominent vasculature. Cancer cell 87 16843262
2014 Polo-like kinase 3 regulates CtIP during DNA double-strand break repair in G1. The Journal of cell biology 84 25267294
2015 CtIP: A DNA damage response protein at the intersection of DNA metabolism. DNA repair 83 25957490
2022 Micropeptide PACMP inhibition elicits synthetic lethal effects by decreasing CtIP and poly(ADP-ribosyl)ation. Molecular cell 77 35219381
2014 FANCD2 binds CtIP and regulates DNA-end resection during DNA interstrand crosslink repair. Cell reports 77 24794430
2022 POLθ prevents MRE11-NBS1-CtIP-dependent fork breakage in the absence of BRCA2/RAD51 by filling lagging-strand gaps. Molecular cell 76 36400008
2014 FANCD2 and CtIP cooperate to repair DNA interstrand crosslinks. Cell reports 76 24794434
2013 The interaction between CtIP and BRCA1 is not essential for resection-mediated DNA repair or tumor suppression. The Journal of cell biology 72 23712259
2014 CtIP mediates replication fork recovery in a FANCD2-regulated manner. Human molecular genetics 70 24556218
2014 APC/C(Cdh1) controls CtIP stability during the cell cycle and in response to DNA damage. The EMBO journal 70 25349192
2011 Cdk1 uncouples CtIP-dependent resection and Rad51 filament formation during M-phase double-strand break repair. The Journal of cell biology 70 21893598
2019 NBS1 promotes the endonuclease activity of the MRE11-RAD50 complex by sensing CtIP phosphorylation. The EMBO journal 69 30787182
2013 BRCA1 and CtIP suppress long-tract gene conversion between sister chromatids. Nature communications 67 23994874
2007 A conserved function for a Caenorhabditis elegans Com1/Sae2/CtIP protein homolog in meiotic recombination. The EMBO journal 67 18007596
2020 CtIP promotes the motor activity of DNA2 to accelerate long-range DNA end resection. Proceedings of the National Academy of Sciences of the United States of America 65 32241893
2015 CtIP tetramer assembly is required for DNA-end resection and repair. Nature structural & molecular biology 64 25558984
2013 A role for BLM in double-strand break repair pathway choice: prevention of CtIP/Mre11-mediated alternative nonhomologous end-joining. Cell reports 64 24095737
2012 CtIP protein dimerization is critical for its recruitment to chromosomal DNA double-stranded breaks. The Journal of biological chemistry 63 22544744
2017 Enhancement of BLM-DNA2-Mediated Long-Range DNA End Resection by CtIP. Cell reports 62 29020620
2012 CtIP-dependent DNA resection is required for DNA damage checkpoint maintenance but not initiation. The Journal of cell biology 62 22733999
2018 Sae2/CtIP prevents R-loop accumulation in eukaryotic cells. eLife 61 30523780
2009 N terminus of CtIP is critical for homologous recombination-mediated double-strand break repair. The Journal of biological chemistry 61 19759395
2002 Ikaros-CtIP interactions do not require C-terminal binding protein and participate in a deacetylase-independent mode of repression. The Journal of biological chemistry 60 11959865
2013 Microsatellite instability induced mutations in DNA repair genes CtIP and MRE11 confer hypersensitivity to poly (ADP-ribose) polymerase inhibitors in myeloid malignancies. Haematologica 58 23349304
2016 Cullin3-KLHL15 ubiquitin ligase mediates CtIP protein turnover to fine-tune DNA-end resection. Nature communications 55 27561354
2015 The Deubiquitylating Enzyme USP4 Cooperates with CtIP in DNA Double-Strand Break End Resection. Cell reports 53 26387952
2006 CtIP activates its own and cyclin D1 promoters via the E2F/RB pathway during G1/S progression. Molecular and cellular biology 51 16581787
2006 TRB3 interacts with CtIP and is overexpressed in certain cancers. Biochimica et biophysica acta 49 17112672
2015 Neddylation inhibits CtIP-mediated resection and regulates DNA double strand break repair pathway choice. Nucleic acids research 48 25567988
2018 PLK1 targets CtIP to promote microhomology-mediated end joining. Nucleic acids research 45 30202980
2013 ATM-dependent MiR-335 targets CtIP and modulates the DNA damage response. PLoS genetics 45 23696749
2017 CtIP/Ctp1/Sae2, molecular form fit for function. DNA repair 44 28623092
2017 DNA end resection requires constitutive sumoylation of CtIP by CBX4. Nature communications 43 28740167
2015 Relative contribution of four nucleases, CtIP, Dna2, Exo1 and Mre11, to the initial step of DNA double-strand break repair by homologous recombination in both the chicken DT40 and human TK6 cell lines. Genes to cells : devoted to molecular & cellular mechanisms 43 26525166
2004 Dimerization of CtIP, a BRCA1- and CtBP-interacting protein, is mediated by an N-terminal coiled-coil motif. The Journal of biological chemistry 43 15084581
2018 Promoter methylation of DNA damage repair (DDR) genes in human tumor entities: RBBP8/CtIP is almost exclusively methylated in bladder cancer. Clinical epigenetics 42 29445424
2009 Derepression of HMGA2 via removal of ZBRK1/BRCA1/CtIP complex enhances mammary tumorigenesis. The Journal of biological chemistry 42 20007691
2020 Human CtIP: A 'double agent' in DNA repair and tumorigenesis. Seminars in cell & developmental biology 39 32950401
2017 Aquarius is required for proper CtIP expression and homologous recombination repair. Scientific reports 39 29061988
2014 Triapine disrupts CtIP-mediated homologous recombination repair and sensitizes ovarian cancer cells to PARP and topoisomerase inhibitors. Molecular cancer research : MCR 37 24413181
2003 SIAH-1 interacts with CtIP and promotes its degradation by the proteasome pathway. Oncogene 37 14654780
2015 SERBP1 affects homologous recombination-mediated DNA repair by regulation of CtIP translation during S phase. Nucleic acids research 36 26068472
2005 CtIP, a candidate tumor susceptibility gene is a team player with luminaries. Biochimica et biophysica acta 36 16249056
2016 Loss of CtIP disturbs homologous recombination repair and sensitizes breast cancer cells to PARP inhibitors. Oncotarget 33 26713604
2021 ATM controls the extent of DNA end resection by eliciting sequential posttranslational modifications of CtIP. Proceedings of the National Academy of Sciences of the United States of America 31 33723063
2020 The SWI/SNF ATPase BRG1 stimulates DNA end resection and homologous recombination by reducing nucleosome density at DNA double strand breaks and by promoting the recruitment of the CtIP nuclease. Cell cycle (Georgetown, Tex.) 30 33044911
2020 USP52 regulates DNA end resection and chemosensitivity through removing inhibitory ubiquitination from CtIP. Nature communications 30 33097710
2019 CSB interacts with BRCA1 in late S/G2 to promote MRN- and CtIP-mediated DNA end resection. Nucleic acids research 30 31501894
2015 BRCA1 and CtIP promote alternative non-homologous end-joining at uncapped telomeres. The EMBO journal 29 25582120
2015 BRCA1 and CtIP Are Both Required to Recruit Dna2 at Double-Strand Breaks in Homologous Recombination. PloS one 29 25909997
2020 Germline RBBP8 variants associated with early-onset breast cancer compromise replication fork stability. The Journal of clinical investigation 28 32379725
2017 And-1 coordinates with CtIP for efficient homologous recombination and DNA damage checkpoint maintenance. Nucleic acids research 28 27940552
2012 CtIP is required to initiate replication-dependent interstrand crosslink repair. PLoS genetics 28 23144634
2020 FANCJ helicase promotes DNA end resection by facilitating CtIP recruitment to DNA double-strand breaks. PLoS genetics 27 32251466
2016 53BP1 Protects against CtIP-Dependent Capture of Ectopic Chromosomal Sequences at the Junction of Distant Double-Strand Breaks. PLoS genetics 27 27798638
2007 CtIP silencing as a novel mechanism of tamoxifen resistance in breast cancer. Molecular cancer research : MCR 26 18171986
2016 Impaired 53BP1/RIF1 DSB mediated end-protection stimulates CtIP-dependent end resection and switches the repair to PARP1-dependent end joining in G1. Oncotarget 25 27494840
2020 Phosphorylated CtIP bridges DNA to promote annealing of broken ends. Proceedings of the National Academy of Sciences of the United States of America 24 32817418

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