| Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells. | Polyubiquitinated PCNA triggers SLX4-mediated break-induced replication in alternative lengthening of telomeres (ALT) cancer cells.
Kim S, Park SH, Kang N, Ra JS, Myung K, Lee KY., Free PMC Article | 11/13/2024 |
| Compartmentalization of the SUMO/RNF4 pathway by SLX4 drives DNA repair. | Compartmentalization of the SUMO/RNF4 pathway by SLX4 drives DNA repair.
Alghoul E, Paloni M, Takedachi A, Urbach S, Barducci A, Gaillard PH, Basbous J, Constantinou A. | 05/22/2023 |
| RNF168 E3 ligase participates in ubiquitin signaling and recruitment of SLX4 during DNA crosslink repair. | RNF168 E3 ligase participates in ubiquitin signaling and recruitment of SLX4 during DNA crosslink repair.
Katsuki Y, Abe M, Park SY, Wu W, Yabe H, Yabe M, van Attikum H, Nakada S, Ohta T, Seidman MM, Kim Y, Takata M., Free PMC Article | 02/12/2022 |
| Coordinated roles of SLX4 and MutSbeta in DNA repair and the maintenance of genome stability. | Coordinated roles of SLX4 and MutSβ in DNA repair and the maintenance of genome stability.
Young SJ, West SC., Free PMC Article | 10/2/2021 |
| Abraxas suppresses DNA end resection and limits break-induced replication by controlling SLX4/MUS81 chromatin loading in response to TOP1 inhibitor-induced DNA damage. | Abraxas suppresses DNA end resection and limits break-induced replication by controlling SLX4/MUS81 chromatin loading in response to TOP1 inhibitor-induced DNA damage.
Wu X, Wang B., Free PMC Article | 08/7/2021 |
| PARP1 modulates telomere sister chromatid exchange and telomere length homeostasis by regulating telomere localization of SLX4 in U2OS cells. | PARP1 modulates telomere sister chromatid exchange and telomere length homeostasis by regulating telomere localization of SLX4 in U2OS cells.
Sadhukhan R, Ghosh U. | 06/26/2021 |
| SLX4-XPF mediates DNA damage responses to replication stress induced by DNA-protein interactions. | SLX4-XPF mediates DNA damage responses to replication stress induced by DNA-protein interactions.
Ishimoto R, Tsuzuki Y, Matsumura T, Kurashige S, Enokitani K, Narimatsu K, Higa M, Sugimoto N, Yoshida K, Fujita M., Free PMC Article | 05/22/2021 |
| SLX4 interacts with RTEL1 to prevent transcription-mediated DNA replication perturbations. | SLX4 interacts with RTEL1 to prevent transcription-mediated DNA replication perturbations.
Takedachi A, Despras E, Scaglione S, Guérois R, Guervilly JH, Blin M, Audebert S, Camoin L, Hasanova Z, Schertzer M, Guille A, Churikov D, Callebaut I, Naim V, Chaffanet M, Borg JP, Bertucci F, Revy P, Birnbaum D, Londoño-Vallejo A, Kannouche PL, Gaillard PHL. | 10/3/2020 |
| The binding of SLX4IP to both SLX4 and XPF-ERCC1 not only is vital for maintaining the stability of SLX4IP protein, but also promotes the interaction between SLX4 and XPF-ERCC1, especially after DNA damage. Collectively, these results demonstrate a new regulatory role for SLX4IP in maintaining an efficient SLX4-XPF-ERCC1 complex in interstrand crosslinks (ICLs) repair. | SLX4IP acts with SLX4 and XPF-ERCC1 to promote interstrand crosslink repair.
Zhang H, Chen Z, Ye Y, Ye Z, Cao D, Xiong Y, Srivastava M, Feng X, Tang M, Wang C, Tainer JA, Chen J., Free PMC Article | 12/14/2019 |
| This review aims at providing an up-to-date and comprehensive view on the key functions that SLX4 fulfills to maintain genome stability as well as to highlight and discuss areas of uncertainty and emerging concepts. [review] | SLX4: multitasking to maintain genome stability.
Guervilly JH, Gaillard PH. | 04/20/2019 |
| RAD52 and SLX4 mediate distinct postreplicative DNA repair processes that maintain ALT telomere stability and cancer cell viability | RAD52 and SLX4 act nonepistatically to ensure telomere stability during alternative telomere lengthening.
Verma P, Dilley RL, Zhang T, Gyparaki MT, Li Y, Greenberg RA., Free PMC Article | 03/2/2019 |
| Using RNAi or FA-P cells complemented with SLX4 mutants that abrogate interaction with MUS81 or SLX1, we show that SLX4 cooperates with MUS81 to introduce DSBs after replication stress but also counteracts pathological targeting of demised forks by GEN1. | SLX4 Prevents GEN1-Dependent DSBs During DNA Replication Arrest Under Pathological Conditions in Human Cells.
Malacaria E, Franchitto A, Pichierri P., Free PMC Article | 11/10/2018 |
| observed aberrant bands of CSMD1 in one case of CRCs and SRPK1 in two cases of colorectal cancers | Rare frameshift mutations of putative tumor suppressor genes CSMD1 and SLX4 in colorectal cancers.
Lee JH, An CH, Kim MS, Yoo NJ, Lee SH. | 11/3/2018 |
| Findings propose a risk variant with high penetrance on the haplotype spanning SLX4/FANCP to be functionally associated to BC predisposition via decreased repair capacity and suggest this variant is carried by a fraction of these haplotypes that is enriched in early onset BC cases. | A low-frequency haplotype spanning SLX4/FANCP constitutes a new risk locus for early-onset breast cancer (<60 years) and is associated with reduced DNA repair capacity.
Surowy H, Varga D, Burwinkel B, Marmé F, Sohn C, Luedeke M, Rinckleb A, Maier C, Deissler H, Volcic M, Wiesmüller L, Hasenburg A, Klar M, Hoegel J, Vogel W. | 08/18/2018 |
| Loss-of-function mutations in SLX4 may contribute to the development of breast cancer in very rare cases | Assessment of SLX4 Mutations in Hereditary Breast Cancers.
Shah S, Kim Y, Ostrovnaya I, Murali R, Schrader KA, Lach FP, Sarrel K, Rau-Murthy R, Hansen N, Zhang L, Kirchhoff T, Stadler Z, Robson M, Vijai J, Offit K, Smogorzewska A., Free PMC Article | 10/14/2017 |
| The BLM-TOP3A-RMI (BTR) dissolvase complex is required for Alternative lengthening of telomeres-mediated telomere synthesis. BLM and SLX4 play opposing roles in recombination-dependent replication at human telomeres. | BLM and SLX4 play opposing roles in recombination-dependent replication at human telomeres.
Sobinoff AP, Allen JA, Neumann AA, Yang SF, Walsh ME, Henson JD, Reddel RR, Pickett HA., Free PMC Article | 10/14/2017 |
| Data suggest that dimeric GEN1 binds with high affinity/selectivity to Holliday junctions, introducing two symmetrical hydrolytic cleavages of phosphodiester backbone; at present, less is known about SLX1-SLX4-MUS81-EME1 resolving enzyme complex. (GEN1 = Holliday junction 5' flap endonuclease; SLX = structure-specific endonuclease subunit; MUS81 = MUS81 endonuclease; EME1 = essential meiotic endonuclease 1) [REVIEW] | Holliday junction-resolving enzymes-structures and mechanisms.
Lilley DMJ. | 08/12/2017 |
| These data also indicate that HIV-1 and HIV-2 Vpr activate the DNA damage response through an SLX4-independent mechanism that remains uncharacterized. | Activation of the DNA Damage Response Is a Conserved Function of HIV-1 and HIV-2 Vpr That Is Independent of SLX4 Recruitment.
Fregoso OI, Emerman M., Free PMC Article | 06/24/2017 |
| The functioning of SLX4 is dependent on its dimerization via an oligomerization motif called the BTB domain. | Dimerization of SLX4 contributes to functioning of the SLX4-nuclease complex.
Yin J, Wan B, Sarkar J, Horvath K, Wu J, Chen Y, Cheng G, Wan K, Chin P, Lei M, Liu Y., Free PMC Article | 05/27/2017 |
| SLX4-SLX1 Protein-independent Down-regulation of MUS81-EME1 Protein by HIV-1 Viral Protein R (Vpr). | SLX4-SLX1 Protein-independent Down-regulation of MUS81-EME1 Protein by HIV-1 Viral Protein R (Vpr).
Zhou X, DeLucia M, Ahn J., Free PMC Article | 05/7/2017 |
| Results identified homozygous mutations in FANCA and FANCP/SLX4 genes, both located on chromosome 16, were the affected recessive FA genes in three and one family respectively. Genotyping with short tandem repeat markers and SNP arrays revealed uniparental disomy of the entire mutation-carrying chromosome 16 in all four patients. | Paternal or Maternal Uniparental Disomy of Chromosome 16 Resulting in Homozygosity of a Mutant Allele Causes Fanconi Anemia.
Donovan FX, Kimble DC, Kim Y, Lach FP, Harper U, Kamat A, Jones M, Sanborn EM, Tryon R, Wagner JE, MacMillan ML, Ostrander EA, Auerbach AD, Smogorzewska A, Chandrasekharappa SC., Free PMC Article | 12/31/2016 |
| SLX4 (FANCP) and XPF (FANCQ) proteins interact with each other and play a vital role in the Fanconi anemia (FA) DNA repair pathway. Study has revealed that the global minor allele, SLX4(Y546C), is defective in this interaction. | Physical interaction between SLX4 (FANCP) and XPF (FANCQ) proteins and biological consequences of interaction-defective missense mutations.
Hashimoto K, Wada K, Matsumoto K, Moriya M., Free PMC Article | 06/28/2016 |
| SUMOylation and PARylation cooperate to recruit and stabilize SLX4 at DNA damage sites. | SUMOylation and PARylation cooperate to recruit and stabilize SLX4 at DNA damage sites.
González-Prieto R, Cuijpers SA, Luijsterburg MS, van Attikum H, Vertegaal AC., Free PMC Article | 12/26/2015 |
| Identification and characterization of MUS81 point mutations that abolish interaction with the SLX4 scaffold protein. | Identification and characterization of MUS81 point mutations that abolish interaction with the SLX4 scaffold protein.
Nair N, Castor D, Macartney T, Rouse J., Free PMC Article | 10/24/2015 |
| Vpr recruits the SLX4 endonuclease complex and Vpr-induced inappropriate activation of this complex leads to cell cycle arrest at the G2 phase. | How SLX4 cuts through the mystery of HIV-1 Vpr-mediated cell cycle arrest.
Blondot ML, Dragin L, Lahouassa H, Margottin-Goguet F., Free PMC Article | 10/17/2015 |