Fancp/Slx4

Cybulski, Kelly E; Howlett, Niall G.

doi:10.4161/cc.10.11.15818

Cited by 49 publications

(22 citation statements)

References 80 publications

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“…Together, these results suggest Vpr as an antagonist of innate sensing of HIV-1 infection. The recent landmark study by Laguette and colleagues suggested a first molecular explanation for this activity by unraveling the interaction of Vpr with SLX4, a nuclease scaffold with important roles in DNA damage and repair (44,73). Via this interaction, Vpr prematurely activates SLX4 complexes, which results in cell cycle arrest but also reduces the proinflammatory cytokine response to HIV infection (44,59,74).…”

Section: Discussionmentioning

confidence: 99%

Sensing of HIV-1 Infection in Tzm-bl Cells with Reconstituted Expression of STING

Trotard

Tsopoulidis

Tibroni

et al. 2016

J Virol

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Section: Discussionmentioning

confidence: 99%

Sensing of HIV-1 Infection in Tzm-bl Cells with Reconstituted Expression of STING

Trotard

Tsopoulidis

Tibroni

et al. 2016

J Virol

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“…Of the fifteen FA genes/candidate genes currently identified [9] ( Table 1 ), two ( FANCM, FANCJ ) encode DNA-dependent ATPases. FANCM regulates replication fork progression [10,11] and is thought to remodel stalled replication forks through its ATP-dependent branch migration activity [12-15].…”

Section: Chromosomal Instability Disorders Fanconi Anemia and Bloom'smentioning

confidence: 99%

Fanconi anemia and Bloom's syndrome crosstalk through FANCJ–BLM helicase interaction

Suhasini

Brosh

2012

Trends in Genetics

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Fanconi anemia (FA) and Bloom's syndrome (BS) are rare hereditary chromosomal instability disorders. FA displays bone marrow failure, acute myeloid leukemia, and head and neck cancers, whereas BS is characterized by growth retardation, immunodeficiency, and a wide spectrum of cancers. The BLM gene mutated in BS encodes a DNA helicase that functions in a protein complex to suppress sister chromatid exchange. Of the fifteen FA genetic complementation groups implicated in interstrand cross-link repair, FANCJ encodes a DNA helicase involved in recombinational repair and replication stress response. Based on evidence that BLM and FANCJ interact, we put forward that crosstalk between BLM and FA pathways is more complex than previously thought. We propose testable models for how FANCJ and BLM coordinate to help cells deal with stalled replication forks or double strand breaks. Understanding how BLM and FANCJ cooperate will help to elucidate an important pathway to maintain genomic stability.

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“…Upon damage, the monoubiquitinated FANCD2-I complex is then recruited to the chromatin where it interacts with downstream FA proteins [FANCD1/BRCA2, FANCJ/BACH1, FANCN/PALB2, FANCO/RAD51C, and FANCP/SLX4 along with the FA-associated nuclease 1 (FAN1)] that are all involved in promoting HR repair (Howlett et al 2002; Litman et al 2005; Reid et al 2007; Xia et al 2007; Shen et al 2009; Liu et al 2010; Smogorzewska et al 2010; Vaz et al 2010; Crossan et al 2011; Stoepker et al 2011). Monoubiquitinated FANCD2 also provides binding sites for SLX4 and FAN1, which are structure specific endonucleases that play roles in unhooking the ICL, HR repair, and potentially facilitating TLS (Liu et al 2010; Cybulski and Howlett 2011; Sengerova et al 2011; Yamamoto et al 2011). Deficiencies in any of these proteins results in the characteristic deficiency in DSB resolution following exposure to DNA crosslinking agents, as well as reductions in gene conversion efficiencies, identical to what has have observed in REV1 or Polζ-depleted cells (Hicks et al 2010; Sharma et al 2012a).…”

Section: The Fa Pathway: Regulator Of Rev1 and Polζmentioning

confidence: 99%

REV1 and DNA polymerase zeta in DNA interstrand crosslink repair

Sharma

Canman

2012

Environ and Mol Mutagen

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DNA interstrand crosslinks (ICLs) are covalent linkages between two strands of DNA and their presence interfere with essential metabolic processes such as transcription and replication. These lesions are extremely toxic and their repair is essential for genome stability and cell survival. In this review, we will discuss how the removal of ICLs requires interplay between multiple genome maintenance pathways and can occur in the absence of replication (replication-independent ICL repair) or during S phase (replication-coupled ICL repair), the latter being the predominant pathway used in mammalian cells. It is now well recognized that translesion DNA synthesis (TLS), especially through the activities of REV1 and DNA polymerase zeta (Polζ), is necessary for both ICL repair pathways operating throughout the cell cycle. Recent studies suggest that the convergence of two replication forks upon an ICL initiates a cascade of events including unhooking of the lesion through the actions of structure-specific endonucleases thereby creating a DNA double stranded break (DSB). TLS across the unhooked lesion is necessary for restoring the sister chromatid prior to homologous recombination (HR) repair. Biochemical and genetic studies implicate REV1 and Polζ as being essential for performing lesion bypass across the unhooked crosslink and this step appears to be important for subsequent events to repair the intermediate DSB. The potential role of Fanconi anemia pathway in the regulation of REV1 and Polζ-dependent TLS and the involvement of additional polymerases, including DNA polymerases kappa, nu, and theta, in the repair of ICLs is also discussed in this review.

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Fancp/Slx4

Cited by 49 publications

References 80 publications

Sensing of HIV-1 Infection in Tzm-bl Cells with Reconstituted Expression of STING

Sensing of HIV-1 Infection in Tzm-bl Cells with Reconstituted Expression of STING

Fanconi anemia and Bloom's syndrome crosstalk through FANCJ–BLM helicase interaction

REV1 and DNA polymerase zeta in DNA interstrand crosslink repair

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