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1 FANCI and EYA4 were identified as candidate DNA repair-r
2 FANCI and FANCD2 form the "ID" complex that loads onto c
3 FANCI is in close proximity to SF3B1 in the nucleoplasm
4 FANCI is integral to the Fanconi anemia (FA) pathway of
5 FANCI shares sequence similarity with FANCD2, likely evo
6 FANCI switches from FANCD2/repair to PIDD1/apoptosis sig
7 FANCI was localized in spermatocytes and spermatids and
8 FANCI:FANCD2 monoubiquitination is a critical event for
11 ions with RNA polymerase II on the BRCA1 and FANCI genes suggest a transcriptional defect in the abse
12 lized to viral replication compartments, and FANCI-D2 interacted with a multisubunit complex containi
16 e model of the FXDs, but that the FANCD2 and FANCI associated nuclease 1 (FAN1), a component of the F
23 dimerization of monoubiquitinated FANCD2 and FANCI in chromatin is mediated in part through a noncova
24 ut cells display a unique lack of FANCD2 and FANCI localization to chromatin in exponentially growing
26 he role of a proper DNA ligand in FANCD2 and FANCI monoubiquitination, and reveal regulatory mechanis
28 via the monoubiquitination of the FANCD2 and FANCI proteins, targeting these proteins to discrete nuc
30 ty of RAD18 in the recruitment of FANCD2 and FANCI to chromatin and the events leading to their ubiqu
32 s require Fanconi anemia proteins FANCD2 and FANCI, as well as Blm helicase, but not canonical DDR si
33 coni anemia (FA) pathway members, FANCD2 and FANCI, contribute to the repair of replication-stalling
34 rotein complex that ubiquitinates FANCD2 and FANCI, leading to formation of DNA repair structures.
35 lso play a role in mitosis, since FANCD2 and FANCI, the 2 key FA proteins, are localized to the extre
37 is positioned at the interface of FANCD2 and FANCI, where it acts as a covalent molecular pin to trap
54 romosome 15, likely underlain by FANCD2- and FANCI-associated nuclease 1 (FAN1), a nuclease involved
56 clude FANCD2, FANCA, FANCG, ERCC4, FANCE and FANCI, while DNA mismatch repair genes MSH3 and PMS1 out
57 stic insight into the functions of FANCL and FANCI in the catalysis of FANCD2 monoubiquitination.
60 g these genes, eight, including CHEK1, CDC6, FANCI, GINS2, MAD2L1, ORC1, RACGAP1, and SMC4, have demo
61 x monoubiquitinates and recruits the central FANCI and FANCD2 proteins that subsequently coordinate I
64 cient for FA complementation group I and D2 (FANCI and FANCD2) that function as part of the FA I-D2 c
65 y is the Fanconi anemia I-Fanconi anemia D2 (FANCI-FANCD2) (ID) complex, which is activated by DNA da
67 Here, we focus on an FA-I patient-derived FANCI mutant protein, R1299X (deletion of 30 residues fr
70 o germline mutations in FANCA, FANCB, FANCC, FANCI or BRIP1/FANCJ or proficient due to correction wit
74 which requires pathway activation by FANCD2-FANCI monoubiquitination and upstream FANC core complex
75 anched DNA-binding mode that enhances FANCD2-FANCI monoubiquitination through FA core complex interac
78 n of a pseudosymmetric heterodimer of FANCD2-FANCI(4,5) by the FA core complex-a megadalton multiprot
81 ults uncover the mechanism of how the FANCD2-FANCI complex activates the FA pathway, and explains the
86 k repair is monoubiquitination of the FANCD2-FANCI heterodimer, which then recruits nucleases to remo
87 essive mutations in the gene encoding FANCD2/FANCI-associated nuclease 1 (FAN1) cause KIN in humans.
92 each carried nonsense variant in the FANCD2/FANCI-associated nuclease 1 gene (FAN1), which encodes a
93 biquitination and deubiquitination of FANCD2:FANCI heterodimer is central to DNA repair in a pathway
94 s for temporal and spatial control of FANCD2:FANCI monoubiquitination that is critical for chemothera
102 e report the functions of FANCONI ANAEMIA I (FANCI), an Arabidopsis thaliana homologue of the mammali
103 itylation of the FA complementation group I (FANCI)-FANCD2 (ID) complex by FA complementation group L
109 -dependent mechanisms, we generated isogenic FANCI-, FANCD2- and FANCI:FANCD2 double-null cells.
115 nology, we knocked out the expression of lnc-FANCI-2 in the HPV16-positive cervical cancer cell line,
119 We show that in plant cells, as in mammals, FANCI forms a nuclear localised complex with FANCD2.
121 recruited to lesions by a monoubiquitinated FANCI-FANCD2 (ID) complex and participates in ICL repair
122 Our results reveal how monoubiquitinated FANCI:FANCD2, defective in many cancer types and all cas
123 n microscopy that purified monoubiquitinated FANCI:FANCD2 forms filament-like arrays on long dsDNA.
125 E motif, that is critical for the ability of FANCI to properly monoubiquitinate FANCD2 and promote DN
129 ly, removing key endonucleases downstream of FANCI/FANCD2, increasing ICL levels, or allowing damaged
131 pressed in insect cells, a small fraction of FANCI forms a stable complex with FANCD2 (Fanconi anemia
132 highlights common and distinct functions of FANCI and FANCD2 during mouse development, meiotic recom
134 hat, although proper nuclear localization of FANCI is crucial for robust FANCD2 monoubiquitination, t
135 The 7.8 angstrom electron-density map of FANCI-DNA crystals and in vitro data show that each prot
137 significantly precedes monoubiquitination of FANCI; moreover, monoubiquitination responses of FANCD2
140 hway activation relies on phosphorylation of FANCI by the ataxia telangiectasia and Rad3-related (ATR
145 nuclear speckles in a manner that depends on FANCI and on the activity of the checkpoint kinase ATR.
146 2 sequence of UAF1 or mutation of the SIM on FANCI disrupts UAF1/FANCI binding and inhibits FANCD2 de
152 the Fanconi anemia (FA) DNA repair pathway, FANCI, as a key effector of dormant origin firing in res
154 ssociate from FANCD2, whereas phosphomimetic FANCI cannot interact with FANCD2, indicating that FANCI
156 ere, we provide evidence that the FA protein FANCI also functions in ribosome biogenesis, the process
158 nd crosslinks (ICLs), the ICL-repair protein FANCI heterodimerizes with FANCD2 to initiate ICL excisi
160 n monoubiquitination of FA effector proteins FANCI and FANCD2 (FANCI-D2) and required the viral DNA p
161 epair pathway, the tumor suppressor proteins FANCI and FANCD2 (the ID complex), are SUMOylated in res
165 bust FANCD2 monoubiquitination, the putative FANCI EDGE motif is important for DNA crosslink repair.
166 istent with a role in meiotic recombination, FANCI interacted with RAD51 and stimulated D-loop format
170 n the absence of FANCD2, DNA also stimulates FANCI monoubiquitination, but in a FANCL-independent man
171 s also deubiquitinated at a faster rate than FANCI, which can result in a FANCI-ubiquitinated ID2 com
175 tation with purified proteins indicates that FANCI interacts with FANCD2 through its C-terminal amino
176 cannot interact with FANCD2, indicating that FANCI phosphorylation is the molecular trigger for FANCD
178 ir of CRISPR-Cas9-induced DSBs revealed that FANCI promotes single nucleotide insertions and reduces
182 ng super-resolution microscopy, we show that FANCI co-localizes with MCM-bound chromatin in response
184 Using a cell-free system, we showed that FANCI-FANCD2 is required for replication-coupled ICL rep
187 associates with FANCD2 and, together, as the FANCI-FANCD2 (ID) complex, localize to chromatin in resp
190 his pathway is the monoubiquitination of the FANCI-FANCD2 (ID) complex by the multiprotein "core comp
191 ty responsible for monoubiquitination of the FANCI-FANCD2 (ID) complex, which in turn initiates a cas
193 ia pathway is the mono-ubiquitylation of the FANCI-FANCD2 complex, but how this complex confers ICL r
194 onjugase is in the monoubiquitination of the FANCI-FANCD2 heterodimer, a central step in the Fanconi
197 ain and monoubiquitin covalently attached to FANCI, and that this interaction shields monoubiquitinat
198 on forks collide with the lesion, leading to FANCI-FANCD2-dependent unhooking and formation of a doub
199 study, we report that the purified wild-type FANCI (Fanconi anemia complementation group I) protein d
200 r mutation of the SIM on FANCI disrupts UAF1/FANCI binding and inhibits FANCD2 deubiquitination and D
203 ts respective partner, it is unclear whether FANCI has any additional domains that may be important i
205 dress the clinical phenotype associated with FANCI and the epistatic relationship with FANCD2, we cre
206 CUE domain is required for interaction with FANCI, retention of monoubiquitinated FANCD2, and FANCI