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1 SCC cell lines derived from patients without Fanconi anemia.
2 sensitivity to DNA crosslinking agents, and Fanconi anemia.
3 associated with diseases such as cancer and Fanconi anemia.
4 and genetically heterogeneous BMF syndrome: Fanconi anemia.
5 y identified in hereditary breast cancer and Fanconi anemia.
6 associated with breast cancer and linked to Fanconi anemia.
7 , Li-Fraumeni and Bloom syndrome, as well as Fanconi anemia.
8 ailure is a nearly universal complication of Fanconi anemia.
9 ed to uncover a novel pathway linking HPV to Fanconi anemia.
10 opoietic stem cell defects characteristic of Fanconi anemia.
11 e sequence-related FANCJ helicase mutated in Fanconi anemia.
12 reatment, unlike cells from individuals with Fanconi anemia.
13 ny key features of the human genetic illness Fanconi anemia.
14 strand crosslinks is the defining feature in Fanconi anemia.
15 alive but die of malignancy associated with Fanconi anemia.
16 of malignancies, including breast cancer and Fanconi anemia.
17 for chemotherapy responses and prevention of Fanconi anemia.
18 hen biallelic, result in a severe subtype of Fanconi anemia.
19 at least sixteen FANC genes (FANCA-Q) cause Fanconi anemia, a disorder characterized by sensitivity
20 response in cells derived from patients with Fanconi anemia, a hereditary disorder characterized by b
23 Cancer Cell, Schlacher et al. show that the Fanconi anemia and BRCA2 tumor suppressor pathways coope
27 se therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nucl
29 re coordinated by the combined action of the Fanconi anemia and homologous recombination pathways.
30 hich is accompanied by downregulation of the Fanconi anemia and homologous recombination pathways.
31 cle arrest and uncovered a critical role for Fanconi anemia and homologous recombination proteins in
32 minor groove adducts normally recognized by Fanconi anemia and nucleotide excision repair machinery,
33 ndividuals with typical clinical features of Fanconi anemia and show that the cellular defects in the
34 g the pathogenesis of bone marrow failure in Fanconi anemia and suggest possible therapeutic approach
35 tudy included 330 patients (235 acquired, 85 Fanconi anemia, and 10 Diamond-Blackfan anemia) and thei
36 rth defects and bone marrow failure occur in Fanconi anemia, and may have implications for fetal well
37 es the S-phase accumulation of the BRCA1 and Fanconi anemia-associated DNA helicase FANCJ to sites of
38 omplex consists of eight FA proteins and two Fanconi anemia-associated proteins (FAAP24 and FAAP100).
42 ream HSP90-dependent regulatory point in the Fanconi anemia/BRCA DSB/ICL repair pathway, illuminate t
43 tions in BRCA1, BRCA2, or other genes in the Fanconi anemia/BRCA pathway, and these tumors have been
46 rare disorder related to cohesinopathies and Fanconi anemia, caused by bi-allelic mutations in DDX11.
53 rcomes inherent TNFalpha hypersensitivity of Fanconi anemia complementation group C deficient progeni
54 tivates the FA pathway by monoubiquitinating Fanconi anemia complementation group D2 (FANCD2) for the
55 complex acts on DNA-bound, monoubiquitinated Fanconi anemia complementation group D2 (FANCD2) protein
56 itivity to replication-blocking lesions than Fanconi anemia complementation group L (FANCL)-null muta
58 which encodes the DNA translocase FANCM (for Fanconi anemia complementation group M), which is requir
59 l cells depleted of alphaIISp by siRNA or in Fanconi anemia, complementation group A (FA-A) cells, wh
60 ules using TLR agonist-stimulated FANCC- and Fanconi anemia, complementation group A (FANCA)-deficien
62 his model leads to the discovery that Fancl (Fanconi anemia, complementation group L) is downregulate
63 AAP20 UBZ is required for recruitment of the Fanconi anemia complex to interstrand DNA crosslink site
64 ger module, toward ubiquitin recognition and Fanconi anemia complex-mediated DNA interstrand crosslin
67 s essential for viability, yet patients with Fanconi anemia-D1 subtype are born alive with biallelic
70 way analysis, we observed that both cAMP and Fanconi anemia DNA damage repair pathways were affected
73 plicate a functional interaction between the Fanconi anemia DNA repair and FOXO3a pathways in HSC mai
74 g enzyme that promotes the activation of the Fanconi anemia DNA repair pathway and facilitates replic
75 s the E2 ubiquitin-conjugating enzyme of the Fanconi anemia DNA repair pathway and it is overexpresse
76 t data have shown that HIV-1 Vpr targets the Fanconi anemia DNA repair pathway by interacting with an
79 eins and that the ability to dysregulate the Fanconi anemia DNA repair pathway is an essential functi
80 at the ability to dysregulate members of the Fanconi anemia DNA repair pathway is essential for HIV/S
82 link colorectal cancer predisposition to the Fanconi anemia DNA repair pathway, supporting the connec
84 and in the unfractionated BM of healthy and Fanconi anemia donors, resulting in the correction of CD
90 er of repair proteins including those of the Fanconi anemia (FA) and the homologous recombination (HR
94 In response to DNA cross-linking damage, the Fanconi anemia (FA) core complex activates the FA pathwa
95 so associates with FANCM, a component of the Fanconi anemia (FA) core complex that is important for r
96 tute a complex involved in the activation of Fanconi anemia (FA) DNA damage response mechanism, but n
103 ietic stem cell function and are part of the Fanconi anemia (FA) double-strand break DNA repair pathw
104 oteins disabled in the cancer-prone disorder Fanconi anemia (FA) ensure the maintenance of chromosoma
105 d the double-stranded break (DSB) repair and Fanconi anemia (FA) factors active in the S/G2 phase as
108 c stem and progenitor cells with inactivated Fanconi anemia (FA) genes, FANCA and FANCC, are hypersen
158 the bone marrow failure (BMF) mechanisms in Fanconi anemia (FA) may improve current therapeutic stra
163 viously reported intrinsic activation of the Fanconi anemia (FA) pathway in a tumor-prone mouse model
173 Moreover, we have identified several new Fanconi anemia (FA) pathway SNPs that are likely to modu
174 the possibility that HELQ is involved in the Fanconi anemia (FA) pathway, a dominant mechanism for in
181 hematopoietic cell transplantation (HCT) for Fanconi anemia (FA) patients resulted in excessive morbi
188 skews HSC differentiation in mouse models of Fanconi anemia (FA), a genetic disorder associated with
189 athogenesis of many human diseases including Fanconi anemia (FA), a genetic disorder associated with
191 is the predominant clinical manifestation of Fanconi anemia (FA), a rare, recessively inherited disor
192 d activities of translesion synthesis (TLS), Fanconi anemia (FA), and homologous recombination repair
193 icient mice, while phenotypically resembling Fanconi anemia (FA), are also hypersensitive to replicat
195 suffering from a rare human genetic disease, Fanconi anemia (FA), demonstrates the importance of FA g
196 he only curative treatment for patients with Fanconi anemia (FA), published series mostly refer to si
197 t underlying progressive BM failure (BMF) in Fanconi anemia (FA), the most frequent inherited BMF dis
200 ell proliferation, whereas the expression of Fanconi anemia (FA)-complex genes was correlated with el
201 line mutations in RAD51C are known to cause Fanconi anemia (FA)-like disorder and breast and ovarian
202 Current methods for detecting mutations in Fanconi anemia (FA)-suspected patients are inefficient a
216 marrow failure syndromes: (1) defects in the Fanconi anemia (FA)/BRCA DNA repair pathway, (2) defects
218 Surprisingly, depleting BRCA1 or FANCD2 (Fanconi anemia [FA] proteins) or BRG1, a mSWI/SNF subuni
219 etic screens for homologous recombination or Fanconi anemia factors indicates that our evolution-base
221 deleterious c.2715 + 1G > A mutation in the Fanconi anemia gene, FANCD2, was over two times more com
223 describe a previously unappreciated role of Fanconi anemia group A protein (Fanca) during the endomi
227 t other DNA helicases [Bloom syndrome (BLM), Fanconi anemia group J (FANCJ), RECQ1, RecQ, UvrD, or Dn
228 3 ubiquitin-protein ligase RNF168-deficient, Fanconi anemia group J protein (FACJ, BRIP1)-deficient,
229 ion of aldehydes as endogenous genotoxins in Fanconi anemia has provided new insight into disease cau
232 how that Mph1, the budding yeast ortholog of Fanconi anemia helicase FANCM, prevents precocious DSB s
234 ceptibility gene, BRCA2, are associated with Fanconi anemia, implying that some persons who inherit 2
235 Examining the cancer predisposition syndrome Fanconi anemia in depth revealed that mutant FANCA prote
246 ni anemia, we propose collaborations between Fanconi anemia, NER, and MMR are necessary to initiate c
247 FANCD2 and FANCI function together in the Fanconi anemia network of deoxyribonucleic acid (DNA) cr
248 disabling the mismatch, nucleotide excision, Fanconi anemia, nonhomologous end joining, or translesio
249 ndently of the previously identified anti-CO Fanconi anemia of complementation group M (FANCM) helica
251 demonstrated that chronic GVHD (P = .02) and Fanconi anemia (P = .03) negatively impacted survival.
253 owever, were incomplete or low magnitude for Fanconi anemia pathway (FANC) gene mutations relevant to
255 ts elucidate the functional link between the Fanconi anemia pathway and the recombination machinery d
258 we investigated whether and to which extent Fanconi anemia pathway inactivation underlies CIN in HNS
260 CD2 and provide a novel mechanism of how the Fanconi anemia pathway modulates DNA damage response and
262 dy, a role that we show is not shared by the Fanconi anemia pathway or the Slx4-Slx1 nuclease also in
263 define the molecular mechanism by which the Fanconi anemia pathway promotes a key event in replicati
264 ced downregulation of a key component of the Fanconi anemia pathway, FANCD2 through mTOR regulation o
265 of the defects seen in cells impaired in the Fanconi anemia pathway, including a pronounced G2-M cell
266 e that FANCL, the E3 ubiquitin ligase of the Fanconi anemia pathway, is constitutively targeted for d
267 s recombination, postreplication repair, the Fanconi anemia pathway, polymerase beta, and FEN1 are cr
274 ment, including single-strand DNA repair and Fanconi anemia pathways, suggesting that DNA repair afte
279 separately and with loss of staining for the Fanconi anemia protein FANCD2 (corrected Fisher's exact
280 show that the monoubiquitinated form of the Fanconi Anemia protein FANCD2 acts in opposition to the
282 The USP1/UAF1 complex deubiquitinates the Fanconi anemia protein FANCD2, thereby promoting homolog
287 epair activities that are independent of the Fanconi anemia proteins and that this activity is redund
288 phenotype raises the question of whether the Fanconi anemia proteins are stabilized or recruited as p
289 acentric chromosomes, papillar cells require Fanconi anemia proteins FANCD2 and FANCI, as well as Blm
290 rons, from 27 samples from the International Fanconi Anemia Registry at The Rockefeller University.
293 r onset and a loss of blood cells similar to Fanconi anemia.See related article by Park et al., p.
294 utations in the PALB2 tumor suppressor cause Fanconi anemia subtype FA-N, monoallelic mutations predi
295 ) have been identified in patients, with the Fanconi anemia subtype J (FA-J) resulting from homozygou
297 ical processes, including DNA damage repair (Fanconi anemia), telomere maintenance (dyskeratosis cong
298 promising initial hit compound targeting the Fanconi anemia ubiquitin-conjugating enzyme Ube2T and de
299 iven that, mutations in XPF can also lead to Fanconi anemia, we propose collaborations between Fancon