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1 sensitivity to DNA crosslinking agents, and Fanconi anemia.
2 and genetically heterogeneous BMF syndrome: Fanconi anemia.
3 y identified in hereditary breast cancer and Fanconi anemia.
4 associated with breast cancer and linked to Fanconi anemia.
5 ailure is a nearly universal complication of Fanconi anemia.
6 ed to uncover a novel pathway linking HPV to Fanconi anemia.
7 opoietic stem cell defects characteristic of Fanconi anemia.
8 e sequence-related FANCJ helicase mutated in Fanconi anemia.
9 reatment, unlike cells from individuals with Fanconi anemia.
10 ny key features of the human genetic illness Fanconi anemia.
11 strand crosslinks is the defining feature in Fanconi anemia.
12 alive but die of malignancy associated with Fanconi anemia.
13 for chemotherapy responses and prevention of Fanconi anemia.
14 SCC cell lines derived from patients without Fanconi anemia.
15 at least sixteen FANC genes (FANCA-Q) cause Fanconi anemia, a disorder characterized by sensitivity
16 response in cells derived from patients with Fanconi anemia, a hereditary disorder characterized by b
20 Cancer Cell, Schlacher et al. show that the Fanconi anemia and BRCA2 tumor suppressor pathways coope
24 se therefore establishes a disease model for Fanconi anemia and genetically links a regulator of nucl
26 hich is accompanied by downregulation of the Fanconi anemia and homologous recombination pathways.
27 re coordinated by the combined action of the Fanconi anemia and homologous recombination pathways.
28 cle arrest and uncovered a critical role for Fanconi anemia and homologous recombination proteins in
29 minor groove adducts normally recognized by Fanconi anemia and nucleotide excision repair machinery,
30 ndividuals with typical clinical features of Fanconi anemia and show that the cellular defects in the
31 g the pathogenesis of bone marrow failure in Fanconi anemia and suggest possible therapeutic approach
32 tudy included 330 patients (235 acquired, 85 Fanconi anemia, and 10 Diamond-Blackfan anemia) and thei
33 rth defects and bone marrow failure occur in Fanconi anemia, and may have implications for fetal well
34 es the S-phase accumulation of the BRCA1 and Fanconi anemia-associated DNA helicase FANCJ to sites of
35 omplex consists of eight FA proteins and two Fanconi anemia-associated proteins (FAAP24 and FAAP100).
38 radiation or UVB, UVA does not activate the Fanconi anemia/BRCA DNA damage response pathway or the "
39 ream HSP90-dependent regulatory point in the Fanconi anemia/BRCA DSB/ICL repair pathway, illuminate t
47 rcomes inherent TNFalpha hypersensitivity of Fanconi anemia complementation group C deficient progeni
48 tivates the FA pathway by monoubiquitinating Fanconi anemia complementation group D2 (FANCD2) for the
49 /EBPdelta promotes monoubiquitination of the Fanconi anemia complementation group D2 protein (FANCD2)
50 we report that the purified wild-type FANCI (Fanconi anemia complementation group I) protein directly
51 itivity to replication-blocking lesions than Fanconi anemia complementation group L (FANCL)-null muta
53 which encodes the DNA translocase FANCM (for Fanconi anemia complementation group M), which is requir
54 l cells depleted of alphaIISp by siRNA or in Fanconi anemia, complementation group A (FA-A) cells, wh
55 ules using TLR agonist-stimulated FANCC- and Fanconi anemia, complementation group A (FANCA)-deficien
57 his model leads to the discovery that Fancl (Fanconi anemia, complementation group L) is downregulate
58 AAP20 UBZ is required for recruitment of the Fanconi anemia complex to interstrand DNA crosslink site
59 ger module, toward ubiquitin recognition and Fanconi anemia complex-mediated DNA interstrand crosslin
62 s essential for viability, yet patients with Fanconi anemia-D1 subtype are born alive with biallelic
63 tral to this pathway is the Fanconi anemia I-Fanconi anemia D2 (FANCI-FANCD2) (ID) complex, which is
68 plicate a functional interaction between the Fanconi anemia DNA repair and FOXO3a pathways in HSC mai
69 g enzyme that promotes the activation of the Fanconi anemia DNA repair pathway and facilitates replic
70 s the E2 ubiquitin-conjugating enzyme of the Fanconi anemia DNA repair pathway and it is overexpresse
71 t data have shown that HIV-1 Vpr targets the Fanconi anemia DNA repair pathway by interacting with an
74 eins and that the ability to dysregulate the Fanconi anemia DNA repair pathway is an essential functi
75 at the ability to dysregulate members of the Fanconi anemia DNA repair pathway is essential for HIV/S
77 link colorectal cancer predisposition to the Fanconi anemia DNA repair pathway, supporting the connec
79 and in the unfractionated BM of healthy and Fanconi anemia donors, resulting in the correction of CD
85 basis of the phenotypic similarities between Fanconi Anemia (FA) and Bloom's Syndrome, identifying FA
88 The hallmarks of the rare inherited disorder Fanconi anemia (FA) are progressive bone marrow failure
89 In response to DNA cross-linking damage, the Fanconi anemia (FA) core complex activates the FA pathwa
91 so associates with FANCM, a component of the Fanconi anemia (FA) core complex that is important for r
92 n vertebrates, FANCM-MHF associates with the Fanconi anemia (FA) core complex, promotes FANCD2 monoub
93 tute a complex involved in the activation of Fanconi anemia (FA) DNA damage response mechanism, but n
96 F1 complex is required for regulation of the Fanconi anemia (FA) DNA repair pathway, less is known ab
99 ietic stem cell function and are part of the Fanconi anemia (FA) double-strand break DNA repair pathw
100 oteins disabled in the cancer-prone disorder Fanconi anemia (FA) ensure the maintenance of chromosoma
103 c stem and progenitor cells with inactivated Fanconi anemia (FA) genes, FANCA and FANCC, are hypersen
155 the bone marrow failure (BMF) mechanisms in Fanconi anemia (FA) may improve current therapeutic stra
161 viously reported intrinsic activation of the Fanconi anemia (FA) pathway in a tumor-prone mouse model
166 along with a second report, describe how the Fanconi anemia (FA) pathway is involved in preventing ab
171 Moreover, we have identified several new Fanconi anemia (FA) pathway SNPs that are likely to modu
172 the possibility that HELQ is involved in the Fanconi anemia (FA) pathway, a dominant mechanism for in
179 hematopoietic cell transplantation (HCT) for Fanconi anemia (FA) patients resulted in excessive morbi
189 skews HSC differentiation in mouse models of Fanconi anemia (FA), a genetic disorder associated with
190 athogenesis of many human diseases including Fanconi anemia (FA), a genetic disorder associated with
192 is the predominant clinical manifestation of Fanconi anemia (FA), a rare, recessively inherited disor
193 d activities of translesion synthesis (TLS), Fanconi anemia (FA), and homologous recombination repair
194 icient mice, while phenotypically resembling Fanconi anemia (FA), are also hypersensitive to replicat
196 suffering from a rare human genetic disease, Fanconi anemia (FA), demonstrates the importance of FA g
198 he only curative treatment for patients with Fanconi anemia (FA), published series mostly refer to si
201 ell proliferation, whereas the expression of Fanconi anemia (FA)-complex genes was correlated with el
202 line mutations in RAD51C are known to cause Fanconi anemia (FA)-like disorder and breast and ovarian
203 Current methods for detecting mutations in Fanconi anemia (FA)-suspected patients are inefficient a
218 marrow failure syndromes: (1) defects in the Fanconi anemia (FA)/BRCA DNA repair pathway, (2) defects
219 Surprisingly, depleting BRCA1 or FANCD2 (Fanconi anemia [FA] proteins) or BRG1, a mSWI/SNF subuni
221 tein levels of the DNA repair protein BRIP1 [Fanconi anemia gene J (FANC J)] are upregulated after IR
222 deleterious c.2715 + 1G > A mutation in the Fanconi anemia gene, FANCD2, was over two times more com
224 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
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
248 ni anemia, we propose collaborations between Fanconi anemia, NER, and MMR are necessary to initiate c
249 FANCD2 and FANCI function together in the Fanconi anemia network of deoxyribonucleic acid (DNA) cr
250 disabling the mismatch, nucleotide excision, Fanconi anemia, nonhomologous end joining, or translesio
252 ndently of the previously identified anti-CO Fanconi anemia of complementation group M (FANCM) helica
254 demonstrated that chronic GVHD (P = .02) and Fanconi anemia (P = .03) negatively impacted survival.
256 owever, were incomplete or low magnitude for Fanconi anemia pathway (FANC) gene mutations relevant to
258 ts elucidate the functional link between the Fanconi anemia pathway and the recombination machinery d
261 we investigated whether and to which extent Fanconi anemia pathway inactivation underlies CIN in HNS
264 CD2 and provide a novel mechanism of how the Fanconi anemia pathway modulates DNA damage response and
266 dy, a role that we show is not shared by the Fanconi anemia pathway or the Slx4-Slx1 nuclease also in
267 define the molecular mechanism by which the Fanconi anemia pathway promotes a key event in replicati
269 ced downregulation of a key component of the Fanconi anemia pathway, FANCD2 through mTOR regulation o
270 of the defects seen in cells impaired in the Fanconi anemia pathway, including a pronounced G2-M cell
271 e that FANCL, the E3 ubiquitin ligase of the Fanconi anemia pathway, is constitutively targeted for d
272 s recombination, postreplication repair, the Fanconi anemia pathway, polymerase beta, and FEN1 are cr
283 separately and with loss of staining for the Fanconi anemia protein FANCD2 (corrected Fisher's exact
284 show that the monoubiquitinated form of the Fanconi Anemia protein FANCD2 acts in opposition to the
286 ence, Knipscheer et al. demonstrate that the Fanconi Anemia protein FANCD2 promotes multiple steps of
287 The USP1/UAF1 complex deubiquitinates the Fanconi anemia protein FANCD2, thereby promoting homolog
292 epair activities that are independent of the Fanconi anemia proteins and that this activity is redund
293 phenotype raises the question of whether the Fanconi anemia proteins are stabilized or recruited as p
294 acentric chromosomes, papillar cells require Fanconi anemia proteins FANCD2 and FANCI, as well as Blm
295 rons, from 27 samples from the International Fanconi Anemia Registry at The Rockefeller University.
297 ) have been identified in patients, with the Fanconi anemia subtype J (FA-J) resulting from homozygou
299 promising initial hit compound targeting the Fanconi anemia ubiquitin-conjugating enzyme Ube2T and de
300 iven that, mutations in XPF can also lead to Fanconi anemia, we propose collaborations between Fancon
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