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1 ongly associated with an ability to modulate BRCA1 protein.
2 xpression, localization, and function of the BRCA1 protein.
3 2 controls the intracellular localization of BRCA1 protein.
4 EZH2 knockdown upregulated BRCA1 protein.
5 RCA1 siRNA, thus silencing the expression of BRCA1 protein.
6 minant negative inhibitor of the full-length BRCA1 protein.
7 onserved and rapidly evolving regions in the BRCA1 protein.
8 transcription factor NF-kappaB, binds to the BRCA1 protein.
9 he RING finger domain of the 1863 amino acid BRCA1 protein.
10 37 breast cancer cells, which contain mutant BRCA1 protein.
11 d the exon 11-deleted isoforms of the murine Brca1 protein.
12 e due to lack/decreased levels of functional BRCA1 proteins.
13 overexpression of EZH2 and downregulation of BRCA1 proteins.
14 equired for the tumor suppressor function of BRCA1 proteins.
15 olated centrosomes now provide evidence that BRCA1 protein, a suppressor of tumorigenesis in breast a
16 pithelial cells results in nuclear export of BRCA1 protein, aberrant mitoses with extra centrosomes,
17 lation and focus formation of ATM, NBS1, and BRCA1 proteins after IR, they exhibit a defective S-phas
20 gs reveal a tissue-specific function for the BRCA1 protein and raise the possibility that antiprogest
22 ssion of p53 resulted in a rapid decrease in BRCA1 protein and RNA levels and BRCA1 promoter-driven l
24 esence of a second p53 interaction domain in BRCA1 proteins and suggests that BRCA1a and BRCA1b prote
25 transcriptional coactivator function for the BRCA1 protein, and more recently, BRCA1 has been implica
26 SKOV-3 CDDP/R, we found increased levels of BRCA1 protein, and we determined that the SKOV-3 CDDP/R
28 , these results indicate that RING-deficient BRCA1 proteins are hypomorphic and capable of contributi
32 s work we demonstrate that recombinant human Brca1 protein binds strongly to DNA, an activity conferr
33 lls resistant to DNA damage; while truncated BRCA1 proteins blocked the wtBRCA1-induced chemoresistan
35 We have also characterized two new variant BRCA1 proteins (BRCA1a/p110 and BRCA1b/ p100) which are
36 d not affect the expression of the truncated BRCA1 protein, but caused a loss of transcriptional acti
37 express low or undetectable basal levels of BRCA1 protein, but not in cells with high basal expressi
40 t the identification of a DNA damage-induced BRCA1 protein complex containing BCLAF1 and other key co
42 ticular, several carboxyl-terminal truncated BRCA1 proteins conferred chemoresistance, decreased susc
45 om normal thymocytes and found two different BRCA1 proteins, derived from translation of the first an
48 thermore the subcellular localization of the BRCA1 protein does not change throughout the cell cycle.
50 ven amino acids as compared to human, bovine BRCA1 protein exhibited a similar cell cycle-regulated n
56 rotein co-localizes in nuclear foci with the BRCA1 protein following DNA damage and during S-phase, r
57 the N-terminal protein sequence of purified BRCA1 protein from normal thymocytes and found two diffe
58 xic stress, resulting in the displacement of BRCA1 protein from the BRCA1 promoter and subsequent upr
61 suggest that one of the mechanisms by which BRCA1 proteins function is through recruitment of CBP/p3
63 ce presented here indicates that full-length BRCA1 protein generated by in vitro translation interact
66 death, while overexpressing miR-182 reduces BRCA1 protein, impairs homologous recombination-mediated
67 the possibility that the mislocation of the BRCA1 protein in breast cancer cells may be due to a def
69 BRCA1) missense mutations on the function of BRCA1 protein in DNA recombination have been little stud
70 is finding may reflect a direct role for the BRCA1 protein in double strand break (DSB) repair and in
71 investigation, immunohistological studies of BRCA1 protein in frozen breast cancer tissue and MCF7 an
73 n this study, we investigate the role of the BRCA1 protein in modulating a 6-TG-induced MMR damage re
74 ls were deficient in their ability to reduce BRCA1 protein in response to DNA damage, whereas the wil
76 ochemically confirmed restored expression of BRCA1 protein in two cases with secondary mutations.
81 sphorylations, cytoplasmic relocalization of BRCA1 protein is a mechanism whereby BRCA1 function is r
82 ent with this hypothesis, we showed that the BRCA1 protein is absent in 29% of human ULMS and that BR
84 ependent manner, and, in addition, a pool of BRCA1 protein is constitutively associated with the ER u
85 ts in multiple mouse tissues, and that human BRCA1 protein is expressed and stabilized following expo
90 It is clear that one of the roles of the Brca1 protein is to facilitate cellular responses to DNA
91 requires fully functional BRCA1 as a mutant BRCA1 protein is unable to localize to the FOXC1 promote
92 l domain (BRCT) of the Breast Cancer Gene 1 (BRCA1) protein is an evolutionarily conserved module tha
93 be functionally important because a mutated Brca1 protein lacking two phosphorylation sites failed t
94 to be a growth suppressor gene, no change in BRCA1 protein level was found when MCF10A cells were arr
99 mino-17-demethoxygeldanamycin reduced mutant BRCA1 protein levels and restored their sensitivity to P
100 us recombination, probably by regulating the BRCA1 protein levels and the generation of single strand
102 n and secretion we hypothesized that altered BRCA1 protein levels in breast tumors could affect hypox
104 no changes were detected in CstF, BARD1, and BRCA1 protein levels, increased amounts of a CstF/BARD1/
108 estrogen-stimulated MCF7 cells demonstrated BRCA1 protein localization in the granular components of
109 mRNA expression was unaffected; and (2) the BRCA1 protein loss was also observed in DU-145 cells tha
111 lls containing reduced amounts of endogenous BRCA1 protein (obtained by transfecting with BRCA1 siRNA
114 ild-type allele and the cancer cells express Brca1 protein, precluding the chromosomal mechanism for
116 breast and ovarian cancer cells, most of the BRCA1 protein redistributed to the nucleus revealing a n
117 This surprising phenotype suggests that the BRCA1 protein regulates two functions in the control of
118 Here we show that the steady-state levels of BRCA1 protein remain elevated throughout mitosis but beg
119 sy regarding the subcellular localization of BRCA1 proteins, reports of which have ranged from exclus
120 Small interfering RNA-mediated knockdown of BRCA1 protein resulted in decreased immunofluorescence s
124 of the breast cancer susceptibility gene-1 (BRCA1) protein, starting at approximately 1 h after the
126 due to a deficiency of the cells, wild-type BRCA1 protein tagged with the flag epitope was ectopical
128 cifically recognize an approximately 220-kDa BRCA1 protein that is predominantly expressed in the nuc
129 alternative start codon to generate a novel BRCA1 protein that lacks the first 17 amino acids (Delta
130 interesting new gene domain-less (RING-less) BRCA1 protein that mediated resistance to HRD-targeted t
132 ing BRCA1 variants M18T and I42V resulted in BRCA1 proteins that caused centrosome amplification.
133 In studies using epitope-tagged truncated BRCA1 proteins, the ability to stimulate the HSP27 promo
134 ntial mechanism for the nuclear transport of BRCA1 protein, three regions of highly charged, basic re
135 proteasome, calpain, and cathepsins, caused BRCA1 protein to accumulate in the nucleus of several hu
138 istent with the reported localization of the BRCA1 protein to the nucleus, a cytoplasmic localization
139 at lack or impaired binding of the disrupted BRCA1 proteins to E2F, cyclins/CDKs in patients with mut
140 cated (aa 1-100) and full-length (aa 1-1863) BRCA1 proteins to interact with and/or repress ER-alpha
142 diated stabilization of a BRCT domain mutant BRCA1 protein under PARP inhibitor selection pressure.
144 The inhibition of expression of endogenous BRCA1 protein was detected in NIH3T3 transfectants by We
146 Ai to knockdown expression of the endogenous BRCA1 protein, we assessed the level of repression depen
149 s, raised against three regions of the human BRCA1 protein, were characterized and revealed BRCA1 as
150 BRCA1 that restored the reading frame of the BRCA1 protein, whereas none of the three platinum-sensit
154 Delta9,10 transcripts predicted to encode a BRCA1 protein with tumor suppression function.We confirm
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