ライフサイエンスコーパス: HAC

1 HAC and RS patients had higher maximum standardized upta

2 HAC are important vectors for investigating the organiza

3 HAC have so far been obtained in immortalized or tumour-

4 HACs avoid the limited cloning capacity, lack of copy nu

5 HACs have been used to complement gene deficiencies in h

6 II-4 cells at ratios of 4:1, 12:1, and 50:1 (HAC:II-4) when compared with coculture with normal human

7 Like mammalian APAF-1, HAC-1 can activate caspases in a dATP-dependent manner i

8 ere histologically classified as: 95 RS, 117 HAC, and 120 histologically indolent CLL (HIC).

9 The 17alpha HAC vectors generated artificial minichromosomes in 32-7

10 The 17alpha HAC vectors produced megabase-sized, circular HACs conta

11 hogen-inoculated seedlings revealed that Z-3-HAC boosts JA-dependent defenses during the necrotrophic

12 Interestingly, analysis of the effect of Z-3-HAC pretreatment on SA- and JA-responsive gene expressio

13 scenario whereby the green leaf volatile Z-3-HAC protects wheat against Fusarium head blight by primi

14 green leaf volatile Z-3-hexenyl acetate (Z-3-HAC) primed wheat (Triticum aestivum) for enhanced defen

15 ioassays showed that, after priming with Z-3-HAC, wheat ears accumulated up to 40% fewer necrotic spi

16 clinically significant HAC (4 thromboses, 35 HACs requiring IVI) was found in 2.9% (n = 1/34), 32.1%

17 AC carrying a gene of interest to generate a HAC vector.

18 Here, a HAC (human artificial chromosome) module with a regulate

19 conversion of any genomic BAC target into a HAC vector by transposon-mediated modification with synt

20 a, or PMA; conditioned medium from activated HAC contained all the MMPs demonstrated by immunohistoch

21 Notably, all HAC-PD1 radiotracer variants enabled much earlier detect

22 ciation between hospital characteristics and HAC program penalization.

23 Survival of patients with RS and HAC was similar among patients with SUVmax <10 or >/=10.

24 tween the hospital quality summary score and HAC program penalization was examined.

25 ells by lipid-mediated DNA transfection, and HACs were identified that bound the active kinetochore p

26 gnificantly advance the utility of BAC-based HACs for functional annotation of the genome and for app

27 en degradation of human articular cartilage (HAC) in vivo.

28 In addition, human articular chondrocytes (HAC) were treated in vitro with either IL-1beta, TNFalph

29 Human articular chondrocytes (HACs) and SW-1353 chondrosarcoma cells were treated with

30 a nonessential human artificial chromosome (HAC) carrying a constitutively expressed EGFP transgene.

31 ions to support human artificial chromosome (HAC) formation was assessed by transfection into human H

32 Human artificial chromosome (HAC) technology has developed rapidly over the past four

33 We have used a human artificial chromosome (HAC) to manipulate the epigenetic state of chromatin wit

34 A human artificial chromosome (HAC) vector was constructed from a 1-Mb yeast artificial

35 y, we show that human artificial chromosome (HAC) vectors based on alpha-satellite (alphoid) DNA from

36 de novo formed Human Artificial Chromosome (HAC) was analyzed.

37 Human artificial chromosome (HAC)-based vectors offer a promising system for delivery

38 Human artificial chromosome (HAC)-based vectors represent an alternative technology f

39 Human artificial chromosome (HAC)-based vectors represent an alternative technology f

40 of a synthetic human artificial chromosome (HAC).

41 ESc) utilizing human artificial chromosomes (HAC), which behave as autonomous endogenous host chromos

42 Human artificial chromosomes (HACs) can be formed de novo by transfection of large fra

43 Human artificial chromosomes (HACs) provide a unique opportunity to study kinetochore

44 n of BAC-based human artificial chromosomes (HACs) requires optimization of each key functional unit

45 development of human artificial chromosomes (HACs).

46 AC vectors produced megabase-sized, circular HACs containing multiple copies of alphoid fragments (60

47 a sign of hepatic artery (HA) complication (HAC).

48 h to dispose halogenated aromatic compounds (HACs).

49 instituted the Hospital-Acquired Condition (HAC) Reduction Program, which reduces payments to the lo

50 isplatin were the top 10 drugs demonstrating HAC loss at a high frequency.

51 ed green fluorescent protein gene-expressing HAC at high frequency, which were stably maintained with

52 allows identifying patients at low risk for HAC, for whom CTA could be avoided, and helps choosing b

53 e 17 but not the Y chromosome regularly form HACs in HT1080 human cells.

54 s can produce these 6 MMPs was obtained from HAC cultures treated with either IL-1beta, TNFalpha, or

55 ta for hospitals participating in the FY2015 HAC Reduction Program were obtained from CMS' Hospital C

56 In order to generate HACs carrying a gene of interest, one can either co-tran

57 ally inadequate in 23%, 29%, and 53% of HIC, HAC, and RS, respectively.

58 either vector or HPRT1 DNA.The 17alpha-HPRT1 HACs were less stable than those with 17alpha only, and

59 ted through its detailed characterization in HAC explants as well as in the urine of human and other

60 The synthetic arrays are competent in HAC formation when transformed into human cells.

61 ytokine-induced MMP1 and MMP13 expression in HACs.

62 elationship in centromeric tandem repeats in HACs requires the ability to manipulate repeat substruct

63 f the drugs based on their ability to induce HAC loss revealed that paclitaxel, gemcitabine, dactylol

64 Microdissected HACs used as fluorescence in situ hybridization probes l

65 different trends, liquid-phase HDH of mixed HACs over Pd/C and Raney Ni catalysts were studied, and

66 ated in hyaluronic acid-based nanoparticles (HAC/DOX) and intravenously administered with TRAILPEG, D

67 hese results may influence the design of new HAC gene transfer vectors.

68 In the new HAC vector, a tTS-EYFP cassette is inserted into a gene-

69 cessfully generating gene expressing de novo HAC in hESc, and is a significant step towards the genet

70 enotypic changes attributed to expression of HAC-encoded genes.

71 the structural requirements for formation of HAC vectors that might have a potential for therapeutic

72 1 amplicon system for efficient transfer of HAC DNA into two hESc.

73 m DeltaYq74 did not support the formation of HACs, indicating that the requirements for the existence

74 In presence of HACs (10(-9) mol/plate), C. lechleri essential oil was t

75 be the main reason why the HDH reactivity of HACs in the presence of NaI is rather low.

76 es on the HAC without significant effects on HAC segregation.

77 ssive chronic lymphocytic leukemia (CLL), or HAC, has not been studied.

78 ly significant HAC, defined as thrombosis or HAC requiring IVI.

79 lphoid(tetO)-HAC has an advantage over other HAC vectors because it can be easily eliminated from cel

80 lphoid(tetO)-HAC has an advantage over other HAC vectors because it can be easily eliminated from cel

81 The resultant HAC vector was introduced into human cells by lipid-medi

82 l high-affinity engineered protein scaffold (HAC-PD1).

83 A clinically significant HAC (4 thromboses, 35 HACs requiring IVI) was found in 2

84 erformance of DUS for clinically significant HAC after OLT.

85 s strategy to predict clinically significant HAC, defined as thrombosis or HAC requiring IVI.

86 were associated with clinically significant HAC.

87 We constructed four structurally similar HAC vectors, two with chromosome 17 or Y alphoid DNA (17

88 Since HACs are known as possible colon and liver cancer induce

89 For liquid-phase HDH of single HACs, hydrogenolytic scission reactivity of C-X bonds de

90 oarenes and bromoarenes in the HDH of single HACs.

91 Six HAC-PD1 radiotracer variants were developed and used in

92 able CENP-B motifs formed mitotically stable HACs in the absence of drug selection without detectable

93 We previously described a synthetic HAC that can be easily eliminated from cell populations

94 eously targeted to a synthetic alphoid(tetO) HAC centromere.

95 The alphoid(tetO)-HAC elimination is highly efficient when a high level of

96 To adopt the alphoid(tetO)-HAC for routine gene function studies, we constructed a

97 The recently developed alphoid(tetO)-HAC has an advantage over other HAC vectors because it c

98 The recently developed alphoid(tetO)-HAC has an advantage over other HAC vectors because it c

99 ding into the loxP site of the alphoid(tetO)-HAC in hamster CHO cells from where the HAC may be MMCT-

100 approach to re-engineering the alphoid(tetO)-HAC that allows verification of phenotypic changes attri

101 tuating heterochromatin on the alphoid(tetO)-HAC that induces fast silencing of the genes on the HAC

102 The newly modified alphoid(tetO)-HAC-based system has multiple applications in gene funct

103 duced by genes loaded into the alphoid(tetO)-HAC.

104 Recent reports show that HACs are useful gene transfer vectors in expression stud

105 The HAC has a dimeric alpha-satellite repeat containing one

106 y and causes spreading of H3K9me3 across the HAC, ultimately inactivating the centromere.

107 te expression of NBS1 and VHL genes from the HAC at physiological levels.

108 P16 domain constitutively expressed from the HAC is capable to generate chromatin changes in the HAC

109 s attributed to expression of genes from the HAC without a transfection step.

110 s attributed to expression of genes from the HAC without a transfection step.

111 capable to generate chromatin changes in the HAC kinetochore that are not compatible with its functio

112 Of the 3284 hospitals participating in the HAC program, 721 (22.0%) were penalized.

113 oach for assessing hospital penalties in the HAC Reduction Program merits reconsideration to ensure i

114 Among hospitals participating in the HAC Reduction Program, hospitals that were penalized mor

115 Penalization in the HAC Reduction Program.

116 pping of replication initiation sites in the HAC revealed that replication preferentially initiated i

117 phenotypes induced by genes loaded into the HAC.

118 Our ability to manipulate the HAC vector by recombinant genetic methods should allow u

119 an be reversed when cells are "cured" of the HAC by inactivating its kinetochore in proliferating cel

120 Importantly, no integration of the HAC DNA was observed in the hESc lines, compared with th

121 However, inactivation of the HAC kinetochore requires transfection of cells by a retr

122 eliminated from cells by inactivation of the HAC kinetochore via binding of chromatin modifiers, tTA

123 eliminated from cells by inactivation of the HAC kinetochore via binding of tTS chromatin modifiers t

124 This silencing of the HAC-encoded genes can be readily recovered by adding dox

125 lencer caused missegregation and loss of the HAC.

126 t induces fast silencing of the genes on the HAC without significant effects on HAC segregation.

127 enous human chromosomes, suggesting that the HAC was not formed by telomere fragmentation.

128 n situ hybridization probes localized to the HAC itself and not to the arms of any endogenous human c

129 etO)-HAC in hamster CHO cells from where the HAC may be MMCT-transferred to the recipient human cells

130 This HAC exhibits normal kinetochore protein composition and

131 Here, we demonstrate the utility of this HAC, which has a unique gene acceptor site, for delivery

132 s with reduced systemic toxicity compared to HAC/DOX or free DOX combined with TRAILPEG (80% vs. 40%

133 Patients with HAC show different characteristics and worse prognosis c

134 ed with only approximately 4% for the Yalpha HAC vectors, indicating that Yalpha is inefficient at fo