ライフサイエンスコーパス: HindIII

1 three restriction enzymes, EcoRI, PstI, and HindIII.

2 esent in overall gene frequencies of .39 for HindIII, .04 for BamHI, and .02 for EcoRI.

3 agments (AFs) generated with the primer pair HindIII+A and HhaI+A were compared.

4 In CAD patients (>60% stenosis; n = 483), HindIII (+) allelic carriage was increased (93.8% of pat

5 Topical application of liposomal HindIII also induced TNF-alpha in the epidermis of mice.

6 anephora were constructed using two enzymes, HindIII and BstYI.

7 digested with restriction enzymes BamHI and HindIII and cloned in bacteriophage M13mp18.

8 ccus faecium (VRE) isolates was cleaved with HindIII and HaeIII and subjected to agarose gel electrop

9 S. pneumoniae were cloned and used to probe HindIII and HindIII-plus-ApaI genomic DNA digests from o

10 wn shoots of J. regia cv. Chandler using the HindIII and MboI cloning sites.

11 ard arrow AAA, 1 inhibited DNA hydrolysis by HindIII and PspOMI at A downward arrow AGCTT and G downw

12 sis (PFGE) and automated ribotyping by using HindIII and PvuII.

13 to specifically label the HindIII termini in HindIII and Sau3AI restriction digests of clones that ar

14 or plasminogen activator inhibitor-1 (PAI-1) HindIII and tissue plasminogen activator (TPA) EcoRI res

15 urpose of this study was to test whether the HindIII (+) and PvuII (-) or (+) restriction enzyme-defi

16 In no-CAD control subjects (n = 168), HindIII (-) and (+) allelic frequencies were 28.6% and 7

17 ng: type I (EcoBI, EcoAI, Eco124I), type II (HindIII) and type III (EcoP1I).

18 e-site enzymes (BamHI, EcoRI, EcoRV, HaeIII, HindIII, and DNaseI).

19 ng of the different UGPase-cDNAs with BamHI, HindIII, and EcoRI revealed that at least two mRNA popul

20 BAC clones were digested with HindIII, and fragments were size separated on analytical

21 ctrophoretically after digestion with BamHI, HindIII, and MfeI.

22 ints, generated from each clone using BamHI, HindIII, and PstI endonucleases, were combined and used

23 p, the entire library was fingerprinted with HindIII, and the fingerprinted clones were assembled int

24 bridization experiments detected polymorphic HindIII, BamHI, and EcoRI sites.

25 fewer than 10% of the rRNA genes at NOR2 are HindIII-bearing variants.

26 These ORFs, in the HindIII C fragment of MCMV, are colinear with the UL82,

27 CAD risk factors and the other polymorphism, HindIII (+) carriage was associated with an OR = 2.86, C

28 The liposome-encapsulated HindIII caused double strand breaks in DNA and induced I

29 -bacteriophage with the fragments of its own HindIII digest, a standard DNA ladder, was sized by leng

30 ng this new protocol, accurate histograms of HindIII digested lambda DNA were demonstrated for DNA co

31 Class I SSRs in end-sequences of EcoRI- and HindIII-digested BAC clones was one SSR per 40 Kb, where

32 Southern blot analysis of the HindIII-digested chromosomal DNA demonstrated the presen

33 Restriction fragment length polymorphisms of HindIII-digested DNAs from six OspA-negative isolates di

34 Southern blot analysis of HindIII-digested genomic DNA indicated that amplificatio

35 ved alterations in the patterns of PstI- and HindIII-digested proviral DNA were found to be due to th

36 enome was end sequenced and fingerprinted by HindIII digestion.

37 gulator gene (fur) as a probe, a 2.6-kb SalI/HindIII DNA fragment from an A. hydrophila chromosome wa

38 s, made using different restriction enzymes (HindIII, EcoRI, and MboI, respectively), were evaluated

39 tion efficiencies severalfold, while Asp718, HindIII, EcoRI, SalI, SmaI, HpaI, MscI, and SnaBI do not

40 A 3.1-kb HindIII-EcoRI fragment found in both cosmids was shown t

41 obe (395-bp G217B yps 21:E-9 probe or 512-bp HindIII-EcoRI-labelled Downs yps21:E-9).

42 llowed by a multiple restriction digest with HindIII, EcoRV, and AspI to generate restriction fragmen

43 second outbreak with eight patient isolates, HindIII found six were the same type and two were unique

44 The strong effect of a 1.9-kilobase HindIII fragment containing HS3 after, but not prior to,

45 If for a given isolate the HindIII fragment detected by the probe was reduced in si

46 intronless genes contained on a common 8-kb HindIII fragment in a "head-to-head" orientation.

47 A 3.0-kb HindIII fragment of the 24.7-kb linear plasmid was used

48 kb of its promoter were isolated on a 5.4-kb HindIII fragment of this cosmid.

49 ous probe, revealed the presence of a 6.4 kb HindIII fragment that was detectable at only low stringe

50 However, a 1.18-kb HindIII fragment was common among 18 of the 20 biotype 1

51 The GSTM1-0 deletion produces a novel 7.4-kb HindIII fragment with the loss of 10.3- and 11.4-kb Hind

52 A 572-bp SacI-HindIII fragment, BmScH, that was previously shown to ex

53 A 4.4-kb HindIII fragment, encoding an unusual rubredoxin (denote

54 6.2-kb SacI fragment, P </= 0.05 and a 19-kb HindIII fragment, P </= 0.03).

55 range, 24 to 36 kb) that hybridized with the HindIII fragment.

56 wo CR1 alleles that differ in having genomic HindIII fragments of either 7.4 or 6.9 kb and that deter

57 (Zn2+ and Cu2+) interacting with lambda-DNA-HindIII fragments ranging from 2,027 to 23,130 bp in Tri

58 of Mg2+, Ca2+, and Co(NH3)63+ to lambda-DNA-HindIII fragments ranging from 2.0 to 23.1 kbp was used

59 fragment with the loss of 10.3- and 11.4-kb HindIII fragments.

60 termined the nucleotide sequence of a 5.2-kb HindIII genomic DNA fragment which contains the complete

61 ed with HaeIII (cna and fnbA-fnbB probes) or HindIII (hlb probe).

62 B radiation, however, treatment of mice with HindIII in liposomes before contact sensitization did no

63 Unlike UV-B irradiation, however, HindIII in liposomes failed to induce suppressor T cell

64 Topical application of HindIII in liposomes to murine skin in vivo impaired the

65 Another chimeric enzyme, mBE I-II HindIII, in which the amino-terminal end of mBE II was r

66 Automated ribotyping with HindIII is an accurate method for genetic fingerprinting

67 The common LPL polymorphic allele, HindIII (+), is moderately associated with CAD, and the

68 es demonstrate that deletion of sequences in HindIII-J and -I confer altered cell and tissue tropism.

69 deletion of 7.7 kb spanning portions of MCMV HindIII-J and -I.

70 ifference was observed between the BstYI and HindIII libraries (14.9 vs. 8.8 %).

71 re markers were hybridized to filters of the HindIII library, representing 6x coverage of the genome,

72 A HindIII M. pneumoniae fragment containing the lambda MP

73 om those of ESRVs upon digestion with EcoRI, HindIII, NdeI, KpnI, and ScaI.

74 two whole-genome restriction maps (EcoRI and HindIII) of R. sphaeroides strain 2.4.1 were constructed

75 Liposomes containing heat-inactivated HindIII or an endonuclease specific for pyrimidine dimer

76 somes, but not liposomes containing inactive HindIII or an irrelevant endonuclease, to the skin of C3

77 ae were cloned and used to probe HindIII and HindIII-plus-ApaI genomic DNA digests from other isolate

78 ily demonstrated that the segregation of the HindIII polymorphic site is consistent with Mendelian in

79 We also report EcoRI and HindIII polymorphisms that may prove to be useful in dis

80 DNA, standard electrophoresis of BamHI- and HindIII-restricted DNA, Southern hybridization, restrict

81 al DNA damage in immune suppression, we used HindIII restriction endonuclease encapsulated in liposom

82 nd breaks in the DNA of epidermal cells with HindIII restriction endonuclease encapsulated in liposom

83 y primed polymerase chain reaction (AP-PCR), HindIII restriction enzyme analysis (REA), and pulsed-fi

84 ar to that of Co53, and the ApaI, BamHI, and HindIII restriction fingerprints of the total cellular D

85 This probe hybridized with a 4.0-kb HindIII restriction fragment from all 13 strains of S. g

86 We also identified a HindIII restriction fragment length polymorphism of F8A

87 hich were physically mapped to five distinct HindIII restriction fragments.

88 One aphid clone bore a variant HindIII restriction site in the Buchnera leucine plasmid

89 be due to the appearance of PstI and loss of HindIII restriction sites in the pol region as a result

90 The HindIII RFLP and 3 of the latter 6 sites were analyzed i

91 HindIII ribotypes correlated well with PFGE.

92 ysis, single-copy landmark content analysis, HindIII-Sau3AI fingerprinting, and sequencing of PCR pro

93 From Dam methylation and HindIII sensitivity tests, the methylation loci were pre

94 identified in the 5'-flanking region (from a HindIII site at position -1641).

95 es at NOR4 are homogeneous with respect to a HindIII site occurring once per gene.

96 on approximately 1.5 kbp downstream from the HindIII site of 5'Sgamma2 on chromosome 14q32 and identi

97 hloramphenicol resistance cassettes into the HindIII site of the kpsF coding sequence.

98 The presence of the polymorphic HindIII site results in a 7.0-kilobase (kb) band, and th

99 onstruct is extended by 600 bp beyond the 3' HindIII site to include a previously identified regulato

100 ' sequence information beyond the A gamma 3' HindIII site.

101 A 10.0 kb HindIII subclone (Hind10) of this insert yields a high f

102 agged dideoxy ATPs to specifically label the HindIII termini in HindIII and Sau3AI restriction digest

103 In contrast, mBE I-II HindIII transferred more long chains (with a degree of p

104 ining only the RNA coding portion of the OAX HindIII unit both produce OAX RNA transcripts.

105 into Xenopus oocyte nuclei of either the OAX HindIII unit or a subclone containing only the RNA codin

106 NA transcript has been mapped within the OAX HindIII unit using S1 nuclease.

107 he complete DNA sequence of one of these OAX HindIII units is reported here.

108 OAX DNA is present in tandemly repeated HindIII units of 752 bp.

109 cribed from the bovine herpesvirus 4 (BHV-4) HindIII W fragment, in a region of the genome not conser

110 HaeIII was partly inhibited and cleavage by HindIII was enhanced, whereas BamHI, EcoRI, and DNaseI w

111 When HindIII-X and EcoRI-D primer sets were used, CMV DNA fro

112 148 specimens, primer pairs directed to the HindIII-X fragment region of CMV detected target DNA wit

113 In conclusion, primers directed to the HindIII-X fragment region were the most optimal for the

114 with symptomatic infection ranged from 100% (HindIII-X) to 20% (MIE gene); however, specificity was i

115 however, specificity was inversely related (HindIII-X, 45%; MIE gene, 91%) to primers directed to th