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1 tion, because a Deltaisu1Deltaisu2 strain is inviable.
2 or growth, but mga2 spt23 double mutants are inviable.
3 hich either of these motifs is disrupted are inviable.
4 e interaction of the J domain with Hsp70 are inviable.
5  combinations of spt3 and mot1 mutations are inviable.
6 sporulate poorly and the spores produced are inviable.
7  of the XY sex are preferentially sterile or inviable.
8 olynucleotide phosphorylase were found to be inviable.
9 n cell growth, spt23 mga2 double mutants are inviable.
10  and that spt3 delta toa1 double mutants are inviable.
11 n2 cln3 triple mutant is Start defective and inviable.
12 yeast cells lacking both Bem2p and Dbm1p are inviable.
13 e fraction that are either female sterile or inviable.
14 use pfy1-111, but not wild-type, cells to be inviable.
15 is essential as trf4 trf5 double mutants are inviable.
16  Tyr residues mutated to Phe (Rpb1-Y1F) were inviable.
17 placing the wild-type gene, the cells became inviable.
18 s in yeast, and spa2delta cdc10-10 cells are inviable.
19 s of selfing, but selfed progeny were mostly inviable.
20 F(1), and almost all hybrid self-progeny are inviable.
21 the progeny of these divisions are typically inviable.
22 lpha1 and alpha2 together rendered the cells inviable.
23 le but sterile: the gametes they produce are inviable.
24 etions, cln3 delta ccr4 delta cells are also inviable.
25 ng the killer element fail to mature and are inviable.
26 s carrying null mutations of either gene are inviable.
27 in "crisis," a period when most cells become inviable.
28 knockout mutations in them are by definition inviable.
29 tants lacking both atToc120 and atToc132 are inviable.
30 phorylase (PNPase) and RNase R activities is inviable.
31 ants are viable whereas the double mutant is inviable.
32 s and fertility, but the double mutants were inviable.
33                     Null mutants of each are inviable.
34  mutants gradually died, and the plants were inviable.
35 ell because a strain lacking both kinases is inviable.
36 ts combining mutations in two RFC genes were inviable.
37 in region II in Pol delta or Pol epsilon are inviable.
38 nd pcl1 Delta pcl2 Delta cdc42-1 strains are inviable.
39 ve, temperature-sensitive, and anaerobically inviable.
40          We found that rpaA-null mutants are inviable after several hours in the dark and compared th
41 elta dnf2Delta dnf3Delta quadruple mutant is inviable, although any one member of this group can main
42 ding these hydrolytic enzymes are considered inviable, although their exact nature has not been studi
43      Strains lacking both NCS1 and NOH1 were inviable and arrested as unbudded cells, implying that P
44                    Clb2p-depleted cells were inviable and arrested with hyper-elongated projections c
45 g individual mcd1 or smc3 mutant alleles are inviable and defective for both sister chromatid cohesio
46                         ppc89Delta cells are inviable and exhibit defects in SPB integrity, and hence
47 over, cells lacking Clb5, Clb6, and Pds1 are inviable and lose cohesion during an unperturbed S phase
48  ada3 swi1, and gcn5 swi1 double mutants are inviable and that mutations in SIN1 allow viability of t
49 GTP or that bind but cannot hydrolyze it are inviable and unable to support nuclear transport of RNAP
50 nations of FG-nups from the pore to simulate inviable and viable NPCs that were previously studied ex
51 helicase and the Mus81/Mms4 endonuclease are inviable, and indirect studies implicate homologous reco
52 metophytes lacking both DRP2A and DRP2B were inviable, arresting prior to the first mitotic division
53                       Mutants of dnaAcos are inviable at 30 degrees C because DnaAcos hyperinitiates,
54 pe A and serotype D calcineurin mutants were inviable at 37 degrees C and avirulent in mice, whereas
55  We found that Deltaelm1 Deltaswe1 cells are inviable at 37 degrees C and that a large proportion of
56                           The null mutant is inviable at 37 degrees C, demonstrating that the OST4 ge
57 were alive but misshapen at 30 degrees C and inviable at 37 degrees C.
58       Cells from which BEM4 was deleted were inviable at 37 degrees C.
59 ells, but it rendered the nup116 null strain inviable at all temperatures and coincidentally resulted
60 ls accumulate toxic 4-carboxysterols and are inviable at high temperature.
61    Homozygous cdc28-4(ts) clb5 diploids were inviable at room temperature.
62 ine; consequently, many meiotic products are inviable because of aneuploidy.
63 Hybrids between species are often sterile or inviable because the long-diverged genomes of their pare
64                           sbp1(-) yeast were inviable but could be rescued by all four exogenous prot
65 Delta cln1 Delta cln2 Delta strains are also inviable, but are rescued by osmotic stabilization with
66         An oxidase-deficient Mia40 mutant is inviable, but can be partially rescued by the addition o
67 imals defective in both sag-1 and eat-16 are inviable, but reducing function in egl-30 restores viabi
68 ession of eIF2 subunits rescued an otherwise inviable cdc123 deletion mutant.
69 e-induced genes, and a morphologically mixed inviable cell fate.
70 uction box resulted in rapid accumulation of inviable cells, frequently multiply budded, with DNA con
71 nondisjunctional progeny, to account for the inviable classes.
72 bition is likely due to the formation of an "inviable complex" which becomes degraded, rather than by
73 and mutants lacking both Elo2p and Elo3p are inviable confirming that the very long-chain fatty acids
74 ble mutant in calcineurin (CNB1) and FKS1 is inviable due to a deficiency in FKS2 expression.
75                     apn1 apn2 rad1 yeast are inviable due to accumulation of abasic sites and strand
76 Embryos from mex-5 single-mutant mothers are inviable due to the misexpression of SKN-1, a transcript
77  All of the transgenic lines were homozygote inviable, dying neonatally and exhibiting heart malforma
78                        However, they produce inviable embryos that succumb to failure of mitosis caus
79 cking Heterochromatin Protein 1E (HP1E) sire inviable embryos that undergo catastrophic mitosis.
80 , by observing uric acid deposits in unfixed inviable embryos, we identified five previously describe
81 propriately processed, leading to permeable, inviable embryos.
82 ssion of UvsW allows growth of an (otherwise inviable) Escherichia coli recG rnhA double mutant, cons
83                  Whereas vti1Delta cells are inviable, expression of hVti1 allows vti1Delta cells to
84 umption that genotype fitness can only be 0 (inviable genotype) or 1 (viable genotype).
85 escued by mutations known to rescue normally inviable hybrid males.
86 Drosophila melanogaster mutation Hmr rescues inviable hybrid sons from the cross of D. melanogaster f
87 educing Hmr(+) activity can rescue otherwise inviable hybrids.
88 nsiently hypermutable fraction that would be inviable if cells were haploids.
89                  Cells depleted of Pfh1 were inviable if they also lacked the human TIMELESS homolog
90 (R275Q, E295K, and A302D) caused cells to be inviable in an in vivo assay in which the mutant beta' i
91 dentified in a screen for mutations that are inviable in combination with a top1 null mutation.
92 constant light conditions, but renders cells inviable in cycling conditions when light and dark perio
93                             UBR2-/- mice are inviable in some strain backgrounds and are defective in
94 vation that if only one gender is sterile or inviable in species hybrids, it is nearly always the het
95 s of wild-type morphology, but the mutant is inviable in the absence of fixed nitrogen and unable to
96 d to as "petite-positive" and those that are inviable in the absence of mitochondrial DNA are termed
97 mperature-sensitive growth phenotype and are inviable in the absence of mitochondrial DNA.
98 ing, we screened for yeast mutants that were inviable in the absence of sterol esterification.
99 ed and polysumoylated proteins, and they are inviable in the absence of the Sgs1 DNA helicase.
100        Many pollen grains were collapsed and inviable in the gsl1-1/gsl1-1 gsl5/+ and gsl1-1/+ gsl5/g
101           Haploid cells lacking cdc24(+) are inviable, indicating that cdc24(+) is an essential gene.
102   dna2-1 rad27/rth1 delta double mutants are inviable, indicating that the mutations are syntheticall
103 riately progress through meiosis, generating inviable meiotic products.
104 de the pore does not exceed 185 mg/mL in the inviable NPCs, whereas for the wild-type and viable NPCs
105        An inp51 inp52 inp53 triple mutant is inviable on standard medium, but can grow weakly on medi
106 ell aneuploidy and subsequent development of inviable or abnormal progeny.
107 ne chromosome, is deleterious and results in inviable or defective progeny if passed through the germ
108 s": those alleles whose interaction produces inviable or infertile interspecific hybrids but does not
109 ses the production of diploid males that are inviable or infertile, imposing a high cost on matings b
110 arp7 delta and arp9 delta mutants are either inviable or show greatly impaired growth and Swi-/Snf- m
111                     Diploid males, which are inviable or sterile in almost all cases studied, are the
112                    The rate of male-specific inviable or sterile mutations is 5 x 10(-4)/generation,
113  the heterogametic sex are more likely to be inviable or sterile than the homogametic sex because som
114            Diploid males are developmentally inviable or sterile, and the likelihood of diploid male
115 the rate at which homogametic hybrids become inviable or sterile.
116 nd represent a genetic load because they are inviable or sterile.
117 males are genetic dead ends because they are inviable or sterile.
118 ocus become diploid males, which are usually inviable or sterile.
119  of the paternal genome that renders embryos inviable or unable to complete diploid development in cr
120                 These microbial partners are inviable outside of specialized host tissues, and theref
121 ot package any DNA, (4) four mutants, though inviable, package the entire lambda chromosome, and (5)
122        Expression of human PDK1 in otherwise inviable pkh1Delta pkh2Delta cells permitted growth.
123 h convert a basal proliferative cell into an inviable rigid squame.
124 ngation-defective and termination-proficient inviable rpoB alleles that affect highly conserved resid
125 ploid A. lyrata and A. arenosa causes mainly inviable seed formation, revealing a strong postzygotic
126 4 plants have diminished stature and produce inviable seeds.
127 ng diploid males, which are often sterile or inviable, sl-CSD can generate substantial inbreeding dep
128 her a red nor a hop1 mutation can rescue the inviable spores produced by a rad52 spo13 strain; this p
129              Finally, mum4-1 mutants produce inviable spores.
130 nes, fail to secrete AcbA and, thus, produce inviable spores.
131 eferentially forms viable spores rather than inviable stalk cells.
132 t the ybr159Deltaayr1Delta double mutant was inviable, suggesting that Ayr1p is responsible for the r
133 the ER-mitochondria encounter structure) are inviable, suggesting that the EMC also functions as a te
134                          Deltapch1 cells are inviable, therefore S. pombe has two essential genes tha
135                                              Inviable TRA1 mutants all showed defects in SAGA and NuA
136 elicases with Deltarep DeltauvrD cells being inviable under rapid growth conditions.
137  with an inactive endogenous vma-1 gene were inviable unless a functional copy of the gene cosegregat
138                                    Cells are inviable upon BRCA2 loss, which leads to replication str
139  to methylmethane sulfonate, and they become inviable upon introducing either the sgs1Delta or rad54D
140 vertebrates, and mouse Nbs1-null mutants are inviable, we tested the hypothesis that the NBS1 657del5
141  haploid and heterozygous tub1-724 cells are inviable when another microtubule effector, PAC2, is ove
142 m30) allele become sterile and their progeny inviable when fed Q7-containing bacteria.
143 f Saccharomyces cerevisiae mutants that were inviable when present in a rad52 null mutation backgroun
144 s involved in morphogenesis are specifically inviable when the Pho85-associated G1 cyclins encoded by
145         Double mutants of dpl1 and ysr2 were inviable, whereas dpl1 ysr2 lcb4 triple mutants were via
146                         rdgB recBC cells are inviable, whereas rdgB recF cells are healthy, suggestin
147 ila simulans are mated, the male progeny are inviable, whereas the female progeny display manifold ma
148  of endosperm development and are completely inviable, while others develop relatively normally at fi
149 re isolated in a screen for mutants that are inviable with deletions in the G1 cyclins CLN1 and CLN2.
150 le in the presence of full-length Ent1p, but inviable with only Ent1DeltaCBMp; these strains were nam
151 eins are genetically redundant, as cells are inviable without at least one of the two BDF genes.
152        Cells lacking all three nucleases are inviable without RecG.
153  value of males, caused by the production of inviable Y0 embryos in X0 x X'Y matings, can outweigh an
154                                    Otherwise inviable ypk1Delta ykr2Delta cells were fully rescued by

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