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1  is insufficient to cause cells to be GM-CSF hypersensitive.
2      ACC2 knockout mutants, by contrast, are hypersensitive.
3 e of 10 patients with CRU (10%) were aspirin hypersensitive.
4 ined tolerant; all Group B patients remained hypersensitive.
5      Here we describe an expanded search for hypersensitive accessions of Arabidopsis, evaluate wheth
6 nucleotide resolution, coincident with DNase hypersensitive and ATAC-seq sites at a low sequencing bu
7                                         Both hypersensitive and control glutamatergic terminals were
8                             HCM mutants were hypersensitive and DCM mutants were hyposensitive to Ca(
9  the DSB-induced G2-M checkpoint, inducing a hypersensitive and prolonged arrest.
10 d by the insulator protein CTCF, are DNase I hypersensitive and represent only a small minority of th
11 T cells are equivalent to the ones formed in hypersensitive and tolerant patients, which indicates th
12 NCODE database showed the presence of DNaseI hypersensitive and transcription factors binding sites i
13 gene encoding PTP1B (Ptpn1) are lean, leptin-hypersensitive, and resistant to high fat diet-induced (
14 reening for suppressors of the aluminum (Al) hypersensitive Arabidopsis thaliana mutant als3-1, it wa
15 ase was designed and used as the basis for a hypersensitive assay.
16  a strong level of rescue to the Arabidopsis hypersensitive bzip19 bzip23 double mutant under Zn defi
17  effector strongly suppresses both basal and hypersensitive cell death innate immune responses, and i
18  oxygen species and enhancement of localized hypersensitive cell death.
19 ative genomic analysis was performed between hypersensitive cells and cells categorized as least sens
20                                              Hypersensitive cells underwent early S-phase arrest at d
21 jective of this study was to define 'aspirin-hypersensitive' children and adolescents in a clearly de
22 putationally designed mutant, E181K, that is hypersensitive, confirming predictions derived from in s
23 e, we describe a DCAF protein, ABD1 (for ABA-hypersensitive DCAF1), that negatively regulates abscisi
24 ructs, corresponding to roughly 3500 DNase I hypersensitive (DHS) sites, into the mouse retina by ex
25                            The KRAS nuclease-hypersensitive element (NHE) region contains a G-rich el
26 uman KRAS proto-oncogene contains a nuclease-hypersensitive element located upstream of the major tra
27                                              Hypersensitive footprints were enriched at the 5' and 3'
28 ene expression was linked to tissue-specific hypersensitive footprints.
29 a strain and identified many novel rapamycin-hypersensitive genes.
30                We also describe a set of 37 'hypersensitive' genes which were frequently targeted by
31 clade A of type 2C protein phosphatases: ABA-HYPERSENSITIVE GERMINATION 1 (AHG1) and AHG3.
32                        Here we show that ABA-hypersensitive germination3 (AHG3), encoding a protein p
33           ANT1-deficient animals are insulin-hypersensitive, glucose-tolerant, and resistant to high
34                  Unexpectedly, the rapamycin hypersensitive growth arrest of vip1-1 cells was depende
35 e filtrates that have the capacity to elicit hypersensitive (HR) cell death and disease resistance in
36            The peanut proteins however cause hypersensitive immunogenic responses in certain individu
37                                  Arabidopsis hypersensitive-induced reaction (AtHIR) proteins functio
38  gene encoding a putative protein similar to hypersensitive-induced response proteins (HIR) was ident
39 es in a cell-autonomous manner, leading to a hypersensitive innate immune response to lipopolysacchar
40 hat this ultrafine nanorod material exhibits hypersensitive intense red emission (610 nm) with good b
41 often render an addict's brain reward system hypersensitive, leaving the individual more susceptible
42  associated with virulence, whereas necrotic hypersensitive-like response was not.
43 -based mechanism of resistance, six showed a hypersensitive-like response while three had elevated SA
44                     We find that maize MNase-hypersensitive (MNase HS) regions localize around active
45 llination-independent fruit set in the auxin hypersensitive mutant iaa9-3.
46 tified eed1Delta/Delta as the first farnesol hypersensitive mutant of C. albicans.
47         Accordingly, ABA-insensitive and ABA-hypersensitive mutants were more susceptible and resista
48               In contrast, other putative Pb hypersensitive mutants were unaffected under these condi
49                        All of the 15 aspirin-hypersensitive patients (aged between 6.6 and 17.4 years
50 ll response induced in the blood and skin of hypersensitive patients and healthy volunteers.
51 y volunteers, and the mycobiome signature of hypersensitive patients differed from that of normally s
52  570, 84% CD4(+)) from blood of piperacillin-hypersensitive patients proliferated and secreted TH1/TH
53                      Analysis of plasma from hypersensitive patients revealed the same pattern and le
54 o define the epitopes formed in tolerant and hypersensitive patients taking the beta-lactam antibioti
55 period, 182 positive DPT (accounting for 171 hypersensitive patients) were analysed.
56                                 B cells from hypersensitive patients, but not controls, were stimulat
57          T-cell clones were generated from 4 hypersensitive patients.
58  T lymphocytes are activated in piperacillin-hypersensitive patients.
59 nd an up-regulation of the genes involved in hypersensitive PCD triggered by nonhost-pathogen interac
60 ivation of salicylic acid (SA) signaling and hypersensitive PCD, BiP overexpression further induced N
61            Our data indicate that during the hypersensitive PCD, BiP positively regulates the NRP cel
62      Loss of SDG7 results in a vernalization-hypersensitive phenotype, as well as more rapid cold-med
63      OsHAC4 is the causal gene for the As(V)-hypersensitive phenotype.
64 nhibitor fluridone rescued the mybs1 glucose-hypersensitive phenotype.
65 nd mutations in ABD1 result in ABA- and NaCl-hypersensitive phenotypes.
66 e receptor Tim50 to promote the transport of hypersensitive precursors into the matrix.
67 hether BiP also controlled developmental and hypersensitive programmed cell death (PCD).
68               Administration of fungicide to hypersensitive rats reduced their visceral hypersensitiv
69 of HvSod1 impeded Mla-triggered H(2)O(2) and hypersensitive reaction (HR) at barley-Bgh interaction s
70       However, a durable polymer may provoke hypersensitive reaction, delayed artery healing, and eve
71          This association requires a DNase I hypersensitive region (RHS6) at the Th2 locus.
72 were referenced against enhancer and DNase I hypersensitive regions from ENCODE and Roadmap Epigenomi
73 ing at enhancers, promoters, and other DNase hypersensitive regions not marked with canonical histone
74 d over-representation of enhancers and DNAse hypersensitive regions when compared against all SNPs of
75 , ORC binds nonspecifically to open (DNase I-hypersensitive) regions containing active chromatin mark
76                                         This hypersensitive regulatory switch is entirely dependent o
77                                          The hypersensitive response (HR) is a localized programmed c
78 that expression of AdVPE was associated with hypersensitive response (HR) like cell death.
79 , effector recognition by the host elicits a hypersensitive response (HR) that overcomes the inhibiti
80 ene, PAD4, and salicylate, are disabled, the hypersensitive response (HR) typical of ETI is abolished
81 rigger a rapid localized cell death called a hypersensitive response (HR) upon pathogen recognition.
82 ecreted effector proteins often triggers the hypersensitive response (HR), a complex multicellular de
83 ulation of reactive oxygen species (ROS) and hypersensitive response (HR), a rapid programmed death o
84 unction results in reduced growth and yield, hypersensitive response (HR)-like lesions, accumulation
85  cell death of the infected area through the hypersensitive response (HR).
86 taneous lesions that show characteristics of hypersensitive response (HR).
87 onents (hrpRS, hrpV and PhrpL) from the hrp (hypersensitive response and pathogenicity) gene regulato
88 SERK3 is required for the effector-triggered hypersensitive response and resistance of tomato against
89  overexpression of SINA3 interferes with the hypersensitive response cell death triggered by multiple
90 PM1) P. syringae strains, conserving typical hypersensitive response features.
91          The lipase/esterase also elicited a hypersensitive response in grapevine.
92                      XA23 can trigger strong hypersensitive response in rice, tobacco and tomato.
93                    XA23 can trigger a strong hypersensitive response in rice, tobacco, and tomato.
94          Induction of a Pm3 allele-dependent hypersensitive response in transient assays in Nicotiana
95 lence (Avr) genes in pathogens can produce a hypersensitive response of localized programmed cell dea
96  Furthermore, the csrA mutant did not induce hypersensitive response on tobacco or cause disease on i
97 t analysis method on a small set of bacteria hypersensitive response phenotypes and identified a sing
98 ence under normal conditions and accelerated hypersensitive response triggered by Pseudomonas syringa
99 saic virus (TMV) resistance gene N induces a hypersensitive response upon TMV infection and protects
100  response generally encompasses a defensive 'hypersensitive response' (HR) that involves programmed c
101 en interactions are well known to induce the hypersensitive response, a localized cell death.
102 ylation significantly relieved ER stress and hypersensitive response, and facilitated the folding/ass
103 he major dominant gene for simple resistance hypersensitive response, Cr1 We describe new markers and
104 bacterial mutant strains, and assays for the hypersensitive response, salicylic acid (SA) accumulatio
105 nt dead and dying tissues due to an aberrant hypersensitive response.
106 ce that hexose is involved in triggering the hypersensitive response.
107   Plant genets varied widely for an induced 'hypersensitive' response in which meristem cells become
108 sgr mutant and alfalfa SGR-RNAi lines showed hypersensitive-response-like enhanced cell death upon in
109 lergens and autoantigens and demonstrate how hypersensitive responses to environmental antigens may t
110 ades, as well as prominent genes involved in hypersensitive responses, cell wall fortification, and h
111    Here we present PlantDHS, a plant DNase I hypersensitive site (DHS) database that integrates histo
112 ce, which leverages cell-type specific DNAse Hypersensitive Site (DHS) information from the NIH Epige
113 d that allows us to generate maps of DNase I-hypersensitive site (DHS) of mouse preimplantation embry
114 element (MARE) in locus control region (LCR) hypersensitive site 2 (HS2) reveals a remarkably high de
115  in various cells using Encode Roadmap DNase-hypersensitive site data.
116 co-occurring DNA motifs in 349 human DNase I hypersensitive site datasets.
117             However, GATA-1 binding, DNase I hypersensitive site formation and several histone modifi
118  nucleosome positioning for MNase-seq, DNase hypersensitive site mapping, site annotation and motif i
119 ing (snDrop-seq) and single-cell transposome hypersensitive site sequencing (scTHS-seq).
120 n sequencing and microarray data and DNase I hypersensitive site sequencing data.
121 In this study, we applied DNase-seq (DNase I hypersensitive site sequencing) to study changes of chro
122 of the KRAS gene contains a GC-rich nuclease hypersensitive site with three potential DNA secondary s
123          The Lockd promoter contains a DNase-hypersensitive site, binds numerous transcription factor
124 folds from 1.36 to 3.1) as well as the DNase hypersensitive sites (1.58-2.42 fold), H3K4Me1 (1.23-1.4
125                                      DNase I hypersensitive sites (DHSs) are a hallmark of chromatin
126 tory elements; therefore, mapping of DNase I hypersensitive sites (DHSs) enables the detection of act
127 , we mapped >1.3 million deoxyribonuclease I-hypersensitive sites (DHSs) in 45 mouse cell and tissue
128 drive gene-expression changes though DNase-I hypersensitive sites (DHSs) near transcription start sit
129                                      DNase I hypersensitive sites (DHSs) provide important informatio
130               Over half of embryonic DNase I hypersensitive sites (DHSs) were annotated as noncoding,
131  AP-1 which created thousands of new DNase I-hypersensitive sites (DHSs), enabling ETS-1 and RUNX1 re
132 ave created genome-scale catalogs of DNase I hypersensitive sites (DHSs), which demark potentially fu
133 ory DNA elements are associated with DNase I hypersensitive sites (DHSs).
134 bility and DNA methylation patterns at DNase hypersensitive sites (DHSs).
135                        Sequencing of DNase I hypersensitive sites (DNase-seq) is a powerful technique
136 by two partially overlapping sets of DNase I hypersensitive sites (HSs) that constitute the pituitary
137 isruptive mutations within fetal CNS DNase I hypersensitive sites (i.e., putative regulatory regions)
138 DNA fragment including only its four DNase I hypersensitive sites (lacking the large spacer regions)
139  gene RAD50, containing several RAD50 DNase1-hypersensitive sites (RHS), have been robustly associate
140 which is characterized by four Rad50 DNase I hypersensitive sites (RHS4-7).
141 a shared region of 39 kb that contains DNAse hypersensitive sites active at a restricted time window
142                   Global analyses of DNase I-hypersensitive sites and 3D genome architecture, linking
143 ssible chromatin by global mapping of DNaseI hypersensitive sites and analyzed enriched TF-binding mo
144 in wild-type cells, suggesting that the four hypersensitive sites contain most of the CSR-promoting f
145  with, and maintain the intensity of DNase I hypersensitive sites genome wide, in resting but not in
146 s information from H3K27ac signal at DNase I hypersensitive sites identified from published human and
147 his technique enables genome-wide mapping of hypersensitive sites in a wide range of cell populations
148 erization of the most highly mutated DNase I hypersensitive sites in breast cancer (using in silico a
149 didate noncoding driver mutations in DNase I hypersensitive sites in breast cancer and experimentally
150 enoc7arcinoma cell line (LNCaP) or by DNaseI hypersensitive sites in cancer cell lines.
151 e observed significant enrichment in DNase I hypersensitive sites in fetal heart and lung.
152  we profile parental allele-specific DNase I hypersensitive sites in mouse zygotes and morula embryos
153 ld tend to contain more micrococcal nuclease hypersensitive sites in their promoters, a proxy for ope
154         Bound regions covered 80% of DNase I hypersensitive sites including 99.7% of TSS and 98% of e
155  In the vicinity of active genes and DNase I hypersensitive sites nucleosomes are organized into peri
156 s strong enhancer regions containing DNase I hypersensitive sites overlapping the rs874040 linkage di
157  were capable of pinpointing the most likely hypersensitive sites related to cell-type-specific expre
158                     We present a transposome hypersensitive sites sequencing assay for highly sensiti
159 sequence alone, with the highest accuracy at hypersensitive sites shared across cell types.
160 single guide RNA libraries to target DNase I hypersensitive sites surrounding a gene of interest, we
161  genes with paternal allele-specific DNase I hypersensitive sites that are devoid of DNA methylation
162                      We identify ten DNase I hypersensitive sites that are significantly mutated in b
163 occurs primarily within narrow, highly DNase hypersensitive sites that frequently coincide with trans
164                     By analyzing the DNase I hypersensitive sites under 349 experimental conditions,
165   Enrichment of SNPs associated with DNase I-hypersensitive sites was also found in many tissue types
166           However, correlations with DNase I hypersensitive sites were different for all vectors, ind
167 veral traits, and cell-type-specific DNase-I hypersensitive sites were enriched with SNPs associated
168              We found that 40% DHSs (DNaseI hypersensitive sites) were diminished under darkness.
169 for 17 TFs, 3 histone modifications, DNase I hypersensitive sites, and high-resolution promoter-enhan
170 site methylation, CGIs, co-localized DNase I hypersensitive sites, transcription factor binding sites
171 sitions of 4 histone modifications and DNase hypersensitive sites, Wilson et al reveal many more of t
172 ma cells by inducing and maintaining DNase I hypersensitive sites.
173 and termination sites, enhancers and DNase I hypersensitive sites.
174 r chromatin binding and induction of DNase I hypersensitive sites.
175 C with target-sequence enrichment of DNase I hypersensitive sites.
176 ct through binding events located in DNase I hypersensitive sites.
177 accessible regulatory DNA defined by DNase I hypersensitive sites.
178 n transcription-factor-binding-sites and DNA-hypersensitive-sites.
179 events per bombarded sample in spectinomycin-hypersensitive Slavice and Columbia acc2 knockout backgr
180                      Cells lacking USP45 are hypersensitive specifically to UV irradiation and DNA in
181 sensory signals from visceral organs produce hypersensitive spots on the skin (neurogenic spots), cau
182 tivity and MAs(III) resistance to an arsenic-hypersensitive strain of Escherichia coli, demonstrating
183 um toxicity was investigated using a cadmium-hypersensitive strain of Saccharomyces cerevisiae.
184               In our study, 21 patients with hypersensitive teeth were tested using nonpainful and pa
185  aim was to determine whether these putative hypersensitive terminals could constitute a significant
186 king Snf1 (AMP-activated protein kinase) are hypersensitive to 2DG.
187 ordered cortical microtubule arrays that are hypersensitive to a microtubule-depolymerizing drug.
188 ells, memory B cells, and plasmablasts, were hypersensitive to a range of H2O2 concentrations and res
189 t in the rgs1 mutant background makes plants hypersensitive to a subset of abscisic acid-mediated res
190                           The era1 mutant is hypersensitive to ABA during seed germination and shows
191    In addition, the rgga knockout mutant was hypersensitive to ABA in root growth and survival tests
192 hat the two PLCgamma2 mutants are strikingly hypersensitive to activation by Rac2 such that even wild
193  a dominant negative effect, rendering cells hypersensitive to agents that cause DNA double-strand br
194     The authors found that these lesions are hypersensitive to Akt inhibitors which bind to the ATP b
195 are defective in ASCC foci formation and are hypersensitive to alkylating agents.
196 ts indicate that the angustifolia1 mutant is hypersensitive to alterations in microtubule dynamics.
197                Arabidopsis atm3 mutants were hypersensitive to an inhibitor of glutathione biosynthes
198           Mutants of gamma-ECS and PCS1 were hypersensitive to As and had higher root-to-shoot As tra
199                                A rice mutant hypersensitive to As(V), but not to As(III), was isolate
200 er of children and adolescents with CSU were hypersensitive to aspirin.
201 hesis that hypertrophic cardiomyopathies are hypersensitive to Ca(2+) activation, and dilated cardiom
202 uggesting that TSC2-deficient cells would be hypersensitive to ceramide.
203 C) cell lines and report that nearly 20% are hypersensitive to CHKi monotherapy.
204 A (Csa(-/-)) and group B (Csb(-/-)) mice are hypersensitive to cisplatin, in contrast to global genom
205 R) branch of nucleotide excision repair, are hypersensitive to cisplatin-induced hearing loss and sen
206 -R273H-expressing cancer cells renders cells hypersensitive to cisplatin.
207 ivated GIRK currents in only DA neurons were hypersensitive to cocaine and could be restored to a nor
208 r the polarity gene scribble (scrib(KD)) are hypersensitive to compaction, that interaction with wild
209 ts from Nuclear Magnetic Resonance (NMR) are hypersensitive to conformational changes and ensembles i
210 c overexpression of ARR10, Arabidopsis lines hypersensitive to cytokinin were generated and used to c
211                     K-H deficient cells were hypersensitive to cytotoxic agents that induce DSBs, una
212 oxically, this inhibition renders stem cells hypersensitive to cytotoxic stress, as tumour regenerati
213 d that DNA sequences at RNA splice sites are hypersensitive to digestion by MNase but not by MPE-Fe(I
214               cyp86a2 and lacs2 mutants were hypersensitive to diphenyleneiodonium but could be rever
215 -deficient cells, devoid of most miRNAs, are hypersensitive to DISE, suggesting cellular miRNAs prote
216 g a Pst phosphate uptake system component is hypersensitive to diverse stress conditions in vitro and
217                             sav6 mutants are hypersensitive to DNA damage induced by ultraviolet (UV)
218             Cells devoid of Set2/H3K36me are hypersensitive to DNA-damaging agents and site-specific
219 omologous recombination and consequently are hypersensitive to DNA-damaging agents, including cisplat
220 nogenic and biallelic mutations in SPRTN are hypersensitive to DPC-inducing agents due to a defect in
221 ture, the neo1-1(ts) mutant became extremely hypersensitive to duramycin, although the sensitivity to
222 tions in iron homeostasis-related genes were hypersensitive to E9591 and LMT.
223 or activity whose erythroid progenitors were hypersensitive to EPO.
224 lso have a fragile cuticle and are generally hypersensitive to exogenous agents, a phenotype that is
225                      The silenced lines were hypersensitive to exogenous auxin, while levels of endog
226         The yuc1, yuc4, and ahp6 mutants are hypersensitive to exogenous cytokinin and 1-napthylphtha
227                       mtp8 mutants were only hypersensitive to Fe deficiency when Mn was present in t
228 2-deficient ovarian cancer cell line that is hypersensitive to floxuridine, we show that GSK-3 phosph
229 fective mutants of Arabidopsis thaliana were hypersensitive to freezing before and after cold acclima
230           Moreover, CTCF-deficient cells are hypersensitive to genotoxic stress such as ionizing radi
231                      Sam68 deleted cells are hypersensitive to genotoxicity caused by DNA damaging ag
232 ted that Sam68-deleted cells and animals are hypersensitive to genotoxicity caused by DNA-damaging ag
233       CDKAL1 mutant insulin+ cells were also hypersensitive to glucolipotoxicity.
234 ll populations in the BM and spleen that are hypersensitive to granulocyte macrophage-CSF due to hype
235 ic uptake regulator (Fur) renders mstA cells hypersensitive to H2O2 Conversely, induction of chromoso
236  on respiration for growth but they were not hypersensitive to H2O2.
237 red with the wild type, the rcf2-1 mutant is hypersensitive to heat stress and because the reduced th
238 th Ala substitutions of Cys276 or Cys303 are hypersensitive to high-light conditions during greening.
239 utant in heme biosynthesis, hem13-1, that is hypersensitive to HU.
240 uperoxide dismutase 2 and catalase, and were hypersensitive to hydrogen peroxide.
241               Chicken cells lacking Rnf4 are hypersensitive to hyroxyurea, DNA alkylating drugs and D
242 L-15, and deletion of Cish rendered NK cells hypersensitive to IL-15, as evidenced by enhanced prolif
243 eukemic Tp53-/-Lnk-/- pro-B progenitors were hypersensitive to IL-7, exhibited marked self-renewal in
244 oting cell growth or survival and may become hypersensitive to inactivation of key components within
245 reases genomic instability, and renders mice hypersensitive to IR.
246  presynaptic excitatory neurotransmission is hypersensitive to isoflurane in Ndufs4(KO) mice due to t
247 d JAK2 protein levels and signaling and were hypersensitive to JAKi.
248 D)-deficient mutants of Escherichia coli are hypersensitive to killing by exogenous cytidine, adenosi
249 lmonella strains with mutations of phoPQ are hypersensitive to killing by RNS generated in vitro.
250    Here, we identified and characterized the HYPERSENSITIVE TO LATRUNCULIN B1 (HLB1) protein isolated
251 l gene, Retinoic acid induced-1 (Rai1), were hypersensitive to light such that light eliminated alert
252                    A Us3-deficient virus was hypersensitive to low-energy-induced stress as infected
253 3 kinase binding and Akt activation, and are hypersensitive to MEK inhibition.
254 e demonstrate that SIRT1-deficient mESCs are hypersensitive to methionine restriction/depletion-induc
255             The Arabidopsis fen1-1 mutant is hypersensitive to methyl methanesulfonate and shows redu
256                      Their lymphoblasts were hypersensitive to MMC and MMC-induced monoubiquitination
257 tion to identify protein footprints that are hypersensitive to MNase digestion, an approach we term d
258 nuclease that specifically repairs ICLs, are hypersensitive to most ABQ prodrugs, a phenotype exacerb
259 deficient plants senesce prematurely and are hypersensitive to nitrogen and fixed-carbon limitations.
260 ium tuberculosis result in bacteria that are hypersensitive to NO and attenuated for growth in vivo,
261                         Subjects with asthma hypersensitive to nonsteroidal anti-inflammatory drugs w
262 matin that is covered by nucleosomes and not hypersensitive to nuclease probes such as DNase I.
263 e rare population variant G241R are uniquely hypersensitive to nucleosome complexes in the vicinity o
264 utants exhibited altered morphology and were hypersensitive to nutrient-limiting conditions.
265               XP-C patients are specifically hypersensitive to ocular damage, and XP-F and XP-G patie
266 dopsis thaliana amy3 bam1 double mutants are hypersensitive to osmotic stress, showing impaired root
267            These mutant parasites were often hypersensitive to other PfDHODH inhibitors, which immedi
268 tiated BAK activation, rendering tumor cells hypersensitive to otherwise sublethal doses of clinicall
269       Offspring of mice exposed to DEPs were hypersensitive to OVA, as indicated by airway inflammati
270 ramatic premature aging, and their cells are hypersensitive to oxidative stress.
271 displayed reduced catalase activity and were hypersensitive to oxidative stress.
272 homologous recombination (HR) deficient, are hypersensitive to PARPi through the mechanism of synthet
273  we identified an Arabidopsis mutant, hps10 (hypersensitive to Pi starvation 10), which is morphologi
274 calize in neurons and that Mrap2 KO mice are hypersensitive to PKR1 stimulation.
275                     HR-deficient cancers are hypersensitive to Poly (ADP ribose)-polymerase (PARP) in
276 ce have normal intestinal morphology but are hypersensitive to radiation injury in the intestine comp
277           We found that mutants in PHO84 are hypersensitive to rapamycin and in response to phosphate
278 mutant phyB(Lys996Arg)-YFP photoreceptor are hypersensitive to red light, (ii) light-induced SUMOylat
279 lly resembling Fanconi anemia (FA), are also hypersensitive to replication inhibitors and predisposed
280           Arabidopsis plants lacking SP1 are hypersensitive to salt, osmotic, and oxidative stresses,
281         Several DNA repair-deficient strains hypersensitive to selenide displayed wild-type growth ra
282                      The Y1F strain was also hypersensitive to several different cellular stresses th
283 ive to ABA in dose-response assays, but also hypersensitive to the GA synthesis inhibitor PAC.
284                   DCDC-deficient mutants are hypersensitive to the genotoxic agent methyl methanesulf
285    Instead, we found that ios1-1 plants were hypersensitive to the plant hormone abscisic acid (ABA),
286 ion of this regulon and notably are strongly hypersensitive to the proteasome inhibitors MG132 and bo
287        Cells depleted of Ube2w alone are not hypersensitive to the same DNA damaging agents.
288 how that cells from affected individuals are hypersensitive to TOP2-induced DSBs and that loss of TDP
289  mutants affected in lignin biosynthesis are hypersensitive to U. maydis infection.
290 icken DT40 cells completely lacking H3.3 are hypersensitive to UV light, a defect that epistasis anal
291          Finally, UBR5 and BMI1 KO cells are hypersensitive to UV, which supports the notion that fau
292 f mitochondrial complex I and are strikingly hypersensitive to VAs yet resistant to the intravenous a
293 on of Blimp1 and that Fancc(-/-) B cells are hypersensitive to Wnt activation during ASC differentiat
294 rans proteobacterial phytochrome (DrBphP) is hypersensitive to X-ray photons used in typical synchrot
295              Such tumors are predicted to be hypersensitive to, yet still depend on, secreted Wnts.
296 s (PECTIN LYASE-LIKE, ASPARTYL PROTEASE, DWD-HYPERSENSITIVE-TO-ABA3, and YELLOW STRIPE-LIKE5) were fu
297 vity during a stepwise cold stimulation of a hypersensitive tooth, as well as nonpainful control stim
298 sequence, loss of diphthamide rendered cells hypersensitive toward TNF-mediated apoptosis.
299                         Applications of this hypersensitive transport for optical and microwave limit
300 ong-Evans rats separated from their mothers (hypersensitive) with non-handled (normally sensitive) ra

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