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1 of EBV gH/gL and the EBV gH/gL-N(69)L/S(71)V mutant.
2        We further generated a lon-2 deletion mutant.
3 y, and in vitro evaluation against the C165S mutant.
4 of for in pr1 cells phenocopies the for null mutant.
5 reas spores were nearly absent in the double mutant.
6 cted with a lytically replicating KSHV BAC16 mutant.
7  into wild-type oocytes phenocopied the MIHR mutants.
8  is upregulated in imbibed seeds of drt111-2 mutants.
9 ke protrusions, which are absent in beta-Pix mutants.
10 ic subunits were affected in the phosphatase mutants.
11 ns in wild type Arabidopsis, but not in msh2 mutants.
12 tenuated colonization caused by the virulent mutants.
13  of apoptosis found in the beta-catenin S45F mutants.
14 morphogenic phenotypes of both cop1 and pifQ mutants.
15 f a library of 484 transcription factor null mutants.
16 lopment but not germ cell induction in Tfap2 mutants.
17 meristems observed in fbl17 loss-of-function mutants.
18 type (Col-0) or rescue of GA-deficient dwarf mutants.
19 more defective than those from larp6a single mutants.
20  formation than seen in either of the single mutants.
21 type, 21 IDH mutant/1p19q intact, and 19 IDH mutant/1p19q codeleted), the classification accuracy was
22 le of 49 gliomas (nine IDH wild type, 21 IDH mutant/1p19q intact, and 19 IDH mutant/1p19q codeleted),
23 responses to both wild-type (D614) and D614G mutant(2) SARS-CoV-2 as well as CD8(+) T cell responses,
24 for an insertional Chlamydomonas reinhardtii mutant affected in theVTC2 gene encoding GDP-l-Gal phosp
25                                  The exo70A1 mutant affected SNARE distribution and suppressed vesicl
26 ein in Arabidopsis and that the fertile ask1 mutant allowed us to uncover a comprehensive set of SCF
27 ble mutants displayed more release than Syt1 mutants alone, indicating SYT7 does not mediate the resi
28 Serratia plymuthica Serratiochelin-producing mutants also displayed a decreased growth rate under iro
29                     Biological profiling and mutant analysis revealed that this compound is a prodrug
30                           Double- and triple-mutant analysis shows that DRT111 controls splicing of A
31 grative strategy including enzymatic assays, mutant analysis, metabolic engineering, isotope labeling
32 p1 were performed by constructing a knockout mutant and analyzing the resulting heterokaryon.
33 ad compound 48c, induced necrosis in several mutant and FLT3-resistant AML cell lines and primary bla
34  contrast, assembly of equimolar mixtures of mutant and wild-type desmin generated chimeric filaments
35 he proteomic landscape of ALS-related Ubqln2 mutants and identifies candidate client proteins that ar
36 ity-stability tradeoffs for the advantageous mutants and provide a mechanistic explanation for Lon's
37   Here we use Arabidopsis thaliana ecotypes, mutants and transgenic lines to determine how control of
38  in extra surviving cells in a weak ced-3(-) mutant, and suppresses the embryonic lethality of a muta
39                Specifically, mac1Delta/Delta mutants are profoundly deficient in mitochondrial respir
40                                        While mutant ATXN1 is expressed throughout the brain, patholog
41 tho, we used the BK/BK mouse (homozygous for mutant Becn1(F121A) ) with increased autophagic flux, an
42 rminus of Brd4, but in all other aspects the mutant behaves differently between the two families of p
43 uired for the longevity of insulin signaling mutants, but surprisingly, loss of PQM-1 increases survi
44 mutated MPNs, defective interactions between mutant calreticulin, ERp57, and STIM1 activated SOCE and
45                           Nevertheless, this mutant can induce early gene expression, suggesting a po
46         It has been shown that the M125Q CaM mutant can mimic the functional effects of methionine ox
47 reshold proliferative advantage, below which mutants cannot persist.
48 Fur protein is ~31% in the E. coli iscA/sufA mutant cells and is decreased to ~4% in WT E. coli cells
49 wn tooth development genes) was perturbed in mutant cells and quite significantly for PAX9 and RUNX2.
50                          In vitro, VE-cadDEE mutant cells displayed defects in polarization and cell
51 t, thus prompting the question of how single mutant cells give rise to neoplasia.
52 rift and can also cause downward invasion of mutant cells in the crypt.
53 ed in both bleached mutants, indicating that mutant cells retain some plastid remnants.
54 t to enable survival and proliferation of CI mutant cells under nutrient stress conditions.
55  stabilization, in Arabidopsis lnp1-1 lnp2-1 mutant cells, the ER becomes a dense tubular network.
56                                         This mutant chimera enabled us to determine the cryoelectron
57 llular context using the thermosensitive CCT-mutant CHO-MT58 cell line.
58 els was weaker for the JNCL-related missense mutant CLN3(R334C) and for a JNCL-related C-terminal del
59 ) and for a JNCL-related C-terminal deletion mutant (CLN3DeltaC).
60  broad loss of neural APA in elav/fne double mutant CNS, the first genetic background to largely abro
61 tivating gene (Rag) failed to show rescue of mutant colonization.
62 h prevented IFN-gamma production and rescued mutant colonization.
63 e approach for treating patients with PIK3CA-mutant colorectal cancers and warrants further clinical
64  of wild-type E-cadherin and cis-interaction mutants combined with simulations demonstrate that both
65      Transcriptomic analysis of multiple myc mutants confirmed that MYCs are required for full expres
66  compared with wild-type, but not in the tt4 mutant, consistent with opposite effects of these mutant
67         Immunoprecipitation of wild-type and mutant constructs showed that IQGAP1 associated with cdc
68 ur menthol binding models with thermodynamic mutant cycle analysis.
69  and suppresses the embryonic lethality of a mutant defective for the apoptotic suppressor ced-9/Bcl-
70 f the model plant Arabidopsis thaliana and a mutant defective in mRNA methylation (m(6)A).
71 -type B anthracis strain or with an isogenic mutant deficient for the protective antigen.
72 omyelitis, we examined survival of S. aureus mutants deficient in central metabolic pathways, includi
73 antly improve the physiology of NPC assembly mutants, despite having only negligible effects when NPC
74 nd rule pathway ubiquitin E3 ligases in NatB mutants did not restore NAD(+) levels.
75  In order to overcome the limitations of the mutant DISC1 model and understand the putative regional
76 g is suppressed in constant light, and PRL-1 mutants display a delayed phase under short, but not lon
77                                   Maize rtn2 mutants display increased autophagy and up-regulation of
78 to the late-onset defects, given that hira-1 mutants display mitochondrial stress, and the induction
79                 The osvoz1 and osvoz2 single mutants display modest but opposite M. oryzae resistance
80                         M120A and background mutants display significantly reduced substrate binding,
81 lutionarily conserved polarity cues, yet Wnt mutants display variable PCP defects; thus, how Wnts reg
82                             Syt1/Syt7 double mutants displayed more release than Syt1 mutants alone,
83                           The two frameshift mutants displayed reduced photosynthesis efficiency and
84                     bhlh121 loss-of-function mutants displayed severe defects in Fe homeostasis that
85  DeGeRing might facilitate the generation of mutant DNA sequences for protein engineering and the fun
86 pts of scyl-1 are greatly decreased in adr-1 mutants due to deficient RNA editing at a single adenosi
87 cture and functional properties of the SERCA mutant E340A.
88 ingly we found that the mitochondrial fusion mutants eat-3 and fzo-1 are more resistant to both heat
89                                              Mutant embryos display epidermal hyperplasia, but also a
90 catenin is enhanced in Med23(fx/fx);Wnt1-Cre mutant embryos, which, together with downregulation of C
91  group received adenovirus type 5 host range mutant empty vector and alum.
92  deficits in gene regulatory activity of the mutant ERalpha proteins.
93                                     The pfl2 mutant exhibited reduced capsule production only in gala
94                   Consistent with this, phyB mutants exhibited a freezing-sensitive phenotype, wherea
95 skin) and distant organs (intestine) in tert mutants exhibited higher levels of senescence and inflam
96  elevated iron levels in the hemolymph, Tsf1 mutants exhibited increased susceptibility to Pseudomona
97        Surprisingly, the gpa-3;nlp-24 double mutants exhibited much higher dauer formation than seen
98 r results with a new Lpar1 conditional mouse mutant expand an understanding of LPA(1) signaling in th
99                              Similarly, DAAM mutants express invariably high levels of Ena in vitro.
100    Patients were categorised by EZH2 status: mutant (EZH2(mut)) or wild-type (EZH2(WT)).
101                      Eggs from larp6b single mutant females showed minor chorion defects, but chorion
102 rions from eggs laid by larp6a;larp6b double mutant females were more defective than those from larp6
103 structure ceases to amplify selection if the mutant fitness advantage r is larger than r .
104                            Finally, knockout mutants for 41 genes belonging to the different function
105    In this study, we engineered and selected mutant forms of uPlm that are both catalytically active
106 th and seed development because of nonviable mutant gametes.
107 Following maxillary tooth injury, Smoc2(-/-) mutants had increased osteoclast activity and bone resor
108 ng can also be observed in single and double mutants harboring vps35Delta.
109                                         This mutant has an unusual mechanism as it depletes normal-fu
110 he salicylic acid-deficient Arabidopsis eds5 mutants have an unnoticed fah1-2 background mutation, wh
111 d-type (WT) background, suggesting that such mutants have the potential to promote tumor karyotype ev
112 s supports the notion that patients with IDH-mutant high-risk LGG regardless of codeletion status rec
113 +) mice, expressing the pathogenic human Tau mutant (hTau-P301L), the hTau S199 phosphorylation was a
114                           Here, we show that mutant huntingtin (mHtt) aggregates associated with Hunt
115                      The mechanisms by which mutant huntingtin (mHTT) leads to neuronal cell death in
116  aggregation of the intrinsically disordered mutant Huntingtin (mHtt) vis-a-vis the pathogenicity of
117 ed and can induce responses in patients with mutant IDH2 myelodysplastic syndromes, including in thos
118 e inhibitor BAY11-7085 and dominant-negative mutant IkappaBalphaM inhibited NF-kappaB activity and in
119 lial cells by expressing a hyperactive STAT5 mutant in the mammary gland during postlactational remod
120  frequently used as a catalytically inactive mutant in vivo (based on in vitro peptide studies) actua
121 ing wild-type SERCA2b or a redox-insensitive mutant in which C674 is replaced by serine (C674S) were
122  showcases the utility of yeast phospholipid mutants in dissecting the phospholipid requirements of i
123                               The fitness of mutants in each gene under each condition was then asses
124 scores the importance of employing true null mutants in genetic complementation studies.
125         We found that the defects of the bon mutants in osmotic stress responses were suppressed by m
126                                              Mutants in other proline-glutamate (PE)/PPE clusters, re
127 e generated high depth RNA-sequencing on FUS mutants in parallel to FUS knockout, allowing us to comp
128                Here, we show that Drosophila mutants in the homolog of the human CYFIP1, a gene linke
129 , NT5C2 mutations in six patients, and PRPS1 mutants in two patients.
130 ies were reduced in cpk3/5/6/11/23 quintuple mutants, in correlation with the stomatal opening phenot
131            Experimental analysis of the DLC1 mutants indicated 7 of 9 mutants whose lesions were loca
132 acylglycerols were detected in both bleached mutants, indicating that mutant cells retain some plasti
133  Conversely, the phosphomimetic IFITM3(Y20E) mutant induced oncogenic PI3K signalling and initiated t
134                                         This mutant interacted with zDHHC17 more strongly but was S-a
135 rrelates with reduced AKT signaling in Pcdhg mutant interneurons, and is rescued by genetic blockade
136         The fixation probability of a single mutant invading a population of residents is among the m
137 ons in the ADAR- and ERI-6/7/MOV10-defective mutant is associated with the induction of the unfolded
138          Retention of phosphomimetic dCENP-A mutants is reduced relative to wildtype, while non-phosp
139   We demonstrate that the scoliosis in dstyk mutants is related to the wavy and malformed notochord s
140       Ivosidenib is an oral inhibitor of the mutant isocitrate dehydrogenase 1 (IDH1) enzyme, approve
141 ite 2-hydroxyglutarate via inhibition of the mutant isocitrate dehydrogenase 1 (IDH1; mIDH1) enzyme.
142            In human cancer cells that harbor mutant KRAS and WT p53 (p53), KRAS contributes to the ma
143 that ATP7A, a copper-exporter upregulated by mutant KRAS, is essential for neoplastic growth.
144 ficantly inhibited the cell proliferation of mutant KRAS-expressing cells.
145 le analyses of surrounding groups for WT and mutant KSIs provided insights into the forces and intera
146                                   Adenovirus mutants lacking E1B55K or E4orf6 display defects in vira
147 Arabidopsis (Arabidopsis thaliana) knock-out mutants lacking either phot2 or chup1 and analyzed the k
148 the best characterized function of mtFAS, as mutants lacking lipoylation have an intact ETC.
149 plete loss of hair-cell function, tmc triple-mutant larvae retain normal gross morphology of hair bun
150 dorferi proteins, lipid immunogens, and live mutants lead the design of canonical vaccines aimed at d
151                In a screen of an insertional mutant library of all 14 annotated PTS permease (EIIC) g
152 ease in membrane saturation in the fat1Delta mutant, likely accounting for UPR induction.
153        Similar to the rgi1/2/3/4/5 quintuple mutant, loss-of-function mutants of MPK3 and MPK6, MKK4
154 erials and Methods Data in patients with IDH-mutant lower-grade gliomas (World Health Organization gr
155 derived from idiopathic patients (AHNPs) and mutant LRRK2 patients showed differences between both ph
156             Supplementing gut-sterilized p53-mutant mice and p53-mutant organoids with gallic acid re
157                                   Homozygous mutant mice develop lethal postnatal inflammation of the
158            Lobular appendages are present in mutant mice lacking BCs, implying that although synchron
159      We also find that the Ttbk2 conditional mutant mice quickly lose cilia throughout the brain.
160 the conduction velocity of sciatic nerves of mutant mice showed an 80% decrease, the mice displayed o
161         Partial loss-of-function Fech(m1Pas) mutant mice showed reduced retinal neovascularization an
162          We crossed diabetic leptin receptor-mutant mice to mice lacking CaMKIIdelta globally.
163 ce and were significantly upregulated in the mutant mice, indicating that pre-translational splicing
164 ed striatal phenotypes in heterozygous Disc1 mutant mice, which could be a promising model of DISC1 h
165 min-positive GABAergic interneurons in Grin1 mutant mice.
166 ble behaviors, respectively, in male PC-Tsc1 mutant mice.
167 , learning, and memory are impaired in these mutant mice.
168 IDH1) enzyme, approved for treatment of IDH1-mutant (mIDH1) acute myeloid leukemia (AML).
169 nse beyond those of the synthetic lethal p53 mutant/MK2 combination alone.
170                                 In a genetic mutant model of retinitis pigmentosa, a lead compound, Q
171 l of the left ventricle of RyR2 wild type or mutant mouse hearts.
172 at this process requires factors involved in mutant mRNA decay, as in zebrafish and mouse.
173  known as "tassel blasting." We identified a mutant, necrotic upper tips1 (nut1), that mimics tassel
174 four major subtypes (i.e., BRAF-mutant, NRAS-mutant, NF1-deficient, and triple wild-type).
175 elanoma into four major subtypes (i.e., BRAF-mutant, NRAS-mutant, NF1-deficient, and triple wild-type
176 pping of digenic interactions for a deletion mutant of each paralog, and of trigenic interactions for
177  the expression of the DNA-binding-deficient mutant of NuMA affects chromatin decondensation at the m
178 roach to score the distribution of the tsO45 mutant of VSVG protein in Rab6 depleted cells, we found
179  mycorrhizal colonization was reduced in mlo mutants of barley, wheat, and M. truncatula, and this wa
180                    Enzymatically-compromised mutants of CypD show reduced abilities to dissociate alp
181 n of TRIF and generated STING-noninteracting mutants of human and mouse TRIFs.
182 1/2/3/4/5 quintuple mutant, loss-of-function mutants of MPK3 and MPK6, MKK4 and MKK5, or YDA show a s
183 upted by the expression of dominant-negative mutants of Rab5 and Rab11.
184 of T3D/T1L L3S2, we screened for hyperstable mutants of T3D/T1L L3S2 and identified three point mutat
185 tants share light-associated phenotypes with mutants of the phytochrome B photoreceptor, such as dela
186 compromised such as in temperature-sensitive mutants of Tim17.
187 t, consistent with opposite effects of these mutants on lateral root emergence.
188 the functional effect of the four stillbirth mutants on TRPM7 ion channel function in heterologous ce
189 nting gut-sterilized p53-mutant mice and p53-mutant organoids with gallic acid reinstated the TCF4-ch
190 (2+) elevation, and Ca(2+) influx in octuple mutant ovules rescues LURE1.2 secretion.
191 istically, the tumour-suppressive effects of mutant p53 were driven by disruption of the WNT pathway,
192 ity was independent of its canonical target, mutant p53, and was better associated with glutathione m
193                                         KRAS mutant pancreatic ductal adenocarcinoma (PDAC) is charac
194 d that Parkinson's disease-associated Parkin mutants, ParkinR42P and ParkinG430D, are selectively exc
195                Consistent with this, the hec mutants partially suppress photomorphogenic phenotypes o
196 ine learning model was able to identify EGFR-mutant patients in multiple validation sets with globall
197                     Interestingly, the PRL-1 mutant period lengthening is suppressed in constant ligh
198                                              Mutant peripheral-blood cells showed decreased ubiquityl
199                               We report that mutant pfk13 has emerged independently in Guyana, with g
200                      Rescue of unc-13/Munc13 mutant phenotypes by overexpressed open UNC-64/syntaxin
201 ssion of KCS1 in akr2a mutants rescued akr2a mutant phenotypes, including chilling sensitivity and a
202 d cause salicylic acid- and EDS5-independent mutant phenotypes.
203 anscriptome analysis of Arabidopsis thaliana mutant plants in PAP-SAL1 pathway revealed that the ferr
204                                        While mutant plants lacking xanthophylls are capable of photoa
205                                In the zmnlp5 mutant plants, loss of the ZmNLP5 function led to change
206 ere further studied by phenotyping knock-out mutant plants.
207 on atlases, variation datasets and sequenced mutant populations, provides a foundation to identify ge
208                                Structures of mutant pre-ribosomes lacking the tunnel domain of uL4 re
209 f Src or overexpression of a kinase-dead Src mutant prevented the effect of leptin, whereas a Src kin
210                                   The Fgpal1 mutant produced conidia with fewer septa and more nuclei
211 f-function JAK1 genetic variant results in a mutant protein with mosaic expression that drives multi-
212  and of trigenic interactions for the double mutant, provides insight into their roles and a quantita
213                                          The mutant quenches light-induced rhodopsin signaling like w
214   Using cells expressing a WT or S838A/T841A mutant RB fragment, we present evidence that deficiency
215  (W571) from its typical pocket in these Env mutants renders the Env insensitive to CD4 binding.
216              Overexpression of KCS1 in akr2a mutants rescued akr2a mutant phenotypes, including chill
217 2 system makes it possible to create a large mutant resource for S. viridis in a rapid and high throu
218  ventral striatum of D2R knockout mice, this mutant restored basal locomotor activity and cocaine-ind
219                        In particular, vps13A mutants result in the neurodegenerative disorder Chorea-
220 Infection of HPCs with an HCMVDeltamiR-US5-2 mutant resulted in decreased TGF-beta expression and res
221 nfection with the recombinant A4G (rA4G) RSV mutant resulted in transcriptional readthrough and lower
222 entally generated C-terminal truncated KCNQ3 mutants retain the ability to assemble with KCNQ2.
223 is shows that rcy1Delta and snx4Delta single mutants retain the ability to recycle Snc1, but a snx4De
224      Crystal structures of arsenic-bound p53 mutants reveal a cryptic allosteric site involving three
225 sformation assays and expression analyses in mutants reveal that, in planta, the majority of these re
226 lysis of the lls1 sgl1 and lls1 palm1 double mutants revealed that SGL1 is epistatic to LLS1, and LLS
227 back, we now know that the analysis of these mutants revealed the molecular mechanisms and logic of t
228 ith normalized secretomes from wild-type and mutant S. marcescens derivatives.
229 ort inhibitors counteracted the CEP receptor mutant's steep GSA phenotype.
230                  Here, through a genome-wide mutant screen of human antigen-presenting cells, we show
231                   We found that multiple myc mutants share light-associated phenotypes with mutants o
232                             Purified UNC-45B mutants showed changes in folding and solubility.
233  observed that rem1.2, orc1a, ppd1, and mcm4 mutants showed different degrees of reduction in rosette
234 tochondrial fission and mitochondrial fusion mutants showed increased sensitivity to osmotic stress a
235 2 (At1g65290), and mtACP3 (At5g47630) single mutants showed no discernible morphological growth pheno
236 h specific cellular potency for either WT or mutant SHP2.
237 homogenous population of transient P. patens mutants specific for our gene targets with zero survivin
238 d with the isocitrate dehydrogenase 2 (IDH2) mutant-specific inhibitor enasidenib, leading to improve
239                Preferential selection of the mutant splice site likely reflects its positioning adjac
240                      Analysis of a zebrafish mutant, spondo, whose spine is dysmorphic, prompted us t
241 lacebo in patients with resected, BRAF(V600)-mutant, stage III melanoma in the phase 3 COMBI-AD trial
242 nt, hopper(Bd-we), isolated from a white eye mutant strain had an intact transposase reading frame an
243 dent growth of the M. smegmatis tam deletion mutant strain.
244 r cell signaling, and the germination of rpf mutant strains could not be stimulated by the addition o
245                                 We show that mutant strains lacking gigC have impaired growth in the
246 urement of the relative fitness of bacterial mutants, strains and species in mixed inocula in the hos
247 ty to recycle Snc1, but a snx4Deltarcy1Delta mutant substantially blocks export.
248 erosis (ALS), in which astrocytes expressing mutant superoxide dismutase-1 (mutSOD1) kill wild-type m
249                                       mmachc mutants survived the embryonic period but perished in ea
250                            A Yersinia pestis mutant synthesizing an adjuvant form of lipid A (monopho
251  of either wild-type (WT) LIN28B or a LIN28B mutant that is unable to inhibit let-7 processing increa
252 -of-function fatty acid oxygenation 2 (fou2) mutant that, even when undamaged, shows JA-dependent lea
253 K) cleavage by SpoIVFB, based on analysis of mutants that bypass the need for relief of SpoIVFB inhib
254 can rapidly and comprehensively characterize mutants that have altered hypothalamic patterning, ident
255 ution of PTEN-null embryoid bodies with PTEN mutants that lack only PTEN's lipid phosphatase activity
256                             Recombinant ZIKV mutants that lack ubiquitination are attenuated in human
257                                              Mutants that shorten SFs cause disoriented BBs.
258 ese results and freezing sensitivity of ost1 mutants, the cold-induced [Ca(2+) ](cyt) elevation in th
259               In cells transfected with FliI mutants, the LRR of FliI, but not its gelsolin-like doma
260 , but overexpression of dapF(Ct) allowed the mutant to overcome growth inhibition.
261 diting and engineered separation-of-function mutants to define how CENP-F contributes to kinetochore
262 m characterizing cancer-associated G-protein mutants to neurotransmitter signaling in primary neurons
263 regulatory function of most of the tested FH mutants to WT FH levels on a human HAP-1 cell line and o
264    We describe the isolation of a yeast top2 mutant (top2-F1025Y,R1128G) the product of which generat
265 ient mice, mAb treatment inhibited growth of mutant TP53, WT PTEN LN-229 tumors, and sensitized LN-22
266 in and tropomyosin showed weakening of actin-mutant tropomyosin binding.
267 ng could be beneficial to patients with KRAS-mutant tumors.
268 synthesis pathways, whereas OXPHOS(low) BAP1 mutant UM cells employ fatty acid oxidation.
269 cular analyses showed that OXPHOS(high) BAP1 mutant UM cells utilize glycolytic and nucleotide biosyn
270                By contrast, in an HLTF-HIRAN mutant, unrestrained replication relies on the TLS prote
271 architecture are minimally perturbed in Jag1 mutants until later stages, when ductal remodeling fails
272 sidues, followed by infection of the labeled mutant virions in mammalian cells in the presence of NAb
273  the replication and pathogenesis of the DUB mutant virus (DUBmut) in cultured macrophages and in mic
274                                 Although the mutant virus showed slightly decreased replication in mi
275 risk of the emergence of treatment-resistant mutant virus.
276                   On the other hand, the two mutant viruses induced lower STAT1 phosphorylation and g
277 stigate the potential threat of serum escape mutant viruses to humans and poultry, the impact of thes
278  although the fitness characteristics of the mutant viruses were not fully defined.
279        To do this we screened the E90K GnRHR mutant vs. a library of 645,000 compounds using a cell-b
280 duced [Ca(2+) ](cyt) elevation in the ost1-3 mutant was reduced.
281 ar synthesis data from different strains and mutants, we identify the general underlying design princ
282             Furthermore, by imaging deletion mutants, we observed functional differences between the
283 und that the phenotypic changes of the dwarf mutant were associated with the physiological responses
284                                          The mutants were also affected in development as they produc
285                                        jmj14 mutants were compromised in both local and systemic defe
286                              Three more FPGS mutants were identified in two patients, NT5C2 mutations
287 ies that of ISC1 Reciprocally, ISC1 deletion mutants were sensitive to benomyl, indicating a SAC defe
288 uration was also defective in the vps27Delta mutant, which had a larger vesicle size as measured by d
289 sensitive growth of the yeast mms19 deletion mutant while expression of the diminutive allele resulte
290 nalysis of the DLC1 mutants indicated 7 of 9 mutants whose lesions were located in the Rho-GAP domain
291 inear IgE epitopes, a hypoallergenic Ara h 2 mutant with abolished IgE binding and anaphylactogenic p
292                        We generated an IL-10 mutant with enhanced affinity for its IL-10Rbeta recepto
293 eta counteracted the interference of D/N Vif mutants with A3G degradation by wild-type Vif.
294 m, besides Arabidopsis thaliana, with viable mutants with an essentially complete loss of methylation
295             Here we employ a series of mouse mutants with constitutive and conditional Sox10 deficien
296 nk between pathological localisation of ANKH mutants with different degrees in mineralization.
297 e, we describe the phenotype of 2 Cdk2 point mutants with elevated or decreased activity, respectivel
298 ions exhibit antibiotic tolerance, bacterial mutants with higher or lower tolerant subpopulation size
299   Phosphoproteomic comparison of TbDYRK null mutants with wild-type parasites identified molecules th
300 by Benjamin and colleagues demonstrates that mutant YAP expression is sufficient to enhance tumor cel
301 tovascular development in wild-type and etv2 mutant zebrafish embryos.

 
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