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1 on of DNA in the cytoplasm of AT and Artemis-deficient cells.
2 to Wipi2-positive puncta are reduced in Optn-deficient cells.
3  in TGFbeta-dependent signaling in Kindlin-2-deficient cells.
4 e to restore antigen processing in human TAP-deficient cells.
5 EDD8 conjugation pathway components in SENP8-deficient cells.
6 entional DSBs is severely compromised in DEK-deficient cells.
7 sites of ICL induction is perturbed in RFWD3-deficient cells.
8 ses that cause genome instability in BRCA1/2-deficient cells.
9 establishes the substrate for MUS81 in BRCA2-deficient cells.
10 type and Niemann-Pick disease type C1 (NPC1) deficient cells.
11 , much smaller vesicles were formed in SphK1-deficient cells.
12 e inflammatory response was altered in MDFIC-deficient cells.
13 posed an abnormal nucleolar structure in Pf1-deficient cells.
14 signaling, rescued barrier function in KRIT1 deficient cells.
15 nist, but remained the same in TLR3- or Trif-deficient cells.
16 s of TIRR restores PARPi resistance in BRCA1-deficient cells.
17 Vs is substantially diminished in Galectin-3-deficient cells.
18 lls, but only reduced proliferation in Nupr1-deficient cells.
19 ulated cells, but replicated normally in ZAP-deficient cells.
20 r, mitosis onset occurs on schedule in MCPH1 deficient cells.
21 Activation of both MAPKs was defective in CL-deficient cells.
22 mentation and transactivation assays in NEMO-deficient cells.
23 tor-operated cAMP signaling in neurofibromin-deficient cells.
24 the impairment of retromer pathway in Parkin-deficient cells.
25 mbryonic stem cells as effectively as in MMR-deficient cells.
26  cell growth and activated apoptosis in LKB1-deficient cells.
27 in lanthanide-treated BMDMs but not in Gsdmd-deficient cells.
28 ociated with VAMP3 coalescence in WT and Fyn-deficient cells.
29 ssion of the Muller marker P27(Kip1) in Lhx2-deficient cells.
30 nduce protein acetylation in liver kinase B1-deficient cells.
31 rom different intracellular sources in ERAAP-deficient cells.
32 te supply during starvation of the autophagy-deficient cells.
33  actin dynamics in early endosomes of BLOC-1-deficient cells.
34  to the pathogenesis of adipogenesis in PKP2-deficient cells.
35 rgizes with BSO and auranofin in killing TSC-deficient cells.
36 te of cell division in comparison with LAG-3-deficient cells.
37 ent and decreased directionality in vinculin-deficient cells.
38 NP-A, does localize to centromeres in RbAp48-deficient cells.
39 , and Erdr1 fails to induce apoptosis in Fas-deficient cells.
40 g FOXM1, as OTUB1 has little effect on FOXM1-deficient cells.
41  self-cells, while enabling killing of MHC I-deficient cells.
42 ory factor 3 phosphorylation in inflammasome-deficient cells.
43  forks are the entry point for MRE11 in BRCA-deficient cells.
44  we determined to mediate cell death in Tsc2-deficient cells.
45 ck of a strong DNA repair phenotype of RAD52-deficient cells.
46 ry defect but not the growth defect of DCAF1-deficient cells.
47 endent degradation of stalled forks in Abro1-deficient cells.
48 roxyurea treatment observed in WRN- or RAD51-deficient cells.
49 on transporter associated with Ag processing-deficient cells.
50 l to preventing ubiquitin deficiency in zinc-deficient cells.
51 e E2F1 pathway, which was suppressed in PKP2-deficient cells.
52 r the endocytic phenotype observed in Parkin-deficient cells.
53 ored mitochondrial membrane potential in p62-deficient cells.
54 ed replication of C. trachomatis even in p53-deficient cells.
55  more base substitution mutations in BRCA1/2-deficient cells.
56 bp deletion rearrangement is enhanced in ATM-deficient cells.
57 ithin the sequence context identified in RER-deficient cells.
58  DDX41 only in p53-proficient but not in p53-deficient cells.
59 to-AMPase activity were elevated in the FADD-deficient cells.
60 A and protein levels were increased in STAT1-deficient cells.
61 ws activation of cell signaling events of HS-deficient cells.
62 sitive phagophores was not decreased in Optn-deficient cells.
63 d a cage-like appearance, occurred in sacsin-deficient cells.
64 o not completely suppress cell death in Tak1-deficient cells.
65 reaks and chromosomal aberrations in BRCA1/2-deficient cells.
66  cellular mechanism, and selectivity for MMR-deficient cells.
67 transients, SOCE, and Orai1 currents in NCLX-deficient cells.
68 mulation of dysfunctional telomeres in RTEL1-deficient cells.
69 lia, and its activity was attenuated in LRP1-deficient cells.
70 ine-induced DNA damage is abolished in ALKBH deficient cells.
71 city and are preferentially cytotoxic to MMR-deficient cells.
72 pe consistent with cortactin- and coronin 1B-deficient cells [2, 7].
73                              Moreover, RECQ5-deficient cells accumulate RAD18 foci and BRCA1-dependen
74  with long dsRNA specifically vaccinates IFN-deficient cells against infection with viruses bearing a
75  associated with CSR can be resolved in NHEJ-deficient cells (albeit at a reduced level) by a poorly
76 rmed during mitosis, a trait of Topo IIalpha-deficient cells and a hallmark of chromosome instability
77 alpha induction was attenuated in AMPKalpha2-deficient cells and accompanied by its enhanced hydroxyl
78  potent antiproliferative activities in TSC2-deficient cells and an immunodeficient mouse xenograft m
79  tolerance, which sustains survival of BRCA2-deficient cells and can be exploited therapeutically thr
80 th cases, NK cells are unresponsive to MHC I-deficient cells and hyporesponsive when stimulated throu
81 on of TERC increased telomere length in PARN-deficient cells and hypothesized that decreasing posttra
82     Phosphorylated TFEB accumulated in STUB1-deficient cells and in tissues of STUB1-deficient mice r
83 f RAD52, suppress growth of BRCA1- and BRCA2-deficient cells and inhibit RAD52-dependent single-stran
84               Both endogenous Rab7 in Parkin-deficient cells and overexpressed K38 R-Rab7 mutant disp
85 nform on mechanism of PARPi resistance in HR-deficient cells and present Dictyostelium as a convenien
86 ctivation of the tyrosine kinase Syk in TSC2-deficient cells and pulmonary nodules from lymphangiolei
87 s3 encoding galectin-3 was increased in Tsc2-deficient cells and serum of Tsc2cKO(Prrx1)-cre mice.
88 nced by the decreased FST expression in Nrf2-deficient cells and the direct binding of Nrf2 to FST pr
89 ER) as a backup pathway for RER in RNase HII-deficient cells and the known mutagenic profile of DnaE,
90                           As a result, GSNOR-deficient cells and tumors are highly sensitive to SDH i
91                                Moreover, Atm-deficient cells and tumors were sensitive to the PARP in
92 lso increased ubiquitin accumulation in zinc-deficient cells, and by using a ubiquitin-independent pr
93 essed by the RIP1/RIP3/MLKL signaling in TSC-deficient cells, and could be a promising therapeutic ta
94   Tau is overexpressed in cytidine deaminase-deficient cells, and its depletion worsens genome instab
95 n maintaining survival of cytidine deaminase-deficient cells, and ribosomal DNA transcription and sta
96 y conserved residues in the lid region inNCT-deficient cells, and then assessed their impact on gamma
97 l and colony formation were enhanced in PHD3-deficient cells, and this phenotype was associated with
98                                        MYSM1-deficient cells are characterized by increased sensitivi
99  in other regions, the "tumor coldspot" nTSG-deficient cells are extruded toward the basal side and u
100                                      TAX1BP1-deficient cells are highly sensitive to apoptosis in res
101                               Although BRCA1-deficient cells are highly sensitive to treatment with D
102                               Moreover, CTCF-deficient cells are hypersensitive to genotoxic stress s
103 RCA1-proficient cells, PARPi-resistant BRCA1-deficient cells are increasingly dependent on ATR for su
104         Furthermore, we demonstrate that XPC-deficient cells are particularly prone to replication-as
105                  This explains why relA-spoT-deficient cells are sensitive to diverse genotoxic agent
106 etyl-CoA synthesis, which is decreased in CL-deficient cells as a result of a defective PDH bypass pa
107 er TNF mRNA levels were also observed in Fyn-deficient cells as a result of increased transcription a
108 r-free DDT mechanisms are employed by H2Bub1-deficient cells as another means for survival.
109       We show that in both normal and in NMD-deficient cells, AS rates strongly decrease with increas
110 yclin-dependent kinase inhibitor 2B (CDKN2B)-deficient cells, as well as TGFbeta1 upregulation in the
111 dispensable, with all stress defects of Sty1-deficient cells being suppressed by expression of the At
112 trafficking activated the UPR pathway in ULK-deficient cells; both processes were reversed upon expre
113     Pyruvate enables the proliferation of RC-deficient cells but has surprisingly limited effects on
114 ly and efficiently trigger apoptosis in Tsc2-deficient cells but not wild-type cells.
115 tosis and cytotoxicity were blocked in STAT1-deficient cells but restored in cells simultaneously exp
116             MRE11 is highly unstable in PTEN-deficient cells but stability can be significantly resto
117 es RTC4 and RAD27 increases markedly in zinc-deficient cells but, surprisingly, their protein levels
118  ARID1B preserves SWI/SNF function in ARID1A-deficient cells, but defects in SWI/SNF targeting and co
119 ox9 promoted amacrine cell formation in Lhx2-deficient cells, but not in wildtype retinas.
120 inhibitors (PARPis) selectively kill BRCA1/2-deficient cells, but their efficacy in BRCA-deficient pa
121 sized to induce synthetic lethality in BRCA2 deficient cells by PARP inhibition.
122  development and suppressive function of Itk deficient cells can be restored by the expression of the
123              Sodium permeation in alpha-SNAP-deficient cells cannot be corrected by tethering multipl
124 in false alarm and miss probabilities in A20-deficient cells, caused by cell's inability to inhibit T
125                Because fork stalling in FAN1-deficient cells causes chromosomal instability, we reaso
126 K4me1 from enhancers in Mll3/4 catalytically deficient cells causes partial reduction of H3K27ac, but
127              Re-expression of PAR-1 in PAR-1-deficient cells combined with a limiting-dilution transp
128 dance of the corresponding protein in copper-deficient cells concomitant with CRR1-dependent increase
129 action of MHC-associated peptides from ERAAP-deficient cells contained N-terminal extensions and had
130                                  Unlike Coa6 deficient cells, copper supplementation fails to rescue
131            Hyperactivation of mTORC1 in SZT2-deficient cells could be partially corrected by overexpr
132 composition and improved FA resistance of LD-deficient cells cure autophagy and cell survival.
133 kines during TCR stimulation, while in Ndfip-deficient cells cytokine responsiveness persists, promot
134  robust structures on their basal side, nTSG-deficient cells delaminate from the apical side of the e
135       Reconstitution experiments in the JAK1-deficient cells demonstrate that the impaired JAK1 funct
136         Compared to WT macrophages, p58(IPK) deficient cells demonstrated significantly stronger acti
137 he identification of pathways upon which p53-deficient cells depend could reveal therapeutic targets
138                             Drosha and Dicer-deficient cells, devoid of most miRNAs, are hypersensiti
139          In contrast to control cells, SMAD4-deficient cells did not migrate against the direction of
140                             Strikingly, HIR1-deficient cells display altered transcriptional amplitud
141                                       TRIM21-deficient cells display an enhanced antioxidant response
142                      We report here that Nf2-deficient cells display elevated expression levels of ke
143                          Consistently, SIRT7-deficient cells display increased replication stress and
144    Notably, N-linked glycans produced by GNE-deficient cells displayed enhanced binding to galectin-1
145  cell population is short-lived, with the HC-deficient cells displaying signs of an unfolded protein
146  effects of the knockout are impaired, NLRX1-deficient cells do not display significant differences i
147    The pattern of NF-kappaB dynamics in TRIF-deficient cells does not, however, directly reflect the
148 it fails to localize to the midbody in SCCRO-deficient cells during abscission, and its inactivation
149 TP/AMP accumulation was observed in the FADD-deficient cells during necroptosis, but not during apopt
150 bustness of the observed phenotype in Torsin-deficient cells enables a structural analysis via electr
151  RNase L activity promotes survival of ADAR1 deficient cells even in the presence of MDA5 and MAVS, s
152 between PAK4 and p85alpha and find that PAK4 deficient cells exhibit a reduction in Akt phosphorylati
153                                        TRMT1-deficient cells exhibit decreased proliferation rates, a
154 due to lack of inhibition of PFKFB3, IKKbeta-deficient cells exhibit elevated aerobic glycolysis and
155 ent survival differences, we found that Wwox-deficient cells exhibit enhanced homology directed repai
156                  Remarkably, nearly all KRAS deficient cells exhibit phosphoinositide 3-kinase (PI3K)
157                             Cultured Clec16a-deficient cells exhibited a striking accumulation of LC3
158                                           CL-deficient cells exhibited decreased GFP-tagged mitochond
159                 Compared with controls, ULK1-deficient cells exhibited decreased tumor necrosis facto
160                                         LKB1-deficient cells exhibited enhanced sensitivity to erloti
161                                        PHGDH-deficient cells exhibited increased oxidant levels and a
162 d membrane extensions, whereas RhoA- or RhoB-deficient cells exhibited mild phenotypes.
163 odel of irradiated breast cancer cells; Wwox-deficient cells exhibited significantly shorter tumor la
164                                          Ska-deficient cells fail to biorient and display chromosome
165                  When exposed to cWnts, Bmp2-deficient cells fail to progress through the Runx2/Osx1
166 tent with reduced MRN complex function, PTEN-deficient cells fail to resect DNA double-strand breaks
167 hromatin localization is decreased in FANCD2 deficient cells, FANCD2 siRNA knockdown cells and RAD51
168   We also report evidence that in human MGMT-deficient cell-free extracts, CAF-1-dependent packaging
169 L3/4 complex protein, PTIP, protects Brca1/2-deficient cells from DNA damage and rescues the lethalit
170                           In contrast, smArf-deficient cells from mice of the Arf(M45A) strain are as
171                                        NLRX1-deficient cells generate an amplified STING-dependent ho
172                         We found that RAD51D-deficient cells had a reduced capacity for HR-mediated g
173    RNA-Seq analysis revealed that the DNMT3a-deficient cells had deactivated gene networks involved i
174         Decreased cellular responses in WASp-deficient cells have been interpreted to mean that WASp
175                             Conversely, HSF1-deficient cells have increased autophagic flux under bot
176                              Indeed, RNase H-deficient cells have increased chromosomal rearrangement
177              We showed previously that Trex1-deficient cells have reduced mammalian target of rapamyc
178                    Depletion of Prmt1 in p53-deficient cells impaired tumor initiation and maintenanc
179 drial damage, and necrotic cell death in TSC-deficient cells in a highly synergistic and cell context
180 pivot rescues gamma-secretase activity inNCT-deficient cells in a manner indistinguishable from WT NC
181  from the screen, repressed survival of BCL6-deficient cells in vitro and reduced growth and prolifer
182 is have selective deleterious effects on TSC-deficient cells, including in mouse tumor models.
183 mpromised the aggressive phenotype of Merlin-deficient cells indicating a clear dependence of cells o
184 ency of reactivation from latency in miR-155-deficient cells, indicating an important role for miR-15
185       Upon RA-mediated differentiation, Oct1-deficient cells induce lineage-appropriate developmental
186 of palmitic acid from malonyl-CoA, drove NF2-deficient cells into apoptosis.
187 anced degradation of PAR1 observed in Rab11B-deficient cells is blocked by depletion of Rab11A and th
188        The increased ICL sensitivity of PTEN-deficient cells is caused, in part, by elevated PLK1 kin
189 o co-transcriptionally formed G4 DNA in Top1-deficient cells is significantly augmented and that its
190  with canonical repair pathways but, in NHEJ-deficient cells, is engaged more frequently and protects
191 he survival of homologous recombination (HR) deficient cells, it represents a promising new cancer dr
192 ith the retromer are maintained in autophagy-deficient cells, leading to GLUT1 mis-sorting into endol
193           Failure of RipA processing in MarP-deficient cells leads to cell elongation and chain forma
194 rease of N(6)-methyladenine levels in Alkbh1-deficient cells leads to transcriptional silencing.
195 C-disparate mouse strains with costimulation-deficient cells led to robust cytotoxicity mediated by c
196                We have established that PTEN-deficient cells, like FA cells, exhibit increased cytoto
197                                     In MICOS-deficient cells, limiting PS transfer by Ups2-Mdm35 and
198 enesis or homeostasis and establish a Torsin-deficient cell line as a valuable experimental platform
199                        However, in the ErbB3-deficient cell line MIAPaCa-2, no such effects were obse
200 onversely, reconstitution of MTAP in an MTAP-deficient cell line rescued PRMT5 dependence.
201 n triggered rapid programmed necrosis in VHL-deficient cell lines and primary ccRCC tumor cells, but
202                       Certain DNA DSB repair-deficient cell lines are sensitized toward 1, and 1 is u
203 and lack of TCR signaling restoration in LAT-deficient cell lines reconstituted with a synthetic LAT
204                                       TRIM14-deficient cell lines showed both resistance to hypoxia-i
205 minished the Warburg-like phenotype in SIRT3-deficient cell lines, and this effect is largely depende
206 ous ChIP-seq and microarray analyses in Isl1-deficient cell lines, we found that Slit2 transcript was
207 unoblotting and immunoprecipitation in STAT1-deficient cell lines.
208 cate that nascent DNA degradation in BRCA1/2-deficient cells occurs as a consequence of MRE11-depende
209 ly enriched, relative to random in LEDGF/p75 deficient cells, other host factors likely contribute to
210 s and stalled forks in PARPi-resistant BRCA1-deficient cells, overcoming both resistance mechanisms.
211 olite that accumulates in fumarate hydratase-deficient cells, plays a key role in cell transformation
212 onfirmed diminished neurogenesis in the MCT8-deficient cell population as well as aberrant migration
213                   However, LmRad9 and LmHus1-deficient cells present markedly opposite phenotypes, wh
214 ed" peptides was lost in WT cells, and ERAAP-deficient cells presented a unique "unedited" repertoire
215  viral glycoproteins fail to mature in SPCA1-deficient cells preventing viral spread, which is eviden
216                              However, how HR-deficient cells process DSBs is not clear.
217 to exhibiting low levels of sialylation, GNE-deficient cells produced distinct N-linked glycan struct
218 urvival and sensitivity to ER stress in USF3-deficient cells provide avenues for therapeutic and adju
219  accumulation and lipid peroxidation in Gpx4-deficient cells remain high.
220 ugs that selectively affect viability of TSC-deficient cells, representing promising candidates for r
221 e that replication fork progression in BRCA2-deficient cells requires MUS81.
222   Furthermore, TBC1D5 depletion in autophagy-deficient cells rescues retromer recruitment to endosoma
223                                However, ULK1-deficient cells responded normally to DMXAA, indicating
224                 Reexpression of SCAP in SCAP-deficient cells restored SREBP2 protein expression and p
225 netic prevention of ROS accumulation in Oma1-deficient cells restores this defective TOR signaling.
226 accumulation of phosphorylated TFEB in STUB1-deficient cells resulted in reduced autophagy and reduce
227  to replication stress is impaired in DONSON-deficient cells, resulting in decreased checkpoint activ
228 ion induced by Rh-PPO is not repaired in MMR-deficient cells, resulting in selective cytotoxicity.
229 by the tmeA strain of Chlamydia, since AHNAK-deficient cells revealed no invasion phenotype.
230 ifferentially expressed in wild-type and Pf1-deficient cells revealed the impact of Pf1 in multiple r
231        Overexpression of ID1 or ID2 in STAT5-deficient cells reversed osteoclast development recovere
232                                      In zinc-deficient cells, RTC4 RNA with longer transcript leaders
233 d that allosensitization with "costimulation-deficient" cells should induce DSA synthesis but not nai
234                                        BRCA1-deficient cells show defects in DNA repair and rely on o
235                                     Munc13-4-deficient cells show increased numbers of significantly
236                  Here, we report that Spata2-deficient cells show resistance to RIPK1-dependent apopt
237 in ligands, was severely impaired, and CYTH1-deficient cells showed a reduced integrin beta1 activati
238                                      RASGRP1-deficient cells showed decreased activation of the GTPas
239                                         ASS1-deficient cells showed preferential sensitivity to ADI-P
240         Results obtained for normal and GAGs-deficient cells showed that the recombinant proteins mai
241  (PDS) increases telomere fragility in BRCA2-deficient cells, suggesting that G4 formation drives tel
242 Gli2, restored Hh pathway activation in Intu-deficient cells, suggesting that INTU functions upstream
243 e midbody was deficient in SCCRO- and KLHL21-deficient cells, suggesting that it is the target of Cul
244 wild-type (wt) cells compared to that in PKR-deficient cells, suggesting that PKR or PKR activation d
245 sed secretion of exosomes observed in Parkin-deficient cells, suggesting that Rab7 deregulation may b
246 ding Cul3(KLHL9/KLHL13), was intact in SCCRO-deficient cells, suggesting that SCCRO selectively, rath
247 icularly accumulate in HSP70- and proteasome-deficient cells, suggesting that SUMOylation participate
248       The protective effects are lost in CMA-deficient cells, suggesting that they are mediated throu
249 me trafficking and ALR, accumulated in GCase deficient cells, supporting the notion that lysosomal re
250 dia with beta-mercaptoethanol rescues CD98hc-deficient cell survival.
251 levation in TNFalpha expression rendered VHL-deficient cells susceptible to necrosis triggered by cys
252                                      In TSC2-deficient cells, Syk signaling increased the expression
253 ity in chimeric mice reconstituted with TET2-deficient cells than in nonchimeric mice.
254                                Moreover, VHL-deficient cells that expressed activating mTOR mutants g
255 t-expressing cells, and an increase in MCPH1-deficient cells that was suppressed by the loss of peric
256  and cadC are substantially increased in Tdg-deficient cells, those of both AP- and betaE-sites are u
257 ation complex Arp2/3 is reduced in dysbindin-deficient cells, thus affecting actin-dependent phenotyp
258 vivo analysis with mycobacteria-infected MR1-deficient cells to demonstrate the presence of functiona
259 esion, Mn(2+) enabled talin- but not kindlin-deficient cells to initiate spreading on FN.
260 e mechanisms that drive resistance of the HR-deficient cells to PARPi.
261 ective checkpoint surveillance enables BRCA2-deficient cells to progress through mitosis with under-r
262 TNFalpha associated with VHL loss forced VHL-deficient cells to rely on intact RIPK1 to inhibit apopt
263 ling BLM-deficient and/or cytidine deaminase-deficient cells to tolerate constitutive DNA damage and
264  targeted gene deletion of Ifitm3 as well as deficient cells transcomplemented with Ifitm3.
265                          Mice receiving 5-LO-deficient cell transplant or zileuton treatment had prol
266 control Jurkat cells and necroptosis in FADD-deficient cells; treatment of both lines with chemothera
267 activated ectopically in these coldspot nTSG-deficient cells, tumorigenesis is induced.
268 ensation and cell cycle progression in MCPH1 deficient cells under undamaging conditions.
269                 Nevertheless, TLR4- and TRIF-deficient cells undergo significant apoptosis, implicati
270       We showed that as a consequence, AP1S3-deficient cells up-regulate IL-1 signaling and overexpre
271 gradation and genomic instability in BRCA1/2-deficient cells upon replication stress.
272                 Subsequent selection for MMR-deficient cells using the guanine analog 6-thioguanine a
273 icroscopy revealed that mHtt toxicity in RQC-deficient cells was accompanied by multiple mHtt aggrega
274   While starvation survival of the autophagy-deficient cells was not rescued by the general antioxida
275 atopoietic differentiation capacity of Hdac8-deficient cells was observed.
276 ges showed that IL-4-induced fusion of Mac-1-deficient cells was strongly reduced compared with wild-
277 partial bone marrow reconstitution with TET2-deficient cells was sufficient for their clonal expansio
278                   Expression of NRP1 in NRP1-deficient cells was sufficient to induce NE uptake.
279 Thus, while olaparib efficiently kills BRCA2-deficient cells, we demonstrate that it can also contrib
280                   Using transcription factor-deficient cells, we demonstrate that RORgammat and Tbet
281                                      In LKB1-deficient cells, we found AMPK activation to be predomin
282 terations in the endocytic pathway in Parkin-deficient cells, we found that Parkin regulates the leve
283 cs of proteins accumulating in GABARAP/L1/L2-deficient cells, we identified C18orf8/RMC1 as a new sub
284 in LEs similar to that seen in NPC- and LAMP-deficient cells, we show that the restriction of parasit
285                                       C-NAP1-deficient cells were capable of signaling through the ci
286                      In support of this, SPL-deficient cells were defective in mounting an effective
287                        In contrast, the RIP1-deficient cells were defined by increased expression of
288                                         Ku70-deficient cells were exposed to 150 muM BPA, 20 mM KBrO3
289                                          DEK-deficient cells were impaired for gammaH2AX phosphorylat
290                                        PHGDH-deficient cells were relatively weakly tumorigenic and t
291 g of Rad51, a protein critical for HDR, Wwox-deficient cells were resensitized to radiation.
292 formations after transmigration in lamin-A/C-deficient cells, whereas the wild-type cells show much l
293 ion of autophagy by HBB2 is impaired in NRF2-deficient cells, which have reduced autophagic flux and
294 drial respiration is perturbed in TORC2-Ypk1-deficient cells, which results in the accumulation of mi
295 d IFN response in JUNV- or MACV-infected PKR-deficient cells, which was inversely correlated with vir
296 ng why R-tracts do not accumulate in RNase H-deficient cells, while double-strand breaks do.
297     Correction of abscission delays in SCCRO-deficient cells with addition of an Aurora B inhibitor a
298 further demonstrate selective killing of p53-deficient cells with camptothecin while sparing isogenic
299 ictor or Sin1 compared with parent or rictor-deficient cells with re-expression of ectopic rictor.
300                                      In zinc-deficient cells, Zap1 binds to zinc responsive elements

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