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1 l only in the acute liver-specific Hnf4alpha-null mouse.
2 in a neural cell line derived from a PrP(C)-null mouse.
3 7(rsq1) is a bona fide phenocopy of the TLR7 null mouse.
4 nd imbalanced glucose metabolism in the Igf2 null mouse.
5 create the hepatic microsomal cytochrome b5 null mouse.
6 ment were examined using a conditional Wnt7b-null mouse.
7 bed the generation of a mast cell protease-6-null mouse.
8 nce of Nodal reported in the LPM of the Pkd2-null mouse.
9 sion to alleviate dystrophy in the delta sgc-null mouse.
10 created a conditional and cell-specific TLR null mouse.
11 in the vascular endothelial cells of the Ace null mouse.
12 exclusively in a single cell type of an Ace null mouse.
13 hese alterations are reproduced in the Kv1.1-null mouse.
14 AFP repression during development of the p53-null mouse.
15 frontal cortex of the dopamine D(1) receptor null mouse.
16 gy of NCB5OR and the phenotype of the Ncb5or-null mouse.
17 cted based on the phenotype of the AP-2alpha-null mouse.
18 yopathy, but were recapitulated in a cMyBP-C null mouse.
19 spontaneous thymic tumor found in a CD45-AP-null mouse.
20 alabsorption and, more recently, by the Pcft-null mouse.
21 cantly elevated in the kidneys of the miR-22 null mouse.
22 increased in the processing-deficient (PC1/3 null) mouse.
23 and mast cell degranulation in the annexin 1(null) mouse.
24 for comparison, a fully EXO1-deficient (Exo1(null)) mouse.
25 periodontal defect was observed in the Dmp1 null mouse, a mouse model of hypophosphatemic rickets.
26 g cells, we examined secretion from Munc18-1-null mouse adrenal chromaffin cells expressing Munc18-1
28 n two genetic models of hemochromatosis (HFE-null mouse and HJV-null mouse) and in two nongenetic mod
30 reduced during early lactation in the AFAP1-null mouse and the localization of active cSrc at the ap
31 s of hemochromatosis (HFE-null mouse and HJV-null mouse) and in two nongenetic models of iron overloa
32 ly detected abnormal remodeling in the Cox-1 null mouse, and clearly demonstrated that the cervix pla
34 y expressing human apoE3 or human apoE4 on a null mouse apoE background revealed that apoE4 expressio
35 s and lack of a cancer phenotype in the TP73 null mouse are inconsistent with a suppressor function b
38 in RAW264.7 cells as well as the use of Hsf1 null mouse bone marrow cells demonstrated that 17-AAG-en
39 ry Mk cells from cultures initiated with p53-null mouse bone marrow mononuclear cells displayed highe
40 e MKS3, we analyzed phenotypes in the Tmem67 null mouse (bpck) and in zebrafish tmem67 morphants.
42 d in the maturation stage enamel of the Klk4 null mouse, but not in the Klk4 heterozygous or wild-typ
43 PHR1 function and expression, we made a Phr1 null mouse by inserting a beta-galactosidase/neor casset
44 sors and neurogenesis normalized in the nNOS null mouse by P6W, there was an overgrowth of mitral or
46 ve shown that mTOR is hyperactivated in Pkd1-null mouse cells due to failure of the HGF receptor c-Me
47 ane fusion can be readily visualized in OPA1-null mouse cells in vivo, but these events do not progre
56 a7beta1 integrin expression in the delta sgc-null mouse did not alleviate muscular dystrophy in these
58 f ADAR in PyV infection, we used genetically null mouse embryo fibroblast cells deficient in either A
59 , by using purified soluble Pref-1 in Pref-1 null mouse embryo fibroblasts (MEF), we show that Pref-1
60 target gene RAR-beta2 are impaired in ASC-2-null mouse embryo fibroblasts (MEFs) or in MEFs expressi
65 We conclude that late passage IGF-I receptor null mouse embryo fibroblasts can be transformed by SV40
68 es of wild-type and HIF-1alpha- or AMPKalpha-null mouse embryo fibroblasts to determine whether AMPK
69 result from the loss of Pin1 predispose Pin1 null mouse embryo fibroblasts to undergo more rapid geno
70 ifferentiation of 3T3-L1 cells and in Pref-1-null mouse embryo fibroblasts transduced with Pref-1A.
71 with >2-fold differential expression in Egr1-null mouse embryo fibroblasts, including 143 known genes
75 H-beta by short hairpin RNA and P4H-alpha(I) null mouse embryonic fibroblast cells showed reduced sta
79 ression was severely abrogated in C/EBP-beta-null mouse embryonic fibroblasts (MEFs) and primary C/EB
80 ne 27 trimethylation (H3K27me3) in both Pten null mouse embryonic fibroblasts (MEFs) and Pten null mo
81 compare the gene expression profiles of Pten null mouse embryonic fibroblasts (MEFs) cell lines and t
82 st-induced NFAT activation is reduced in p65 null mouse embryonic fibroblasts (MEFs) compared with wi
84 genes, we compared gene expression in STAT3-null mouse embryonic fibroblasts (MEFs) stably expressin
85 NA damage, we exposed wild-type and PKCdelta null mouse embryonic fibroblasts (MEFs) to UV radiation.
86 also reduced in Ras(V12)-expressing p19(Arf) null mouse embryonic fibroblasts (MEFs), and overall Egr
88 ore and after oxidative stress in caveolin-1-null mouse embryonic fibroblasts (MEFs), which do not ex
91 CDC3 expression is markedly reduced in TAp63-null mouse embryonic fibroblasts and brown adipose tissu
92 nscription assays were performed with IQGAP1-null mouse embryonic fibroblasts and HEK293 cells with I
94 well as STAT3 activation, we examined STAT5-null mouse embryonic fibroblasts and primary hepatocytes
95 d the spontaneous transformation of MdmX/p53-null mouse embryonic fibroblasts in vitro and with an in
96 ion, we showed that the loss of RNPC1 in p53-null mouse embryonic fibroblasts leads to reduced expres
97 ver, inhibition of deregulated TORC1 in TSC2-null mouse embryonic fibroblasts or in 293 cells by down
100 ng-deficient mutants of vinculin in vinculin-null mouse embryonic fibroblasts revealed that PIP2 bind
101 d Ca(2+) imaging experiments with presenilin-null mouse embryonic fibroblasts to analyze ER Ca(2+) le
105 cally expressed in oxidatively stressed OGG1-null mouse embryonic fibroblasts, suggests that acetylat
107 junction (HJ) resolution activity in Rad51c-null mouse embryonic fibroblasts, we propose that this l
110 ddress biology we previously generated trex2(null) mouse embryonic stem (ES) cells and expressed in t
111 performed a microarray analysis using Mef2c-null mouse embryos and identified a novel MEF2-regulated
113 ution of prostaglandins from the uterus: COX null mouse embryos develop normally during embryogenesis
115 ssential for mouse development, as most Bmp4-null mouse embryos die at the onset of gastrulation and
116 ome, which commence early in gestation, MMP9-null mouse embryos exhibit deficiencies in trophoblast d
122 Here, we show that removal of Gli3 in Ihh-null mouse embryos restored normal proliferation and mat
123 tient cells, and in tissues from Flna(Dilp2) null mouse embryos results in cellular phenotypes identi
127 y in Xenopus as well as the analysis of Dkk1-null mouse embryos transform the anterior neural fold in
128 ity partially rescued the phenotypes in Chd7-null mouse embryos, demonstrating that p53 contributes t
130 from chromatin remodeling ATPase LSH (HELLS)-null mouse embryos, which lack DNA methylation from cent
131 unctions in vivo, we have generated Aurora A null mouse embryos, which show severe defects at 3.5 d.p
135 ight percent of mature mineral in the MMP-20 null mouse enamel was only 7-16% less than that in contr
136 portance of UTX in bivalency resolution, Utx-null mouse ESCs and UTX-depleted NT2/D1 cells displayed
142 pression of mutated caveolin-1 in caveolin-1-null mouse fibroblasts failed to induce formation of cav
147 ack of cell surface cadherin 11, cadherin 11-null mouse FLS cells still formed intimate cell-cell con
149 knockdown of miR-491-5p in primary Ink4a-Arf-null mouse glial progenitor cells exacerbated cell proli
152 Echocardiography of Mybphl heterozygous and null mouse hearts exhibited a 36% reduction in fractiona
154 eat-containing E3 ubiquitin protein ligase 1-null mouse hearts was associated with increased PLN leve
157 processed CRS4C in protein extracts of MMP-7-null mouse ileum demonstrates the in vivo requirement fo
158 on-overlapping phenotypes with the TGF-beta2 null mouse, implying the existence of TbetaRIII independ
159 ed in a dose-dependent phenocopy of the Tbx1 null mouse including loss of caudal pa and pharyngeal ar
160 ein complex-lacking Scgd (delta-sarcoglycan) null mouse, indicating that dysferlin functionality is n
162 inflammatory cells into vital organs of the null mouse is accompanied by increased gene expression o
167 s reduced throughout collecting ducts of AE1-null mouse kidney, where increased fractional excretion
168 It was reported previously that Pkd1(null/null) mouse kidney epithelial cells are unresponsive to
171 erized a genuine estrogen receptor (ER) beta-null mouse line (named ERbeta(ST)(L-/L-)) and showed tha
177 immunoprecipitation assays of normal and p53-null mouse liver tissue showed that TA-p73 binds at a pr
178 bserved in the sphingolipid profile of CerS2 null mouse liver, including elevated C16-ceramide and sp
179 otein levels in wild-type, but not PPARalpha-null, mouse livers, with no changes in HNF4alpha mRNA.
181 endothelial cell deficiency, isolated CD151-null mouse lung endothelial cells showed diminished supp
187 This system relies on the transplant of p53 null mouse mammary epithelial cells into the cleared mam
190 mmary tumors derived from transplantable p53 null mouse mammary outgrowth lines revealed significant
192 , we demonstrate that TICs isolated from p53 null mouse mammary tumors repair DNA damage following in
193 mammary epithelial cells isolated from Cav-1 null(-/-)/mouse mammary tumor virus-CR-1 transgenic anim
195 in invertebrates and suggest that the Dlgh-1 null mouse may be a useful animal model to study certain
197 D, with distinct defects from both the Aipl1-null mouse mimicking LCA and the Aipl1-hypomorphic mice
202 s question, we used a conditional p16(INK4a) null mouse model and determined the impact of p16(INK4a)
204 O(6)MeG-dependent apoptosis, we used an Mgmt-null mouse model combined with either the Msh6-null muta
206 In accordance, cells derived from a parkin-null mouse model exhibited increased levels of cyclin D1
207 omplete ablation of Dicer activity in a Pten null mouse model for prostate cancer significantly halts
208 Our findings using a VGLUT2 conditional-null mouse model indicate that glutamate is essential fo
211 Dietary restriction does not affect a PTEN-null mouse model of prostate cancer, but it significantl
214 this scar analysis approach, a fibromodulin-null mouse model that heals with increased scar was also
217 pecifically designed Drosha-null/conditional-null mouse model, generated using the conditional by inv
219 resent results of a study using a novel GHSR-null mouse model, in which ghrelin administration fails
220 ific ligand (L165041) and the PPARbeta/delta-null mouse model, that PPARbeta/delta enhances postnatal
229 ion, we used the humanized NOD/SCID/gamma(c)(null) mouse model, which becomes populated with human B
232 utilized conditional expression and genetic-null mouse models of Spry1 in adipocytes using the fatty
233 To address this question, we generated H3.3-null mouse models through classical genetic approaches.
236 bserved in immune cells cultured from Samhd1 null mouse models, these mice are physically healthy, sp
241 ent, based on clinical score, of conditional null mouse mutants lacking S1P(1) in CNS cell lineages a
245 rocarbon core nanoparticles (PFC-NP) in ApoE null mouse plaques with [(19)F] magnetic resonance spect
246 d secretion responses were diminished in HS1-null mouse platelets after stimulation of GPVI and prote
248 duced platelet functional responses in GIRK2-null mouse platelets, suggesting that functional channel
249 and hair phenotype of a whole-body PPARgamma-null mouse (Pparg(Delta/Delta)), obtained by preserving
251 5) in tooth development using laminin alpha5-null mouse primary dental epithelium and tooth germ orga
254 gression might be activated in indolent Pten-null mouse prostate tumours and that inactivation of suc
256 after adoptive transfer into NOD scid gammac(null) mouse recipients, verifying the effects in vivo.
257 esults in embryonic lethality, the calpain-1 null mouse remains the only experimental model available
258 of either Msh6 or Exo1 function in the Mgmt-null mouse renders these rapidly proliferating tissues a
260 , ShH10, transduces Muller cells in the Dp71-null mouse retina efficiently and specifically (2,3).
263 cological and behavioral studies in the D(1) null mouse should be interpreted in the context of possi
264 Thy-1, we discuss the phenotype of the Thy-1 null mouse, signaling pathways modulated by Thy-1, the r
265 Furthermore, Ras-transformed p53- and Cry-null mouse skin fibroblasts are more sensitive than p53
266 COX-2) is significantly greater, in PPARbeta-null mouse skin in response to TPA compared with wild-ty
268 his study, we show that MSUC occurs in Spo11-null mouse spermatocytes with extensive asynapsis but la
270 in-2 receptor-gamma-null (NOD-SCID IL2Rgamma(null)) mouse strain that expressed human stem cell facto
271 ure ghrelin in various prohormone convertase null mouse strains generated in our laboratory and have
272 ls and patterns are not altered in the SPARC null mouse, suggesting that SC1 does not compensate for
273 red with the more permissive NOD/SCID beta2M null mouse, suggesting that the ALDH(hi)Lin(-) populatio
274 ntly generated a ceramide synthase 2 (CerS2) null mouse that cannot synthesize very long acyl chain (
277 luble extracts from various C57BL/6J and Ahr-null mouse tissues were also analyzed for the presence o
278 ific alterations of mtDNA copy number in ATM null mouse tissues, the latter being recapitulated in ti
281 SAGE mammary cancer data validates this p53 null mouse tumor model as a useful system closely resemb
286 as caused by EP1 receptor inhibition, an EP1-null mouse was generated using a "hit-and-run" strategy
291 glia to spongiform degeneration in the Fig4 null mouse, we expressed Fig4 under the control of the n
292 transduced embryonic fibroblasts from a CSL-null mouse, we generated cell lines that express either
293 ific epidermal growth factor receptor (EGFR) null mouse, we show that exendin-4 induced an increase i
296 SFRP1 (secreted frizzled-related protein-1)-null mouse, which exhibits activated WNT signaling and a
298 aling by using a ceramide synthase 2 (CerS2) null mouse, which is unable to synthesize very long acyl
300 manner, and have attempted to rescue the Ihh-null mouse with the Gli2 activator, either alone or in c
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