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1 issue polarity as it is deleted in a weak fy hypomorph.
2 P1 expression and therefore generated a NRP1 hypomorph.
3 s shown by mig-38 RNAi with the mig-15(rh80) hypomorph.
4 xpression pattern using heterozygosity and a hypomorph.
5 ng partner Csk, unmasks the risk allele as a hypomorph.
6 t ventral branch migration in the breathless hypomorph.
7 was compromised in neurons cultured from the hypomorphs.
8 equency of vascular defects reported in Fgf8 hypomorphs.
9 solated new vn mutations including nulls and hypomorphs.
10 crepancies between receptor mutants and Ntn1 hypomorphs.
11 for persistent attraction to the midline in hypomorphs.
12 um channel are markedly increased in the 10% hypomorphs.
13 e in inflammatory cytokine expression in the hypomorphs.
14 d this phosphorylation is compromised in CK2 hypomorphs.
15 source of lethality in irradiated Smc5-Smc6 hypomorphs.
16 -associated Six3 mutant proteins function as hypomorphs.
17 ation when breaks are reduced in yeast spo11 hypomorphs.
18 proach was used to generate a series of Plk1 hypomorphs.
19 nstrated by the myeloerythroid bias in Dnmt1 hypomorphs, a comprehensive DNA methylation map of haema
20 permorphs at age 12 wk to 400% normal in the hypomorphs accompanied with proportionate changes in pla
21 and male reproductive tract, but served as a hypomorph allele in the development of the appendicular
22 bly, the reduced Elmo1 expression in the 30% hypomorphs almost abolishes the pathological features of
23 y defects, the mutant protein is both a mild hypomorph and a potent antimorph as determined by the ef
26 idence that the aphakia allele of Pitx3 is a hypomorph and that Pitx3 is required for the regulation
27 is indicated protein-coding alterations in 8 hypomorphs and 6 amorphs, with mild-moderate phenotypes
28 , moderate, umbrous-like, severe) for the 18 hypomorphs and a single category for the 7 amorphs (null
29 penetrance of mutant phenotypes in signaling hypomorphs and explains available experiments with no ad
31 ison of the mutant phenotypes of dpp and gbb hypomorphs and null clones shows that both BMPs act loca
33 homozygous lethal in midgestation, but Mpc1 hypomorphs and tissue-specific deletion of Mpc1 presente
34 s stages up through metamorphosis (synthetic hypomorphs) and displayed prepupal and pupal phenotypes
35 us: a 5' deletion, with reduced Sno protein (hypomorph), and an exon 1 deletion removing half the pro
37 ies: inactivation of tumor suppressor genes (hypomorph, antimorph or amorph) or activation of oncogen
38 phs showed only slight G2/M arrest, a medium hypomorph arrested with 4N DNA content, followed later b
41 icant improvement in serum creatinine in the hypomorphs at 3 and 10 days after injury, and renal fibr
44 uppress the DNA damage sensitivity of Smc5/6 hypomorphs but not that of HR mutants and remarkably dec
45 ro, suggesting that the mutants are actually hypomorphs, but must be above certain concentration to e
46 dated peptides were largely absent in strong hypomorphs, but peptide precursors, a nonamidated neurop
48 ve previously reported generation of an Orc2 hypomorph cell line (Delta/-) that expresses very low le
51 ional exposure, the patent DV in AHR or ARNT hypomorphs could be efficiently closed by dioxin exposur
53 scued by L. major glf, which behave as glf-1 hypomorphs, display resistance to infection by Microbact
56 toxicity studies demonstrated that the ARNT hypomorphs exhibited resistance to the end points of dio
62 which we believe is either a null or severe hypomorph, has an IRES-lacZ-neomycin resistance cassette
63 ver perfusion studies demonstrated that ARNT hypomorphs have a patent ductus venosus, identical to th
70 ssion from low to high in the tubules of the hypomorphs increased their albumin excretion more than 1
71 ion and dMYC-dependent overgrowth in the Hfp hypomorph is further impaired in the C-terminal Hay/XPB
72 The altered phenotypic landscape in our adar hypomorph is paralleled by an unexpected dichotomous res
73 ean number of supercoil domains, this gyrase hypomorph is prone to fork collapse and topological chao
77 s LDH-A and rescue expression of a catalytic hypomorph LDH-A mutant, Y10F, demonstrate increased resp
78 showed that the BALB/c allele of Ube2l6 is a hypomorph leading to the lack of UBE2L6 protein expressi
79 hat B. burgdorferi-infected hearts from CD18 hypomorph mice express increased levels of MCP-1 RNA com
81 increased severity of Lyme carditis in CD18 hypomorph mice is caused by deficiency in CD11a or CD11c
82 e demonstrate that dendritic cells from CD18 hypomorph mice secrete higher levels of monocyte/macroph
91 anscription of Sema3c in the OFT, whereas, a hypomorph of Tbx1, a key SHF transcription factor, resul
94 R localization in metaphase-II Mater(tm/tm) (hypomorph) oocytes and found ER clusters to be less abun
95 sion of phosphorylation-deficient, catalytic hypomorph PDHK1 mutants in cancer cells leads to decreas
98 tinct from RAG nullizygosity, the RAG1-S723C hypomorph results in aberrant DNA double-strand breaks w
101 otype induced in the PV myocardium in Nkx2-5 hypomorphs reverted back to a working myocardial phenoty
104 posis Coli 2 (APC2) rescued GSC loss in chic hypomorphs, suggesting an additive role of APC2 and F-ac
105 pression was attenuated or reversed in Keap1 hypomorphs, suggesting that protection in these mice was
106 throid maturation was deficient in these Scl hypomorphs, supporting that Scl was required both for th
107 passenger complex (CPC), AURKC p.C229Y is a hypomorph that cannot fully support cell-cycle progressi
108 an N-terminal GFP-Foxp3 fusion protein, is a hypomorph that causes profoundly accelerated autoimmune
109 , with NPC1, we have generated a murine NPC2 hypomorph that expresses 0-4% residual protein in differ
113 lizability of our findings, we subjected the hypomorphs to unilateral ureteral obstruction (UUO) and
114 genetic model of brd2 lo mice, a BET protein hypomorph, to show that Brd2 is essential for proinflamm
117 mRNA enhances the Daf-c phenotype of a daf-4 hypomorph, whereas the same transgene with a nonsense mu
119 strongly enhanced phenotype relative to Ntn1 hypomorphs, which retain many axons with normal trajecto
120 e-trap mouse (Pikfyve(beta-geo/beta-geo)), a hypomorph with ~10% of the normal level of Pikfyve prote
121 amage, since the synthetic lethality of smc6 hypomorphs with a topoisomerase II mutant, defective in
122 ectrolytes are markedly decreased in the 10% hypomorphs without significant change in the glomerular
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