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1 c mutations in its Brd and GY boxes exhibits hypermorphic activity that results in characteristic def
4 ssion of TEC1, by expression of the dominant hypermorphic allele STE11-4 or by deletion of HOG1, Ty1
5 ay inform future gene-editing strategies for hypermorphic alleles and have advanced the pursuit of ge
8 e identified three of four such mutations as hypermorphic alleles of Gnaq and Gna11, which encode wid
12 st, a common T108M polymorphism in GPR35 was hypermorphic and had the opposite effects to Gpr35 delet
14 vo, resulting in phenotypic suppression of a hypermorphic bin2 mutation and enhanced resistance to a
16 atient we identified two rare, recessive and hypermorphic coding variants in GPATCH3, a gene of unide
18 aracterization in patients' blood revealed a hypermorphic effect of this Sp1 variant, triggering supe
19 l and histologic analyses established if the hypermorphic Egfr(Dsk5) allele can rescue the woe embryo
22 ified as a dominant suppressor of EgfrElp, a hypermorphic form of the Drosophila Epidermal growth fac
23 suggest that CLN4 alleles resemble dominant hypermorphic gain of function mutations that drive exces
24 s were likely caused by either neomorphic or hypermorphic gain-of-function mutations in the BIN2 gene
27 rmant studies confirmed that the mutation is hypermorphic in vivo, but the DER function was elevated
28 with previous results, PLCG2(R665W) confers hypermorphic induction of downstream signaling events.
30 Here we show that a previously characterized hypermorphic mutant FtsA (FtsA*) partially disassembled
32 hed using an anergy model in which the Zap70 hypermorphic mutant W131A is coexpressed with the OTII T
33 ome (BAC)-based transgenic system in which a hypermorphic mutation has been introduced into the murin
35 A study of drug-resistant lymphomas with hypermorphic mutations in PRC2 has identified a 'methyla
36 morphic mutations in STAT3 and patients with hypermorphic mutations in STAT1 share several clinical a
39 5F be referred to as allomorphic rather than hypermorphic mutations of PLCG2 Rerouting of the transme
40 m of fixation in the presence of amorphic or hypermorphic mutations, we consider a diallelic model at
41 ral vector to drive expression of wild-type, hypermorphic, or hypomorphic MYC in bone marrow that exp
43 ,C186S) not targeted to membranes produced a hypermorphic phenotype and stimulated mitogen-activated
45 the highly conserved Lys-774 residue induced hypermorphic phenotypes that mimicked the loss of phosph
46 ons of this cleavage site produced the first hypermorphic point mutation within the Apaf1/Ced-4 gene
50 ress, was evoked in zebrafish expressing the hypermorphic Ser482Cys-GLS and could be alleviated by in
53 xpress oncogenic Kras and null, wild-type or hypermorphic Trp53 alleles in alveolar type 2 (AT2) cell