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1 ed Ctf19 complex (Ctf19c) in pericentromeric CO suppression.
2 tion mutants obtained by RNA interference or co-suppression.
3 nscriptional control, and extent of endogene co-suppression.
4 lly inactive, and as such is recalcitrant to co-suppression.
5 nly occurred in plants where the outcome was co-suppression.
6 ansgenic lines of CSN3 produced through gene co-suppression also accumulate multi-ubiquitinated prote
10 is approach, we query sufficiency in meiotic CO suppression, and identify Ctf19 as a mediator of kine
12 lored in transgenic plants showing inducible co-suppression following infection with a cytoplasmicall
13 el mechanisms such as RNA interference, gene co-suppression, gene silencing, imprinting and DNA demet
14 idopsis resulted in delayed flowering, while co-suppression lines and a transferred DNA (T-DNA) knock
17 often occur together in human lymphomas and co-suppression of both genes promotes lymphomagenesis in
19 Many of these plants were wilty, suggesting co-suppression of endogenous gene activity; however thre
20 echanism functioned through mir-302-targeted co-suppression of four epigenetic regulators, AOF2 (also
22 reover, overexpression of PKC-delta, without co-suppression of PKC-alpha and beta, is not apoptotic t
25 xhibit IKZF1 high expression and dependency, co-suppression of WDR5 and Ikaros by MS40 is superior in
26 rongly suggest that the infection produced a co-suppression response; the endogenous level of ubiquit
27 home gland and used both antisense and sense co-suppression strategies to investigate its function.