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1 enomic DNA that was previously thought of as junk.
2 lue paradox involves perhaps 15% of genomic 'junk,' and encompasses the bulk of the introns, thought
5 We explain known balanced distributions of junk DNA within genomes and between subgenomes in allopo
6 SINEs and LINEs, which have been considered "junk DNA", are among the repeat sequences that would app
9 ons are not simply buffers of nonfunctional 'junk DNA' next to the molecular telomere, but are instea
11 ms implicated are not proved to apply to all junk DNA, and the continuous nature of the centromeric a
12 Despite often being classified as selfish or junk DNA, transposable elements (TEs) are a group of abu
13 the genome that had heretofore been deemed "junk DNA," yet no one could answer the obvious question:
21 t thereby ascribes an important function to "junk DNA." This model arose from analysis of a serendipi
22 their initial characterization as selfish or junk DNA; however, it is now known that they may acquire
23 uch as mVL30 apparently evolved not only as "junk" DNA but also as transcriptionally active noncoding
24 tions that promote the formation of useless "junk" DNA sequences or multimeric sequences containing m
26 s, while the remaining 98%, once considered "junk" DNA, codes for regulatory/epigenetic elements that
27 heterochromatin, while often considered as "junk" DNA, plays important functions in chromosome biolo
28 What is in the rest of the genome, or the "junk" DNA, that, in Homo sapiens, is estimated to be alm
30 ackground or noisy transcripts derived from "junk" DNA, whose production may be inherent to the proce
31 ions for the way in which we view so-called 'junk' DNA and our understanding of eukaryotic gene regul
34 ed to a complete or near-complete removal of junk Env from many viral strains, leaving trimers and vi
35 he face of harsh conditions, suggesting that junk Env is unlikely to arise by trimer dissociation or
36 we sought to better understand the nature of junk Env with a view to devising strategies for its remo
37 We have shown previously that a maternal junk food diet during pregnancy and lactation plays a ro
38 o showed that offspring from mothers fed the junk food diet in pregnancy and lactation, and which wer
39 This study therefore shows that a maternal junk food diet promotes adiposity in offspring and the e
40 t rat offspring born to mothers fed the same junk food diet rich in fat, sugar and salt develop exace
41 ot Glut 4 mRNA expression in females fed the junk food diet throughout the study compared with female
42 and LPL being up-regulated in those fed the junk food diet throughout the study compared with males
44 red with offspring also given free access to junk food from weaning but whose mothers were exclusivel
45 es of the food industry, such as engineering junk food to make it addictive and marketing it to young
49 neurobiological consequences of exposure to junk-food diets and the potential contribution of incent
51 occurred rapidly, persisted for weeks after 'junk-food' consumption ceased, and preceded the developm
53 PAR expression and function is increased by 'junk-food' diet consumption in obesity-susceptible vs -r
55 to cocaine in rats that gained weight on a 'junk-food' diet, consistent with greater responsivity of
59 ternal intake of high-fat and/or high-sugar "junk foods" during pregnancy and lactation can alter the
62 used a model of individual susceptibility to junk-foods diet-induced obesity to determine whether the
64 virus-like particles (VLPs) bear nonnative "junk" forms of envelope (Env) glycoprotein that may unde
68 the rest of the DNA of larger genomes to be junk or, at least, assign it a different sort of role (s
72 , and having done that, it discards what is "junk." To accomplish these many and varied tasks, the GI
73 unclear function that has been regarded as "junk." Yet, persistence of these tandem highly repetitiv
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