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1  indicates that most of the produced RNA are junk.
2 enomic DNA that was previously thought of as junk.
3 lue paradox involves perhaps 15% of genomic 'junk,' and encompasses the bulk of the introns, thought
4            Cryptic prophages are not genomic junk but instead enable cells to combat myriad stresses
5 t for uncertainty or do not include null and junk clusters.
6 ausal estimates, and it includes 'null' and 'junk' clusters, to provide protection against the detect
7 ements (ENCODE) project render the notion of junk DNA obsolete?
8 ults in the conceptual transfer of so-called junk DNA to the domain of functional DNA.
9   We explain known balanced distributions of junk DNA within genomes and between subgenomes in allopo
10 SINEs and LINEs, which have been considered "junk DNA", are among the repeat sequences that would app
11                       Thus, the presence of "junk DNA", through co-determining the (higher or lower)
12 ansposable elements (TEs) - long considered 'junk DNA' - challenge the binary of threat and therapeut
13 nd transposons have earned epithets such as 'junk DNA' and 'molecular parasites'.
14 w insights into the function and dangers of 'junk DNA' in the human genome.
15 ons are not simply buffers of nonfunctional 'junk DNA' next to the molecular telomere, but are instea
16 ements in the human genome, once considered 'junk DNA', are now known to adopt more than a dozen alte
17 sing from what was previously thought to be 'junk DNA'.
18 ms implicated are not proved to apply to all junk DNA, and the continuous nature of the centromeric a
19                  Though initially derided as junk DNA, they have been widely hypothesized to contribu
20 Despite often being classified as selfish or junk DNA, transposable elements (TEs) are a group of abu
21  the genome that had heretofore been deemed "junk DNA," yet no one could answer the obvious question:
22 irs-the remaining sequence was classified as junk DNA.
23 CG/GC sites that are the major components of junk DNA.
24 uld be called genomic scrap yard rather than junk DNA.
25 enome, they are often quoted as a selfish or junk DNA.
26 mposition of isochores and large sections of junk DNA.
27 , it is a good candidate for a repository of junk DNA.
28 an short interspersed elements, prototypical junk DNA.
29 t thereby ascribes an important function to "junk DNA." This model arose from analysis of a serendipi
30 their initial characterization as selfish or junk DNA; however, it is now known that they may acquire
31 uch as mVL30 apparently evolved not only as "junk" DNA but also as transcriptionally active noncoding
32 tions that promote the formation of useless "junk" DNA sequences or multimeric sequences containing m
33  evidence for chromosome-wide regulation of "junk" DNA transcription.
34 s, while the remaining 98%, once considered "junk" DNA, codes for regulatory/epigenetic elements that
35  heterochromatin, while often considered as "junk" DNA, plays important functions in chromosome biolo
36   What is in the rest of the genome, or the "junk" DNA, that, in Homo sapiens, is estimated to be alm
37 removes all transposons and other so-called "junk" DNA, which comprise ~95% of the germline.
38 ackground or noisy transcripts derived from "junk" DNA, whose production may be inherent to the proce
39 ions for the way in which we view so-called 'junk' DNA and our understanding of eukaryotic gene regul
40 ryotic genomes containing much more of this 'junk' DNA than actual coding DNA.
41 ch was initially largely thought of as mere 'junk' DNA.
42 ed to a complete or near-complete removal of junk Env from many viral strains, leaving trimers and vi
43 he face of harsh conditions, suggesting that junk Env is unlikely to arise by trimer dissociation or
44 we sought to better understand the nature of junk Env with a view to devising strategies for its remo
45     We have shown previously that a maternal junk food diet during pregnancy and lactation plays a ro
46 o showed that offspring from mothers fed the junk food diet in pregnancy and lactation, and which wer
47   This study therefore shows that a maternal junk food diet promotes adiposity in offspring and the e
48 t rat offspring born to mothers fed the same junk food diet rich in fat, sugar and salt develop exace
49 ot Glut 4 mRNA expression in females fed the junk food diet throughout the study compared with female
50  and LPL being up-regulated in those fed the junk food diet throughout the study compared with males
51 th offspring which were never exposed to the junk food diet.
52 red with offspring also given free access to junk food from weaning but whose mothers were exclusivel
53 d girls' implicit positive associations with junk food marketing and substantially improves boys' dai
54 es of the food industry, such as engineering junk food to make it addictive and marketing it to young
55 nd health (high fat, high sugar, high salt, "junk food", sugar-sweetened-beverages, and meats plus su
56 reating positive emotional associations with junk food(1-6).
57 cents are exposed to extensive marketing for junk food, which drives overconsumption by creating posi
58  compared with females never given access to junk food.
59 dy compared with males never given access to junk food.
60                                We found that junk-food consumption increases silent synapses and subs
61               In addition, a brief period of junk-food deprivation is needed for the synaptic inserti
62                                 In contrast, junk-food did not induce AMPAR plasticity in females but
63                           In addition, after junk-food diet exposure, those rats that developed obesi
64  neurobiological consequences of exposure to junk-food diets and the potential contribution of incent
65 ies reveal sex differences in the effects of junk-food on NAc synaptic plasticity.
66           In contrast, prolonged exposure to junk-food resulted in cross-sensitization to amphetamine
67 occurred rapidly, persisted for weeks after 'junk-food' consumption ceased, and preceded the developm
68 ral 'read out' of mesolimbic function after 'junk-food' consumption.
69 PAR expression and function is increased by 'junk-food' diet consumption in obesity-susceptible vs -r
70  enhanced in obesity-susceptible rats after 'junk-food' diet consumption.
71  to cocaine in rats that gained weight on a 'junk-food' diet, consistent with greater responsivity of
72                         In addition, eating 'junk-food' increased NAc calcium-permeable-AMPAR (CP-AMP
73 etabolic, cellular and molecular response to junk-food-diet-induced adiposity.
74 tions between sales of tobacco, alcohol, and junk foods and the predicted probability of implementing
75 ems, and program an increased preference for junk foods in the offspring.
76 collated sales data on tobacco, alcohol, and junk foods to examine the association between changes in
77 ternal intake of high-fat and/or high-sugar "junk foods" during pregnancy and lactation can alter the
78 tables, and fiber and high mean purchases of junk foods, saturated fat, and sodium.
79               Pavlovian cues associated with junk-foods (caloric, highly sweet, and/or fatty foods),
80 used a model of individual susceptibility to junk-foods diet-induced obesity to determine whether the
81                  Further, overconsumption of junk-foods leading to the development of obesity may its
82                      Furthermore, effects of junk-foods on glutamatergic plasticity in females are un
83 n can be induced by cocaine or sugary, fatty junk-foods.
84  virus-like particles (VLPs) bear nonnative "junk" forms of envelope (Env) glycoprotein that may unde
85           Here, I review older arguments for junk grounded in the C-value paradox and propose a thoug
86 , in animals but not in plants, most of the "junk" is intron DNA.
87            Is it possible that much of this "junk" is intron DNA?
88  the rest of the DNA of larger genomes to be junk or, at least, assign it a different sort of role (s
89 e elements (TEs) as 'useless', 'selfish' or 'junk' pieces of DNA is not an accurate one.
90 ease specificities but continuing to degrade junk proteins, cells modify the abundance of particular
91          While once thought of primarily as "junk," recent studies indicate that a large number of th
92 that terminates the synthesis of damaged and junk RNAs that are not translated by the ribosome.
93 o one could answer the obvious question: if "junk," then why still around?
94 , and having done that, it discards what is "junk." To accomplish these many and varied tasks, the GI
95                             On the contrary, junk transcripts provide the raw material for the evolut
96            Despite long being considered as "junk", transposable elements (TEs) are now accepted as c
97  unclear function that has been regarded as "junk." Yet, persistence of these tandem highly repetitiv