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1 h accessible chromatin regions that lack enhancer activity, were enriched for enhancer RNAs (eRNAs) and preferentially in
2 eins were significantly altered by Abeta42 accumulation and were enriched for AD-associated processes.
4 atory elements, were located near established SAN genes and were enriched for distinct sets of TF (transcription factor)
5 ) and early memory precursor (CCR7(+)CD127(+)) subsets, and were enriched for the transcription factors IRF4 and c-Maf.
6 infected macaques revealed that the MUC16-eluted antibodies were enriched for certain specific epitopes, including region
7 c centrality in both the weighted and unweighted approaches were enriched for pathways previously associated with autism,
8 Genes showing a similar expression profile to Arg1 were enriched for STAT6 transcription factor recognition elem
9 In contrast, biallelic deletions in individuals with ASD were enriched for overlap with regulatory regions, with 23/28
12 rons, glia, bulk brain, T cells, monocytes, and whole blood were enriched for genes supported by genome-wide association
13 The fusion transcripts in fetal brain were enriched for genes for long-term depression; while those
14 Cells derived from milk from the breast with cancer were enriched for CD49f(+)/EpCAM(-), CD44(+)/CD24(-), and CD2
15 Proteins less abundant in these cells were enriched for constituents of granules, supporting a role
16 from the largest genetic study of anorexia nervosa to date were enriched for expression in the arcuate nucleus of the hy
19 Genes abnormally expressed in major depressive disorder were enriched for innate immune-related functions, coded for
20 that fetal-enhancer regions methylated by Dnmt3a and Dnmt3b were enriched for kidney disease genetic risk loci.
21 al profiling by mass spectrometry showed that placental EVs were enriched for proteins that function in transport and vir
22 eover, the DEGs associated with parental Holocaust exposure were enriched for glucocorticoid-regulated genes and immune p
23 ctor enrichment analysis revealed that genes in this factor were enriched for androgen receptor binding sites.
24 e >4000 genes displaying altered expression during fibrosis were enriched for proinflammatory and profibrotic pathways.
25 Positively weighted (downregulated) genes were enriched for neuronal, specifically interneuronal, affil
26 , prenatal and age-dependent differentially expressed genes were enriched for genes implicated in non-syndromic autism sp
27 ghest-ranked gene, and several functionally plausible genes were enriched for rare variants, although no gene achieved st
29 Conversely, the most negatively weighted genes were enriched for genes that were transcriptionally upregulat
31 ression map colocated with schizotypy-related magnetization were enriched for genes that were significantly downregulated
32 identified using GPWAS with 260 phenotypic traits in maize were enriched for genes independently linked to phenotypic va
33 The genes under genetic regulation in human and mouse were enriched for oxidative phosphorylation and adipogenesis.
34 tin affected by dopamine depletion within GPe PV(+) neurons were enriched for hypoxia-inducible factor family binding mot
36 HPC expression and GC-affected DNAm profiles were enriched for changes observed during human fetal brain d
37 gnatures in non-progressors, and found that non-progressors were enriched for proteomic processes involving regulation of
38 PU.1, and CEBP cis elements, whereas NIPBL-bound promoters were enriched for GC-rich DNA sequences.
39 ncluded the following steps: trypsin-digested tumor samples were enriched for phosphopeptides through immobilized metal i
40 Genes whose expression correlate with schizophrenia were enriched for those involved in abnormal CNS synaptic tra
41 riants in the PLASMA credible sets for RNA-seq and ChIP-seq were enriched for open chromatin and chromatin looping, respe
42 orrelates of depression-linked brain function and structure were enriched for disorder-relevant molecular pathways.
45 own to have breast cancer, two of them contained cells that were enriched for the CSC phenotype and carried mutations in
46 ifferences were largely driven by prenatal differences that were enriched for pathways previously implicated in addiction
47 mately a quarter of mutant-enriched accessible regions that were enriched for other DNA binding factors, including FOXA1,
48 ets of FMRP, derived from studies of multiple tissue types, were enriched for common schizophrenia risk alleles, as well
49 our knowledge previously unreported (P < 5 x 10(-8)), which were enriched for cell signaling pathways, including the NEK6
50 l tissue-specific enhancers, the human orthologues of which were enriched for disease-associated genetic variants.