kwic
novel
novel
right
off
ON
215
1
100
500
strict
ELIZA cgi-bash version rev. 1.90
- Medical English LInking keywords finder for the PubMed Zipped Archive (ELIZA) -
return
kwic search for novel out of >500 occurrences
330250 occurrences (No.59 in the rank) during 5 years in the PubMed. [cache]
--- ABSTRACT ---
--- ABSTRACT END ---
[frequency of next (right) word to novel]
330250 occurrences (No.59 in the rank) during 5 years in the PubMed. [cache]
| 215) We demonstrate a novel CTCF-binding site in BCL6 exon1A within a potential CpG island, which is unmethylated both in cell lines and in primary lymphoma samples. |
| PMID:24362533 DOI:10.1038/onc.2013.535 |
| 2015 Oncogene |
| * Novel CTCF binding at a site in exon1A of BCL6 is associated with active histone marks and a transcriptionally active locus. |
| - BCL6 is a zinc-finger transcriptional repressor, which is highly expressed in germinal centre B-cells and is essential for germinal centre formation and T-dependent antibody responses. Constitutive BCL6 expression is sufficient to produce lymphomas in mice. Deregulated expression of BCL6 due to chromosomal rearrangements, mutations of a negative autoregulatory site in the BCL6 promoter region and aberrant post-translational modifications have been detected in a number of human lymphomas. Tight lineage and temporal regulation of BCL6 is, therefore, required for normal immunity, and abnormal regulation occurs in lymphomas. CCCTC-binding factor (CTCF) is a multi-functional chromatin regulator, which has recently been shown to bind in a methylation-sensitive manner to sites within the BCL6 first intron. We demonstrate a novel CTCF-binding site in BCL6 exon1A within a potential CpG island, which is unmethylated both in cell lines and in primary lymphoma samples. CTCF binding, which was found in BCL6-expressing cell lines, correlated with the presence of histone variant H2A.Z and active histone marks, suggesting that CTCF induces chromatin modification at a transcriptionally active BCL6 locus. CTCF binding to exon1A was required to maintain BCL6 expression in germinal centre cells by avoiding BCL6-negative autoregulation. Silencing of CTCF in BCL6-expressing cells reduced BCL6 mRNA and protein expression, which is sufficient to induce B-cell terminal differentiation toward plasma cells. Moreover, lack of CTCF binding to exon1A shifts the BCL6 local chromatin from an active to a repressive state. This work demonstrates that, in contexts in which BCL6 is expressed, CTCF binding to BCL6 exon1A associates with epigenetic modifications indicative of transcriptionally open chromatin. |
[
right
kwic]
(1)22  therapeutic |
(17)3 mutation |
(33)2 approaches |
(49)2 information |
| (2)11 and |
(18)3 paradigm |
(34)2 autosomal |
(50)2 inhibitors |
| (3)8 mechanism |
(19)3 role |
(35)2 candidate |
(51)2 learning |
| (4)8 method |
(20)3 strain |
(36)2 cardiac |
(52)2 modulators |
| (5)7 approach |
(21)3 target |
(37)2 clinical |
(53)2 object |
| (6)7 mutations |
(22)3 targeted |
(38)2 compounds |
(54)2 oral |
| (7)6 therapies |
(23)3 targets |
(39)2 data |
(55)2 polymer |
| (8)5 technique |
(24)3 treatment |
(40)2 described |
(56)2 potent |
| (9)4 strategies |
(25)3 type |
(41)2 dual |
(57)2 prognostic |
| (10)4 strategy |
(26)3 words |
(42)2 electroporation |
(58)2 putative |
| (11)4 surgical |
(27)2 *null* | (43)2 finding |
(59)2 recombinants |
| (12)3 antibacterial |
(28)2 anti-tumor |
(44)2 findings |
(60)2 results |
| (13)3 drug |
(29)2 antibiotic |
(45)2 form |
(61)2 therapeutical |
| (14)3 homozygous |
(30)2 anticancer |
(46)2 genetic |
(62)2 titanium |
| (15)3 insights |
(31)2 application |
(47)2 imaging |
(63)2 treatments |
| (16)3 mechanisms |
(32)2 applications |
(48)2 in |
add keyword
--- WordNet output for novel ---