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Example sentences for: krc
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KRC binds to the signal sequences of V(D)J recombination (RSS) [ 14 28 ] . αACRYBP1 binds to a sequence in the type II collagen gene enhancer [ 5 ] . MIBP1 binds to a TC-rich element present in the somatostatin type II receptor gene enhancer [ 3 ] .
These data suggest that with respect to the RSS canonical elements, KRC/ZAS-N binds the nonamer more efficiently while KRC/ZAS-C binds the heptamer more efficiently, and that two KRC molecules may be needed to bind a single RSS element.
Our finding that KRC binds to the RSS as well as the κB motif may also provide a link between transcription and recombination in the context of the accessibility model [ 58 59 ] . Enhancer or promoter elements are important for the recombination process in cell lines and animal models [ 60 ] . Similarly, expression of transcription factors, in conjunction with the recombination activating genes, has been shown to induce V(D)J recombination in non-lymphoid tissues by rendering RSS accessible to the recombinase [ 61 ] . The κB motif, first found in the Igκ light chain [ 62 ] , and later in the TCR β2 locus [ 31 ] , has been shown to promote V(D)J recombination by modulating locus accessibility [ 63 ] . In addition to influencing recombination by binding of RSS, KRC binding of the κB motif may modulate accessibility and transcription of target loci.
For example, the KRC/ZAS-C consensus sequence "ATTTTGTGG" matches completely with 6 nucleotides of the RSS nonamer and 3 flanking nucleotides of the human IgH D1, D2, D3 and D4 gene segments [ 35 ] . Furthermore, the MAST search identified KRC-selected motifs near two chromosomal breakpoints: between a t(11:14) translocation of the Ig DH2-2 gene segment and the B cell lymphoma 1 ( BCL-1 ) gene in a mantle cell lymphoma [ 36 ] , and at a t(11:19) translocation of the myeloid lymphoid leukemia ( MLL ) gene and the ENL/MLLT1/LTG19 gene in a T-cell acute lymphoblastic leukemia [ 37 ] . The other hits were derived from loci of cellular genes, pseduogenes, or DNA fragments [ 41 42 43 44 ] . The expression of those genes has not been shown to be regulated by KRC or other family members, therefore, the biological significance of those MAST results is unknown.
We had previously shown by methylation interference analysis that KRC/ZAS-C bound specifically to the sequence TGTGG within the context of the canonical RSS heptamer plus the immediately flanking guanine [ 14 ] . Because the pentamer motif for KRC/ZAS-C predicted by MEME completely matched with the empirical results, we conclude that the two pentameric motifs discovered by MEME are likely authentic binding sites for KRC/ZAS-N as well.
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