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At least 577 records · Page 32Linked to original sources
PubMed2005

Association by guilt: identification of DLX5 as a target for MeCP2 provides a molecular link between genomic imprinting and Rett syndrome.

Rett syndrome (RTT) is an X-linked dominant neurodevelopmental disorder affecting almost exclusively girls. Although mutations in methyl-CpG-binding protein (MeCP2) are known to be associated with RTT, gene expression patterns are not significantly altered in MeCP2-deficient cells. A recent study1 identified MeCP2-mediated histone modification and formation of a higher-order chromatin loop structure specifically associated with silent chromatin at the Dlx5-Dlx6 locus in normal cells, and its absence thereof in RTT patients. This altered expression of Dlx5 through loss of silent chromatin loop formation provides a molecular mechanism underlying RTT and proposes a novel role for MeCP2 in chromatin organization and imprinting.

Animals↗
PubMedDate not supplied

Guilt by association?

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Anesthesia, Conduction↗
PubMed1990

Guilt by association: HLA-B27 and ankylosing spondylitis.

The remarkable association between HLA-B27 and ankylosing spondylitis (AS) remains an enigma. While previous reviews have discussed the controversies surrounding the involvement of bacteria in the etiology of this disease and the sequence variability between subtypes of HLA-B27, concepts of disease mechanism remain ill-defined. In this article Richard Benjamin and Peter Parham synthesize new data on the structure and function of HLA class I molecules into possible mechanisms that might underly the pathogenesis of AS.

Amino Acid Sequence↗
PubMed2005

Guilt by association? p53 and the development of aneuploidy in cancer.

Aneuploidy is one of the most frequent genetic alterations in solid tumors. It is commonly caused by cell division errors that are induced by oncogene activation or loss of tumor suppressor functions. In addition, certain viral oncoproteins have been implicated in the induction of chromosome copy number changes. Aneuploidy and inactivation of p53 frequently coincide in human cancers but there is increasing evidence that loss of p53 by itself is not a primary cause of aneuploidy. Nonetheless, p53 inactivation synergizes with additional oncogenic events to promote aneuploidy and may facilitate chromosomal imbalances through indirect mechanisms. This review summarizes the current knowledge about the association between aneuploidy and p53, and discusses two of the most controversial mechanisms that have been implicated in genomic instability associated with loss of p53: subversion of ploidy control and aberrant centrosome duplication.

Aneuploidy↗