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A purpose-built high-resolution array with 93.75% breakpoint accuracy was used to map 4000 patients with diverse diagnoses and identify eight probands harboring microdeletions at TP53 (17p13.1), a DNA copy-number variations (CNVs) which might cause childhood-onset developmental delay (DD) and cancer. The results revealed a possible association of 17p13.1 CNVs with distinct phenotypes depending on the position of the breakpoint with respect to TP53 and called for further studies to determine if other loci in the genome also give rise to phentotypically distinct disorder.

Research demonstrates that immunostimulatory effect of bacterial DNA and synthetic oligonucleotides stimulate innate immunity. Data point out that DNA-dependent protein kinase and IKKbeta produce cytokine during immunostimulation suggesting a possible link between DNA repair and innate immunity.

The mitotically regulated manner of interaction between vesicle docking protein p115 and cis-Golgi matrix protein GM130 was analyzed through utilization of deletion analysis which revealed that p115 specifically interacts with the N-terminus while GM130 with C-terminus. Mitotically modified GM130 and N-terminus peptide failed to bind with p115, significantly implying that interactions were mitotically regulated.

The p53 tumor plays a direct role in cellular metabolism and this suppressor pathway coordinates DNA repair, cell-cycle arrest, apoptosis, and senescence to preserve genomic stability and prevent tumor formation. The product of a p53 target gene, TIGAR (TP53-induced glycolysis and apoptosis regulator), is identified and the discovery of three new target genes for p53 reveals unexpected functions for this tumor suppressor in the regulation of glucose metabolism and autophagy.

The 3.2 A-resolution X-ray crystal structure of Escherichia coli transcription-repair coupling factor (TRCF) is discussed. A compact arrangement of eight domains, a translocation module and a region of structure similarity to UvrB is observed in the structure.