Disease relevance of SNORD106

• In particular, there was no significant difference between the two groups in the frequency of apo E2 homozygosity, a condition that is associated with type III hyperlipoproteinemia [1].
• However, all E2 homozygote survivors of myocardial infarction had hyperlipoproteinemia type III (cholesterol 269 +/- 29 mg/dl; triglyceride 419 +/- 150 mg/dl; age 54 +/- 14 years; N = 5) [1].
• During adenovirus infection, there is induction of a form of E2F that binds cooperatively to the pair of sites in the E2 control region [2].
• After separation from the low-molecular-weight protein, colicin E2 retained the original in vivo killing activity, and in addition showed a high activity in vitro in cleaving various DNA molecules, such as a ColE1 hybrid plasmid and DNAs from Escherichia coli, lambda phage, chiX174 phage, and simian virus 40 [3].
• Herpes simplex virus 1 mutant in which the ICP0 HUL-1 E3 ubiquitin ligase site is disrupted stabilizes cdc34 but degrades D-type cyclins and exhibits diminished neurotoxicity [4].

Psychiatry related information on SNORD106

• Apolipoprotein E (apoE) and its three major alleles (APOE2, E3, and E4) have been implicated in Alzheimer's disease and other neurological disorders [5].
• Molecular epidemiological research has identified the association of a common apolipoprotein E (apo E) isoform (E4 as opposed to E3), with risk both of coronary artery disease and of Alzheimer dementia [6].
• The patients with E4/4 also showed lowest scores on delayed memory tests and differed from E3/3, 3/2 patients in the list learning test (< 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)[7]
• E1/E2 dimers and the HCV-LPs of 1b did not bind CD81-LEL, consistent with the notion that CD81 recognition by E2 is strain-specific and does not correlate with permissiveness of infection [8].
• In men, there was a significant correlation between systolic blood pressure and alcohol consumption in the E2/3 phenotype (rs = 0.71, P < .01) and in the E3/3 phenotype (rs = 0.25, P < .01), but not in the E4/3 phenotype (rs = 0.03, NS) [9].

High impact information on SNORD106

• We report that, at limiting E1 and E2 levels, the enhancer proteins GAL4-VP16 and GAL4-p53(1-73) stimulate BPV in vitro DNA replication [10].
• For papillomavirus DNA replication, the E2 enhancer protein cooperatively assists in binding of the E1 helicase to the origin [10].
• The adenovirus type 2 encoded protein E3/19K binds to human histocompatibility class I antigens (HLA) [11].
• Treatment of cells with 100 microM anisomycin inhibits 99.6% of protein synthesis and substantially depresses (by 20--200 fold) the levels of the conventional early mRNAs from regions E1A, E1B, E2, E3 and E4 [12].
• Each E1 activity is specified by a domain: an adenylation domain resembling bacterial adenylating enzymes, an E1-specific domain organized around the catalytic cysteine, and a domain involved in E2 recognition resembling ubiquitin [13].

Chemical compound and disease context of SNORD106

• This is in contrast to the Eukarya and most aerobic bacteria, which use the pyruvate dehydrogenase multienzyme complex [PDHC], consisting of multiple copies of three component enzymes: E1 (pyruvate decarboxylase), E2 (lipoate acetyl-transferase) and E3 (dihydrolipoamide dehydrogenase, DHLipDH) [14].
• E2 transacylase-deficient (type II) maple syrup urine disease. Aberrant splicing of E2 mRNA caused by internal intronic deletions and association with thiamine-responsive phenotype [15].
• Structurally related class I and class II receptor protein tyrosine kinases are down-regulated by the same E3 protein coded for by human group C adenoviruses [16].
• Mutations in the parkin gene, encoding an E3 ubiquitin-protein ligase, are a frequent cause of autosomal recessive parkinsonism and are also involved in sporadic Parkinson's disease [17].
• Our study suggests that urinary E1, E2, and E3 reflect the differences in breast cancer risk between Singapore Chinese and United States women to a stronger degree than the estrogen metabolites 2OHE(1) and 16alpha-OHE(1) or the ratio of 2OHE(1):16alpha-OHE(1.)[18]

Biological context of SNORD106

• The primary structure of apolipoprotein E (apo E) was investigated in seven type III hyperlipoproteinemic patients with the apo E-2/2 phenotype [19].
• At baseline, the apo E 2/3 genotype was associated with the lowest, and apo E 3/4 and E4/4 with the highest low-density liporpotein (LDL) cholesterol and apo B levels in men and women of both races, while female (not male) carriers of apo E3 had higher high-density lipoprotein (HDL) cholesterol levels than carriers of other genotypes [20].
• Although RING finger proteins constitute an important family of E3 ligases, only a few post-transcriptional modifications, including phosphorylation, proline hydroxylation and glycosylation, are known to function as recognition signals for E3 [21].
• Competition experiments revealed that E2F did not recognize and bind to the E1B, E3, E4, or major late promoter sequences [22].
• In one class of E3 ubiquitin ligases, the catalytic domain contains a zinc-binding RING finger motif [23].

Anatomical context of SNORD106

• One of these patients had an enzymatically demonstrable deficiency in the E2 dihydrolipoyl transacetylase segment of the complex and very low observable E2 protein component on Western blotting of fibroblast proteins [24].
• We have detected a HeLa cell factor, termed E2 promoter binding factor (E2F), that appears to mediate the transcriptional stimulation of the viral E2 promoter [22].
• We have previously shown that a major M2"a" antigen is the E2 component of the pyruvate dehydrogenase multienzyme complex located within mitochondria [25].
• Peripheral blood T-cell responses to E2/X are thus strongly associated with early PBC [26].
• Injection of the human E1, E2, and E3 genes into Xenopus oocytes generated sequence-specific transcripts of the approximate sizes of the respective snoRNAs [27].

Associations of SNORD106 with chemical compounds

• His very low-density lipoprotein contained approximately five times more apo E2 (136 Arg----Ser) than apo E2 (158 Arg----Cys), as determined by cysteamine treatment and peptide mapping [19].
• As in normal persons with phenotype E3/3, the apolipoprotein E of affected members appears to have a single residue of cysteine [28].
• This is the first time that defects in either the E2 or the X component of the pyruvate dehydrogenase complex have been observed in the human population [24].
• The RING finger protein Ring1B is an E3 ligase that participates in the ubiquitination of lysine 119 of histone H2A, and the binding of Bmi-1 stimulates the E3 ligase activity [29].
• Moreover, incubation of nNOS with a purified system containing an E1 ubiquitin-activating enzyme, an E2 ubiquitin carrier protein conjugating enzyme (UbcH5a), CHIP, glutathione S-transferase-tagged ubiquitin, and an ATP-generating system leads to the ubiquitylation of nNOS [30].

Enzymatic interactions of SNORD106

• Additionally, we provide biochemical and in vivo evidence that TRAF6 serves as an E3 to directly ubiquitinate NEMO [31].

Other interactions of SNORD106

• Consistent with previous studies (Kahyo, T., Nishida, T., and Yasuda, H. (2001) Mol. Cell 8, 713-718), the RING finger-like domain of the SUMO-E3 was required for ligase activity [32].
• Staring binds and recruits the brain-enriched E2 ubiquitin-conjugating enzyme UbcH8 to syntaxin 1 and facilitates the ubiquitination and proteasome-dependent degradation of syntaxin 1 [33].
• Structural analysis of Siah1-Siah-interacting protein interactions and insights into the assembly of an E3 ligase multiprotein complex [34].
• We conclude that the ICP0 HUL-1 domain acts in infected cells to degrade cdc34 and that this function requires the interaction of cdc34 with sequences in exons 2 and 3 but does not involve the HUL-2 RING finger E3 domain [4].
• The RanBP2 SUMO E3 ligase is neither HECT- nor RING-type [35].

Analytical, diagnostic and therapeutic context of SNORD106

• The frequencies of genetic apo E isoforms E2, E3 and E4 were determined in 523 patients with myocardial infarction and compared to those in a control group (1031 blood donors) [1].
• We have observed the typical clinical and biochemical characteristics of this disorder in five members of a family, in all of whom the apolipoprotein E phenotype, as determined by isoelectric focusing electrophoresis, is E3/3 [28].
• Enzyme-linked immunosorbent assays demonstrated that PHF-tau was 38% less reactive with E-2 and 79% more reactive with E-3 than normal tau [36].
• We examined the molecular epidemiology and evolution of Ross River (RR) virus in Australia and the Pacific Islands. Nucleotide sequences of the E2 and E3 genes of five RR virus strains revealed remarkable conservation between 1959 and 1989 with a maximum divergence of only 3.3% [37].
• Titration of E2E3 subcomplexes with E1 resulted in maximum complex activity at an E1/E2 ratio of 1.5-1 [38].

References