Disease relevance of ERDA1

• These repeats localize to an intron in transcription factor gene SEF2-1B at 18q21, a site named ERDA1 on 17q21 with no associated coding region, and the 3' end of a gene on 13q21, SCA8, that is believed to be responsible for a form of spinocerebellar ataxia [1].
• Analysis of ERDA1, CTG18.1, and uncloned CAG/CTG repeat sequences in familial Parkinson's disease with anticipation [2].

Psychiatry related information on ERDA1

• We conclude that expanded alleles at the CTG18.1 locus confers an odds ratio of 2.6-2.8 and may thus act as a vulnerability factor for affective disorder, while the ERDA1 locus seems unrelated to disease [3].
• At present no strong evidence exists that large repeat alleles at either SEF2-1B or ERDA1 are involved in the etiology of schizophrenia or bipolar disorder [1].
• Intergenerational CAG repeat expansion at ERDA1 in a family with childhood-onset depression, schizoaffective disorder, and recurrent major depression [4].
• The project Epidemiology Research on Dementia in Antwerp (ERDA) estimated the prevalence of dementia in a random, population-based sample, stratified for age and sex [5].

High impact information on ERDA1

• Two unstable CAG/CTG repeats, SEF2-1B and ERDA1, have recently been cloned, and studies indicate that the majority of individuals with large repeats as detected by repeat-expansion detection (RED) have large repeat alleles at these loci [6].
• A highly polymorphic CAG repeat locus, ERDA1, was recently described on human chromosome 17q21.3, with alleles as large as 50-90 repeats and without any disease association in the general population [7].
• We analyzed 20 FSP families, including four for which there is evidence for linkage to SPG4, and found that in most cases the repeat expansion detected by RED is due to non-pathogenic expansions of the chromosome 18q21.1 SEF2-1 or 17q21.3 ERDA1 locus [8].
• Association and linkage studies between bipolar affective disorder and the polymorphic CAG/CTG repeat loci ERDA1, SEF2-1B, MAB21L and KCNN3 [9].
• Here we report that 89% of RED products (CAG/CTG repeats) > 120 nt (n = 202) detected in affective disorder patients as well as unaffected family members and controls correlate with expansions at two repeat loci, ERDA1 on chromosome 17q21.3 and CTG18.1 on 18q21 [3].

Biological context of ERDA1

• Alleles at two recently discovered unstable trinucleotide repeat loci at 18q21.1 (SEF2-1B) and 17q21.3 (ERDA1) have also been analysed in affecteds and matched controls [10].
• Our results demonstrate that unstable CAG/CTG expansions corresponding to uncloned or cloned sequences (ERDA1, CTG18.1) are not involved in the etiology of rare familial case of PD with genetic anticipation [2].
• The purpose of the present study was to further test if expanded CAG repeats detected by the repeat expansion detection (RED) method in bipolar affective disorder (BPAD) are correlated with ERDA1 (17q21.3) and/or CTG18.1 (18q21.1) loci expansions, and changes of phenotype severity in successive generations (anticipation) [11].

Associations of ERDA1 with chemical compounds

• Elastic recoil detection analysis (ERDA) was used to determine the surface excesses of fluorocarbon end-capped polystyrene (hPSF) and poly(styrene-b-dimethylsiloxane) (hPS-PDMS) in deuterated polystyrene (dPS) films [12].
• DLC coatings deposited by PACVD and FAD, were analysed with respect to sp(3) content (EELS), hydrogen content (ERDA), surface composition (XPS), surface roughness (AFM), surface energy, albumin:fibrinogen adsorption ratio, and macrophage viability and attachment [13].
• UV-VIS, Raman spectroscopy, RBS (Rutherford backscattering) and ERDA (Elastic Recoil Detection Analysis) techniques were used for the characterization of the layers [14].

Other interactions of ERDA1

• Polymorphic expansions at SEF2-1 and ERDA1 appear frequent and may confound RED studies in the search for genes causing disorders demonstrating anticipation [8].
• In six FSP families, however, CAG repeat expansion was detected in a subset of affected and at-risk individuals that did not result from expansion of the SEF2-1 and ERDA1 loci [8].

Analytical, diagnostic and therapeutic context of ERDA1

• METHODS: CAG/CTG repeat distribution in KCNN3, CTG 18.1 and ERDA1 was examined and the copy number of ligation product in repeat expansion detection (RED) was measured in Korean bipolar patients in comparison to ethnically matched healthy controls [15].
• Repeat expansion detection (RED) technique was used to measure genomic CAG/CTG repeat size, and PCR for CAG repeat size at the ERDA-1 and CTG 18.1 loci [16].
• The ERDA total artificial heart was shown to successfully fit the fiftieth percentile adult male human [17].

References