Disease relevance of EED

• Recent studies have revealed the intrinsic histone methyltransferase (HMTase) activity of the EED-EZH2 complex and its role in Hox gene silencing, X inactivation, and cancer metastasis [1].
• The human polycomb group EED protein interacts with the integrase of human immunodeficiency virus type 1 [2].
• In the present study, EED was found to interact with HIV-1 integrase (IN) both in vitro and in vivo in yeast [2].
• In vitro, data from mutagenesis studies, pull-down assays, and phage biopanning suggested that EED-binding site(s) are located in the C-terminal domain of IN, between residues 212 and 264 [2].
• The potential use of EED data in parkinsonism is discussed [3].

Psychiatry related information on EED

• They were randomly assigned to four conditions: (1) one-session (E1); or (2) five-sessions of exposure (E5); (3) five-sessions of cognitive therapy (C5); and (4) Wait-list for 5 weeks [4].
• Mental health. Wait not, want not [5]?
• This study extends the compliance literature through: (1) an analysis of the effects of compliance training in long-term institutionalized mentally retarded adults, (2) the investigation of a third response class "Wait" requests, and (3) an assessment of stimulus generalization [6].
• Seventy-eight motor vehicle accident survivors with chronic (greater than 6 months) PTSD, or severe sub-syndromal PTSD, completed a randomized controlled comparison of cognitive behavioral therapy (CBT), supportive psychotherapy (SUPPORT), or a Wait List control condition with two detailed assessments [7].

High impact information on EED

• Finally, the histone deacetylase inhibitor trichostatin A (ref. 17) relieves transcriptional repression mediated by EED, but not by HPC2, a human homologue of polycomb [8].
• SUZ12 is required for both the histone methyltransferase activity and the silencing function of the EED-EZH2 complex [1].
• We further find that overexpression of SUV39H1 induces selective nuclear relocalization of HPC/HPH PcG proteins but not of the EED/EZH2 PcG proteins [9].
• The present study interrogated the genetic, biochemical and molecular interaction of BMI1 and EED, pivotal constituents of heterologous Polycomb complexes, in the regulation of vertebral identity during mouse development [10].
• Strikingly, methylated lysine 27 of histone H3 (H3-K27), a mediator of Polycomb complex recruitment to target genes, stably associated with the EED complex during the maintenance phase of Hox gene repression [10].

Chemical compound and disease context of EED

• Human EED, a member of the superfamily of WD-40 repeat proteins and of the Polycomb group proteins, has been identified as a cellular partner of the human immunodeficiency virus type 1 (HIV-1) matrix (MA) protein (R. Peytavi et al., J. Biol. Chem. 274:1635-1645, 1999) [2].
• The aim of our study was to evaluate the efficacy and toxicity of a bi-weekly chemohormonal regimen consisting of epirubicin, etoposide, and low-dose dexamethasone (EED) in patients with hormone-refractory prostate cancer (HRPC) [11].

Biological context of EED

• EZH2 is a component of the PRC2 histone methyltransferase complex, which also contains EED and SUZ12 and is required for the silencing of HOX gene expression during embryonic development [12].
• Polycomb group proteins of both the HPC/HPH and the EED/EZH2 complexes, which are involved in the heritable repression of gene activity, are not recruited to the amplified chromosome region by HP1alpha and HP1beta in vivo targeting [13].
• Furthermore, in contrast with a recent study suggesting that Embryonic Ectoderm Development EED isoforms may affect substrate specificity, we found that EZH2 complexes reconstituted with different EED isoforms exhibit similar substrate preference and specificity [14].
• The binding site for WAIT-1 was mapped to a short membrane-proximal region of the beta7 cytoplasmic tail with Tyr-735 being of critical importance [15].
• Despite evidence implicating the Polycomb group protein, Eed (embryonic ectoderm development protein) in imprinted X inactivation, a similar role in random X inactivation in the embryo has remained an open question [16].

Anatomical context of EED

• Northern blot analysis revealed multiple WAIT-1-related transcripts with differential expression in circulating leukocytes, tissue-resident cells of diverse origin, and lymphoid malignancies [15].
• Canadian Association of General Surgeons and American College of Surgeons evidence based reviews in surgery. 13. Wait-and-see policy or laparoscopic cholecystectomy after endoscopic sphincterotomy for bile-duct stones [17].

Associations of EED with chemical compounds

• In EED, two putative discrete IN-binding sites were mapped to its N-terminal moiety, at a distance from the MA-binding site, but EED-IN interaction also required the integrity of the EED last two WD repeats [2].
• Please Wait until I Finish [18].

Physical interactions of EED

• SUZ12 is a Polycomb group protein that forms Polycomb repressive complexes (PRC2/3) together with EED and histone methyltransferase EZH2 [19].

Other interactions of EED

• Two distant topological sorting signals were required for efficient nuclear import of the 4.1R80 isoform: a basic peptide, KKKRER, encoded by alternative exon 16 and acting as a weak core nuclear localization signal (4.1R NLS), and an acidic peptide, EED, encoded by alternative exon 5 [20].

Analytical, diagnostic and therapeutic context of EED

• In 19 patients who had cardiac catheterization druing the follow-up period, the discharge EED/PR-AC ratio correlated inversely with the angiographic ejection fraction (r = 0.79; p less than 0.001) [21].
• The third patient, with the most severe arteriopathy, had to wait 1 year for a donor, and the attempted transplantation was complicated by ventricular tachycardia; death occurred 2 days after surgery [22].
• As part of its Wait Time Strategy, the Ontario Ministry of Health and Long-Term Care provided significant amounts of money to perform more cases with the understanding that improving access by reducing wait times is not just a matter of increasing funding [23].
• METHODS: Wait lists from 4 Canadian transplantation centers were examined for causes of living kidney donor exclusion [24].
• METHODS: Of the 120 residents from a home for the aged, 69 were stratified based on age (five year intervals) and randomly allocated to three groups i.e., Yoga (physical postures, relaxation techniques, voluntarily regulated breathing and lectures on yoga philosophy), Ayurveda (a herbal preparation), and Wait-list control (no intervention) [25].

References