Disease relevance of ENC1

• In other experiments, overexpression of ENC1 in HT-29 colon cancer cells suppressed the usual increase of two differentiation markers, in response to treatment with sodium butyrate, a differentiation-inducible agent [1].
• Up-regulation of the ectodermal-neural cortex 1 (ENC1) gene, a downstream target of the beta-catenin/T-cell factor complex, in colorectal carcinomas [1].
• Disruption of a novel ectodermal neural cortex 1 antisense gene, ENC-1AS and identification of ENC-1 overexpression in hairy cell leukemia [2].
• Cloning of human ENC-1 and evaluation of its expression and regulation in nervous system tumors [3].
• These results suggest that ENC-1 expression plays a role during differentiation of neural crest cells and may be down regulated in neuroblastoma tumors [3].

High impact information on ENC1

• Altogether, these results suggest that upregulation of ENC-1 contributes to the development of HCL and provides new information on the possible dysregulation of ENC-1 including expression of a novel antisense gene, ENC-1AS [2].
• In addition, we have also found tissue-specific methylation of a 1.2 kb segment encompassing the overlapping ENC-1/ENC-1AS 5' exons, adding to the complexity of the regulation of this locus [2].
• Importantly, subsequent analysis of ENC-1 in purified primary HCL tumor cells revealed a striking upregulation of ENC-1 in all 26 patients examined, compared with normal peripheral blood lymphocytes from healthy donors [2].
• These data suggest that ENC1 is regulated by the beta-catenin/Tcf pathway and that its altered expression may contribute to colorectal carcinogenesis by suppressing differentiation of colonic cells [1].
• In an attempt to study molecules that play a regulatory role early in adipocyte differentiation, we identified by differential display ENC-1, a Drosophila kelch-related protein [4].

Biological context of ENC1

• Assignment of the ectodermal-neural cortex 1 gene (ENC1) to human chromosome band 5q13 by in situ hybridization [5].
• To gain insight into a potential role for ENC-1 gene in the processes of cell differentiation and malignant transformation in the human nervous system, we first cloned and characterized the human homologue of ENC-1 [3].
• In the present study, several key features of early ENC1 development were characterized as a necessary foundation for further experimental studies on the mechanisms underlying ENC1 development and its physiological role during embryogenesis [6].
• Furthermore, decreasing the endogenous ENC-1 levels by stable antisense transfection, thereby preventing the transient induction, effectively inhibits 3T3-L1 adipocyte differentiation [4].
• These effector genes, including Grp, Trpc3, Pcp4, and Enc1, have been implicated in synaptic transmission, calcium homeostasis, and structural function and thus may have similar roles in the dorsal horn [7].

Anatomical context of ENC1

• The human ENC-1 gene appeared to be highly expressed in adult brain and spinal cord, and in a number of cell lines derived from nervous system tumors we detected low steady-state levels of ENC-1 mRNA [3].
• Although the proximal neurite outgrowth of ENC1 appeared unaffected by the pCPA treatment at both of these time points, the distal outgrowth in the target cell region appeared more profuse [8].
• The ENC-1 induction correlates with the subsequent differentiation of primary stroma-vascular cells into adipocytes [4].
• Guidance on exposure to such fields has been published by NRPB and ICNIRP, which is based on the avoidance of acute effects in the central nervous system [9].

Associations of ENC1 with chemical compounds

• In contrast, 5-HTP treatment resulted in an increase in embryonic serotonin content and a significant decrease in the number of ENC1 branch points [8].
• Treatment with dopamine had no effect on the pattern of ENC1 neurite outgrowth [8].
• NADPH diaphorase histochemistry on stage E25-E30 embryos revealed NOS expression in the protonephridia, buccal mass, dorsolateral ciliary cells and the sensory dendritic knobs of ENC1 [10].
• Treatment with the adipogenic inducers dexamethasone and methylisobutylxanthine causes an increase in ENC-1 mRNA levels specifically in preadipocytes, and methylisobutylxanthine is the main effector of ENC-1 expression [4].
• The study is based on a collaboration between the Cancer Registry of Norway, the Norwegian Radiation Protection Authority, and National Radiological Protection Board (NRPB, UK) [11].

Other interactions of ENC1

• We used a neuroblastoma differentiation model, the retinoic acid-induced neuronal differentiation of SMS-KCNR cells, to study the regulation of the ENC-1 gene during neural crest cell differentiation [3].

Analytical, diagnostic and therapeutic context of ENC1

• High-performance liquid chromatography with electrochemical detection was used to measure the effects of these treatments on serotonin content, and serotonin immunohistochemistry was carried out to quantify the extent of neurite outgrowth of ENC1 [8].
• ENC1 morphology was determined by confocal microscopy of serotonin-immunostained embryos and by differential-interference contrast (DIC) microscopy of live embryos [6].
• With consistent under-response, the NRPB TLD and film badge were found to generally be unsuitable for sites such as Devonport [12].
• The increasing popularity of pantographic dental radiography and particularly its recent use for routine screening of asymptomatic patients have prompted the NRPB to compare the risks to patients from this technique with those from more conventional dental diagnostic procedures [13].
• In 1997, a collaboration between British Nuclear Fuels plc (BNFL), Westlakes Research Institute and NRPB started, with the aim of producing IMBA (Integrated Modules for Bioassay Analysis), a suite of software modules that implement the new ICRP models for estimation of intakes and doses [14].

References