Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.10.1 (ERK)
 95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Actinomycin D (ACT-D), an inhibitor of transcription, was added to chick muscle cultures to study its effect on the synthesis of acetylcholine receptor (ACHR) and acetylcholinesterase (ACHE, EC 3.1.1.7). Doses of ACT-D (1.85-18.5 nM), which inhibited uridine incorporation up to 80%, increased ACHR, ACHE, and creatine kinase (CK, EC 2.7.3.2) levels without affecting general cell protein. Degradation of ACHR was slower in ACT-D treated cultures than controls, resulting in a twofold increase in receptor half-life. Uridine incorporation was inhibited by ACT-D in both mononucleated cells and myotubes and [3H]uridine nuclear grain distribution were shifted to values lower than controls. The results indicate that posttranscriptional effects of ACT-D increase levels of ACHR, ACHE, and CK and that decreased degradation could account for the increase in the number of surface ACH receptors.
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PMID:Alteration of acetylcholine receptor and acetylcholinesterase metabolism by actinomycin D in cultured muscle cells. 617 Apr 4

The chromosome localizations for 159 gene and DNA segments have been refined to one of five intervals in the 7q21-132 region through hybridization analysis with a panel of somatic cell hybrid lines. Seventy-two of these chromosome 7 markers are also mapped on common or overlapping yeast artificial chromosome (YAC) clones. In addition, the breakpoints of chromosome rearrangement contained in five of the somatic cell hybrid lines have been defined by flanking probes within YAC contigs. To provide a framework for further mapping of the 7q21-q32 region, we have established the physical order of a set of reference markers: cen-(COL1A2-D7S15-CYP3A4-PON)-D7S456-(brea kpoint contained in cell hybrid 1EF2/3/K017)-GUSB-D7S186-ASL-(PGY1-PGY3 -GNB2-EPO-ACHE)-D7S238-(proximal breakpoint in GM1059-Rag5)-D7S240-(CUTL1-PLANH1)-(breakp oints in 1CF2/5/K016 and 2068Rag22-2)-(PRKAR2B-D7S13)-LAMB1-(breakpoint in JSR-17S)-DLD-D7S16-MET-WNT2-CFTR-D7S8-tel.
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PMID:Refined localization and yeast artificial chromosome (YAC) contig--mapping of genes and DNA segments in the 7q21-q32 region. 835 94

Tension - type headache is one of the widely spread types of idiopathic headaches. The pathogenesis of the disease includes depression and change in brain serotonin level. The aim of the research is to study the characteristics of ache and the level of serotonin in blood serum in tension-type headache. The intensity of ache, complex psychometric parameters and the level of serotonin in blood serum were investigated in 100 patients (75% females and 25% males from 17 to 55 years old) with tension-type headache. The average period of the illness was 6-5 years. The diagnosis has been determined according to MKGB (2003) criteria. According to the duration of anamnesis of ache the patients were divided into 3 groups: the first - 66 patients, the second - 24 patients, the third - 10 patients with tension-type headache and migraine. Ache status and its impact on different spheres of activity were assessed according to international 150 millimeters visual analogous scale. The research showed that all patients with tension-type headache had moderate ache syndrome, depression and anxiety of the middle or high rate which were in inverse dependence on serotonin rate in the blood. Intensity of episodic tension-type headache (n=24) was 52 mm according to visual analogous scale, the high rate of anxiety (51,08+/-4,2 scores), moderate rate of depression (12,9 scores according to Bek scale) and tendency of serotonin decreasing in blood (205,72+/-6,74 ng ml) was noted. The research of 76 patients with chronic tension-type headache with cephalgy intensity according to VASH 62 mm the high indicators of reactive (46,81+/-2,68 scores) and personal anxiety, the rate of depression (22,4+/-1,64 according to Bek scale) were associated with the displayed decreasing of serotonin amount in blood (119,38+/-9,42 ng/ml). It was concluded that, tension-type headache and moderate ache syndrome leads to depression decreased self-control of pain and life quality. The quality of serotonin in blood decreases in patients with tension-type headache. The relationship between the intensity of pain syndrome, decrease of work capacity, life quality, and quantity of serotonin in patients with ageing was revealed. It is concluded that serotonin level in blood serum may be considered as pain intensity, degree of depression and index of efficacy of depression treatment. Serotonin is an extremely important neurohormone and its metabolism further study will show new characteristic features of its activity in cerebral neurochemical processes. Scientists thought, that the increased activity caused the psychological disorder, changes in the mood and depression. But the results of the last studies show that the person with the abnormal activity of serotonin does not realize the sense of danger and accordingly the main instinct of self-preservation is broken.
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PMID:[Relationship between serum blood serotonin and tension--type headache]. 1957 13

Increasing evidence supports the involvement of acetylcholinesterase and butyrylcholinesterase in cell proliferation control and differentiation, reinforcing the hypothesis that these enzymes might have an influence in tumorigenesis. It has already been shown that the cholinesterase genes are structurally altered or aberrantly expressed in a variety of tumor types. In this study, amplifications and deletions in the ACHE and BCHE genes were investigated in sporadic breast tumors using real-time polymerase chain reaction and the relative quantification method. The majority of the tumor tissues showed a notable number of both deletions and amplifications: 65.7% and 22.9%, respectively, in BCHE and 45.7% and 31.4%, respectively, in ACHE. Deletion of the ACHE gene was significantly correlated with amplification of the protooncogene ERBB2. Tumor size was significantly higher when the ACHE gene was amplified, and the total number of alterations (amplifications plus deletions) of the BCHE gene was positively correlated with tumor malignancy grade.
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PMID:Amplification and deletion of the ACHE and BCHE cholinesterase genes in sporadic breast cancer. 2019 49

Studies in vertebrate neuromuscular synapses have revealed previously that ATP, via P2Y receptors, plays a critical role in regulating postsynaptic gene expressions. An equivalent regulatory role of ATP and its P2Y receptors would not necessarily be expected for the very different situation of the brain synapses, but we provide evidence here for a brain version of that role. In cultured cortical neurons, the expression of P2Y(1) receptors increased sharply during neuronal differentiation. Those receptors were found mainly colocalized with the postsynaptic scaffold postsynaptic density protein 95 (PSD-95). This arises through a direct interaction of a PDZ domain of PSD-95 with the C-terminal PDZ-binding motif, D-T-S-L of the P2Y(1) receptor, confirmed by the full suppression of the colocalization upon mutation of two amino acids therein. This interaction is effective in recruiting PSD-95 to the membrane. Specific activation of P2Y(1) (G-protein-coupled) receptors induced the elevation of intracellular Ca(2+) and activation of a mitogen-activated protein kinase/Raf-1 signaling cascade. This led to distinct up-regulation of the genes encoding acetylcholinesterase (AChE(T) variant), choline acetyltransferase, and the N-methyl-d-aspartate receptor subunit NR2A. This was confirmed, in the example of AChE, to arise from P2Y(1)-dependent stimulation of a human ACHE gene promoter. That involved activation of the transcription factor Elk-1; mutagenesis of the ACHE promoter revealed that Elk-1 binding at its specific responsive elements in that promoter was induced by P2Y(1) receptor activation. The combined findings reveal that ATP, via its P2Y(1) receptor, can act trophically in brain neurons to regulate the gene expression of direct effectors of synaptic transmission.
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PMID:ATP induces synaptic gene expressions in cortical neurons: transduction and transcription control via P2Y1 receptors. 2084 60

Gene amplifications and deletions are common changes in human cancer cells. Previous studies indicate that the regions, where the ACHE (7q22) and BCHE (3q26.1-q26.2) genes are localized, are suffering such structural modifications in breast cancer. Therefore, the products of these genes, acetylcholinesterase and butyrylcholinesterase, respectively, are related to the process of cell differentiation and proliferation, as well as apoptosis. This study also included two other genes involved in tumorigenesis, the EPHB4 (7q22.1) and MME (3q21-27). The aim of this study was to verify amplification and/or deletion in the ACHE, BCHE, EPHB4 and MME genes in 32 samples of sporadic breast cancer. The gene alterations were detected using real-time PCR and determined by relative quantification with the standard curve method. All samples presented genetic alterations, showing a higher tendency for amplification of the ACHE (62.5% vs. 37.5%; p>0.1) and EPHB4 (53.13% vs. 46.88%; p>0.5) genes, and for deletions of the BCHE and MME genes (56.25% vs. 43.75% for both; p>0.5). A positive correlation was found between alterations in ACHE-EPHB4 and BCHE-MME pairs (r(s) = 0.5948; p = 0.0004; r(s) = 0.3581; p = 0.0478, respectively) indicating that these changes comprise a wide region. In conclusion, the results suggest that these genomic regions may contain important genes for this pathology, such as the oncogenes MET (7q31) and PIK3CA (3q26), and thus being interesting targets for future studies in breast cancer research.
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PMID:Copy number variation in ACHE/EPHB4 (7q22) and in BCHE/MME (3q26) genes in sporadic breast cancer. 2306 27

Acetylcholine (ACh) in the ovary and its actions were linked to survival of human granulosa cells in vitro and improved fertility of rats in vivo. These effects were observed upon experimental blockage of the ACh-degrading enzyme (ACH esterase; ACHE), by Huperzine A. We now studied actions of Huperzine A in a three-dimensional culture of macaque follicles. Because a form of programmed necrotic cell death, necroptosis, was previously identified in human granulosa cells in vitro, we also studied actions of necrostatin-1 (necroptosis inhibitor). Blocking the breakdown of ACh by inhibiting ACHE, or interfering with necroptosis, did not improve the overall follicle survival, but promoted the growth of macaque follicles from the secondary to the small antral stage in vitro, which was correlated with oocyte development. The results from this translational model imply that ovarian function and fertility in primates may be improved by pharmacological interference with ACHE actions and necroptosis.
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PMID:Acetylcholine and necroptosis are players in follicular development in primates. 2967 Jan 72