Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.25.1 (proteasome)
 28,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Prolactin (PRL) levels were studied in 5 women with Sheehan syndrome before and after metoclopramide (MCP, 10 mg i.v.) and domperidone (MOT, 10 mg i.v.) stimulation. The levels of PRL were measured by RIA method. The obtained results were compared with control group (10 female volunteers). Decreased serum level of PRL was found in 3 women before stimulation in comparison with control group. The highest serum concentration of PRL was found 30 min after MOT and MCP injection. In group of women with Sheehan syndrome the level of PRL was not significantly increased in MCP-test. In MOT-test the level of this hormone did not change. The findings of the present investigation suggest that measurement of PRL serum levels in MOT-test could be of value in early diagnosis of Sheehan syndrome.
Ginekol Pol 1992 May
PMID:[Importance of prolactin level indication in detection of Sheehan syndrome]. 130 15

It was found that the acid protease of Fusarium culmorum can hydrolyze various proteins of plant origin including polygalacturonase inhibitor from bean (BPI) and soybean trypsin inhibitor (STI). The highest hydrolysis extent of BPI and STI by the enzyme was only 5% and 3% respectively. The partially hydrolyzed BPI lost its inhibition ability to fungal polyglacturonases. Similarly, the partially hydrolyzed STI lost its inhibition ability to trypsin and fungal alkaline protease. The F. culmorum acid protease showed broad substrate specificity towards synthetic dipeptides.
Acta Microbiol Pol 1984
PMID:Hydrolytic ability of acid protease of Fusarium culmorum and its possible role in phytopathogenesis. 620 29

The authors present results of 9 replantation after circular saw transmetacarpal injuries. All the replanted fingers with the exception of one index and one little finger survived. Internal muscles disfunction and restricted range of motion in MCP joints have been observed in all cases.
Chir Narzadow Ruchu Ortop Pol 1995
PMID:[Trans-metacarpal hand replantation]. 767 41

A case of inveterate dorsal dislocation of the MCP joint of the thumb treated by open reduction and tendon reinforcement of the volar capsule. The paper reports rare cases of inveterate, complete dorsal dislocation of the thumb MCP joint. After open reduction there was a full passive flexion but dorsal dislocation recurred. The tendency to return of dislocation was abolish by tendon reinforcement of the capsule of the joint described by Kessler. Follow up studies revealed no significant instability, the range of motion was between 20 degrees and 55 degrees of flexion.
Chir Narzadow Ruchu Ortop Pol 1996
PMID:[A case of inveterate metacarpo-phalangeal dislocation of the thumb treated surgically by the Kessler method]. 864 97

We have shown previously that UV radiation and other DNA-damaging agents induce the ubiquitination of a portion of the RNA polymerase II large subunit (Pol II LS). In the present study UV irradiation of repair-competent fibroblasts induced a transient reduction of the Pol II LS level; new protein synthesis restored Pol II LS to the base-line level within 16-24 h. In repair-deficient xeroderma pigmentosum cells, UV radiation-induced ubiquitination of Pol II LS was followed by a sustained reduction of Pol II LS level. In both normal and xeroderma pigmentosum cells, the ubiquitinated Pol II LS had a hyperphosphorylated COOH-terminal domain (CTD), which is characteristic of elongating Pol II. The portion of Pol II LS whose steady-state level diminished most quickly had a relatively hypophosphorylated CTD. The ubiquitinated residues did not map to the CTD. Importantly, UV-induced reduction of Pol II LS level in repair-competent or -deficient cells was inhibited by the proteasome inhibitors lactacystin or MG132. These data demonstrate that UV-induced ubiquitination of Pol II LS is followed by its degradation in the proteasome. These results suggest, contrary to a current model of transcription-coupled DNA repair, that elongating Pol II complexes which arrest at intragenic DNA lesions may be aborted rather than resuming elongation after repair takes place.
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PMID:Ultraviolet radiation-induced ubiquitination and proteasomal degradation of the large subunit of RNA polymerase II. Implications for transcription-coupled DNA repair. 947 72

The clinical studies show that heparin, well known as an anticoagulant, inhibits early asthmatic response (EAR) and bronchial hyperactivity after allergen challenge in allergic patients. We have previously shown that heparin attenuates also the late phase of allergic reaction (LAR) Recently it has been shown that heparin modulates mastocyte mediator release. This could explain the beneficial role of heparin in EAR. The goal of this study was to explore the protective mechanism of heparin on LAR. Basophils are important cells in the development of LAR. We studied the effect of heparin on histamine release from basophils induced by anti-IgE and monocyte chemotactic-activating factor/monocyte chemotactic protein (MCAF/MCP-I). MCAF belongs to the chemokine family and is the most potent histamine releasing factor. Basophils were isolated from peripheral blood of 12 asthmatic patients. The cells were incubated with heparin in various concentrations: 10, 25, 50 and 100 U. Histamine was measured by spectrophotofluorometric method. We observed that incubation of basophils with heparin inhibits histamine release as shown in the table: [table: see text] Preincubation of anti-IgE or MCAF/MCP-I with heparin did not induce any changes in histamine release. The suggest that action of heparin depends on interaction with the cells but not with the agonists.
Pneumonol Alergol Pol 1997
PMID:[The effect of heparin on release of histamine from basophils under the influence of MCAF/MCP-I in patients with bronchial asthma]. 948 30

An efficient vaccine against human immunodeficiency virus (HIV) must induce good cellular immune responses. To do this, it must be processed and presented by dendritic cells, which are required for primary T-lymphocyte stimulation. We have previously shown that a model lipopeptide containing a short epitopic peptide from HIV-1 was endocytosed and presented in association with major histocompatibility complex class I molecules by human dendritic cells to specific CD8(+) T lymphocytes, but the cross-presentation pathway needed to be precisely determined. We have studied a longer lipopeptide (Pol(461-484)) and another lipopeptide (Nef(66-97)) currently being used in vaccine trials. Like the shorter lipopeptide, the rhodamine-labeled Pol(461-484) lipopeptide was internalized by endocytosis, as assessed by confocal microscopy. The lipopeptides were processed by dendritic cells and presented to CD8(+) T cells specific for the HLA-A*0201-restricted Pol(476-484) and the HLA-A*0301-restricted Nef(73-82) epitope, respectively. Presentation of both lipopeptides was inhibited by brefeldin A. Presentation of the Pol lipopeptide was inhibited by epoxomycin, a proteasome-specific inhibitor, but not by monensin. This shows that it gained access to the cytosol to be digested by the proteasome. In contrast, presentation of the Nef lipopeptide was not inhibited by epoxomycin but was inhibited by monensin, a classical inhibitor of acid-dependent endosomal enzyme activity, indicating an endocytic processing pathway yielding to major histocompatibility complex class I-restricted presentation. Therefore, the two lipopeptides followed different cross-presentation pathways, both resulting in efficient presentation to CD8(+) T lymphocytes.
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PMID:Two human immunodeficiency virus vaccinal lipopeptides follow different cross-presentation pathways in human dendritic cells. 1250 69

The ubiquitin-related protein SUMO-1 is covalently attached to proteins by SUMO-1 ligases. We have performed a proteome-wide analysis of sumoylated substrate proteins in yeast. Employing the powerful affinity purification of Protein A-Smt3 (Smt3 is the yeast homologue of SUMO-1) from yeast lysates in combination with tandem liquid chromatography mass spectrometry, we have isolated potential Smt3-carrying substrate proteins involved in DNA replication and repair, chromatin remodeling, transcription activation, Pol-I, Pol-II, and Pol-III transcription, 5' pre-mRNA capping, 3' pre-mRNA processing, proteasome function, and tubulin folding. Employing tandem affinity purifications or a rapid biochemical assay referred to as "SUMO fingerprint," we showed that several subunits of RNA polymerases I, II, and III, members of the transcription repression and chromatin remodeling machineries previously not known to be sumoylated, are modified by SUMO-1. Thus, the identification of a broad range of SUMO-1 substrate proteins is expected to lead to further insight into the regulatory aspects of sumoylation.
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PMID:A proteome-wide approach identifies sumoylated substrate proteins in yeast. 1529 83

Cancer cachexia is a serious and life-treating syndrome that appears in most solid tumor patients. The syndrome is associated with anorexia, loss of protein mass, wasting of lipids, and disturbances of carbohydrate metabolism. Moreover, psychological distress and lower quality of life are often seen in patients with cancer cachexia. The latter is a multimodality process in which cytokine interactions, action of enzymes playing a key role in lipid metabolism, and activity of proteolytic proteinases are the complex net that are responsible for destruction of an organism suffering from cancer cachexia. Recently, it has been shown a growing role of ubiquitin-proteasome pathway in cachexia. Biochemical interactions are crucial for further study, mainly, when a novel target therapy appears to treat cancer in different modalities. In case of proteasome, PS-341 (bortezomib, Velcade) an inhibitor of proteasome is under investigation in clinical trials phase I.
Pol Merkur Lekarski 2004
PMID:[The role of proteasome in pathophysiology of cancer cachexia]. 1560 47

The c-Myc oncoprotein regulates transcription of genes that are associated with cell growth, proliferation and apoptosis. c-Myc levels are modulated by ubiquitin/proteasome-mediated degradation. Proteasome inhibition leads to c-Myc accumulation within nucleoli, indicating that c-Myc might have a nucleolar function. Here we show that the proteins c-Myc and Max interact in nucleoli and are associated with ribosomal DNA. This association is increased upon activation of quiescent cells and is followed by recruitment of the Myc cofactor TRRAP, enhanced histone acetylation, recruitment of RNA polymerase I (Pol I), and activation of rDNA transcription. Using small interfering RNAs (siRNAs) against c-Myc and an inhibitor of Myc-Max interactions, we demonstrate that c-Myc is required for activating rDNA transcription in response to mitogenic signals. Furthermore, using the ligand-activated MycER (ER, oestrogen receptor) system, we show that c-Myc can activate Pol I transcription in the absence of Pol II transcription. These results suggest that c-Myc coordinates the activity of all three nuclear RNA polymerases, and thereby plays a key role in regulating ribosome biogenesis and cell growth.
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PMID:c-Myc associates with ribosomal DNA and activates RNA polymerase I transcription. 1573 72


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