Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.7 (DNA polymerase)
17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The binding activity of polymerized human serum albumin was determined in 202 HBsAg carriers. The presence of polymerized human serum albumin receptor sites was tested by hemagglutination and differentiated from antihuman albumin antibodies by immunofluorescence, isolation of IgG and IgM fractions and testing of HBsAg anti-HBs immune complexes. A granular pattern with anti-HBs was specific for polymerized human serum albumin receptor sites as demonstrated with purified HBsAg. In addition, a linear pattern with fluoresceinated antihuman immunoglobulins might suggest the presence of antihuman albumin antibodies (which was generally due to an IgG antibody). However, a granular pattern with fluoresceinated antihuman immunoglobulins may indicate the presence of HBsAg anti-HBs immune complexes. A weak linear pattern was also observed simultaneously in these cases, probably due to IgM antihuman albumin antibodies or an antipolymerized human serum albumin receptor site antibody. Of 202 HBsAg-positive patients, 71 showed polymerized human serum albumin receptor sites activity. The highest percentage of polymerized human serum albumin receptor sites was found among patients showing HBeAg and hepatitis B virus DNA polymerase positivity (96%), followed by HBeAg positivity and hepatitis B virus DNA polymerase negativity (48%), and anti-HBe positivity and hepatitis B virus DNA polymerase negativity (17%). In addition, a significant correlation between polymerized human serum albumin titers and hepatitis B virus DNA polymerase was found (r = 0.573, p less than 0.01). However, at similar HBeAg titer, patients who were positive for hepatitis B virus DNA polymerase had a higher polymerized human serum albumin receptor sites titer than those who were negative for hepatitis B virus DNA polymerase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hemagglutination and immunofluorescence studies on polymerized human serum albumin binding activity in chronic hepatitis B virus infection. 300 39

Polymerized human serum albumin virus receptors (pHSA-R) HBsAg, HBeAg, antiHBc-IgM, hepatitis B virus (HBV) DNA polymerase activity and HBV-DNA were studied in 47 acute hepatitis B patients, divided into three groups: 26 HBeAg(+) initially, with favorable outcome; 4 HBeAg (+), with chronic outcome; and 17 antiHBe (+), with favorable outcome. In the basal sample only 2 and 8 patients in Group I were HBV-DNAp and HBV-DNA positive, respectively, and became negative during the follow-up. In contrast all patients in Group II remained positive to both HBV-markers. After a one-month follow-up 100% of the patients in Group II were positive for pHSA-R and HBeAg, in contrast to 25% among those with a favorable outcome in Group I (p less than 0.005). Meanwhile, only 6 out of 17 patients in Group III remained positive for pHSA-R. A significant decrease in pHSA-R and HBsAg concentrations was observed in patients from Group I (p less than 0.005 and p less than 0.05, respectively) 15 days after the onset of the disease, while concentrations of both parameters did not vary in Group II. A significant decrease in HBsAg and pHSA-R concentrations was found in patients from Group III after 15 days (p less than 0.05) and one month follow-up (p less than 0.05), respectively. As a result, pHSA-R and HBeAg are the best prognostic indicators in acute hepatitis B. A decrease in HBsAg and pHSA-R concentrations two weeks after the onset may have predictive value.
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PMID:Receptors for polymerized human serum albumin and other hepatitis B virus markers during acute hepatitis B--predictive value of the outcome of the disease. 302 41

The effect of alpha-1-antichymotrypsin (ACT), which is known as an efficient serum protease inhibitor and is detected in tumor cell nuclei, on DNA synthesis was studied. ACT inhibited the activity of DNA polymerase alpha purified from human stomach adenocarcinoma. Other human serum proteins including serum albumin, alpha-1-acidglycoprotein, alpha-1-antitrypsin, and immunoglobulin G, as well as other protease inhibitors, such as leupeptin, pepstatin, PMSF and chymostatin, did not affect the activity of DNA polymerase alpha. It was therefore concluded that the inhibitory action of ACT on DNA polymerase alpha was direct phenomenon unrelated to its protease inhibitory activity. Furthermore, the effect of ACT on DNA synthesis was also studied using lysolecithin-permeabilized cultured human stomach carcinoma cells. ACT added in the medium inhibited DNA synthesis and the degree of inhibition depended on incubation time. It was proportional to ACT concentration and the concentration of ACT required for 50% inhibition was 0.8 mg/ml.
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PMID:Inhibition of DNA synthesis by alpha-1-antichymotrypsin. 327 75

The present experiments were conducted to determine the effects of cyclophosphamide (150 mg/kg) on the pathophysiology of RIF-1 solid tumors and to determine the temporal relationship between treatment mediated changes in tumor vascular physiology, cell proliferation, and chemoresponsiveness in vivo. Capillary permeability and plasma and extracellular water volumes were determined by a 125I-bovine serum albumin, 51Cr-EDTA double isotope dilution assay at various intervals after cyclophosphamide. Tumor blood flow and exchangeable erythrocyte vascular volumes were determined by 86RbCl distribution and 51Cr-labeled erythrocyte dilution methods. Cell proliferation in RIF-1 tumors, assessed by [3H]thymidine labeling index and tumor growth fraction (primer-dependent DNA polymerase labeling assay) measurements, was inhibited for up to 3 days by cyclophosphamide. Although tumor regrowth was not apparent until Day 10, cell kinetic studies indicated proliferative recovery in the surviving cell population on Days 4 and 5 after treatment. Increases in tumor blood flow and tumor vascular volumes were temporally coincident with this proliferative response. In split-dose experiments, the time-dependent increases in the chemoresponsiveness of RIF-1 tumors, after cyclophosphamide, may be due not only to the increased proliferation of repopulating cells, but also to vascular responses attendant with cytoreduction.
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PMID:Effect of cyclophosphamide on the pathophysiology of RIF-1 solid tumors. 339 Aug 14

alpha 1-Antichymotrypsin (ACT), which is known as an efficient serum protease inhibitor and is detected in tumor cell nuclei, was found to inhibit the activity of DNA polymerase alpha purified from human stomach adenocarcinoma. The concentration of ACT required for 50% inhibition was 1.0 mg/ml and the manner of its inhibition showed the partially competitive relationship between ACT and DNA in the assay system. Furthermore the removal of ACT by anti-ACT antibody lost its antichymotryptic and anti-DNA polymerase activities in parallel. On the other hand, it did not inhibit the activity of human DNA polymerase beta. Other human serum proteins including serum albumin, alpha 1-acid glycoprotein, alpha 1-antitrypsin, and immunoglobulin G as well as other protease inhibitors such as leupeptin, pepstatin, phenylmethylsulfonyl fluoride, and chymostatin did not affect the activity of DNA polymerase alpha. Furthermore ACT heated at 60 degrees C did not inhibit DNA polymerase alpha, although it could still bind to DNA as well as native ACT. It was therefore concluded that the inhibitory action of ACT on DNA polymerase alpha was a direct phenomenon unrelated to its protease inhibitory or DNA binding activities.
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PMID:Inhibition of human DNA polymerase alpha by alpha 1-antichymotrypsin. 349 Sep 7

The binding between hepatitis B surface antigen (HBsAg) and polymerized human serum albumin (poly-HSA) was studied in HBsAg-negative (25) and HBsAg-positive (92) sera by a sensitive enzyme-linked immunosorbent assay technique, and a correlation of binding activity was made with HBe-markers and hepatitis B virus-specific DNA polymerase. The binding could be detected only in HBsAg-positive sera and was found to be independent of the presence of HBe-markers and DNA polymerase activity. Further, binding was noted in significantly higher proportions of sera samples from the patient group compared with the healthy carrier group (p less than 0.01).
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PMID:Relation between HBsAg binding with polymerized human serum albumin and HBV replication. 366 86

Inactivation of Hepatitis B virus associated DNA polymerase was studied in factor IX concentrate (coagulation factors II, VII, IX and X) by heat pasteurization (60 degrees C, 10 hr) and by alkylating agents iodoacetic acid and iodoacetamide. DNA polymerase appeared to reach a residual level which occurred in human serum albumin at 60 degrees C, 10 hr under comparable spike level of hepatitis B virus. Of the four coagulation factors, factor IX activity was most susceptible to inactivation procedures with 40-50% recovery across heat pasteurization and approximately 70% recovery across iodoacetic acid treatment. Factor IX specific activities of the treated concentrates were greater than or equal to 70% of the untreated controls with no appreciable change of corresponding NAPTT values. Factor IX concentrates subjected to such inactivation procedures should reduce the potential for hepatitis B virus transmission.
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PMID:Hepatitis B virus associated DNA polymerase inactivation in factor IX concentrates. 370 11

Binding sites for polymerized albumin on hepatitis B virus components were reported in human hepatitis B virus chronic carriers predominantly with active viral replication (HB e antigen positive). The presence of comparable albumin-binding sites in the woodchuck hepatitis virus (WHV) model was examined on WHV components obtained from woodchucks with active viral replication (DNA polymerase positive). Binding sites for polymerized woodchuck serum albumin were not detected on the intact WHV virion, on 22-nm woodchuck hepatitis surface antigen (WHsAg), or on WHsAg polypeptides. Woodchuck albumin was not detected in purified 22-nm WHsAg, and anti-albumin antibodies were not detected in WHV chronic-carrier woodchucks. Our results in the WHV model argue against a role for viral polyalbumin-binding sites in tissue- and host-specific virus infectivity.
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PMID:Failure to detect polyalbumin-binding sites on the woodchuck hepatitis virus surface antigen: implications for the pathogenesis of hepatitis B virus in humans. 378 21

Hepatitis B immune globulin was given intramuscularly to 102 staff members of a dialysis unit within 48 h after the accidental needlestick exposure to blood containing hepatitis B surface antigen (HBsAg). Hepatitis B virus (HBV) infection developed in 11 of 56 persons (20%) who had been exposed to blood containing hepatitis B e antigen (HBeAg). Among 56 HBeAg-positive inocula, HBsAg-associated deoxyribonucleic acid polymerase activity in the 11 inocula that transmitted HBV infection was significantly higher than that in the remaining 45 inocula that did not (log counts per minute 3.27 +/- 0.57 vs. 2.09 +/- 1.19, p less than 0.001). These 11 HBeAg-positive inocula revealed higher hemagglutination titers of HBsAg (geometric mean 13.5 +/- 1.4 vs. 11.2 +/- 3.2, p less than 0.001). The receptor for polymerized human serum albumin was detected significantly more often in the inocula that transmitted HBV infection than those that did not (10/11 vs. 24/45, p less than 0.05). Based on the results obtained, the failure in protecting all of those exposed to HBeAg-positive blood would be attributable to a high concentration of HBV in some HBeAg-positive inocula and the inability of intramuscular injection to raise a protective level of antibody in the circulation immediately.
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PMID:Factors influencing postexposure immunoprophylaxis of hepatitis B virus infection with hepatitis B immune globulin. High deoxyribonucleic acid polymerase activity in the inocula of unsuccessful cases. 396 63

Blood samples containing antibodies to DNA were obtained from patients with systemic lupus erythematosus (SLE) and rabbits immunized with denatured DNA complexed to methylated bovine serum albumin. The immunoglobulin fractions from these sources did not decrease the over-all template activity of singlestranded DNA with DNA polymerase or DNA-dependent RNA polymerase. In competition studies, both DNA polymerase and DNA-dependent RNA polymerase inhibited the binding of DNA antibodies to single-stranded DNA, as evidenced by inhibition of micro-complement fixation. These findings suggest that antibodies to DNA fail to decrease denatured DNA template activity because the enzymes which use a single-stranded DNA template can displace or block the antibodies from the denatured DNA as a result of greater binding affinity to the denatured DNA. The anti-DNA antibodies associated with SLE, therefore, may not be involved in the pathogenesis of the intracellular abnormalities associated with the disease.
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PMID:In vitro effect of antibodies to DNA on the template activity of DNA. 417 49


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