Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.2 (endonuclease)
18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Multiple flat wart-like lesions of a renal allograft recipient were shown to contain HPV 3 or a serologically crossreacting virus by indirect immunofluorescence with monospecific animal antisera against HPV [1--5]. The patient's serum revealed virus specific antibodies (immunofluorescence titer 1/80). Papillomaviruses were isolated and after in vitro iodination 3 major proteins (MW 70.000, 56.000 and 43.000) were detected by SDS polyacryalmide gel electrophoresis. DNA was extracted from the warts and cleaved with the restriction endonuclease Hae III. Distinct bands were discernible within the background of cellular DNA and these fragments were identified as papillomavirus DNA by blot hypbridization with 32P-labeled viral DNA.
J Invest Dermatol 1979 Nov
PMID:Characterization of human papillomavirus 3 in warts of a renal allograft patient. 22 66

Rapid advances have occurred in the characterization of human papilloma virus (HPV) types applying the new advanced techniques of restriction endonuclease analysis and molecular hybridization to human wart virus. Human papilloma virus can no longer be viewed as a single, homogeneous virus producing all varieties of clinical warts. At least three antigenically heterogeneous HPV types have been associated with common and plantar warts. Two additional HPV types have been found in patients with epidermodysplasia verruciformis. Condylomata acuminata and laryngeal papillomas contain viruses which are also distinct from the preceding viruses and may represent additional HPV types. This antigenic heterogeneity of HPV has important implications concerning the immunology of human warts which have not been taken into account in most previously published studies. Both antibody and cell-mediated responses may be seen in patients with active warts, but many patients with warts have no demonstrable immune reactions. The role of immunity in wart regression remains poorly understood. Nevertheless, the increased frequency of warts in patients receiving immunosuppressive drugs and with immune deficiency states and the immunologic alterations which occur in patients with regressing or cured warts compared to patients with active warts, particularly the increased frequency of cell-mediated responses and antibodies specific for viral antigens, support a possible role for immunity in the resolution of warts. The evidence to date, however, does not prove that immune mechanisms are directly responsible for the elimination of warts.
J Am Acad Dermatol 1979 Oct
PMID:Immunology of human warts. 22 34

Pure cultures of dermal fibroblasts and epidermal keratinocytes have been obtained from a single biopsy of newborn foreskin. The cells were labeled, exposed to several doses of UV light, and allowed to repair in the dark for 16 hr. The number of pyrimidine dimers before and after repair was assessed by measuring the numbers of sites in the DNA sensitive to a specific UV endonuclease. At all doses used, the extent of repair was similar in the cultured keratinocytes and cultured fibroblasts.
J Invest Dermatol 1979 Sep
PMID:Repair of ultraviolet light damage to the DNA of cultured human epidermal keratinocytes and fibroblasts. 46 74

The capability of guinea pig epidermal extracts to hydrolyze deoxyribonucleic acid has been studied. The results of investigation by gel filtration on Sephadex G-75 column and by viscometry on the mode of hydrolysis of deoxyribonucleic acid by epidermal extracts revealed that deoxyribonucleic acid was degraded by both endonuclease and exonuclease activities. The exhaustive digestion by epidermal extracts yielded the complete degradation of deoxyribonucleic acid to mononucleosides or further metabolites. The enzyme systems involved in the deoxyribonucleic acid degradation include at least an endonuclease, an exonuclease and a phosphatase.
Arch Dermatol Res 1975 Nov 14
PMID:Degradation of deoxyribonucleic acid by guinea pig epidermal extracts. 120 Jul 14

The alkaline plasmid DNA extraction method of Birnboim and Doly was applied for the isolation of human papillomavirus (HPV) from warts. Tissue from common and plantar warts was digested with proteinase K, and the extrachromosomal circular covalently-closed form of HPV-DNA was rapidly extracted by alkaline sodium dodecyl sulphate and phenol-chloroform treatment. Recovery of HPV-DNA from the tissue was sufficient for determination of endonuclease restriction patterns by agarose gel electrophoresis.
Arch Dermatol Res 1990
PMID:Human papillomavirus DNA from warts for typing by endonuclease restriction patterns: purification by alkaline plasmid methods. 196 33

One prominent lesion induced in DNA by ultraviolet (UV) radiation is the cyclobutyl pyrimidine dimer formed between adjacent pyrimidines on the same DNA strand. We investigated whether people who have developed basal cell carcinoma on sun-exposed skin have an altered ability to repair UV-induced pyrimidine dimers in DNA. Twenty-two patients with at least one basal cell carcinoma, aged 31-84 years, and 19 healthy volunteers, aged 25-61 years, took part in the study. Both groups were given one minimal erythema dose (MED) of simulated solar radiation on the lower back. DNA was extracted from the irradiated skin 0 to 6 h later, and the number of UV-induced pyrimidine dimers was determined using a dimer-specific endonuclease. At time 0, the average number of dimers per unit of DNA was similar in the two groups. After 6 h, an average of 22 +/- 4% of the dimers were removed in the group with basal cell carcinoma compared to 33 +/- 4% in the cancer-free group. In the basal cell carcinoma group, only 23% of the patients repaired more than 30% of the dimers after 6 h, compared with 53% of the cancer-free subjects (p less than 0.05). We conclude that patients who develop basal cell carcinoma on sun-exposed skin may have a decreased ability to repair pyrimidine dimers induced in skin exposed to simulated solar radiation.
J Invest Dermatol 1990 Nov
PMID:Excision repair of pyrimidine dimers induced by simulated solar radiation in the skin of patients with basal cell carcinoma. 223 Feb 12

We have limited the scope of this article to those disorders that have already been successfully diagnosed or excluded in utero. We currently have the potential to diagnose a number of others for which the opportunity has not yet arisen. If a biochemical, morphologic, chromosomal, or DNA alteration is known for a specific condition and is likely to be expressed in one of the fetal tissues or secretions, attempt at prenatal diagnosis is reasonable. Our ability to detect the inherited disorders of the skin in utero will continue to improve both in the number of specific disorders successfully diagnosed or excluded and in the increasingly earlier stages of pregnancy at which the disorder can be detected. Advances in instrumentation will, it is hoped, decrease the risk of the invasive methods of prenatal diagnosis, and improvement in noninvasive methods, such as maternal serum screening, may eliminate the need for invasive procedures altogether. Detection of useful DNA polymorphisms linked to genes for specific genodermatoses and development of specific gene probes will improve the accuracy of diagnosis and reduce the need for specific fetal tissues. The entire genome of an individual is present in each cell, even though a specific gene product may not be expressed in that cell. Thus, DNA restriction endonuclease studies can be performed on amniotic fluid cells, chorionic villi, fetal cells in maternal circulation, and fetal tissues with equal facility. The usefulness of prenatal diagnosis will always be limited by the ability to detect pregnancies at risk. If carrier detection is unavailable, the only way to identify couples at risk for offspring with an autosomal recessive condition is by the birth of an affected child. For autosomal dominant and X-linked recessive and dominant conditions, new mutations will continue to occur. As mentioned previously, screening of all pregnancies for all defects is not possible now and is unlikely ever to be feasible, either economically or technically. The reliability of prenatal diagnosis will continue to depend upon accurate diagnosis in the index case and upon the availability of a specific and sensitive test (or tests), with no overlap in values between heterozygotes and homozygotes for autosomal recessive conditions or between normal and affected fetuses with autosomal dominant and X-linked recessive disorders. Correct interpretation of test results is subject to experience, recognition of artifact, and variation in the expression of a given disorder in utero.(ABSTRACT TRUNCATED AT 400 WORDS)
Dermatol Clin 1987 Jan
PMID:Prenatal diagnosis and screening. 243 40

Laboratory tests for herpetic infections can be divided into (1) morphologic, (2) immunomorphologic, (3) serologic, and (4) virologic. Tzanck smears are easy to do, inexpensive, and compare favorably with cultures and immunofluorescence tests for specificity and sensitivity, but they require considerable experience to interpret accurately and they cannot differentiate between herpes type 1, herpes type 2, and varicella zoster infections. Biopsies are useful when clues to a diagnosis are being sought. Peroxidase-antiperoxidase and avidin-biotin tests present technical difficulties but interpretational difficulties are low and the results are available in a few hours. They can distinguish between herpes type 1, herpes type 2, and varicella zoster virus, as can immunofluorescence using monoclonal antibodies. Serologic tests are used primarily to distinguish between primary and recurrent herpes simplex infections. Virus isolation in tissue cultures is the gold standard for identifying herpes simplex virus but it is not 100% specific or 100% sensitive. Restriction endonuclease analysis identifies types and strains of virus by their deoxyribonucleic acid composition and it is very useful in epidemiologic studies. Ability to find virus by whatever method is influenced by the stage of the lesion. As lesions age, less infectivity and antigen result in less sensitivity of the tests.
J Am Acad Dermatol 1988 Jan
PMID:New diagnostic tests for herpes simplex and varicella zoster infections. 244 53

The endonuclease digest patterns of viral DNA from 48 genital and 45 non-genital molluscum contagiosum virus (MCV) lesions were examined. The overall ratio of MCVI to MCVII was 3.23:1. There was no predominance of either MCV type in genital lesions. No obvious morphological differences were seen between MCVI and MCVII lesions. MCVII was not found in any patient under 15 years old.
Br J Dermatol 1989 Jan
PMID:Molluscum contagiosum virus types in genital and non-genital lesions. 263 15

Young and old rats were compared with respect to the capacity of their skin fibroblasts and epidermal keratinocytes to remove low levels of ultraviolet light (UV) induced UV-endonuclease sensitive sites (pyrimidime dimers) from their DNA, in vitro and in vivo, respectively. In vitro, over a 24-h time period, fibroblasts from both young and old rats were found to remove about 20% of the pyrimidine dimers originally induced by 4.6 J/m2 of UV-C. In vivo, after 2.6 kJ/m2 of UV-B hardly any UV lesions were found to be present in fibroblasts, as demonstrated by immunohistochemistry using an anti-thymine dimer antibody. As reported earlier (Mullaart et al., J. Invest. Dermatol., 90 (1988) 346-349) cultured epidermal keratinocytes do not differ from cultured fibroblasts in UV repair kinetics, whereas in vivo they remove at least 50% of the pyrimidine dimers induced by 4 kJ/m2 of UV-B within 3 h. We now show that epidermal keratinocytes from old rats are not deficient in their in vivo repair characteristics upon this low UV-B dose. However, since a considerable fraction of the pyrimidine dimers appeared to be persistent in fibroblasts and keratinocytes, demonstrated by both enzymatic and immunochemical assays, the possibility is discussed that long-term exposure of skin cells to UV may lead to an accumulation of DNA damage with age.
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PMID:The removal of UV-induced pyrimidine dimers from DNA of rat skin cells in vitro and in vivo in relation to aging. 271 71


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