Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protease acrosin is widely considered to be an essential component of a zona lysin which enables sperm to penetrate the zona pellucida of the egg. Sperm form a characteristic penetration slit little wider than the sperm head itself and this has long suggested that any zona lysin is attached to the sperm surface after an acrosome reaction. This paper provides the first ultrastructural evidence that this is the case. The protein acrosin inhibitor, Kunitz soybean trypsin inhibitor, has been covalently attached to the electron-dense marker, ferritin, and the conjugate incubated with guinea-pig sperm which have undergone an A23187-induced acrosome reaction. Electron microscopy shows that ferritin is distributed unevenly over the outer surface of the newly exposed inner acrosomal membrane but does not extend to the equatorial segment. This is further evidence that acrosin can be considered as a candidate for the role of zona lysin. The mechanism of sperm penetration of the zona is discussed in the light of these observations.
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PMID:The histochemical localization of acrosin in guinea-pig sperm after the acrosome reaction. 35 79

Ferritin-conjugated soybean trypsin inhibitor was used for the ultrastructural localization of acrosin in bull spermatozoa following acrosomal disruption. The ferritin label was observed in the anterior segment of the acrosome in disrupted cells only. Emptied acrosomes were labeled, mostly on the external surface of their outer membrane. Labeling was also found on the material bound to detached acrosomal caps. However, at no time could the ferritin label be found on the inner acrosomal membrane. It is concluded that acrosin activity is not present on the inner acrosomal membrane but is lost from the acrosomal matrix as the acrosomal reaction proceeds.
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PMID:Acrosin does not appear to be bound to the inner acrosomal membrane of bull spermatozoa. 49 Jan 28

Although the etiology of rheumatic diseases has not been elucidated, it seems to be involved in excessive autoimmune responses. In 1976, we began to research rheumatic diseases, especially rheumatoid arthritis. Anti-human immunoglobulin allotype antibodies in Japanese sera were collected from blood donors or patients by hemagglutination and the hemagglutination inhibition method using anti-D sensitized erythrocytes. Many rheumatoid factors without any specificity to IgG allotypes (Gm allotypes) were detected in patient sera. On the other hand, so-called anti-antibodies, Andresen type but not Milgrom type, were mainly detected in blood donors. Thirty-nine sera possessing anti-Gm and anti-Km antibody specificities were finally obtained by screening about 80,000 Japanese. The antibody to G1m (f) was most frequently detected, but the antibody to G1m (z), which is an allele of G1m (f), was not obtained. Quantitative evaluation of rheumatoid factors (RF) and anti-citrullinated protein antibodies (ACPA) was adopted in the 2010 ACR/EULAR classification criteria for rheumatoid arthritis; however, quality management of RF has been incompletely implemented in Japan. We therefore mounted an effort to standardize the cutoff value. We found marked hyperferritinemia in patients with active adult Still's disease in 1987. Additionally, ratios of glycosylated ferritin in the patients were extremely reduced, even if they came into the inactive phase. This depressive production of glycosylated ferritin might be a marked characteristic of this disease. Finally, the development of musculoskeletal ultrasonography in rheumatic diseases is introduced.
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PMID:[Rheumatic diseases and research on laboratory medicine: new applications of old knowledge]. 2241 55

Giant cell arteritis still results in high morbidity related to systemic complications involving the eyes, the central nervous system, the heart and the aorta. Therefore, reliable diagnostic criteria are required in giant cell arteritis and polymyalgia rheumatica (PMR), to detect and manage at early stages patients with giant cell arteritis and PMR. Indeed, diagnostic criteria of giant cell arteritis and PMR have been validated. Taken together, first we propose to review the diagnostic criteria of giant cell arteritis (ACR, GRACG) and PMR (Bird, Jones-Hazleman, Chuang-Hunder, Dasgupta). Second, more recent diagnostic criteria of GCA and PMR are further reviewed, including biochemical/immunological data (especially anti-ferritin antibodies), temporal artery biopsy and imaging findings (artery ultrasonography, angio-CT-scan, angio-MRI, PET-scan, joint echography, and MRI).
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PMID:[Giant cell arteritis and polymyalgia rheumatica: diagnostic criteria]. 2349 14