Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The structural properties of cardiac isomyosins from several species were compared using native gel electrophoresis, analysis of proteolytic digests, analysis of monoclonal antibody reactivity to specific proteolytic fragments on electroblots and S1 nuclease mapping with cDNA probes. The structure of specific regions of the myosin molecule was analyzed by reacting monoclonal antibodies with chymotryptic peptides of myosin separated by two-dimensional electrophoresis. The pattern of fragments reactive with antibody CCM-52 (epitope in LMM) was identical in all types of V3 isomyosin examined, and different in each type of V1 isomyosin. Peptides reactive with RCM-79 (epitope in HMM) were different from those reactive with CCM-52 and were also significantly different in each type of myosin examined. Thus, HC-alpha is structurally similar in the LMM portion of the molecule in all animals examined, while in the HMM region there are significant structural differences. HC-alpha differs from HC-beta, with structural differences in both LMM and HMM. We have also shown that atrial myosin HC and ventricular HC-alpha in the rabbit are indistinguishable both by RIA and peptide mapping analysis. The same conclusion was derived after analysis of the myosin HC mRNA expressed in rabbit atria and ventricles. Using cDNA probes specific for the alpha and beta myosin HC mRNA, we could not distinguish between the atrial myosin mRNA and ventricular HC alpha (V1 isomyosin) mRNA by S1 nuclease mapping experiments. Classification of different cardiac myosins is largely based on their mobility on native gel electrophoresis, immunological cross-reactivity, and ATPase activities.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Classification and characterization of cardiac isomyosins. 653

Defining the regulatory mechanisms promoting differentiation and proliferation of cementoblasts has not been well understood, because of the lack of cell models in vitro. To establish an in vitro cell model for the cementoblasts, extracted rat molars obtained from 8-week-old rats were used. Cells lining the root surface (cemetoblasts) were obtained by an enzymatic digestion method, and immediately immortalized by transfection of thermolabile SV40 T-antigen gene. The transfected cementum lining cell clones, RCM-C3 and -C4, were maintained for more than 200 population doublings (PD), while the original cells stopped their growth at 60 PD. Thus, immortalized cell lines decreased expression of SV40 T-antigen and subsequently cell proliferation at non-permissive temperature (39 degrees C). Reverse-transcribed-polymerase chain reaction indicated expression of gene for type I collagen, alkaline phosphatase (ALP), osteopontin, and osteocalcin mRNA at both permissive (33 degrees C) and non-permissive (39 degrees C) temperatures. RCM-C4 expressed higher bone siaploprotein (BSP) mRNA than RCM-C3, and further RCM-C4 showed higher BSP mRNA at 39 degrees C than 33 degrees C. High ALP activity and mineralized nodule formation were observed at 39 degrees C in both cell lines. These findings suggested that the cell lines, RCM-C3 and -C4, are useful model for studying the regulatory mechanisms of differentiation and proliferation of cementoblasts.
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PMID:Establishment of cementoblast cell lines from rat cementum lining cells by transfection with temperature-sensitive simian virus-40 T-antigen gene. 1598 73

Troponin (Tn) is a critical regulator of muscle contraction in cardiac muscle. Mutations in Tn subunits are associated with hypertrophic, dilated and restrictive cardiomyopathies. Improved diagnosis of cardiomyopathies as well as intensive investigation of new mouse cardiomyopathy models has significantly enhanced this field of research. Recent investigations have showed that the physiological effects of Tn mutations associated with hypertrophic, dilated and restrictive cardiomyopathies are different. Impaired relaxation is a universal finding of most transgenic models of HCM, predicted directly from the significant changes in Ca(2+) sensitivity of force production. Mutations associated with HCM and RCM show increased Ca(2+) sensitivity of force production while mutations associated with DCM demonstrate decreased Ca(2+) sensitivity of force production. This review spotlights recent advances in our understanding on the role of Tn mutations on ATPase activity, maximal force development and heart function as well as the correlation between the locations of these Tn mutations within the thin filament and myofilament function.
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PMID:Mutations in Troponin that cause HCM, DCM AND RCM: what can we learn about thin filament function? 1991 56

A partial bioinspired as well as the total synthesis of archazolid F, a highly potent V-ATPase inhibitory, antiproliferative polyketide macrolide, is described. Key features of the synthetic routes include a highly stereoselective aldol condensation of two elaborate fragments and macrocyclizations either by a Shiina macrolactonization or by a challenging RCM reaction of an octaene substrate. The syntheses unequivocally confirm the full architecture of this very scarce archazolid.
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PMID:Total Synthesis of Archazolid F. 3054 75