Troponin I, the Story

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Troponin I, the story.

Featured Article: Bodor GS, Porter S, Landt Y, Ladenson JH. Development of monoclonal antibodies for an assay of cardiac troponin I and preliminary results in suspected cases of myocardial infarction. Clin Chem 1992;38:2203–14. In the early 1980s, David N. Dietzer and I started building a team to develop monoclonal antibodies to the isoenzymes then used for detecting cardiac damage: creatine ki...

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The relevance of periprocedural troponin rise: the never ending story!

1 Fröhlich GM, Leistner DM. Open Heart 2017;4:e000590. doi:10.1136/openhrt-2017-000590 High-sensitivity troponin is—per definition—highly sensitive to detect all sorts of myocardial injury. This does not necessarily mean that permanent damage has been done to the myocyte. It is known that the troponin level may well be elevated after exceptional physical exercise, like in marathon runners. Of c...

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The solution structure of a cardiac troponin C-troponin I-troponin T complex shows a somewhat compact troponin C interacting with an extended troponin I-troponin T component.

We have investigated the structure of the cTnC-cTnI-cTnT(198-298) calcium-saturated, ternary cardiac troponin complex by small-angle scattering with contrast variation. Shape restoration was also applied to the scattering information resulting from the deuterated cTnC subunit, the unlabeled cTnI-cTnT(198-298) subunits, and the entire complex. The experimental results and modeling indicate that ...

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Troponin I switching in the developing heart.

Monoclonal antibodies identify two distinct isoforms of troponin I in rat cardiac muscle, one predominant in the embryonic and fetal heart and one predominant in the adult heart. The two isoforms can be resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, with apparent molecular weights of 27,000 and 31,500, respectively. The adult isoform is specifically recognized by a monoc...

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Chimeric cardiac troponin I antibodies

most assay manufacturers take additional measures during the assay development. The most frequent procedure involves suppressing the non-specific binding with blocking reagents, which vary from normal mouse IgG to more refined formulations. Whilst in most cases these measures are adequate, they do result in additional costs in terms of both material and labor. The effect of HAMA can also be sup...

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ژورنال

عنوان ژورنال: Clinical Chemistry

سال: 2010

ISSN: 0009-9147,1530-8561

DOI: 10.1373/clinchem.2009.138255