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골격근 수축기전에 있어서의 Ca++의 역할에 관한 실험적 연구 : The Role of Ca++ on Contractile mechanism of Skeletal Muscle

DC Field Value Language
dc.contributor.author김한진-
dc.date.accessioned2009-09-14T04:20:06Z-
dc.date.available2009-09-14T04:20:06Z-
dc.date.issued1973-06-
dc.identifier.citationSeoul J Med, Vol.14 No.2, pp. 152-160-
dc.identifier.issn0582-6802-
dc.identifier.urihttps://hdl.handle.net/10371/9185-
dc.description.abstractSuperprecipitation of actomyosin has been consi
dered to be an in vitro model of the muscle contraction,
and intimate correlation has been found
between superprecipitation and ATPase activity of
actomyositL
In order to elucidate the precise role of calcium
un interaction of actin-myosin, the effect of the
EGTA on ATPase activity of Perry myosin B"
with or without troponin and/or tropomyosin was
stndied in rabbit skeletal muscle.
The results are as follows:
1) Superprecipitation of Perry myosin B" with
both of troponin and tropomyosin was markedly
delayed by EGTA , and stopped by addition of EGTA
during the reaction.
2) ATPase activity of Perry myosin B" was not
influenced by EGTA.
3) ATPase activity of: Perry myosin B" with only
troponin or tropomyosin was also not influenced by
EGT A. but both of troponin and tropomyosin added
Perry myosin B" revealed depressed ATPase activity
by EGTA.
4) In the system Perry myosin B" with both of
troponin and tropomyosin, addition of EGTA during
the reaction caused depression of ATPase activity.
It is concluded that the actin-myosin interaction is
controled by the minute change of calcium concent
ration only in the presence of both troponin and
tropomyosin through association and dissociation
process.
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dc.language.isoko-
dc.publisher서울대학교 의과대학-
dc.title골격근 수축기전에 있어서의 Ca++의 역할에 관한 실험적 연구-
dc.title.alternativeThe Role of Ca++ on Contractile mechanism of Skeletal Muscle-
dc.typeSNU Journal-
dc.contributor.AlternativeAuthorKim, Han Jin-
dc.citation.journaltitle서울 의대 잡지-
dc.citation.journaltitle서울 의대 학술지-
dc.citation.journaltitleSeoul Journal of Medicine-
dc.citation.endpage160-
dc.citation.number2-
dc.citation.pages152-160-
dc.citation.startpage152-
dc.citation.volume14-
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