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  • Myofibrils
  • Ishiwata's research interests go beyond the mechanical and physiological import of SPOC to bio-motile systems focusing on the structural and functional hierarchy from single molecules (myosin, kinesin, actin) to macromolecular assemblies (myofibrils, meiotic spindle and cells (cardiac, HeLa, etc. (wikipedia.org)
  • isoform
  • The cardiac isoform, encoded by MYBPC3 , has been extensively studied over the last several decades due to its high mutational rate in congenital hypertrophic and dilated cardiomyopathy. (frontiersin.org)
  • The blebbistatin scaffold has been modified in several ways to optimize myosin isoform specificity or to improve the inhibitory properties and to map the structure-activity relationship. (wikipedia.org)
  • Evidence of ALC-1 isoform expression on contractile mechanics of sarcomeres came from experiments studying fibers from patients expressing a higher level of ALC-1 relative to VLC-1 in cardiac left ventricular tissue. (wikipedia.org)
  • The cMyBP-C isoform expressed in cardiac muscle differs from those expressed in slow and fast skeletal muscle (MYBPC1 and MYBPC2, respectively) by three features: (1) an additional immunoglobulin (Ig)-like domain on the N-terminus, (2) a linker region between the second and third Ig domains, and (3) an additional loop in the sixth Ig domain. (wikipedia.org)
  • Only one tissue-specific isoform of TnI is described for cardiac muscle tissue (cTnI), whereas the existence of several cardiac specific isoforms of TnT (cTnT) are described in the literature. (wikipedia.org)
  • TnC in human cardiac muscle tissue is presented by an isoform typical for slow skeletal muscle. (wikipedia.org)
  • Kinetics
  • E258K HCM-causing mutation in cardiac MyBP-C reduces contractile force and accelerates twitch kinetics by disrupting the cMyBP-C and myosin S2 interaction. (nih.gov)
  • Our objective was to define the primary contractile effect and molecular disease mechanisms of the prevalent cMyBP-C E258K HCM-causing mutation in nonremodeled murine engineered cardiac tissue (mECT).Expression of E258K cMyBP-C did not affect cardiac cell survival and was appropriately incorporated into the cardiac sarcomere.Similar to cMyBP-C ablation or phosphorylation, abolition of this inhibitory interaction accelerates contractile kinetics. (nih.gov)
  • Halothane, isoflurane, and sevoflurane increase the kinetics of Ca2+-induced conformational change of recombinant human cardiac troponin C. Anesth Analg. (mayo.edu)
  • Relative to ventricular essential light chain VLC-1, ALC-1 has an additional ~40 amino-acid N-terminal region that contains four to eleven residues that are critical for binding actin and modulating myosin kinetics. (wikipedia.org)
  • Fibers expressing high ALC-1 exhibited a higher maximal velocity and rate of shortening compared to fibers with low amounts of ALC-1, suggesting that ALC-1 increases cycling kinetics of myosin cross-bridges and regulates cardiac contractility. (wikipedia.org)
  • Further biochemical studies unveiled a weaker binding of the Alanine-Proline-rich N-terminus of ALC-1 to the C-terminus of actin relative to VLC-1, which may explain the mechanism underlying the differences in cycling kinetics. (wikipedia.org)
  • Mutations
  • The causes of cardiac arrhythmias are numerous, from structural changes in the conduction system (the sinoatrial and atrioventricular nodes, or His-Purkinje system) and cardiac muscle, to mutations in genes coding for ion channels of the heart. (wikipedia.org)
  • Due to changes in amino acids and binding domains, mutations may also affect the ability of these channels to respond to physiological changes in cardiac demand. (wikipedia.org)
  • Mutations resulting in loss of function of K+ channels can result in delayed repolarization of the cardiac muscle cells. (wikipedia.org)
  • HCM mutations tend to cluster around the N-terminal region and a primary actin binding region known as period 5. (wikipedia.org)
  • fibers
  • The muscle type discussed earlier in this chapter is striated muscle because the fibers' overlapping actin and myosin filaments give it a banded appearance (see Figure 27-2). (cliffsnotes.com)
  • Consistent with this notion, cMyBP-C knockout mice exhibit an abnormal systolic timecourse, with a shortened elastance timecourse and lower peak elastance in vivo, and an accelerated force development in isolated, skinned cardiac fibers suggesting that cMyBP-C is required to constrain the crossbridges in order to sustain a normal ejection. (wikipedia.org)
  • citation needed] An increase in filling of the ventricle increases the load experienced by each cardiac muscle fiber, stretching the fibers toward their optimal length. (wikipedia.org)
  • The force that any single cardiac muscle fiber generates is proportional to the initial sarcomere length, and the stretch on the individual fibers is related to the end-diastolic volume of the left and right ventricles. (wikipedia.org)
  • myofilament
  • Cardiac Myofibril-bundles of contractile myofilament actin & myosin. (majortests.com)
  • Absence of cMyBP-C (Mybpc3-targeted knock-out mice) results in severe cardiac hypertrophy, increased heart-weight-to-body-weight-ratios, enlargement of ventricles, increased myofilament Ca2+ sensitivity and depressed diastolic and systolic function. (wikipedia.org)
  • sarcomere
  • Finally, we have proposed a new structural model of the cardiac muscle sarcomere that includes connectin filaments. (rupress.org)
  • Expression of E258K cMyBP-C did not affect cardiac cell survival and was appropriately incorporated into the cardiac sarcomere. (nih.gov)
  • The action of myosin attachment and actin movement results in sarcomere shortening. (wikipedia.org)
  • cMyBP-C is not essential for sarcomere formation during embryogenesis, but is crucial for sarcomere organization and maintenance of normal cardiac function. (wikipedia.org)
  • Promoter
  • Heart-Specific Targeting of Firefly Luciferase by the Myosin Light Chain-2 Promoter and Developmental Regulation in Transgenic Mice" Circulation Research (1993) 73:629. (freepatentsonline.com)
  • 17 . A therapeutic delivery system of claim 1 , wherein said promoter is a cardiac-specific promoter. (google.es)
  • 18 . A therapeutic delivery system of claim 17 , wherein said promoter is selected from the group consisting of the ANF promoter, alpha-MHC.sub.5.5 promoter, alpha-MHC.sub.87 promoter, and human cardiac actin promoter. (google.es)
  • This recruitment leads to the repression of the MLC2v (Myosin Light Chain 2 v) and βMHC ( β-myosin heavy chain ) promoter. (wikipedia.org)
  • interaction
  • Yeast two-hybrid analysis revealed that E258K cMyBP-C abolished interaction between the N terminal of cMyBP-C and myosin heavy chain sub-fragment 2 (S2). (nih.gov)
  • We show that the E258K mutation in cMyBP-C abolishes interaction between N-terminal cMyBP-C and myosin S2 by directly disrupting the cMyBP-C-S2 interface, independent of cMyBP-C phosphorylation. (nih.gov)
  • A-H) Y2H interaction tests between the WT and E258K C1-C2 region of human cMyBP-C and the 126 distal amino acids of human myosin S2. (nih.gov)
  • I-N) Y2H interaction tests between the WT and E258K C1-C2 region of human cMyBP-C and α cardiac actin (ACTC1), as well as their appropriate control interaction tests. (nih.gov)
  • cMyBP-C regulates the positioning of myosin and actin for interaction and acts as a tether to the myosin S1 heads, limiting their mobility. (wikipedia.org)
  • Strong actin-myosin interaction can further shift the thin filament into the "open" position. (wikipedia.org)
  • myocardial
  • 4,6-12 Because of the difficulty to demonstrate myocardial regeneration in humans in the absence of cardiac biopsies, three possibilities have been raised in the interpretation of the improvement of cardiac function in patients. (ahajournals.org)
  • Several groups have shown that cardiomyocytes can be grafted successfully into myocardial infarcts or cardiac cryoinjuries. (ahajournals.org)
  • weakly bound
  • It also increases the rate of phosphate release from myosin, thereby accelerating the rate-determining step of the cross-bridge cycle, which is the transition of the actin-myosin complex from the weakly bound to the strongly bound state. (wikipedia.org)
  • in this state myosin is in a "cocked" position where heads are weakly bound and not generating force. (wikipedia.org)
  • unique cardiac
  • In conclusion, we have identified a unique cardiac tissue derived cell type that can be isolated and expanded from endomyocardial biopsies and which presents a potential cell source for cardiac repair. (biomedsearch.com)
  • Thus due to the unique cardiac myosin activation mechanism, omecamtiv mecarbil could safely improve cardiac function within tolerated doses. (wikipedia.org)
  • contractile
  • Cardiac autorhythmic cells and cardiac contractile cells. (majortests.com)
  • 2. Before cardiac auto rhythmic and contractile cells depolarize, what is the charge inside and outside the cell. (majortests.com)
  • 3. When cardiac auto rhythmic and contractile cells depolarize, what happens to the charge inside and outside the cell. (majortests.com)
  • Our objective was to define the primary contractile effect and molecular disease mechanisms of the prevalent cMyBP-C E258K HCM-causing mutation in nonremodeled murine engineered cardiac tissue (mECT). (nih.gov)
  • cardiomyocytes
  • 3 4 5 6 In contrast, a recent article by Watanabe et al 7 reported that fetal and neonatal pig cardiomyocytes and the cardiac-derived cell line HL-1 did not survive after grafting into pig infarcts. (ahajournals.org)
  • There are two types of cardiac muscle cell: cardiomyocytes which have the ability to contract easily, and modified cardiomyocytes the pacemaker cells of the conducting system. (wikipedia.org)
  • ventricular
  • Studies have shown celivarone is capable of cardioversion and of maintaining normal sinus cardiac rhythms and that it is effective in hypokalemic, vasotonic, and stretch-induced atrial fibrillation, as well as ischemic and reperfusion ventricular fibrillation. (wikipedia.org)
  • regulate
  • In HeLa cells TEAD1 and SRC induce gene expression, TEAD1 interacts with PARP (Poly-ADP ribose polymerase) to regulate smooth muscle α-actin expression. (wikipedia.org)
  • Physiology
  • Transplantation of Embryonic Stem Cells Improves Cardiac Function in Postinfarcted Rats Journal of Applied Physiology (Bethesda, Md. : 1985). (jove.com)
  • structural
  • 4. What three structural features are found on histological images of cardiac muscle? (majortests.com)
  • The structural domain of cTnC (cCTnC) is anchored to troponin I and T, forming the so-called IT arm, made up of cTnC93-161, cTnI41-135 and cTnT235-286 (in the cardiac complex). (wikipedia.org)
  • contractility
  • Similarly, gain of function of Na+ and Ca2+ channels results in delayed repolarization, and Ca2+ overload causing increased Ca2+ binding to cardiac troponin C, more actin-myosin interactions and causing an increased contractility, respectively. (wikipedia.org)