Browsing by Author "Chalovich, Joseph"
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Localization and Characterization of a 7.3-kDa Region of Caldesmon Which Reversibly Inhibits Actomyosin ATPase Activity
Chalovich, Joseph; Bryan, Joseph; Benson, Caryl E.; Velaz, Laly (East Carolina University, 1992-08-15)Cleavage of caldesmon with chymotrypsin yields a series of fragments which bind both calmodulin and actin and inhibit the binding of myosin subfragments to actin and the subsequent stimulation of ATPase activity. Several ... -
A Long Helix from the Central Region of Smooth Muscle Caldesmon
Wang, C.-L. Albert; Chalovich, Joseph; Graceffa, Philip; Lu, Renne C.; Mabuchi, Katsuhide; Stafford, Walter F. (East Carolina University, 1991-07-25)The central region of smooth muscle caldesmon is predicted to form α-helices on the basis of its primary structure. We have isolated a fragment (CT54) that contains this region. The hydrodynamic properties and the electron ... -
Negative Charges at Protein Kinase C Sites of Troponin I Stabilize the Inactive State of Actin
Mathur, Mohit C.; Kobayashi, Tomoyoshi; Chalovich, Joseph (East Carolina University, 2008-01-15)Alterations in the troponin complex can lead to increases or decreases in contractile activity. Most mutations of troponin that cause hypertrophic cardiomyopathy increase the activity of cardiac muscle fibers. In at least ... -
Purification and Partial Characterization of Relaxin and Relaxin Precursors from the Hamster Placenta
Renegar, R. H.; Owens, C. R.; Chalovich, Joseph (East Carolina University, 1993-07)Previous immunological studies have indicated that the molecular structure of hamster relaxin is quite different from that of porcine relaxin. In the present study, hamster relaxin was purified from placentas and ... -
Some Cardiomyopathy-Causing Troponin I Mutations Stabilize a Functional Intermediate Actin State
Mathur, Mohit C.; Kobayashi, Tomoyoshi; Chalovich, Joseph (East Carolina University, 2009-03-18)We examined four cardiomyopathy-causing mutations of troponin I that appear to disturb function by altering the distribution of thin filament states. The R193H (mouse) troponin I mutant had greater than normal actin-activated ... -
Structural Dynamics of Troponin I during Ca2+-Activation of Cardiac Thin Filaments: A Multi-Site Förster Resonance Energy Transfer Study
Wang, Hui; Chalovich, Joseph; Marriott, Gerard (2012) -
Structural Dynamics of Troponin I during Ca2+-Activation of Cardiac Thin Filaments: A Multi-Site Förster Resonance Energy Transfer Study
Wang, Hui; Chalovich, Joseph; Marriott, Gerard (2012-12)A multi-site, steady-state Förster resonance energy transfer (FRET) approach was used to quantify Ca2+-induced changes in proximity between donor loci on human cardiac troponin I (cTnI), and acceptor loci on human cardiac ... -
The C-terminus of Troponin T Modulates Calcium Regulation of Actin-Myosin Interactions
Johnson, Dylan James (East Carolina University, 2019-05-02)The highly conserved terminal fourteen C-terminal residues of troponin T play a novel role in the regulation of striated muscle contraction. Elimination of the terminal fourteen residues of the C-terminal region of troponin ... -
Tropomyosin Dynamics in Cardiac Thin Filaments: A Multisite Förster Resonance Energy Transfer and Anisotropy Study
Wang, Hui; Mao, Shu; Chalovich, Joseph; Marriott, Gerard (East Carolina University, 2008-06)Cryoelectron microscopy studies have identified distinct locations of tropomyosin (Tm) within the Ca21-free, Ca21-saturated, and myosin-S1-saturated states of the thin filament. On the other hand, steady-state Förster ... -
Troponin-tropomyosin: an allosteric switch or a steric blocker?
Resetar, Andrea M.; Stephens, Jacqueline M.; Chalovich, Joseph (East Carolina University, 2002-08)The interaction of myosin subfragment 1 (S1) with actin-tropomyosin-troponin (regulated actin) is highly nucleotide dependent. The binding of S1 or S1-ADP (but not S1-ATP nor N,N - -phenylenedimaleimide-modified S1-ATP) ...