Pages that link to "Q44684364"

The following pages link to Phosphorylation and mutation of human cardiac troponin I deferentially destabilize the interaction of the functional regions of troponin I with troponin C. (Q44684364):

Displaying 15 items.

• Gene regulation, alternative splicing, and posttranslational modification of troponin subunits in cardiac development and adaptation: a focused review (Q21129229) (← links)
• Structural based insights into the role of troponin in cardiac muscle pathophysiology (Q28235083) (← links)
• Why does troponin I have so many phosphorylation sites? Fact and fancy (Q28274412) (← links)
• A preferred AMPK phosphorylation site adjacent to the inhibitory loop of cardiac and skeletal troponin I (Q28307636) (← links)
• TNNI1, TNNI2 and TNNI3: Evolution, regulation, and protein structure-function relationships. (Q30380968) (← links)
• Combined troponin I Ser-150 and Ser-23/24 phosphorylation sustains thin filament Ca(2+) sensitivity and accelerates deactivation in an acidic environment. (Q33821210) (← links)
• AMP-activated protein kinase phosphorylates cardiac troponin I at Ser-150 to increase myofilament calcium sensitivity and blunt PKA-dependent function. (Q36003703) (← links)
• Low molecular weight fibroblast growth factor-2 signals via protein kinase C and myofibrillar proteins to protect against postischemic cardiac dysfunction (Q36837898) (← links)
• Cardiac troponin structure-function and the influence of hypertrophic cardiomyopathy associated mutations on modulation of contractility (Q38724869) (← links)
• Hypertrophic cardiomyopathy-linked mutation D145E drastically alters calcium binding by the C-domain of cardiac troponin C. (Q40987953) (← links)
• N-terminal phosphorylation of cardiac troponin-I reduces length-dependent calcium sensitivity of contraction in cardiac muscle (Q44281385) (← links)
• Effects of the mutation R145G in human cardiac troponin I on the kinetics of the contraction-relaxation cycle in isolated cardiac myofibrils (Q45271651) (← links)
• Cardiac troponins may be irreversibly modified by glycation: novel potential mechanisms of cardiac performance modulation (Q58091954) (← links)
• Apelin and APJ orchestrate complex tissue-specific control of cardiomyocyte hypertrophy and contractility in the hypertrophy-heart failure transition (Q88726706) (← links)
• Molecular Basis of S100A1 Activation and Target Regulation Within Physiological Cytosolic Ca2+ Levels (Q97529094) (← links)