1. Cardiac remodeling in the mouse model of Marfan syndrome develops into two distinctive phenotypes.

    American Journal of Physiology - Heart and Circ... 310(2):H290 (2016) PMID 26566724 PMCID PMC4747899

    Marfan syndrome (MFS) is a systemic disorder of connective tissue caused by mutations in fibrillin-1. Cardiac dysfunction in MFS has not been characterized halting the development of therapies of cardiac complication in MFS. We aimed to study the age-dependent cardiac remodeling in the mouse mod...
  2. Cardiac Remodeling in the Mouse Model of Marfan Syndrome Develops Independently from Aortic and Valvular Abnormalities

    Biophysical Journal 108(2):595a (2015)

  3. Vessel ultrasound sonographic assessment of soluble receptor for advanced glycation end products efficacy in a rat balloon injury model.

    Current Therapeutic Research 76:110 (2014) PMID 25408789 PMCID PMC4229510

    We aimed to assess the therapeutic efficacy of differentially modified soluble receptor for advanced glycation end products (sRAGE) in vivo using vessel ultrasound sonography and to compare the sonography data with those from postmortem histomorphologic analyses to have a practical reference for...
  4. The N-glycoform of sRAGE is the key determinant for its therapeutic efficacy to attenuate injury-elicited arterial inflammation and neointimal growth.

    Klinische Wochenschrift 91(12):1369 (2013) PMID 24132651 PMCID PMC3846495

    Signaling of the receptor for advanced glycation end products (RAGE) has been implicated in the development of injury-elicited vascular complications. Soluble RAGE (sRAGE) acts as a decoy of RAGE and has been used to treat pathological vascular conditions in animal models. However, previous stud...
  5. Gi-biased β2AR signaling links GRK2 upregulation to heart failure.

    Circulation Research 110(2):265 (2012) PMID 22179058 PMCID PMC3282829

    Phosphorylation of β(2)-adrenergic receptor (β(2)AR) by a family of serine/threonine kinases known as G protein-coupled receptor kinase (GRK) and protein kinase A (PKA) is a critical determinant of cardiac function. Upregulation of G protein-coupled receptor kinase 2 (GRK2) is a well-established...
  6. Striated muscle tropomyosin isoforms differentially regulate cardiac performance and myofilament calcium sensitivity.

    Journal of Muscle Research and Cell Motility 31(3):227 (2010) PMID 20803058 PMCID PMC3805252

    Tropomyosin (TM) plays a central role in calcium mediated striated muscle contraction. There are three muscle TM isoforms: alpha-TM, beta-TM, and gamma-TM. alpha-TM is the predominant cardiac and skeletal muscle isoform. beta-TM is expressed in skeletal and embryonic cardiac muscle. gamma-TM is ...
  7. Molecular and functional characterization of a novel cardiac-specific human tropomyosin isoform.

    Circulation 121(3):410 (2010) PMID 20065163 PMCID PMC2822663

    Tropomyosin (TM), an essential actin-binding protein, is central to the control of calcium-regulated striated muscle contraction. Although TPM1alpha (also called alpha-TM) is the predominant TM isoform in human hearts, the precise TM isoform composition remains unclear. In this study, we quantif...
  8. An internal domain of beta-tropomyosin increases myofilament Ca(2+) sensitivity.

    American Journal of Physiology - Heart and Circ... 297(1):H181 (2009) PMID 19429821 PMCID PMC2711731

    Tropomyosin (TM) is involved in Ca(2+)-mediated muscle contraction and relaxation in the heart. Striated muscle alpha-TM is the major isoform expressed in the heart. The expression of striated muscle beta-TM in the murine myocardium results in a decreased rate of relaxation and increased myofila...
  9. Molecular and Functional Characterization of a Novel Cardiac Specific Human Tropomyosin Isoform

    Biophysical Journal 96(3):224a (2009)

  10. Bitransgenesis with beta(2)-adrenergic receptors or adenylyl cyclase fails to improve beta(1)-adrenergic receptor cardiomyopathy.

    Clinical and Translational Science 1(3):221 (2008) PMID 20443853

    Cardiomyopathic effects of beta-adrenergic receptor (betaAR) signaling are primarily due to the beta(1)AR subtype. beta(1)/beta(2)AR and beta(1)/adenylyl cyclase type 5 (AC5) bitransgenic mice were created to test the hypothesis that beta(2)AR or AC5 co-overexpression has beneficial effects in b...
  11. Tight control of adrenal medulla catecholamine release by alpha 2C-adrenergic receptors influences susceptibility to heart failure.

    Cardiovascular Research 75(4):631 (2007) PMID 17643402

  12. Rescue of tropomyosin-induced familial hypertrophic cardiomyopathy mice by transgenesis.

    American Journal of Physiology - Heart and Circ... 293(2):H949 (2007) PMID 17416600

    Familial hypertrophic cardiomyopathy (FHC) is a disease caused by mutations in contractile proteins of the sarcomere. Our laboratory developed a mouse model of FHC with a mutation in the thin filament protein alpha-tropomyosin (TM) at amino acid 180 (Glu180Gly). The hearts of these mice exhibit ...
  13. Dilated cardiomyopathy mutant tropomyosin mice develop cardiac dysfunction with significantly decreased fractional shortening and myofilament calcium sensitivity.

    Circulation Research 101(2):205 (2007) PMID 17556658

    Mutations in striated muscle alpha-tropomyosin (alpha-TM), an essential thin filament protein, cause both dilated cardiomyopathy (DCM) and familial hypertrophic cardiomyopathy. Two distinct point mutations within alpha-tropomyosin are associated with the development of DCM in humans: Glu40Lys an...
  14. Physiological significance of troponin T binding domains in striated muscle tropomyosin.

    American Journal of Physiology - Heart and Circ... 287(4):H1484 (2004) PMID 15191887

    Striated muscle tropomyosin (TM) plays an essential role in sarcomeric contraction and relaxation through its regulated movement on the thin filament. Previous work in our laboratory established that alpha- and beta-TM isoforms elicit physiological differences in sarcomeric performance. To addre...
  15. A mouse model of familial hypertrophic cardiomyopathy caused by a alpha-tropomyosin mutation.

    Molecular and Cellular Biochemistry 251(1-2):33 (2003) PMID 14575301

    Familial hypertrophic cardiomyopathy, a disease caused by mutations in cardiac contractile proteins, is characterized by left and/or right ventricular hypertrophy, myocyte disarray, fibrosis, and cardiac arrhythmias that may lead to premature sudden death. Five distinct point mutations within al...
  16. Functional importance of the carboxyl-terminal region of striated muscle tropomyosin.

    Journal of Biological Chemistry 278(25):23204 (2003) PMID 12690096

    Striated muscle tropomyosin (TM) interacts with actin and the troponin complex to regulate calcium-mediated muscle contraction. Previous work by our laboratory established that alpha- and beta-TM isoforms elicit physiological differences in sarcomeric performance. Heart myofilaments containing b...
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