Experts and Doctors on sarcomeres in Italy

Summary

Locale: Italy
Topic: sarcomeres

Top Publications

  1. Bagni M, Cecchi G, Colombini B. Crossbridge properties investigated by fast ramp stretching of activated frog muscle fibres. J Physiol. 2005;565:261-8 pubmed
  2. Gallo M, Ramella R, Alloatti G, Penna C, Pagliaro P, Marcantoni A, et al. Limited plasticity of mesenchymal stem cells cocultured with adult cardiomyocytes. J Cell Biochem. 2007;100:86-99 pubmed
  3. Colombini B, Nocella M, Bagni M, Griffiths P, Cecchi G. Is the cross-bridge stiffness proportional to tension during muscle fiber activation?. Biophys J. 2010;98:2582-90 pubmed publisher
    ..These findings call into question the assumption that active force development can be taken as directly proportional to the cross-bridge number. ..
  4. Schiaffino S, Reggiani C. Molecular diversity of myofibrillar proteins: gene regulation and functional significance. Physiol Rev. 1996;76:371-423 pubmed
    ..Both myosin and troponin isoforms contribute to the differences in the resistance to fatigue of muscle fibers...
  5. Valle G, Faulkner G, De Antoni A, Pacchioni B, Pallavicini A, Pandolfo D, et al. Telethonin, a novel sarcomeric protein of heart and skeletal muscle. FEBS Lett. 1997;415:163-8 pubmed
    ..In human, telethonin maps at 17q12, adjacent to the phenylethanolamine N-methyltransferase gene. ..
  6. Faulkner G, Pallavicini A, Formentin E, Comelli A, Ievolella C, Trevisan S, et al. ZASP: a new Z-band alternatively spliced PDZ-motif protein. J Cell Biol. 1999;146:465-75 pubmed
    ..The transcript coding for this Z-band alternatively spliced PDZ motif (ZASP) protein maps on chromosome 10q22.3-10q23.2, near the locus for infantile-onset spinocerebellar ataxia. ..
  7. Kojic S, Medeot E, Guccione E, Krmac H, Zara I, Martinelli V, et al. The Ankrd2 protein, a link between the sarcomere and the nucleus in skeletal muscle. J Mol Biol. 2004;339:313-25 pubmed
    ..Therefore, our findings strengthen the hypothesis that Ankrd2 may be involved in sensing stress signals and linking these to muscle gene regulation. ..
  8. Carta A, Carelli V, D Adda T, Ross Cisneros F, Sadun A. Human extraocular muscles in mitochondrial diseases: comparing chronic progressive external ophthalmoplegia with Leber's hereditary optic neuropathy. Br J Ophthalmol. 2005;89:825-7 pubmed
    ..To compare the ultrastructural aspects of human extraocular muscles in two types of mitochondrial disease: chronic progressive external ophthalmoplegia (CPEO) and Leber's hereditary optic neuropathy (LHON)...
  9. Grazi E. Muscle mechanism: The acceleration of the load. Arch Biochem Biophys. 2010;504:204-9 pubmed publisher
    ..It is sufficient to assume that the stiffness of the same machinery increases with the contractile force. ..

More Information

Publications12

  1. Roncarati R, Latronico M, Musumeci B, Aurino S, Torella A, Bang M, et al. Unexpectedly low mutation rates in beta-myosin heavy chain and cardiac myosin binding protein genes in Italian patients with hypertrophic cardiomyopathy. J Cell Physiol. 2011;226:2894-900 pubmed publisher
    ..This finding, coupled to the clinical diversity of our cohort, emphasizes the complexity of HCM and the need for more inclusive investigative approaches in order to fully understand the pathogenesis of this disease...
  2. Emanueli C, Maestri R, Corradi D, Marchione R, Minasi A, Tozzi M, et al. Dilated and failing cardiomyopathy in bradykinin B(2) receptor knockout mice. Circulation. 1999;100:2359-65 pubmed
    ..01), and reparative fibrosis. The disruption of the bradykinin B(2) receptor leads to hypertension, LV remodeling, and functional impairment, implying that kinins are essential for the functional and structural preservation of the heart. ..
  3. Roncarati R, Viviani Anselmi C, Krawitz P, Lattanzi G, von Kodolitsch Y, Perrot A, et al. Doubly heterozygous LMNA and TTN mutations revealed by exome sequencing in a severe form of dilated cardiomyopathy. Eur J Hum Genet. 2013;21:1105-11 pubmed publisher
    ..In addition, they not only indicate that LMNA and TTN mutational status may be useful in this family for risk stratification in individuals at risk for DCM but also suggest titin as a modifier for DCM. ..