Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Sabrina Friedline"'
Autor:
Yao-Chang Tsan, Samuel J. DePalma, Yan-Ting Zhao, Adela Capilnasiu, Yu-Wei Wu, Brynn Elder, Isabella Panse, Kathryn Ufford, Daniel L. Matera, Sabrina Friedline, Thomas S. O’Leary, Nadab Wubshet, Kenneth K. Y. Ho, Michael J. Previs, David Nordsletten, Lori L. Isom, Brendon M. Baker, Allen P. Liu, Adam S. Helms
Publikováno v:
Nature Communications, Vol 12, Iss 1, Pp 1-16 (2021)
Investigations of human cardiac disease involving human pluripotent stem cell-derived cardiomyocytes are limited by the disorganized presentation of biomechanical cues resulting in cell immaturity. Here the authors develop a platform of micron-scale
Externí odkaz:
https://doaj.org/article/866175855d3a4449bdab9d5e10355c8b
Autor:
Vi T. Tang, Kathryn Ufford, Zhaowen Tong, Allen P. Liu, Sabrina Friedline, Stephanie L. Bielas, Adam S. Helms, Amani S. Dobbs, Yao-Chang Tsan
Publikováno v:
Stem Cell Reports
Summary Disease modeling and pharmaceutical testing using cardiomyocytes derived from induced pluripotent stem cells (iPSC-CMs) requires accurate assessment of contractile function. Micropatterning iPSC-CMs on elastic substrates controls cell shape a
Autor:
Daniel L. Matera, Thomas S. O’Leary, Yu-Wei Wu, Nadab Wubshet, Brendon M. Baker, David Nordsletten, Yao-Chang Tsan, Yan-Ting Zhao, Brynn Elder, Kathryn Ufford, Adela Capilnasiu, Kenneth K. Y. Ho, Isabella Panse, Lori L. Isom, Sabrina Friedline, Adam S. Helms, Michael J. Previs, Samuel J. DePalma, Allen P. Liu
Publikováno v:
Nature Communications
Nature Communications, Vol 12, Iss 1, Pp 1-16 (2021)
Nature Communications, Vol 12, Iss 1, Pp 1-16 (2021)
Human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) allow investigations in a human cardiac model system, but disorganized mechanics and immaturity of hPSC-CMs on standard two-dimensional surfaces have been hurdles. Here, we developed a pla
Autor:
Isabella Panse, Nadab Wubshet, Lori L. Isom, Adela Capilnasiu, Yao-Chang Tsan, Kenneth K. Y. Ho, Brendon M. Baker, David Nordsletten, Adam S. Helms, Sabrina Friedline, Brynn Elder, Yan-Ting Zhao, Thomas S. O’Leary, Michael J. Previs, Yu Wei Wu, Samuel J. DePalma, Allen P. Liu
Human pluripotent stem cell derived cardiomyocytes (hPSC-CMs) allow novel investigations of human cardiac disease, but disorganized mechanics and immaturity of hPSC-CMs on two-dimensional (2D) surfaces have been hurdles for efficient and reproducible
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::aefb37cf4b19c455decfc4dbb9e0826e
https://doi.org/10.1101/2021.05.23.445330
https://doi.org/10.1101/2021.05.23.445330
Autor:
Mick Wauchope, Vi T. Tang, Allen P. Liu, Eric D. Smith, Jordan A Shavit, Xiaoquan Wen, Michael J. Previs, Aaron H Wasserman, Adam S. Helms, Sharlene M. Day, Lap Man Lee, Akul Arora, Sabrina Friedline, Thomas S. O’Leary
Publikováno v:
JCI Insight. 5
Mutations in cardiac myosin binding protein C (MyBP-C, encoded by MYBPC3) are the most common cause of hypertrophic cardiomyopathy (HCM). Most MYBPC3 mutations result in premature termination codons (PTCs) that cause RNA degradation and a reduction o
Autor:
Jonathan Hernandez, Akul Arora, Kathryn Ufford, Sabrina Friedline, Zhaowen Tong, Allen Liu, Adam S Helms
Publikováno v:
Circulation. 138
Introduction: Modeling heart diseases using cardiomyocytes derived from human induced pluripotent stem cells (hiPSC-CMs) enables direct study of cellular and molecular mechanisms. However, the variable phenotypes of individual cells has limited the r
Autor:
Adam S Helms, Vi Tang, Jonathan Hernandez, Mick Wauchope, Akul Arora, Sabrina Friedline, Michael Previs, Sharlene Day
Publikováno v:
Circulation. 138
The mechanism of MYBPC3 (encoding cardiac myosin binding protein C, MyBP-C) truncation mutations, the most common genetic cause of hypertrophic cardiomyopathy, has been incompletely resolved. We hypothesized that truncating MYBPC3 mutations cause myo
Autor:
Randy Strong, Lisa Burmeister, James F. Hejtmancik, Chi-Chao Chan, Sabrina Friedline, Richard A. Miller, Maria A. Woodward, Nancy L. Nadon, David E. Harrison, Lauren K. Wood, Susan V. Brooks, John E. Wilkinson
Publikováno v:
Aging Cell. 11:675-682
Rapamycin increases lifespan in mice, but whether this represents merely inhibition of lethal neoplastic diseases, or an overall slowing in multiple aspects of aging is currently unclear. We report here that many forms of age-dependent change, includ