Zobrazeno 1 - 10
of 81
pro vyhledávání: '"Joshua M. Gorham"'
Autor:
Gabriela Venturini, Juliana M. Alvim, Kallyandra Padilha, Christopher N. Toepfer, Joshua M. Gorham, Lauren K. Wasson, Diogo Biagi, Sergio Schenkman, Valdemir M. Carvalho, Jessica S. Salgueiro, Karina H. M. Cardozo, Jose E. Krieger, Alexandre C. Pereira, Jonathan G. Seidman, Christine E. Seidman
Publikováno v:
Frontiers in Cellular and Infection Microbiology, Vol 13 (2023)
IntroductionChagas cardiomyopathy, a disease caused by Trypanosoma cruzi (T. cruzi) infection, is a major contributor to heart failure in Latin America. There are significant gaps in our understanding of the mechanism for infection of human cardiomyo
Externí odkaz:
https://doaj.org/article/dd5e4d9e31404b4a8296661ca7c6392c
Autor:
Alexander Hsieh, Sarah U. Morton, Jon A. L. Willcox, Joshua M. Gorham, Angela C. Tai, Hongjian Qi, Steven DePalma, David McKean, Emily Griffin, Kathryn B. Manheimer, Daniel Bernstein, Richard W. Kim, Jane W. Newburger, George A. Porter, Deepak Srivastava, Martin Tristani-Firouzi, Martina Brueckner, Richard P. Lifton, Elizabeth Goldmuntz, Bruce D. Gelb, Wendy K. Chung, Christine E. Seidman, J. G. Seidman, Yufeng Shen
Publikováno v:
Genome Medicine, Vol 12, Iss 1, Pp 1-18 (2020)
Abstract Background The contribution of somatic mosaicism, or genetic mutations arising after oocyte fertilization, to congenital heart disease (CHD) is not well understood. Further, the relationship between mosaicism in blood and cardiovascular tiss
Externí odkaz:
https://doaj.org/article/b7f196ef4fc94a1c9c9e2a38f2b299d7
Autor:
Karina N. Gonzalez Herrera, Elma Zaganjor, Yoshinori Ishikawa, Jessica B. Spinelli, Haejin Yoon, Jia-Ren Lin, F. Kyle Satterstrom, Alison Ringel, Stacy Mulei, Amanda Souza, Joshua M. Gorham, Craig C. Benson, Jonathan G. Seidman, Peter K. Sorger, Clary B. Clish, Marcia C. Haigis
Publikováno v:
Cell Reports, Vol 22, Iss 8, Pp 1945-1955 (2018)
Summary: Sirtuin 3 (SIRT3) is a NAD+-dependent deacetylase downregulated in aging and age-associated diseases such as cancer and neurodegeneration and in high-fat diet (HFD)-induced metabolic disorders. Here, we performed a small-molecule screen and
Externí odkaz:
https://doaj.org/article/51a8f19ab26748a8ba8f2357ab0736c7
Autor:
Qi Zhang, Seong Won Kim, Joshua M. Gorham, Daniel M. DeLaughter, Tarsha Ward, Christine E. Seidman, Jonathan G. Seidman
Publikováno v:
Current protocols. 2(10)
This protocol describes a robust pipeline for simultaneously analyzing multiple samples by single-nucleus (sn)RNA-seq. cDNA obtained from each single sample are labeled with the same lipid-coupled oligonucleotide barcode (10X Genomics). Nuclei from a
Autor:
Daniel Reichart, Gregory A. Newby, Hiroko Wakimoto, Mingyue Lun, Joshua M. Gorham, Justin J. Curran, Aditya Raguram, Daniel M. DeLaughter, David A. Conner, Júlia D. C. Marsiglia, Sajeev Kohli, Lukas Chmatal, David C. Page, Nerea Zabaleta, Luk Vandenberghe, David R. Liu, Jonathan G. Seidman, Christine Seidman
Publikováno v:
Nature Medicine. 29:412-421
Dominant missense pathogenic variants in cardiac myosin heavy chain cause hypertrophic cardiomyopathy (HCM), a currently incurable disorder that increases risk for stroke, heart failure and sudden cardiac death. In this study, we assessed two differe
GATA6 mutations in hiPSCs inform mechanisms for maldevelopment of the heart, pancreas, and diaphragm
Autor:
Arun Sharma, Lauren K Wasson, Jon AL Willcox, Sarah U Morton, Joshua M Gorham, Daniel M DeLaughter, Meraj Neyazi, Manuel Schmid, Radhika Agarwal, Min Young Jang, Christopher N Toepfer, Tarsha Ward, Yuri Kim, Alexandre C Pereira, Steven R DePalma, Angela Tai, Seongwon Kim, David Conner, Daniel Bernstein, Bruce D Gelb, Wendy K Chung, Elizabeth Goldmuntz, George Porter, Martin Tristani-Firouzi, Deepak Srivastava, Jonathan G Seidman, Christine E Seidman, Pediatric Cardiac Genomics Consortium
Publikováno v:
eLife, Vol 9 (2020)
Damaging GATA6 variants cause cardiac outflow tract defects, sometimes with pancreatic and diaphragmic malformations. To define molecular mechanisms for these diverse developmental defects, we studied transcriptional and epigenetic responses to GATA6
Externí odkaz:
https://doaj.org/article/de48ca73426c4e9e8cd88b2b87f1b9e5
Autor:
Min Young Jang, Parth N. Patel, Alexandre C. Pereira, Jon A.L. Willcox, Alireza Haghighi, Angela C. Tai, Kaoru Ito, Sarah U. Morton, Joshua M. Gorham, David M. McKean, Steven R. DePalma, Daniel Bernstein, Martina Brueckner, Wendy K. Chung, Alessandro Giardini, Elizabeth Goldmuntz, Jonathan R. Kaltman, Richard Kim, Jane W. Newburger, Yufeng Shen, Deepak Srivastava, Martin Tristani-Firouzi, Bruce D. Gelb, George A. Porter, Christine E. Seidman, Jonathan G. Seidman
Publikováno v:
Circulation: Genomic and Precision Medicine.
BACKGROUND: Known genetic causes of congenital heart disease (CHD) explain METHODS: We tested de novo variants from trio studies of 2649 CHD probands and their parents, as well as rare (allele frequency, − 6 ) variants from 4472 CHD probands in the
Autor:
Mason E. Sweat, Yangpo Cao, Xiaoran Zhang, Ozanna Burnicka-Turek, Carlos Perez-Cervantes, Brynn N. Akerberg, Qing Ma, Hiroko Wakimoto, Joshua M. Gorham, Mi Kyoung Song, Michael A. Trembley, Peizhe Wang, Fujian Lu, Matteo Gianeselli, Maksymilian Prondzynski, Raul H. Bortolin, Jonathan G. Seidman, Christine E. Seidman, Ivan P. Moskowitz, William T. Pu
Publikováno v:
bioRxiv
Understanding how the atrial and ventricular chambers of the heart maintain their distinct identity is a prerequisite for treating chamber-specific diseases. Here, we selectively inactivated the transcription factorTbx5in the atrial working myocardiu
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::44e019c2713c76df1072f0d0d59e6070
https://europepmc.org/articles/PMC10153240/
https://europepmc.org/articles/PMC10153240/
Autor:
Joshua M. Gorham, Christine E. Seidman, Christopher S. Chen, Jonathan G. Seidman, Subramanian Sundaram, Christopher N. Toepfer, Radhika Agarwal, Jourdan K. Ewoldt, Steven P. Gygi, Joao A. Paulo, Steven R. DePalma, Qi Zhang, Anant Chopra
Publikováno v:
Circ Res
Rationale: Dominant heterozygous variants in filamin C ( FLNC ) cause diverse cardiomyopathies, although the underlying molecular mechanisms remain poorly understood. Objective: We aimed to define the molecular mechanisms by which FLNC variants alter
Autor:
Daniel Reichart, Eric L. Lindberg, Henrike Maatz, Antonio M. A. Miranda, Anissa Viveiros, Nikolay Shvetsov, Anna Gärtner, Emily R. Nadelmann, Michael Lee, Kazumasa Kanemaru, Jorge Ruiz-Orera, Viktoria Strohmenger, Daniel M. DeLaughter, Giannino Patone, Hao Zhang, Andrew Woehler, Christoph Lippert, Yuri Kim, Eleonora Adami, Joshua M. Gorham, Sam N. Barnett, Kemar Brown, Rachel J. Buchan, Rasheda A. Chowdhury, Chrystalla Constantinou, James Cranley, Leanne E. Felkin, Henrik Fox, Ahla Ghauri, Jan Gummert, Masatoshi Kanda, Ruoyan Li, Lukas Mach, Barbara McDonough, Sara Samari, Farnoush Shahriaran, Clarence Yapp, Caroline Stanasiuk, Pantazis I. Theotokis, Fabian J. Theis, Antoon van den Bogaerdt, Hiroko Wakimoto, James S. Ware, Catherine L. Worth, Paul J. R. Barton, Young-Ae Lee, Sarah A. Teichmann, Hendrik Milting, Michela Noseda, Gavin Y. Oudit, Matthias Heinig, Jonathan G. Seidman, Norbert Hubner, Christine E. Seidman
Publikováno v:
Science
Science 377:eabo1984 (2022)
Science 377:eabo1984 (2022)
INTRODUCTION Human heart failure is a highly morbid condition that affects 23 million individuals worldwide. It emerges in the setting of an array of different cardiovascular disorders, which has propelled the notion that diverse stimuli converge on