J G Seidman
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Explore the profile of J G Seidman including associated specialties, affiliations and a list of published articles.
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418
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21830
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Recent Articles
1.
Ward T, Morton S, Venturini G, Tai W, Jang M, Gorham J, et al.
J Am Heart Assoc
. 2025 Mar;
14(5):e036860.
PMID: 40028843
Background: SMAD2 is a coregulator that binds a variety of transcription factors in human development. Heterozygous loss-of-function and missense variants are identified in patients with congenital heart disease (CHD) or...
2.
Kim Y, Kim S, Saul D, Neyazi M, Schmid M, Wakimoto H, et al.
J Clin Invest
. 2024 Dec;
135(4).
PMID: 39688912
Heterozygous truncating variants in the sarcomere protein titin (TTN) are the most common genetic cause of heart failure. To understand mechanisms that regulate abundant cardiomyocyte (CM) TTN expression, we characterized...
3.
McKean D, Zhang Q, Narayan P, Morton S, Strohmenger V, Tang V, et al.
J Clin Invest
. 2024 Jun;
134(11.
PMID: 38828726
Trisomy 21 (T21), a recurrent aneuploidy occurring in 1:800 births, predisposes to congenital heart disease (CHD) and multiple extracardiac phenotypes. Despite a definitive genetic etiology, the mechanisms by which T21...
4.
Agarwal R, Wakimoto H, Paulo J, Zhang Q, Reichart D, Toepfer C, et al.
Circulation
. 2022 Nov;
146(22):1674-1693.
PMID: 36321451
Background: encodes α-kinase 3, a muscle-specific protein of unknown function. loss-of-function variants cause cardiomyopathy with distinctive clinical manifestations in both children and adults, but the molecular functions of ALPK3 remain...
5.
Ablation of lysophosphatidic acid receptor 1 attenuates hypertrophic cardiomyopathy in a mouse model
Raja A, Wakimoto H, DeLaughter D, Reichart D, Gorham J, Conner D, et al.
Proc Natl Acad Sci U S A
. 2022 Jul;
119(28):e2204174119.
PMID: 35787042
Myocardial fibrosis is a key pathologic feature of hypertrophic cardiomyopathy (HCM). However, the fibrotic pathways activated by HCM-causing sarcomere protein gene mutations are poorly defined. Because lysophosphatidic acid is a...
6.
Quiat D, Kim S, Zhang Q, Morton S, Pereira A, DePalma S, et al.
Proc Natl Acad Sci U S A
. 2022 May;
119(21):e2203928119.
PMID: 35584116
Microtia is a congenital malformation that encompasses mild hypoplasia to complete loss of the external ear, or pinna. Although the contribution of genetic variation and environmental factors to microtia remains...
7.
Willcox J, Geiger J, Morton S, McKean D, Quiat D, Gorham J, et al.
Am J Hum Genet
. 2022 Apr;
109(5):961-966.
PMID: 35397206
The well-established manifestation of mitochondrial mutations in functional cardiac disease (e.g., mitochondrial cardiomyopathy) prompted the hypothesis that mitochondrial DNA (mtDNA) sequence and/or copy number (mtDNAcn) variation contribute to cardiac defects...
8.
Gonzalez-Teran B, Pittman M, Felix F, Thomas R, Richmond-Buccola D, Huttenhain R, et al.
Cell
. 2022 Feb;
185(5):794-814.e30.
PMID: 35182466
Congenital heart disease (CHD) is present in 1% of live births, yet identification of causal mutations remains challenging. We hypothesized that genetic determinants for CHDs may lie in the protein...
9.
Morton S, Pereira A, Quiat D, Richter F, Kitaygorodsky A, Hagen J, et al.
Circ Genom Precis Med
. 2022 Feb;
15(2):e003500.
PMID: 35130025
Background: Congenital heart disease (CHD) is the most common anomaly at birth, with a prevalence of ≈1%. While infants born to mothers with diabetes or obesity have a 2- to...
10.
Patel P, Ito K, Willcox J, Haghighi A, Jang M, Gorham J, et al.
Circ Genom Precis Med
. 2021 Aug;
14(5):e003389.
PMID: 34461741
Background: Heterozygous truncating variants cause 10% to 20% of idiopathic dilated cardiomyopathy (DCM). Although variants which disrupt canonical splice signals (ie, invariant dinucleotide of the splice donor site, invariant dinucleotide...