3 results match your criteria: "Department of Genetics Albert Einstein College of Medicine Bronx NY.[Affiliation]"

Article Synopsis
  • Endocardial cells are key players in the formation and remodeling of heart valves, and genetic variations can lead to congenital defects in these valves.
  • A study investigated the specific roles of certain genes in endocardial cells by deleting them, which revealed that their absence disrupted heart valve development and remodeling.
  • The results indicated that the deletion of these genes increased cell death, affected extracellular matrix organization, and altered gene expression related to important signaling pathways, suggesting these genes are crucial for proper heart valve formation.
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Background Heart tube looping to form a 4-chambered heart is a critical stage of embryonic heart development, but the gene drivers and their regulatory targets have not been extensively characterized at the cell-type level. Methods and Results To study the interaction of signaling pathways, transcription factors (TFs), and genetic networks in the process, we constructed gene co-expression networks and identified gene modules highly activated in individual cardiomyocytes at multiple anatomical regions and developmental stages using previously published single-cell RNA-seq data. Function analyses of the modules uncovered major pathways important for spatiotemporal cardiomyocyte differentiation.

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Hepatocyte transplantation is an attractive alternative to liver transplantation. Thus far, however, extensive liver repopulation by adult hepatocytes has required ongoing genetic, physical, or chemical injury to host liver. We hypothesized that providing a regulated proliferative and/or survival advantage to transplanted hepatocytes should enable repopulation in a normal liver microenvironment.

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