Posts Tagged: embryonic stem cells

Induced Pluripotent Stem Cells 10 Years Later For Cardiac Applications

Induced Pluripotent Stem Cells 10 Years Later: For Cardiac Applications

Yoshinori Yoshida, Shinya Yamanaka

Factors which possibly cause clonal differences of induced pluripotent stem cells (iPSCs). [Powerpoint File]

Induced Pluripotent Stem Cells 10 Years Later: For Cardiac Applications

Induced Pluripotent Stem Cells 10 Years Later: For Cardiac Applications

Yoshinori Yoshida, Shinya Yamanaka

Patient stratification based on drug responsiveness using induced pluripotent stem cells–derived cardiac myocytes. [Powerpoint File]

Epigenetic Modifications of Stem Cells: A Paradigm for the Control of Cardiac Progenitor Cells

Epigenetic Modifications of Stem Cells: A Paradigm for the Control of Cardiac Progenitor Cells

Yonggang Zhou, Johnny Kim, Xuejun Yuan, Thomas Braun

Epigenetic mechanisms involved in embryonic stem cell self-renewal and differentiation. A, Alteration of epigenetic modifications during ES cell differentiation. In ES cells, transcriptionally active pluripotency genes locate within euchromatin regions marked by H3K4me3 and H3K9ac. Differentiation genes are transcriptionally silent and locate within heterochromatin regions characterized by H3K9me3 and 5mC. Reconfiguration of chromatin structure occurs during ES cell differentiation, whereas euchromatic regions, in particular those associated with pluripotency genes, are transformed to heterochromatin. An inverse picture is seen for chromatin regions associated with differentiation. Chromatin modifiers that confer euchromatin and heterochromatin transition include DNA methyltransferases (DNMTs); histone methyltransferase SETDB1, MLL/Wdr5 complex; histone demethylase Jmjd1a, Jmjd2c, Kdm5b; histone acetyltransferase GCN5; and ATP-dependent chromatin remodeling complex CHD1, Brg1, Tip60–p400 complex. B, Bivalent chromatin domains and epigenetic control of lineage commitment. In pluripotent ES cells, lineage-committed genes are in a transcriptionally poised state and show bivalent epigenetic modifications: active H3K4me3 and repressive H3K27me3. 5hmC occurs in bivalent domains as well. On lineage commitment, genes controlling a distinct cell lineage maintain H3K4me3, remove H3K27me3, and become activated. Genes controlling other lineages maintain H3K27me3, gain H3K9me3 and 5mC, and become fully silenced. Chromatin modifiers that regulate bivalent chromatin domains include DNA methyltransferase DNMT1; TET1; histone methyltransferase/demethylase complex MLL/Dpy-30, MLL2/Jmjd3/UTX complex, PRC2 complex, and LSD1. [Powerpoint File]

Immunogenicity of Pluripotent Stem Cells and Their Derivatives

Immunogenicity of Pluripotent Stem Cells and Their Derivatives

Patricia E. de Almeida, Julia D. Ransohoff, Abu Nahid, Joseph C. Wu

Mechanisms for generating minor histocompatibility antigens in pluripotent stem cells. Polymorphisms induced in embryonic stem (ES) and induced pluripotent stem (iPS) cells can result in expression of proteins and peptides that are distinct from those in the donor cells. On proteolytic degradation, these peptides are transported by the peptide transporter into the endoplasmic reticulum (ER), where they can bind to human leukocyte antigen (HLA) molecules and pass through the Golgi apparatus to be presented at the cell surface as a complex with HLA and can be recognized as foreign by donor T cells. TCR, T-cell receptor. [Powerpoint File]