University of Colorado Denver - Biology
Associate Professor of Molecular Biology, University of Colorado Denver
Higher Education
Christopher
Phiel, PhD
Denver, Colorado
Experienced tenured Associate Professor with 25 years experience working in higher education. Award-winning education professional skilled in Molecular Biology, Embryonic Stem Cells, Signal Transduction, Regulation of Gene Expression, Epigenetics, teaching CRISPR, and Public Speaking.
Assistant Professor
Molecular biology research, focusing on the interface between signal transduction and epigenetics. Special interest in mechanisms of genomic imprinting.
Assistant Professor
Molecular biology research, focusing on the interface between signal transduction, cell biology and epigenetics. Main focus is understanding how Gsk-3 activity is involved in embryonic stem cell pluripotency.
Associate Professor
Christopher worked at University of Colorado Denver as a Associate Professor
Research assistant
Lab assistant in peptide chemistry.
Postdoctoral fellow
Molecular Biology
Ph.D.
Developmental Biology
B.S.
Biology
Ursinus College Rising Star Alumni Award for Professional Achievement and Service to Humanity
Regulation of GSK-3α Activity for Treatment or Prevention of Alzheimer’s Disease
Biology of Reproduction
Biology of Reproduction
Nature Communications
Biology of Reproduction
Nature Communications
Cell Metabolism
Biology of Reproduction
Nature Communications
Cell Metabolism
Journal of Biological Chemistry
Biology of Reproduction
Nature Communications
Cell Metabolism
Journal of Biological Chemistry
Experimental Cell Research
Biology of Reproduction
Nature Communications
Cell Metabolism
Journal of Biological Chemistry
Experimental Cell Research
Molecular Biology of the Cell
Biology of Reproduction
Nature Communications
Cell Metabolism
Journal of Biological Chemistry
Experimental Cell Research
Molecular Biology of the Cell
Molecular Biology of the Cell
Glycogen synthase kinase-3 (Gsk-3) is a key regulator of multiple signal transduction pathways. Recently, we described a novel role for Gsk-3 in the regulation of DNA methylation at imprinted loci in mouse embryonic stem cells (ESCs), suggesting that epigenetic changes regulated by Gsk-3 are likely an unrecognized facet of Gsk-3 signaling. Here, we extend our initial observation to the entire mouse genome by enriching for methylated DNA with the MethylMiner kit and performing next-generation sequencing (MBD-Seq) in wild-type and Gsk-3α-/-;Gsk-3β-/- ESCs. Consistent with our previous data, we found that 77% of known imprinted loci have reduced DNA methylation in Gsk-3-deficient ESCs. More specifically, we unambiguously identified changes in DNA methylation within regions that have been confirmed to function as imprinting control regions (ICRs). In many cases, the reduced DNA methylation at imprinted loci in Gsk-3α-/-;Gsk-3β-/- ESCs was accompanied by changes in gene expression as well. Furthermore, many of the Gsk-3-dependent differentially methylated regions (DMRs) are identical to the DMRs recently identified in uniparental ESCs. Our data demonstrate the importance of Gsk-3 activity in the maintenance of DNA methylation at a majority of the imprinted loci in ESCs, and emphasizes the importance for Gsk-3-mediated signal transduction on the epigenome.
Biology of Reproduction
Nature Communications
Cell Metabolism
Journal of Biological Chemistry
Experimental Cell Research
Molecular Biology of the Cell
Molecular Biology of the Cell
Glycogen synthase kinase-3 (Gsk-3) is a key regulator of multiple signal transduction pathways. Recently, we described a novel role for Gsk-3 in the regulation of DNA methylation at imprinted loci in mouse embryonic stem cells (ESCs), suggesting that epigenetic changes regulated by Gsk-3 are likely an unrecognized facet of Gsk-3 signaling. Here, we extend our initial observation to the entire mouse genome by enriching for methylated DNA with the MethylMiner kit and performing next-generation sequencing (MBD-Seq) in wild-type and Gsk-3α-/-;Gsk-3β-/- ESCs. Consistent with our previous data, we found that 77% of known imprinted loci have reduced DNA methylation in Gsk-3-deficient ESCs. More specifically, we unambiguously identified changes in DNA methylation within regions that have been confirmed to function as imprinting control regions (ICRs). In many cases, the reduced DNA methylation at imprinted loci in Gsk-3α-/-;Gsk-3β-/- ESCs was accompanied by changes in gene expression as well. Furthermore, many of the Gsk-3-dependent differentially methylated regions (DMRs) are identical to the DMRs recently identified in uniparental ESCs. Our data demonstrate the importance of Gsk-3 activity in the maintenance of DNA methylation at a majority of the imprinted loci in ESCs, and emphasizes the importance for Gsk-3-mediated signal transduction on the epigenome.
Biology of Reproduction
Biology of Reproduction
Nature Communications
Cell Metabolism
Journal of Biological Chemistry
Experimental Cell Research
Molecular Biology of the Cell
Molecular Biology of the Cell
Glycogen synthase kinase-3 (Gsk-3) is a key regulator of multiple signal transduction pathways. Recently, we described a novel role for Gsk-3 in the regulation of DNA methylation at imprinted loci in mouse embryonic stem cells (ESCs), suggesting that epigenetic changes regulated by Gsk-3 are likely an unrecognized facet of Gsk-3 signaling. Here, we extend our initial observation to the entire mouse genome by enriching for methylated DNA with the MethylMiner kit and performing next-generation sequencing (MBD-Seq) in wild-type and Gsk-3α-/-;Gsk-3β-/- ESCs. Consistent with our previous data, we found that 77% of known imprinted loci have reduced DNA methylation in Gsk-3-deficient ESCs. More specifically, we unambiguously identified changes in DNA methylation within regions that have been confirmed to function as imprinting control regions (ICRs). In many cases, the reduced DNA methylation at imprinted loci in Gsk-3α-/-;Gsk-3β-/- ESCs was accompanied by changes in gene expression as well. Furthermore, many of the Gsk-3-dependent differentially methylated regions (DMRs) are identical to the DMRs recently identified in uniparental ESCs. Our data demonstrate the importance of Gsk-3 activity in the maintenance of DNA methylation at a majority of the imprinted loci in ESCs, and emphasizes the importance for Gsk-3-mediated signal transduction on the epigenome.
Biology of Reproduction
Nature Communications
Biology of Reproduction
Nature Communications
Cell Metabolism
Journal of Biological Chemistry
Experimental Cell Research
Molecular Biology of the Cell
Molecular Biology of the Cell
Glycogen synthase kinase-3 (Gsk-3) is a key regulator of multiple signal transduction pathways. Recently, we described a novel role for Gsk-3 in the regulation of DNA methylation at imprinted loci in mouse embryonic stem cells (ESCs), suggesting that epigenetic changes regulated by Gsk-3 are likely an unrecognized facet of Gsk-3 signaling. Here, we extend our initial observation to the entire mouse genome by enriching for methylated DNA with the MethylMiner kit and performing next-generation sequencing (MBD-Seq) in wild-type and Gsk-3α-/-;Gsk-3β-/- ESCs. Consistent with our previous data, we found that 77% of known imprinted loci have reduced DNA methylation in Gsk-3-deficient ESCs. More specifically, we unambiguously identified changes in DNA methylation within regions that have been confirmed to function as imprinting control regions (ICRs). In many cases, the reduced DNA methylation at imprinted loci in Gsk-3α-/-;Gsk-3β-/- ESCs was accompanied by changes in gene expression as well. Furthermore, many of the Gsk-3-dependent differentially methylated regions (DMRs) are identical to the DMRs recently identified in uniparental ESCs. Our data demonstrate the importance of Gsk-3 activity in the maintenance of DNA methylation at a majority of the imprinted loci in ESCs, and emphasizes the importance for Gsk-3-mediated signal transduction on the epigenome.
Biology of Reproduction
Nature Communications
Frontiers in Endocrinology