Christopher Phiel

 Christopher Phiel

Christopher J. Phiel

  • Courses2
  • Reviews9

Biography

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.


Experience

  • The Ohio State University

    Assistant Professor

    Molecular biology research, focusing on the interface between signal transduction and epigenetics. Special interest in mechanisms of genomic imprinting.

  • University of Colorado Denver

    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.

  • University of Colorado Denver

    Associate Professor

    Christopher worked at University of Colorado Denver as a Associate Professor

  • Magainin Pharmaceuticals

    Research assistant

    Lab assistant in peptide chemistry.

Education

  • University of Pennsylvania School of Medicine

    Postdoctoral fellow

    Molecular Biology

  • Thomas Jefferson University Hospitals

    Ph.D.

    Developmental Biology

  • Ursinus College

    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



Publications

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Glycogen synthase kinase-3 (GSK3) activity regulates mRNA methylation in mouse embryonic stem cells

    Journal of Biological Chemistry

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Glycogen synthase kinase-3 (GSK3) activity regulates mRNA methylation in mouse embryonic stem cells

    Journal of Biological Chemistry

  • A Simple and Efficient Method for Transfecting Mouse Embryonic Stem Cells Using Polyethylenimine

    Experimental Cell Research

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Glycogen synthase kinase-3 (GSK3) activity regulates mRNA methylation in mouse embryonic stem cells

    Journal of Biological Chemistry

  • A Simple and Efficient Method for Transfecting Mouse Embryonic Stem Cells Using Polyethylenimine

    Experimental Cell Research

  • Immobilization of PRC1 Complex at Mitotic Chromosomes by Cbx2 in a PRC2-Independent Mechanism

    Molecular Biology of the Cell

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Glycogen synthase kinase-3 (GSK3) activity regulates mRNA methylation in mouse embryonic stem cells

    Journal of Biological Chemistry

  • A Simple and Efficient Method for Transfecting Mouse Embryonic Stem Cells Using Polyethylenimine

    Experimental Cell Research

  • Immobilization of PRC1 Complex at Mitotic Chromosomes by Cbx2 in a PRC2-Independent Mechanism

    Molecular Biology of the Cell

  • Glycogen Synthase Kinase-3 (Gsk-3) Plays A Fundamental Role In Maintaining DNA Methylation At Imprinted Loci In Mouse Embryonic Stem Cells

    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.

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Glycogen synthase kinase-3 (GSK3) activity regulates mRNA methylation in mouse embryonic stem cells

    Journal of Biological Chemistry

  • A Simple and Efficient Method for Transfecting Mouse Embryonic Stem Cells Using Polyethylenimine

    Experimental Cell Research

  • Immobilization of PRC1 Complex at Mitotic Chromosomes by Cbx2 in a PRC2-Independent Mechanism

    Molecular Biology of the Cell

  • Glycogen Synthase Kinase-3 (Gsk-3) Plays A Fundamental Role In Maintaining DNA Methylation At Imprinted Loci In Mouse Embryonic Stem Cells

    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.

  • Isoform-Specific Requirement for GSK-3α in Sperm for Male Fertility

    Biology of Reproduction

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Glycogen synthase kinase-3 (GSK3) activity regulates mRNA methylation in mouse embryonic stem cells

    Journal of Biological Chemistry

  • A Simple and Efficient Method for Transfecting Mouse Embryonic Stem Cells Using Polyethylenimine

    Experimental Cell Research

  • Immobilization of PRC1 Complex at Mitotic Chromosomes by Cbx2 in a PRC2-Independent Mechanism

    Molecular Biology of the Cell

  • Glycogen Synthase Kinase-3 (Gsk-3) Plays A Fundamental Role In Maintaining DNA Methylation At Imprinted Loci In Mouse Embryonic Stem Cells

    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.

  • Isoform-Specific Requirement for GSK-3α in Sperm for Male Fertility

    Biology of Reproduction

  • Glycogen Synthase Kinase 3 Controls Migration of the Cranial Neural Crest Lineage in Mouse and Xenopus

    Nature Communications

  • Targeted disruption of GSK-3α affects sperm motility resulting in male infertility

    Biology of Reproduction

  • Live-cell single-molecule dynamics of PcG proteins imposed by the DIPG H3.3K27M mutation

    Nature Communications

  • Glycogen Synthase Kinase-3α Promotes Fatty Acid Uptake and Lipotoxic Cardiomyopathy

    Cell Metabolism

  • Glycogen synthase kinase-3 (GSK3) activity regulates mRNA methylation in mouse embryonic stem cells

    Journal of Biological Chemistry

  • A Simple and Efficient Method for Transfecting Mouse Embryonic Stem Cells Using Polyethylenimine

    Experimental Cell Research

  • Immobilization of PRC1 Complex at Mitotic Chromosomes by Cbx2 in a PRC2-Independent Mechanism

    Molecular Biology of the Cell

  • Glycogen Synthase Kinase-3 (Gsk-3) Plays A Fundamental Role In Maintaining DNA Methylation At Imprinted Loci In Mouse Embryonic Stem Cells

    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.

  • Isoform-Specific Requirement for GSK-3α in Sperm for Male Fertility

    Biology of Reproduction

  • Glycogen Synthase Kinase 3 Controls Migration of the Cranial Neural Crest Lineage in Mouse and Xenopus

    Nature Communications

  • Gene expression profiling in mouse embryonic stem cells reveals glycogen synthase kinase-3-dependent targets of phosphatidylinositol 3-kinase and Wnt/ß-catenin signaling pathways

    Frontiers in Endocrinology

BIOL 3124

4.3(8)