Nerges Winblad

Affiliated to Research
Visiting address: Karolinska Institutet, BioClinicum J10:20, Visionsgatan 4, 17164 Solna
Postal address: K1 Molekylär medicin och kirurgi, K1 MMK Sällsynta diagnoser, 171 76 Stockholm


  • *Exploring Early Human Development and Regenerative Medicine Utilizing the
    CRISPR/Cas Gene Editing System*
    The development of the CRISPR/Cas technology has paved the way for an
    accurate and readily available genome engineering tool. Guided by a small RNA
    molecule, Cas9 is localized to the genomic region of interest where it can
    perform a double-strand break. There are two main repair pathways activated
    upon DNA damage: Homology-Directed Repair (HDR) and Non-Homologous
    End-Joining (NHEJ). The former pathway relies on homology, either endogenous
    or exogenous, to repair the damage in a correcting manner whereas the latter,
    NHEJ, generates insertions or deletions (indels) at the break site. Indels
    generating frameshift mutations prevent normal protein translation usually by
    creating premature stop codon, making it possible to study cellular
    mechanisms and functions in the absence of a protein.
    I am currently utilizing the CRISPR/Cas system to study loss-of-function in
    different contexts of development and regenerative medicine. These projects
    focus on, I) human X chromosome inactivation and II) reducing immunogenicity
    of hESC-derived cell types.
    /I. Human X chromosome inactivation/
    Different species have developed various forms of X chromosome dosage
    compensation, e.g. female preimplantation mouse embryos inactivate the
    paternal X chromosome at the four cell-stage, which is later re-activated in
    the inner cell mass of the blastocyst at which time random X chromosome
    inactivation follows. Human preimplantation embryos do not exhibit the same
    pattern of dosage compensation and although some genes have been previously
    identified as necessary for X chromosome inactivation (XCI) in mouse, their
    function in human dosage compensation is not as well-established. We will
    utilize the CRISPR/Cas system to study loss-of-function of selected genes to
    learn more about early human development.
    /II. Reducing immunogenicity of hESC-derived cell types/
    Immune-mediated rejection of allogenic transplants is an ongoing challenge
    with few long-term sustainable solutions. These transplantations rely on
    donor-host HLA matching to limit rejection of the transplanted tissue. Our
    approach relies on circumventing this response by modifying hESCs using the
    CRISPR/Cas system to reduce their immunological properties.


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  • Affiliated to Research, Department of Molecular Medicine and Surgery, Karolinska Institutet, 2022-2025

Degrees and Education

  • Degree Of Doctor Of Philosophy, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, 2022

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