John Hunt

ORCID: 0000-0003-3095-0122
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About
Contact & Profiles
Research Areas
  • Skin and Cellular Biology Research
  • RNA regulation and disease
  • CRISPR and Genetic Engineering
  • Silk-based biomaterials and applications
  • Mosquito-borne diseases and control
  • Plant Reproductive Biology
  • 3D Printing in Biomedical Research
  • melanin and skin pigmentation
  • Monoclonal and Polyclonal Antibodies Research
  • Wound Healing and Treatments
  • Genomics and Phylogenetic Studies
  • Bioinformatics and Genomic Networks
  • Cell Adhesion Molecules Research
  • Innovation and Socioeconomic Development
  • Virus-based gene therapy research
  • Cellular transport and secretion
  • Microbial Metabolic Engineering and Bioproduction
  • RNA Interference and Gene Delivery

University of Auckland
2022-2025

Maurice Wilkins Centre
2024-2025

Columbia University
2013

Experimental data exists for only a vanishingly small fraction of sequenced microbial genes. This community page discusses the progress made by COMBREX project to address this important issue using both computational and experimental resources.

10.1371/journal.pbio.1001638 article EN cc-by PLoS Biology 2013-08-27

Abstract Gene therapy based on the CRISPR/Cas9 system has emerged as a promising strategy for treating monogenic fragile skin disorder recessive dystrophic epidermolysis bullosa (RDEB). With this approach problematic wounds could be grafted with gene edited, patient‐specific equivalents. Precise editing using homology‐directed repair (HDR) is ultimate goal, however low efficiencies have hindered progress. Reframing strategies highly efficient non‐homologous end joining (NHEJ) aimed at...

10.1002/btm2.10640 article EN cc-by Bioengineering & Translational Medicine 2024-01-17

Gene editing facilitated by homology-directed repair (HDR) holds great potential for treating monogenetic disorders such as recessive dystrophic epidermolysis bullosa (RDEB). However, low efficiency and variability between loci must be overcome its widespread adoption into personalized therapies. To address these challenges, we developed a highly efficient versatile gene strategy RDEB that incorporates the small molecule inhibitor M3814 to enhance HDR. We focused on three causative COL7A1...

10.1016/j.omtn.2025.102472 article EN cc-by Molecular Therapy — Nucleic Acids 2025-02-01

Gene editing therapies are designed to minimise off-target editing. However, it is not widespread practice for common polymorphisms be considered when identifying potential sites in silico. Nevertheless, genetic variants should included as they have the alter existing, or generate new, sites. To facilitate consideration of designing targeted gene we developed PopOff, a web-based tool that integrates minor allele frequencies from gnomAD variant database into an analysis. We used PopOff...

10.1080/03036758.2024.2347968 article EN cc-by-nc-nd Journal of the Royal Society of New Zealand 2024-05-09

One of the key functions human skin is to provide a barrier, protecting body from surrounding environment and maintaining homeostasis internal environment. A mature, stratified epidermis critical achieve barrier function particularly important when producing grafts in vitro for wound treatment. For decades epidermal stratification has been achieved by culturing keratinocytes at an air-liquid interface, triggering proliferating basal differentiate form all layers. We show here that...

10.1016/j.jcyt.2024.12.005 article EN cc-by-nc-nd Cytotherapy 2024-12-01

Gene editing facilitated by homology-directed repair represents a promising strategy for precisely correcting pathogenic variants underlying monogenic disorders, including the life-threatening skin blistering condition junctional epidermolysis bullosa (JEB). Frequent reports of unintended off-target genotoxicity associated with conventional Cas9 nuclease have increasingly led to adoption dual-Cas9 nickases (dual-Cas9n) owing their improved safety profile. However, rates precise obtained such...

10.1016/j.xjidi.2024.100343 article EN cc-by JID Innovations 2024-12-24
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