Itzel Nissen

ORCID: 0000-0002-0741-5730
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About
Contact & Profiles
Research Areas
  • RNA Research and Splicing
  • Genomics and Chromatin Dynamics
  • Protein Degradation and Inhibitors
  • Muscle Physiology and Disorders
  • Cellular Mechanics and Interactions
  • Glioma Diagnosis and Treatment
  • CRISPR and Genetic Engineering
  • Cancer-related molecular mechanisms research
  • Endometriosis Research and Treatment
  • Estrogen and related hormone effects
  • Protein Tyrosine Phosphatases
  • Menopause: Health Impacts and Treatments
  • Calpain Protease Function and Regulation

Umeå University
2022-2024

Universidad Nacional Autónoma de México
2012

Chromatin organization controls transcription by modulating 3D-interactions between enhancers and promoters in the nucleus. Alterations epigenetic states 3D-chromatin result gene expression changes contributing to cancer. Here, we map promoter-enhancer interactome regulatory landscape of glioblastoma, most aggressive primary brain tumour. Our data reveals profound rewiring interactions, chromatin accessibility redistribution histone marks glioblastoma. This leads loss long-range interactions...

10.1038/s41467-023-41919-x article EN cc-by Nature Communications 2023-10-13

Abstract In muscular dystrophies, muscle fibers loose integrity and die, causing significant suffering premature death. Strikingly, the extraocular muscles (EOMs) are spared, functioning well despite disease progression. Although EOMs have been shown to differ from body musculature, mechanisms underlying this inherent resistance dystrophies remain unknown. Here, we demonstrate important differences in gene expression as a response between trunk zebrafish via transcriptomic profiling. We show...

10.1038/s41467-024-46187-x article EN cc-by Nature Communications 2024-03-02

Abstract Background Glioblastoma (GB) is the most aggressive of all primary brain tumours and due to its highly invasive nature, surgical resection nearly impossible. Patients typically rely on radiotherapy with concurrent temozolomide (TMZ) treatment face a median survival ~ 14 months. Alterations in Epidermal Growth Factor Receptor gene ( EGFR ) are common GB tumours, but therapies targeting have not shown significant clinical efficacy. Methods Here, we investigated influence regulatory...

10.1186/s12885-023-11418-9 article EN cc-by BMC Cancer 2023-10-06

Abstract Chromatin organization controls transcription by modulating 3D-interactions between enhancers and promoters in the nucleus. Alterations epigenetic states 3D-chromatin result gene expression changes contributing to cancer pathogenesis. Here, we mapped promoter-enhancer interactome regulatory landscape of glioblastoma, most aggressive primary brain tumour. Our data reveals profound rewiring interactions, chromatin accessibility redistribution histone marks across four glioblastoma...

10.1101/2022.11.16.516797 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2022-11-17

ABSTRACT Glioblastoma (GB) is the most aggressive of all primary brain tumours. Patients typically rely on radiotherapy with concurrent temozolomide (TMZ) treatment and face a median survival ∼14 months. Alterations in Epidermal Growth Factor Receptor gene ( EGFR ) are common GB tumours, but therapies targeting have not shown significant clinical efficacy. Here, we investigated influence regulatory genome cells, identified novel enhancers located an intronic region nearby GB-associated SNP...

10.1101/2023.02.22.529507 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-02-22

Abstract In muscular dystrophies, muscle fibers loose integrity and die, leading to significant suffering a shorter life. Strikingly, the extraocular muscles (EOMs), controlling eye movements, are spared function well despite disease progression. Although EOMs have been shown important differences compared body musculature mechanisms underlying this inherent resistance dystrophies remain largely unknown. Here, we demonstrate in gene expression as response between trunk zebrafish via...

10.1101/2023.10.26.563896 preprint EN bioRxiv (Cold Spring Harbor Laboratory) 2023-10-26
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