Stephanie J. Ellis

ORCID: 0000-0003-3341-3453
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About
Contact & Profiles
Research Areas
  • Cellular Mechanics and Interactions
  • Cell Adhesion Molecules Research
  • Silk-based biomaterials and applications
  • Single-cell and spatial transcriptomics
  • Hippo pathway signaling and YAP/TAZ
  • CRISPR and Genetic Engineering
  • Cancer Cells and Metastasis
  • RNA and protein synthesis mechanisms
  • Developmental Biology and Gene Regulation
  • Cardiomyopathy and Myosin Studies
  • Digestive system and related health
  • Mathematical Biology Tumor Growth
  • Skin and Cellular Biology Research
  • Planarian Biology and Electrostimulation
  • 14-3-3 protein interactions
  • RNA Research and Splicing
  • CAR-T cell therapy research
  • Muscle Physiology and Disorders
  • Marine Invertebrate Physiology and Ecology
  • RNA modifications and cancer
  • Evolution and Genetic Dynamics

Max Perutz Labs
2022-2024

University of Vienna
2022-2024

Vienna Biocenter
2024

Rockefeller University
2019-2022

Howard Hughes Medical Institute
2019-2022

University of British Columbia
2009-2016

The tumour evolution model posits that malignant transformation is preceded by randomly distributed driver mutations in cancer genes, which cause clonal expansions phenotypically normal tissues. Although can remodel entire tissues

10.1038/s41586-024-07663-y article EN cc-by Nature 2024-07-17

The dark proteome includes a rapidly expanding catalog of microproteins with unknown functions that have been historically ignored in genome annotations. Here, we exploit an vivo single-cell CRISPR screening strategy the mouse epidermis to systematically investigate tissue-wide function microproteins. We document global and cell-type-specific roles during epidermal development homeostasis at transcriptomic resolution. Focusing on select candidates, identify novel microprotein Gm10076,...

10.1101/2025.03.17.643322 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2025-03-17

Talin serves an essential function during integrin-mediated adhesion in linking integrins to actin via the intracellular complex. In addition, N-terminal head domain of talin regulates affinity for their ECM-ligands, a process known as inside-out activation. We previously showed that Drosophila, mutating integrin binding site resulted weakened ECM. Intriguingly, subsequent studies canonical activation might not take place flies. Consistent with this, mutation specifically blocks its ability...

10.1371/journal.pgen.1004756 article EN cc-by PLoS Genetics 2014-11-13

Adhesion receptors play diverse roles during animal development and require precise spatiotemporal regulation, which is achieved through the activity of their binding partners. Integrins, adhesion that mediate cell attachment to extracellular matrix (ECM), connect intracellular environment cytoplasmic adapter protein talin. Talin has two essential functions: orchestrating assembly complex (IAC), associates with integrin, regulating affinity integrins for ECM. can bind different...

10.1242/jcs.083337 article EN Journal of Cell Science 2011-05-11

Summary Integrins are heterodimeric adhesion receptors that link the extracellular matrix (ECM) to cytoskeleton. Binding of scaffold protein, talin, cytoplasmic tail β-integrin causes a conformational change domains integrin heterodimer, thus allowing high-affinity binding ECM ligands. This essential process is called activation. Here we report Z-band alternatively spliced PDZ-motif-containing protein (Zasp) cooperates with talin activate α5β1 integrins in mammalian tissue culture and...

10.1242/jcs.103291 article EN Journal of Cell Science 2012-09-20

Somatic stem cells are characterized by their low overall protein synthesis rates, a feature implicated in driving stemness. However, how aging reshapes the translational landscape of and these changes impact regenerative capacity remains poorly understood. Here, we present an vivo single-cell ribosome profiling strategy to monitor tissue-wide landscapes young aged mouse epidermis. By implementing ribosomal elongation-inhibited cell isolation switching RNase I ribonuclease for generating...

10.1101/2024.11.02.621639 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2024-11-03

The tumor evolution model posits that malignant transformation is preceded by randomly distributed driver mutations in cancer genes, which cause clonal expansions phenotypically normal tissues. Although occur frequently human epithelia and can remodel almost entire tissues, the mechanisms behind why only a small number of clones transform into tumors remain enigmatic. Here, we develop an vivo single-cell CRISPR strategy to systematically investigate tissue-wide dynamics 150 most mutated...

10.1101/2023.07.13.548697 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-07-14
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