Yasmin ElMaghloob

ORCID: 0000-0002-5613-0678
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About
Contact & Profiles
Research Areas
  • Genetic and Kidney Cyst Diseases
  • Receptor Mechanisms and Signaling
  • Cellular transport and secretion
  • Pancreatic function and diabetes
  • Cellular Mechanics and Interactions
  • RNA Research and Splicing
  • Hedgehog Signaling Pathway Studies
  • Protein Kinase Regulation and GTPase Signaling
  • Microtubule and mitosis dynamics
  • Protist diversity and phylogeny
  • Fetal and Pediatric Neurological Disorders
  • Nuclear Structure and Function
  • Signaling Pathways in Disease
  • Protein Degradation and Inhibitors
  • Phosphodiesterase function and regulation
  • Angiogenesis and VEGF in Cancer
  • Cancer Cells and Metastasis
  • Genetic Syndromes and Imprinting
  • Renal Diseases and Glomerulopathies

Centre for Genomic Regulation
2024

Children Cancer Hospital
2024

Cancer Research UK Scotland Institute
2017-2022

University of Glasgow
2018

Article10 July 2017Open Access Source DataTransparent process Tumor matrix stiffness promotes metastatic cancer cell interaction with the endothelium Steven E Reid Cancer Research UK Beatson Institute, Glasgow, Search for more papers by this author Emily J Kay Lisa Neilson Anne-Theres Henze Lab of Inflammation and Angiogenesis, Center Biology, VIB, Leuven, Belgium Jens Serneels Ewan McGhee Sandeep Dhayade Colin Nixon John BG Mackey Inflammation, Repair Development, Imperial College London,...

10.15252/embj.201694912 article EN cc-by The EMBO Journal 2017-07-10

Joubert syndrome (JBTS) is a genetically heterogeneous autosomal-recessive neurodevelopmental ciliopathy. We investigated further the underlying genetic etiology of by studying two unrelated families in whom JBTS was not associated with pathogenic variants known JBTS-associated genes. Combined autozygosity mapping both highlighted candidate locus on chromosome 10 (chr10: 101569997–109106128, UCSC Genome Browser hg 19), and exome sequencing revealed missense ARL3 within locus. The encoded...

10.1016/j.ajhg.2018.08.015 article EN cc-by The American Journal of Human Genetics 2018-09-27

Highlights•LCK immune synapse focusing requires its strong interaction with ciliary UNC119A•ARL3Q71L results in unfocused LCK localization and increased T cell stimulation•The ARL3-GEF ARL13B localizes to the synapse•UNC119A regulatory arm interacts kinase domain a phosphoregulated mannerSummaryUpon engagement of receptor an antigen-presenting cell, initiates TCR signaling by phosphorylating activation motifs. However, mechanism specifically at is major question. We show that phosphorylation...

10.1016/j.devcel.2018.08.012 article EN cc-by-nc-nd Developmental Cell 2018-09-13

The ADP-ribosylation factor-like 3 (ARL3) is a ciliopathy G-protein which regulates the ciliary trafficking of several lipid-modified proteins. ARL3 activated by its guanine exchange factor (GEF) ARL13B via an unresolved mechanism. BART described as effector has also been implicated in ciliopathies, although role interaction unknown. Here, we show that, at physiological GTP:GDP levels, human ARL3GDP weakly ARL13B. However, interacts with nucleotide-free and, concert ARL13B, efficiently...

10.7554/elife.64624 article EN cc-by eLife 2021-01-13

RAS is a major anticancer drug target which requires membrane localization to activate downstream signal transduction. The direct inhibition of has proven be challenging. Here, we present novel strategy for targeting by stabilizing its interaction with the prenyl-binding protein PDE6D and disrupting localization. Using rationally designed point mutations, were able stabilize RAS:PDE6D complex increasing affinity PDE6D, resulted in redirection cytoplasm primary cilium oncogenic RAS/ERK...

10.1021/acs.jmedchem.1c01265 article EN cc-by Journal of Medicinal Chemistry 2022-02-02
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