Iliana I. León-Vega

ORCID: 0009-0001-1645-7123
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About
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Research Areas
  • Cardiovascular Effects of Exercise
  • Genetics and Physical Performance
  • Ubiquitin and proteasome pathways
  • CAR-T cell therapy research
  • Cardiovascular and Diving-Related Complications
  • Immune cells in cancer
  • Cancer Immunotherapy and Biomarkers
  • Immune Cell Function and Interaction
  • High Altitude and Hypoxia
  • Adipose Tissue and Metabolism
  • Acute Lymphoblastic Leukemia research
  • Heme Oxygenase-1 and Carbon Monoxide
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Inflammatory Bowel Disease
  • Cell Adhesion Molecules Research
  • Immune Response and Inflammation

Center for Research and Advanced Studies of the National Polytechnic Institute
2023-2025

Instituto Politécnico Nacional
2023-2025

Abstract T cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy that still fatal in many cases. blasts are characterized by hyperactivation and strong proliferative migratory capacities. The chemokine receptor CXCR4 involved mediating malignant properties, cortactin has been shown to control surface localization T-ALL cells. We have previously overexpression correlated with organ infiltration relapse B-ALL. However, the role of biology remains elusive. Here, we...

10.1093/jleuko/qiad001 article EN Journal of Leukocyte Biology 2023-01-19

Abstract Neutrophils infiltrate several types of cancer; however, whether their presence is associated with disease progression remains controversial. Here, we show that colon tumors overexpress neutrophil chemoattractants compared to healthy tissues, leading recruitment the invasive margin and central part tumors. Of note, tumor-associated neutrophils expressing tumor necrosis factor α, which usually represents an antitumoral phenotype, were predominantly located in margin. Tumor-associated...

10.1093/jleuko/qiad123 article EN Journal of Leukocyte Biology 2023-10-11

Abstract The chemokine Cxcl1 plays a crucial role in recruiting neutrophils response to infection. early events chemokine-mediated neutrophil extravasation involve sequence of highly orchestrated steps including rolling, adhesion, arrest, and diapedesis. function is determined by its properties reversible monomer–dimer equilibrium binding Cxcr2 glycosaminoglycans. Here, we characterized how these orchestrate using intravital microscopy the cremaster. Compared WT Cxcl1, which exists as both...

10.1093/jleuko/qiad159 article EN Journal of Leukocyte Biology 2023-12-21

Arpin was discovered as an inhibitor of the Arp2/3 complex localized at lamellipodial tip fibroblasts, where it regulated migration steering. Recently, we showed that arpin stabilizes epithelial barrier in Arp2/3-dependent manner. However, expression and functions endothelial cells (EC) have not yet been described. mRNA protein are expressed EC downregulated by pro-inflammatory cytokines. depletion HUVEC causes formation actomyosin stress fibers leading to increased permeability...

10.7554/elife.90692.2 preprint EN 2024-08-19

Arpin was discovered as an inhibitor of the Arp2/3 complex localized at lamellipodial tip fibroblasts, where it regulated migration steering. Recently, we showed that arpin stabilizes epithelial barrier in Arp2/3-dependent manner. However, expression and functions endothelial cells (EC) have not yet been described. mRNA protein are expressed EC downregulated by pro-inflammatory cytokines. depletion Human Umbilical Vein Endothelial Cells causes formation actomyosin stress fibers leading to...

10.7554/elife.90692.3 article EN cc-by eLife 2024-09-19

ABSTRACT Arpin was discovered as an inhibitor of the Arp2/3 complex localized at lamellipodial tip fibroblasts, where it regulated migration steering. Recently, we showed that arpin stabilizes epithelial barrier in Arp2/3-dependent manner. However, expression and functions endothelial cells (EC) have not yet been described. mRNA protein are expressed EC downregulated by pro-inflammatory cytokines. depletion HUVEC causes formation actomyosin stress fibers leading to increased permeability...

10.1101/2023.05.29.542762 preprint EN cc-by-nc-nd bioRxiv (Cold Spring Harbor Laboratory) 2023-05-31

Arpin was discovered as an inhibitor of the Arp2/3 complex localized at lamellipodial tip fibroblasts, where it regulated migration steering. Recently, we showed that arpin stabilizes epithelial barrier in Arp2/3-dependent manner. However, expression and functions endothelial cells (EC) have not yet been described. mRNA protein are expressed EC downregulated by pro-inflammatory cytokines. depletion Human Umbilical Vein Endothelial Cells causes formation actomyosin stress fibers leading to...

10.7554/elife.90692 article EN cc-by eLife 2023-09-28

Arpin was discovered as an inhibitor of the Arp2/3 complex localized at lamellipodial tip fibroblasts, where it regulated migration steering. Recently, we showed that arpin stabilizes epithelial barrier in Arp2/3-dependent manner. However, expression and functions endothelial cells (EC) have not yet been described. mRNA protein are expressed EC downregulated by pro-inflammatory cytokines. depletion HUVEC causes formation actomyosin stress fibers leading to increased permeability...

10.7554/elife.90692.1 preprint EN 2023-09-28

Abstract T cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy that still fatal in many cases. blasts are characterized by hyperactivation and strong proliferative migratory capacities. The chemokine receptor CXCR4 involved mediating malignant properties cortactin has been shown to control surface localization T-ALL cells. We have previously overexpression correlated with organ infiltration relapse B-ALL. However, the role of biology remains elusive. Here, we...

10.21203/rs.3.rs-1995363/v1 preprint EN cc-by Research Square (Research Square) 2022-10-26
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