Sanda Mimouna

ORCID: 0000-0003-1382-4060
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About
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Research Areas
  • Cancer Research and Treatments
  • Amino Acid Enzymes and Metabolism
  • DNA Repair Mechanisms
  • Cytokine Signaling Pathways and Interactions
  • Cancer, Hypoxia, and Metabolism
  • Pancreatic and Hepatic Oncology Research
  • Autophagy in Disease and Therapy
  • Immune cells in cancer
  • interferon and immune responses
  • Neutrophil, Myeloperoxidase and Oxidative Mechanisms
  • Infective Endocarditis Diagnosis and Management
  • Epigenetics and DNA Methylation
  • Cancer Cells and Metastasis
  • Neuroinflammation and Neurodegeneration Mechanisms
  • Antifungal resistance and susceptibility
  • Developmental Biology and Gene Regulation
  • Estrogen and related hormone effects
  • Cancer-related molecular mechanisms research
  • NF-κB Signaling Pathways
  • Immune Response and Inflammation
  • Inflammasome and immune disorders
  • Adenosine and Purinergic Signaling

Hospital for Special Surgery
2017-2020

Icahn School of Medicine at Mount Sinai
2018

Université Côte d'Azur
2011-2014

Institut de Recherche sur le Cancer et le Vieillissement de Nice
2011-2014

Institute on Aging
2014

Fondation ARC pour la Recherche sur le Cancer
2012-2013

Inserm
2012

Invading bacteria are recognized, captured and killed by a specialized form of autophagy, called xenophagy. Recently, defects in xenophagy Crohn's disease (CD) have been implicated the pathogenesis human chronic inflammatory diseases uncertain etiology gastrointestinal tract. We show here that pathogenic adherent-invasive Escherichia coli (AIEC) isolated from CD patients able to adhere invade neutrophils, which represent first line defense against bacteria. Of particular interest, AIEC...

10.1371/journal.pone.0051727 article EN cc-by PLoS ONE 2012-12-14

Crohn disease (CD) ileal lesions are colonized by adherent-invasive E. coli (AIEC) that locally induce inflammation. Hypoxia inducible factor (HIF)-1alpha protein is expressed in acute and chronically inflamed site; however the molecular basis of this expression not fully understood. The aim study was to access whether AIEC HIF-1α consequence on onset pathogenesis. We show maximally epithelium CD-patients. CEACAM6, a acts as receptor AIEC, particular condition. Using CEABAC 10 transgenic...

10.4161/gmic.18771 article EN Gut Microbes 2011-11-01

The hypoxia inducible transcription factor HIF1 activates autophagy, a general catabolic pathway involved in the maintenance of cellular homeostasis. Dysfunction both autophagy and has been implicated an increasing number human diseases, including inflammatory bowel disease (IBD), such as Crohn (CD). Adherent invasive E. coli (AIEC) colonize ileal mucosa CD patients strongly promote gastrointestinal disorders by activation HIF-dependent responses. Here, we aim to characterize contribution...

10.4161/15548627.2014.984275 article EN Autophagy 2014-11-14

The glucocorticoid (GC) receptor (GR) suppresses inflammation by activating anti-inflammatory and repressing pro-inflammatory genes. GR-interacting protein-1 (GRIP1) is a GR corepressor in macrophages, however, whether GRIP1 mediates GR-activated transcription, what dictates its coactivator versus properties unknown. Here we report that loss macrophages attenuates induction of several targets, GC treatment quiescent globally directs toward binding sites dominated palindromic response...

10.1038/s41467-017-01569-2 article EN cc-by Nature Communications 2017-11-17

// David Dunkin 1, 2 , Alina C. Iuga 3 Sanda Mimouna 4, 5, 6 Carolyn L. Harris 6, 7 Jean-Vianney Haure-Mirande 8 Dominique Bozec 9, 10 Garabet Yeretssian 10, 11, *, ** and Stephanie Dahan 12, 1 Department of Pediatric Gastroenterology, Icahn School Medicine at Mount Sinai, New York, NY 10029, USA The Mindich Child Health Development Institute, Pathology Cell Biology, Columbia University Medical Center, 10032, 4 Precision Immunology 5 Autoimmunity Research Department, Hospital for Special...

10.18632/oncotarget.26086 article EN Oncotarget 2018-09-11

Macrophages (MФ) and microglia (MG) are critical in the pathogenesis of multiple sclerosis (MS) its mouse model, experimental autoimmune encephalomyelitis (EAE). Glucocorticoids (GCs) interferon β (IFN-β) frontline treatments for MS, disrupting each pathway mice aggravates EAE. Glucocorticoid receptor–interacting protein 1 (GRIP1) facilitates both GR type I IFN transcriptional actions; hence, we evaluated role GRIP1 neuroinflammation. Surprisingly, myeloid cell–specific loss dramatically...

10.1084/jem.20192386 article EN cc-by The Journal of Experimental Medicine 2020-10-12
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