Search Results - "Rashed, Fatema"

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    Adipose tissue expression of CCL19 chemokine is positively associated with insulin resistance by Kochumon, Shihab, Al‐Rashed, Fatema, Abu‐Farha, Mohamed, Devarajan, Sriraman, Tuomilehto, Jaakko, Ahmad, Rasheed

    Published in Diabetes/metabolism research and reviews (01-02-2019)
    “…Background Chemokines produced by adipose tissue (AT) are involved in the development of chronic low‐grade inflammation in obese humans and rodents. AT CCL19…”
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    Journal Article
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    TNFα induces matrix metalloproteinase-9 expression in monocytic cells through ACSL1/JNK/ERK/NF-kB signaling pathways by Al-Roub, Areej, Akhter, Nadeem, Al-Rashed, Fatema, Wilson, Ajit, Alzaid, Fawaz, Al-Mulla, Fahd, Sindhu, Sardar, Ahmad, Rasheed

    Published in Scientific reports (01-09-2023)
    “…Studies have established the association between increased plasma levels of matrix metalloproteinase (MMP)-9 and adipose tissue inflammation. Tumor necrosis…”
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    The arsenic bioremediation using genetically engineered microbial strains on aquatic environments: An updated overview by Naiel, Mohammed A.E., Taher, Ehab S., Rashed, Fatema, Ghazanfar, Shakira, Shehata, Abdelrazeq M., Mohammed, Nourelhuda A., Pascalau, Raul, Smuleac, Laura, Ibrahim, Ateya Megahed, Abdeen, Ahmed, Shukry, Mustafa

    Published in Heliyon (15-09-2024)
    “…Heavy metal contamination threatens the aquatic environment and human health. Different physical and chemical procedures have been adopted in many regions;…”
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    The role of TLR2 in exercise-induced immunomodulation in normal weight individuals by Bahman, Fatemah, AlSaeed, Halemah, Albeloushi, Shaima, Al-Mulla, Fahd, Ahmad, Rasheed, Al-Rashed, Fatema

    Published in Scientific reports (03-07-2023)
    “…Toll-like receptors (TLRs) have been targeted for therapeutic drug development for several disorders, including cardiovascular diseases (CVD), and diabetes…”
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    Aryl hydrocarbon receptor: current perspectives on key signaling partners and immunoregulatory role in inflammatory diseases by Bahman, Fatemah, Choudhry, Khubaib, Al-Rashed, Fatema, Al-Mulla, Fahd, Sindhu, Sardar, Ahmad, Rasheed

    Published in Frontiers in immunology (15-08-2024)
    “…The aryl hydrocarbon receptor (AhR) is a versatile environmental sensor and transcription factor found throughout the body, responding to a wide range of small…”
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    LPS Induces GM-CSF Production by Breast Cancer MDA-MB-231 Cells via Long-Chain Acyl-CoA Synthetase 1 by Al-Rashed, Fatema, Thomas, Reeby, Al-Roub, Areej, Al-Mulla, Fahd, Ahmad, Rasheed

    Published in Molecules (Basel, Switzerland) (14-10-2020)
    “…Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a monomeric glycoprotein that has been implicated in the tumor growth and progression of different…”
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    Ceramide kinase regulates TNF-α-induced immune responses in human monocytic cells by Al-Rashed, Fatema, Ahmad, Zunair, Snider, Ashley J., Thomas, Reeby, Kochumon, Shihab, Melhem, Motasem, Sindhu, Sardar, Obeid, Lina M., Al-Mulla, Fahd, Hannun, Yusuf A., Ahmad, Rasheed

    Published in Scientific reports (15-04-2021)
    “…Ceramide kinase (CERK) phosphorylates ceramide to produce ceramide-1-phosphate (C1P), which is involved in the development of metabolic inflammation. TNF-α…”
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    TNF-α Induces a Pro-Inflammatory Phenotypic Shift in Monocytes through ACSL1: Relevance to Metabolic Inflammation by Al-Rashed, Fatema, Ahmad, Zunair, Iskandar, Mina Amin, Tuomilehto, Jaakko, Al-Mulla, Fahd, Ahmad, Rasheed

    “…TNF-α-mediated pro-inflammatory phenotypic change in monocytes is known to be implicated in the pathogenesis of metabolic inflammation and insulin resistance…”
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    TNF-α/Stearate Induced H3K9/18 Histone Acetylation Amplifies IL-6 Expression in 3T3-L1 Mouse Adipocytes by Bahman, Fatemah, Al-Roub, Areej, Akhter, Nadeem, Al Madhoun, Ashraf, Wilson, Ajit, Almansour, Nourah, Al-Rashed, Fatema, Sindhu, Sardar, Al-Mulla, Fahd, Ahmad, Rasheed

    “…Extensive evidence supports the connection between obesity-induced inflammation and the heightened expression of IL-6 adipose tissues. However, the mechanism…”
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