Source: Molecular medicine reports [Mol Med Rep] 2021 Apr; Vol. 23 (4). Date of Electronic Publication: 2021 Jan 26.Publisher: D. A. Spandidos Country of Publication: Greece NLM ID: 101475259 Publication Model: Print-Electronic Cited Medium: Internet ISSN:

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Etidronate down-regulates Toll-like receptor 2 ligand-induced chemokine production by inhibiting MyD88 expression and NF-κB activation.

Authors : Yambe N; Department of Infectious Diseases, Ohu University Graduate School of Dentistry, Koriyama, Japan.; Tamai R

Subjects: Bone Density Conservation Agents/Bone Density Conservation Agents/Bone Density Conservation Agents/*pharmacology ; Chemokines/Chemokines/Chemokines/*antagonists & inhibitors ; Etidronic Acid/Etidronic Acid/Etidronic Acid/*pharmacology

Source: Immunopharmacology and immunotoxicology [Immunopharmacol Immunotoxicol] 2021 Feb; Vol. 43 (1), pp. 51-57. Date of Electronic Publication: 2020 Nov 29.Publisher: Informa Healthcare Country of Publication: England NLM ID: 8800150 Publication Model: Print-Electronic Cited Medium: Internet ISSN:

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Mycobacterium indicus pranii therapy induces tumor regression in MyD88- and TLR2-dependent manner.

Authors : Kumar P; PDC-I, National Institute of Immunology, Aruna Asaf Ali Marg, New Delhi, 110067, India.; Dept. of Preventive Oncology, Dr. B. R. Ambedkar Cancer Hospital, All India Institute of Medical Sciences, Ansari Nagar, New Delhi, 110029, India.

Subjects: Melanoma, Experimental/Melanoma, Experimental/Melanoma, Experimental/*immunology ; Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/*immunology ; Nontuberculous Mycobacteria/Nontuberculous Mycobacteria/Nontuberculous Mycobacteria/*immunology

Source: BMC research notes [BMC Res Notes] 2019 Oct 07; Vol. 12 (1), pp. 648. Date of Electronic Publication: 2019 Oct 07.Publisher: Biomed Central Country of Publication: England NLM ID: 101462768 Publication Model: Electronic Cited Medium: Internet ISSN: 1756-0500

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TLR3-Dependent Activation of TLR2 Endogenous Ligands via the MyD88 Signaling Pathway Augments the Innate Immune Response.

Authors : Teixeira HS; Department of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, PA 19004, USA.; Zhao J

Subjects: Immunity, Innate*; Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/*metabolism ; Signal Transduction/Signal Transduction/Signal Transduction/*genetics

Source: Cells [Cells] 2020 Aug 17; Vol. 9 (8). Date of Electronic Publication: 2020 Aug 17.Publisher: MDPI Country of Publication: Switzerland NLM ID: 101600052 Publication Model: Electronic Cited Medium: Internet ISSN: 2073-4409

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TLR-2, TLR-4 and MyD88 genes expression in renal transplant acute and chronic rejections.

Authors : Sharbafi MH; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.; Assadiasl S

Subjects: Kidney Transplantation*; Graft Rejection/Graft Rejection/Graft Rejection/*metabolism ; Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/*metabolism

Source: International journal of immunogenetics [Int J Immunogenet] 2019 Dec; Vol. 46 (6), pp. 427-436. Date of Electronic Publication: 2019 Jul 09.Publisher: Blackwell Pub Country of Publication: England NLM ID: 101232337 Publication Model: Print-Electronic Cited Medium: Internet ISSN:

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MyD88 Signaling Accompanied by Microbiota Changes Supports Urinary Bladder Carcinogenesis.

Authors : Knezović, Dora¹ (AUTHOR) ; Milić Roje, Blanka¹ (AUTHOR) ; Vilović, Katarina² (AUTHOR)

Subjects: *MYELOID differentiation factor 88; *BACILLUS (Bacteria); *BCG immunotherapy

Source: International Journal of Molecular Sciences. Jul2024, Vol. 25 Issue 13, p7176. 16p.

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Enhanced IL-1β production is mediated by a TLR2-MYD88-NLRP3 signaling axis during coinfection with influenza A virus and Streptococcus pneumoniae.

Authors : Rodriguez AE; Department of Biology, Missouri State University, Springfield, Missouri, United States of America.; Bogart C

Subjects: Coinfection/Coinfection/Coinfection/*immunology ; Influenza A Virus, H1N1 Subtype/Influenza A Virus, H1N1 Subtype/Influenza A Virus, H1N1 Subtype/*immunology ; Interleukin-1beta/Interleukin-1beta/Interleukin-1beta/*immunology

Source: PloS one [PLoS One] 2019 Feb 22; Vol. 14 (2), pp. e0212236. Date of Electronic Publication: 2019 Feb 22 (Print Publication: 2019).Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet

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Candida albicans induces TLR2/MyD88/NF-κB signaling and inflammation in oral lichen planus-derived keratinocytes.

Authors : Liu J; Shandong University Affilicated Qilu Hospital, Jinan, Shandong, China. .; Geng F

Subjects: Candida albicans/Candida albicans/Candida albicans/*pathogenicity ; Keratinocytes/Keratinocytes/Keratinocytes/*microbiology ; Lichen Planus, Oral/Lichen Planus, Oral/Lichen Planus, Oral/*pathology

Source: Journal of infection in developing countries [J Infect Dev Ctries] 2018 Sep 30; Vol. 12 (9), pp. 780-786. Date of Electronic Publication: 2018 Sep 30.Publisher: Open Learning on Enteric Pathogens Country of Publication: Italy NLM ID: 101305410 Publication Model: Electronic Cited Medium: Internet

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Macrophage cytokine responses to commensal Gram-positive Lactobacillus salivarius strains are TLR2-independent and Myd88-dependent.

Authors : Udayan S; APC Microbiome Ireland, University College Cork, Cork, Ireland.; School of Biochemistry and Cell Biology, University College Cork, Cork, Ireland.

Subjects: Cytokines/Cytokines/Cytokines/*metabolism ; Ligilactobacillus salivarius/Ligilactobacillus salivarius/Ligilactobacillus salivarius/*physiology ; Macrophages/Macrophages/Macrophages/*metabolism

Source: Scientific reports [Sci Rep] 2021 Mar 15; Vol. 11 (1), pp. 5896. Date of Electronic Publication: 2021 Mar 15.Publisher: Nature Publishing Group Country of Publication: England NLM ID: 101563288 Publication Model: Electronic Cited Medium: Internet ISSN:

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Investigation of interactions between TLR2, MyD88 and TIRAP by bioluminescence resonance energy transfer is hampered by artefacts of protein overexpression.

Authors : Sampaio NG; Population Health and Immunity Division, Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia.; Department of Medical Biology, University of Melbourne, Parkville, Victoria, Australia.

Subjects: Lipopeptides/Lipopeptides/Lipopeptides/*pharmacology ; Membrane Glycoproteins/Membrane Glycoproteins/Membrane Glycoproteins/*metabolism ; Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/Myeloid Differentiation Factor 88/*metabolism

Source: PloS one [PLoS One] 2018 Aug 23; Vol. 13 (8), pp. e0202408. Date of Electronic Publication: 2018 Aug 23 (Print Publication: 2018).Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet

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نتائج البحث

فلترة النتائج

Involvement of TLR2/4‑MyD88‑NF‑κB signaling pathway in the pathogenesis of intracranial aneurysm.

Etidronate down-regulates Toll-like receptor 2 ligand-induced chemokine production by inhibiting MyD88 expression and NF-κB activation.

Mycobacterium indicus pranii therapy induces tumor regression in MyD88- and TLR2-dependent manner.

TLR3-Dependent Activation of TLR2 Endogenous Ligands via the MyD88 Signaling Pathway Augments the Innate Immune Response.

TLR-2, TLR-4 and MyD88 genes expression in renal transplant acute and chronic rejections.

MyD88 Signaling Accompanied by Microbiota Changes Supports Urinary Bladder Carcinogenesis.

Enhanced IL-1β production is mediated by a TLR2-MYD88-NLRP3 signaling axis during coinfection with influenza A virus and Streptococcus pneumoniae.

Candida albicans induces TLR2/MyD88/NF-κB signaling and inflammation in oral lichen planus-derived keratinocytes.

Macrophage cytokine responses to commensal Gram-positive Lactobacillus salivarius strains are TLR2-independent and Myd88-dependent.

Investigation of interactions between TLR2, MyD88 and TIRAP by bioluminescence resonance energy transfer is hampered by artefacts of protein overexpression.

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