Expression and significance of the TLR4/MyD88 signaling pathway in ovarian epithelial cancers
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- ISSN
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1477-7819
- Extent
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Online-Ressource
- Language
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Englisch
- Notes
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online resource.
- Bibliographic citation
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Expression and significance of the TLR4/MyD88 signaling pathway in ovarian epithelial cancers ; volume:10 ; number:1 ; day:17 ; month:9 ; year:2012 ; pages:1-8 ; date:12.2012
World journal of surgical oncology ; 10, Heft 1 (17.9.2012), 1-8, 12.2012
- Creator
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Kim, Ki Hyung
Jo, Moo Sung
Suh, Dong Soo
Yoon, Man Soo
Shin, Dong Hun
Lee, Jeong Hee
Choi, Kyung Un
- Contributor
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SpringerLink (Online service)
- DOI
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10.1186/1477-7819-10-193
- URN
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urn:nbn:de:101:1-2021082906555977870893
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:19 AM CEST
Data provider
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Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Kim, Ki Hyung
- Jo, Moo Sung
- Suh, Dong Soo
- Yoon, Man Soo
- Shin, Dong Hun
- Lee, Jeong Hee
- Choi, Kyung Un
- SpringerLink (Online service)
Other Objects (12)
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Atractylenolide I modulates ovarian cancer cell-mediated immunosuppression by blocking MD-2/TLR4 complex-mediated MyD88/NF-κB signaling in vitro
Melatonin attenuates the TLR4-mediated inflammatory response through MyD88- and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer
Cryptotanshinone from Salvia miltiorrhiza Bunge (Danshen) inhibited inflammatory responses via TLR4/MyD88 signaling pathway
Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage
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Suppression of TLR4-MyD88 signaling pathway attenuated chronic mechanical pain in a rat model of endometriosis
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The TLR4-MyD88-NF-κB pathway is involved in sIgA-mediated IgA nephropathy
MiR-5195-3p predicts clinical prognosis and represses colorectal cancer progression by targeting TLR4/MyD88 signaling
Prognostic significance of MyD88 expression by human epithelial ovarian carcinoma cells
HPV-transformed cells exhibit altered HMGB1-TLR4/MyD88-SARM1 signaling axis
Hereditary Ovarian Cancers
Atractylenolide I modulates ovarian cancer cell-mediated immunosuppression by blocking MD-2/TLR4 complex-mediated MyD88/NF-κB signaling in vitro
Melatonin attenuates the TLR4-mediated inflammatory response through MyD88- and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer
Cryptotanshinone from Salvia miltiorrhiza Bunge (Danshen) inhibited inflammatory responses via TLR4/MyD88 signaling pathway
Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage
Other Gynecologic Cancers: endometrial, ovarian, vulvar and vaginal cancers
Suppression of TLR4-MyD88 signaling pathway attenuated chronic mechanical pain in a rat model of endometriosis
Stadtjubiläum Akademie D88
The TLR4-MyD88-NF-κB pathway is involved in sIgA-mediated IgA nephropathy
MiR-5195-3p predicts clinical prognosis and represses colorectal cancer progression by targeting TLR4/MyD88 signaling
Prognostic significance of MyD88 expression by human epithelial ovarian carcinoma cells
HPV-transformed cells exhibit altered HMGB1-TLR4/MyD88-SARM1 signaling axis
Hereditary Ovarian Cancers
Atractylenolide I modulates ovarian cancer cell-mediated immunosuppression by blocking MD-2/TLR4 complex-mediated MyD88/NF-κB signaling in vitro
Melatonin attenuates the TLR4-mediated inflammatory response through MyD88- and TRIF-dependent signaling pathways in an in vivo model of ovarian cancer
Cryptotanshinone from Salvia miltiorrhiza Bunge (Danshen) inhibited inflammatory responses via TLR4/MyD88 signaling pathway
Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage
Other Gynecologic Cancers: endometrial, ovarian, vulvar and vaginal cancers
Suppression of TLR4-MyD88 signaling pathway attenuated chronic mechanical pain in a rat model of endometriosis
Stadtjubiläum Akademie D88
The TLR4-MyD88-NF-κB pathway is involved in sIgA-mediated IgA nephropathy