Human U87 glioblastoma cells with stemness features display enhanced sensitivity to natural killer cell cytotoxicity through altered expression of NKG2D ligand

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Location: Deutsche Nationalbibliothek Frankfurt am Main

ISSN: 1475-2867

Extent: Online-Ressource

Language: Englisch

Notes: online resource.

Bibliographic citation: Human U87 glioblastoma cells with stemness features display enhanced sensitivity to natural killer cell cytotoxicity through altered expression of NKG2D ligand ; volume:17 ; number:1 ; day:10 ; month:2 ; year:2017 ; pages:1-9 ; date:12.2017
Cancer cell international ; 17, Heft 1 (10.2.2017), 1-9, 12.2017

Keyword: Krebs
Onkologie

Creator: Oh, Se-Jeong

Contributor: Yang, Jung-In
Kim, Ok
Ahn, Eun-Jung
Kang, Woo Dae
Lee, Jae-Hyuk
Moon, Kyung-Sub
Lee, Kyung-Hwa
Cho, Duck
SpringerLink (Online service)

DOI: 10.1186/s12935-017-0397-7

URN: urn:nbn:de:1111-2017030525706

Rights: Der Zugriff auf das Objekt ist unbeschränkt möglich.

Last update: 14.08.2025, 10:47 AM CEST

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Associated

Oh, Se-Jeong
Yang, Jung-In
Kim, Ok
Ahn, Eun-Jung
Kang, Woo Dae
Lee, Jae-Hyuk
Moon, Kyung-Sub
Lee, Kyung-Hwa
Cho, Duck
SpringerLink (Online service)

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Proteolytic shedding of NKG2D ligands from tumour cells : = Proteolytische Freisetzung von NKG2D-Liganden durch Tumorzellen

Modified dendritic cell-derived exosomes activate both NK cells and T cells through the NKG2D/NKG2D-L pathway to kill CML cells with or without T315I mutation

Cervical cancer cell lines expressing NKG2D-ligands are able to down-modulate the NKG2D receptor on NKL cells with functional implications

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Targeting senescent cells with NKG2D-CAR T cells

Aporphine and isoquinoline derivatives block glioblastoma cell stemness and enhance temozolomide cytotoxicity

Inosine pranobex enhances human NK cell cytotoxicity by inducing metabolic activation and NKG2D ligand expression

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Tumor cell lysis and synergistically enhanced antibody-dependent cell-mediated cytotoxicity by NKG2D engagement with a bispecific immunoligand targeting the HER2 antigen

Autophagic control of cell ‘stemness’

Hochschulschrift

Proteolytic shedding of NKG2D ligands from tumour cells : = Proteolytische Freisetzung von NKG2D-Liganden durch Tumorzellen

Modified dendritic cell-derived exosomes activate both NK cells and T cells through the NKG2D/NKG2D-L pathway to kill CML cells with or without T315I mutation

Cervical cancer cell lines expressing NKG2D-ligands are able to down-modulate the NKG2D receptor on NKL cells with functional implications

Protein quality control of cell stemness

Neural stemness contributes to cell tumorigenicity

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Human U87 glioblastoma cells with stemness features display enhanced sensitivity to natural killer cell cytotoxicity through altered expression of NKG2D ligand

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Other Objects (12)

TLR8 agonist VTX-2337 enhances NKG2D-mediated cytotoxicity of NK cells

Targeting senescent cells with NKG2D-CAR T cells

Aporphine and isoquinoline derivatives block glioblastoma cell stemness and enhance temozolomide cytotoxicity

Inosine pranobex enhances human NK cell cytotoxicity by inducing metabolic activation and NKG2D ligand expression

Tumour stromal cells derived from paediatric malignancies display MSC-like properties and impair NK cell cytotoxicity

Tumor cell lysis and synergistically enhanced antibody-dependent cell-mediated cytotoxicity by NKG2D engagement with a bispecific immunoligand targeting the HER2 antigen

Autophagic control of cell ‘stemness’

Proteolytic shedding of NKG2D ligands from tumour cells : = Proteolytische Freisetzung von NKG2D-Liganden durch Tumorzellen

Modified dendritic cell-derived exosomes activate both NK cells and T cells through the NKG2D/NKG2D-L pathway to kill CML cells with or without T315I mutation

Cervical cancer cell lines expressing NKG2D-ligands are able to down-modulate the NKG2D receptor on NKL cells with functional implications

Protein quality control of cell stemness

Neural stemness contributes to cell tumorigenicity

TLR8 agonist VTX-2337 enhances NKG2D-mediated cytotoxicity of NK cells

Targeting senescent cells with NKG2D-CAR T cells

Aporphine and isoquinoline derivatives block glioblastoma cell stemness and enhance temozolomide cytotoxicity

Inosine pranobex enhances human NK cell cytotoxicity by inducing metabolic activation and NKG2D ligand expression

Tumour stromal cells derived from paediatric malignancies display MSC-like properties and impair NK cell cytotoxicity

Tumor cell lysis and synergistically enhanced antibody-dependent cell-mediated cytotoxicity by NKG2D engagement with a bispecific immunoligand targeting the HER2 antigen

Autophagic control of cell ‘stemness’

Proteolytic shedding of NKG2D ligands from tumour cells : = Proteolytische Freisetzung von NKG2D-Liganden durch Tumorzellen

Modified dendritic cell-derived exosomes activate both NK cells and T cells through the NKG2D/NKG2D-L pathway to kill CML cells with or without T315I mutation

Cervical cancer cell lines expressing NKG2D-ligands are able to down-modulate the NKG2D receptor on NKL cells with functional implications

Protein quality control of cell stemness

Neural stemness contributes to cell tumorigenicity

TLR8 agonist VTX-2337 enhances NKG2D-mediated cytotoxicity of NK cells

Targeting senescent cells with NKG2D-CAR T cells

Aporphine and isoquinoline derivatives block glioblastoma cell stemness and enhance temozolomide cytotoxicity

Inosine pranobex enhances human NK cell cytotoxicity by inducing metabolic activation and NKG2D ligand expression

Tumour stromal cells derived from paediatric malignancies display MSC-like properties and impair NK cell cytotoxicity

Tumor cell lysis and synergistically enhanced antibody-dependent cell-mediated cytotoxicity by NKG2D engagement with a bispecific immunoligand targeting the HER2 antigen

Autophagic control of cell ‘stemness’

Proteolytic shedding of NKG2D ligands from tumour cells : = Proteolytische Freisetzung von NKG2D-Liganden durch Tumorzellen

Modified dendritic cell-derived exosomes activate both NK cells and T cells through the NKG2D/NKG2D-L pathway to kill CML cells with or without T315I mutation

Cervical cancer cell lines expressing NKG2D-ligands are able to down-modulate the NKG2D receptor on NKL cells with functional implications

Protein quality control of cell stemness

Neural stemness contributes to cell tumorigenicity

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