Intracellular application of TNF-alpha impairs cell to cell communication via gap junctions in glioma cells (Q40095603)

17 September 2017

Intracellular application of TNF-alpha impairs cell to cell communication via gap junctions in glioma cells (English)

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17 September 2017

8

Rolf Dermietzel

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17 September 2017

Aiden Haghikia

1

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17 September 2017

Kerstin Ladage

2

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17 September 2017

Pauline Lafênetre

3

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17 September 2017

Arash Haghikia

4

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17 September 2017

Daniel Hinkerohe

5

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17 September 2017

Dirk Smikalla

6

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17 September 2017

Claus G Haase

7

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17 September 2017

Pedro M Faustmann

9

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17 September 2017

10 August 2007

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Journal of Neuro-Oncology

17 September 2017

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17 September 2017

86

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17 September 2017

2

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17 September 2017

143-152

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https://scigraph.springernature.com/pub.10.1007/s11060-007-9462-8

17 September 2017

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Turnover and phosphorylation dynamics of connexin43 gap junction protein in cultured cardiac myocytes.

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Mechanism of v-Src- and mitogen-activated protein kinase-induced reduction of gap junction communication.

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The p55 tumour necrosis factor receptor TNFR1 contains a trans-Golgi network localization signal in the C-terminal region of its cytoplasmic tail.

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Microglia activation influences dye coupling and Cx43 expression of the astrocytic network.

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Protein kinase C-zeta mediates TNF-alpha-induced ICAM-1 gene transcription in endothelial cells

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Direct gap junction communication between malignant glioma cells and astrocytes.

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Connexin 43 enhances the adhesivity and mediates the invasion of malignant glioma cells.

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IL-1beta differentially regulates calcium wave propagation between primary human fetal astrocytes via pathways involving P2 receptors and gap junction channels.

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Two homologous protein components of hepatic gap junctions.

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TNF recruits TRADD to the plasma membrane but not the trans-Golgi network, the principal subcellular location of TNF-R1

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Glucose metabolism and proliferation in glia: role of astrocytic gap junctions

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Soluble TNF-alpha receptors are constitutively shed and downregulate adhesion molecule expression in malignant gliomas.

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The death domain of tumor necrosis factor receptor 1 is necessary but not sufficient for Golgi retention of the receptor and mediates receptor desensitization

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Protein kinase C-zeta regulates transcription of the matrix metalloproteinase-9 gene induced by IL-1 and TNF-alpha in glioma cells via NF-kappa B

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12 December 2020

10.1007/S11060-007-9462-8

Identifiers

DOI

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Dimensions Publication ID

17 September 2017

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