Keratinocyte-specific deletion of the receptor RAGE modulates the kinetics of skin inflammation in vivo (Q34675470)

3 August 2017

title

Keratinocyte-specific deletion of the receptor RAGE modulates the kinetics of skin inflammation in vivo (English)

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3 August 2017

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Julia S Leibold

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3 August 2017

Astrid Riehl

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3 August 2017

Jan Hettinger

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3 August 2017

Michael Durben

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3 August 2017

Jochen Hess

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3 August 2017

Peter Angel

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3 August 2017

language of work or name

English

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publication date

17 April 2013

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Journal of Investigative Dermatology

3 August 2017

published in

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3 August 2017

volume

133

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3 August 2017

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3 August 2017

page(s)

2400-2406

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RAGE: a multi-ligand receptor unveiling novel insights in health and disease

3 August 2017

cites work

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S100P-derived RAGE antagonistic peptide reduces tumor growth and metastasis

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S100B/RAGE-dependent activation of microglia via NF-kappaB and AP-1 Co-regulation of COX-2 expression by S100B, IL-1beta and TNF-alpha

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Bench-to-bedside review: The inflammation-perpetuating pattern-recognition receptor RAGE as a therapeutic target in sepsis

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RAGE (receptor for advanced glycation end products): a central player in the inflammatory response

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Blockade of late stages of autoimmune diabetes by inhibition of the receptor for advanced glycation end products

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RAGE and ICAM-1 differentially control leukocyte recruitment during acute inflammation in a stimulus-dependent manner

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RAGE signaling sustains inflammation and promotes tumor development

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RAGE mediates a novel proinflammatory axis: a central cell surface receptor for S100/calgranulin polypeptides

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beta-Catenin controls hair follicle morphogenesis and stem cell differentiation in the skin

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Advanced glycation end products-induced apoptosis attenuated by PPARdelta activation and epigallocatechin gallate through NF-kappaB pathway in human embryonic kidney cells and human mesangial cells.

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Receptor for advanced glycation end products (RAGE) regulates sepsis but not the adaptive immune response

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7 January 2021

Effects of filaggrin breakdown products on the growth and maturation of keratinocytes

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TNF-alpha inhibits macrophage clearance of apoptotic cells via cytosolic phospholipase A2 and oxidant-dependent mechanisms

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The receptor for advanced glycation end products (RAGE) is a central mediator of the interaction of AGE-beta2microglobulin with human mononuclear phagocytes via an oxidant-sensitive pathway. Implications for the pathogenesis of dialysis-related amyl

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The role of reactive oxygen species in TNFalpha-dependent expression of the receptor for advanced glycation end products in human umbilical vein endothelial cells

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Receptor for AGE (RAGE): signaling mechanisms in the pathogenesis of diabetes and its complications

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Identification of the Rage-dependent gene regulatory network in a mouse model of skin inflammation

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7 January 2021

The mouse keratin 6 isoforms are differentially expressed in the hair follicle, footpad, tongue and activated epidermis

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7 January 2021

The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses

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Phagocyte partnership during the onset and resolution of inflammation.

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The receptor for advanced glycation end products is induced by the glycation products themselves and tumor necrosis factor-alpha through nuclear factor-kappa B, and by 17beta-estradiol through Sp-1 in human vascular endothelial cells

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RAGE, carboxylated glycans and S100A8/A9 play essential roles in colitis-associated carcinogenesis

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The pathophysiology of tumor necrosis factors

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Gene from a psoriasis susceptibility locus primes the skin for inflammation

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7 January 2021

Dermal injection of immunocytes induces psoriasis

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7 January 2021

Identifiers

DOI

10.1038/JID.2013.185

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Dimensions Publication ID

3 August 2017

1033874474

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