Advanced glycation end products increases matrix metalloproteinase-1, -3, and -13, and TNF-alpha in human osteoarthritic chondrocytes (Q38506314)

3 September 2017

Advanced glycation end products increases matrix metalloproteinase-1, -3, and -13, and TNF-alpha in human osteoarthritic chondrocytes (English)

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3 September 2017

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Seong-Su Nah

1

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3 September 2017

In-Young Choi

2

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3 September 2017

Bin Yoo

3

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3 September 2017

Yong Gil Kim

4

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3 September 2017

Hee-Bom Moon

5

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3 September 2017

Chang-Keun Lee

6

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3 September 2017

language of work or name

English

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publication date

9 April 2007

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3 September 2017

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3 September 2017

581

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3 September 2017

9

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3 September 2017

1928-1932

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https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

3 September 2017

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AGEing and osteoarthritis: a different perspective

21 January 2018

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https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Accumulation of advanced glycation end products as a molecular mechanism for aging as a risk factor in osteoarthritis

21 January 2018

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https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Crosslinking by advanced glycation end products increases the stiffness of the collagen network in human articular cartilage: a possible mechanism through which age is a risk factor for osteoarthritis

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Induction of advanced glycation end products and alterations of the tensile properties of articular cartilage

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Accumulation of advanced glycation end products decreases collagen turnover by bovine chondrocytes

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Articular chondrocytes express the receptor for advanced glycation end products: Potential role in osteoarthritis

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Activation of receptor for advanced glycation end products in osteoarthritis leads to increased stimulation of chondrocytes and synoviocytes

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Changes in the ratio of type-I and type-II collagen expression during monolayer culture of human chondrocytes.

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

The receptor for advanced glycation end-products (RAGE) directly binds to ERK by a D-domain-like docking site

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Requirement for p38 and p44/p42 mitogen-activated protein kinases in RAGE-mediated nuclear factor-kappaB transcriptional activation and cytokine secretion

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Amphoterin stimulates myogenesis and counteracts the antimyogenic factors basic fibroblast growth factor and S100B via RAGE binding

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Receptor for advanced glycation end products (RAGE)-mediated neurite outgrowth and activation of NF-kappaB require the cytoplasmic domain of the receptor but different downstream signaling pathways

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Role of receptor for advanced glycation end-product (RAGE) and the JAK/STAT-signaling pathway in AGE-induced collagen production in NRK-49F cells

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

Blockade of RAGE–amphoterin signalling suppresses tumour growth and metastases

21 January 2018

1 reference

https://api.crossref.org/works/10.1016%2FJ.FEBSLET.2007.03.090

10.1016/J.FEBSLET.2007.03.090

21 January 2018

Identifiers

DOI

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3 September 2017

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