scispace - formally typeset
Journal ArticleDOI

Mitogen-Activated Protein Kinase Pathways Mediated by ERK, JNK, and p38 Protein Kinases

Gary L. Johnson, +1 more
- 06 Dec 2002 - 
- Vol. 298, Iss: 5600, pp 1911-1912
Reads0
Chats0
TLDR
Multicellular organisms have three well-characterized subfamilies of mitogen-activated protein kinases (MAPKs) that control a vast array of physiological processes, and inhibitors of these enzymes are being explored as anticancer agents.
Abstract
Multicellular organisms have three well-characterized subfamilies of mitogen-activated protein kinases (MAPKs) that control a vast array of physiological processes. These enzymes are regulated by a characteristic phosphorelay system in which a series of three protein kinases phosphorylate and activate one another. The extracellular signal-regulated kinases (ERKs) function in the control of cell division, and inhibitors of these enzymes are being explored as anticancer agents. The c-Jun amino-terminal kinases (JNKs) are critical regulators of transcription, and JNK inhibitors may be effective in control of rheumatoid arthritis. The p38 MAPKs are activated by inflammatory cytokines and environmental stresses and may contribute to diseases like asthma and autoimmunity.

read more

Citations
More filters
Journal ArticleDOI

Comprehensive molecular portraits of human breast tumours

Daniel C. Koboldt, +355 more
- 04 Oct 2012 - 
TL;DR: The ability to integrate information across platforms provided key insights into previously defined gene expression subtypes and demonstrated the existence of four main breast cancer classes when combining data from five platforms, each of which shows significant molecular heterogeneity.
Journal ArticleDOI

Cisplatin in cancer therapy: molecular mechanisms of action

TL;DR: This comprehensive review highlights the physicochemical properties of cisplatin and related platinum-based drugs, and discusses its uses (either alone or in combination with other drugs) for the treatment of various human cancers.
Journal ArticleDOI

The cancer genome

TL;DR: This work has shown that the complete DNA sequence of large numbers of cancer genomes will be possible to obtain and will provide a detailed and comprehensive perspective on how individual cancers have developed.
Journal ArticleDOI

Targeting the Raf-MEK-ERK mitogen-activated protein kinase cascade for the treatment of cancer.

TL;DR: The current status of the different approaches and targets that are under evaluation and development for the therapeutic intervention of this key signaling pathway in human disease are summarized.
Journal ArticleDOI

AP-1: a double-edged sword in tumorigenesis

TL;DR: This work focuses on the JUN and FOS proteins and aims to offer a new perspective on the molecular mechanisms that regulate the oncogenic and anti-oncogenic effects of AP-1 in tumour development.
References
More filters
Journal ArticleDOI

A protein kinase involved in the regulation of inflammatory cytokine biosynthesis.

TL;DR: Production of interleukin-1 and tumour necrosis factor from stimulated human monocytes is inhibited by a new series of pyridinyl-imidazole compounds, suggesting that the CSBPs are critical for cytokine production.
Journal ArticleDOI

Mitogen-Activated Protein Kinase: Conservation of a Three-Kinase Module From Yeast to Human

TL;DR: All known MAPK module kinases from yeast to humans are defined, what is known about their regulation, defined MAPK substrates, and the function of MAPK in cell physiology are defined.
Journal ArticleDOI

The stress-activated protein kinase subfamily of c-Jun kinases.

TL;DR: The kinase p54s are the principal c-Jun N-terminal kinases activated by cellular stress and tumour necrosis factor (TNF)-α, hence they are designated stress-activated protein kinases, or SAPKs.
Journal ArticleDOI

Requirement of JNK for Stress- Induced Activation of the Cytochrome c-Mediated Death Pathway

TL;DR: It is shown here that JNK is required for UV-induced apoptosis in primary murine embryonic fibroblasts, and data indicate that mitochondria are influenced by proapoptotic signal transduction through the JNK pathway.
Journal ArticleDOI

c-Jun N-terminal kinase is required for metalloproteinase expression and joint destruction in inflammatory arthritis

TL;DR: The novel JNK inhibitor SP600125 completely blocked IL-1--induced accumulation of phospho-Jun and induction of c-Jun transcription in synoviocytes and in joint arthritis, indicating that JNK is an important therapeutic target for RA.
Related Papers (5)