Exploring the function of the JNK (c-Jun N-terminal kinase) signalling pathway in physiological and pathological processes to design novel therapeutic strategies
Published 2012 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Exploring the function of the JNK (c-Jun N-terminal kinase) signalling pathway in physiological and pathological processes to design novel therapeutic strategies
Authors
Keywords
-
Journal
BIOCHEMICAL SOCIETY TRANSACTIONS
Volume 40, Issue 1, Pages 85-89
Publisher
Portland Press Ltd.
Online
2012-01-19
DOI
10.1042/bst20110641
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Development of JNK2-Selective Peptide Inhibitors That Inhibit Breast Cancer Cell Migration
- (2011) Tamer S. Kaoud et al. ACS Chemical Biology
- Functional variant (−1304T>G) in the MKK4 promoter is associated with decreased risk of acute myeloid leukemia in a southern Chinese population
- (2011) Lan Jiang et al. CANCER SCIENCE
- RASSF7 negatively regulates pro-apoptotic JNK signaling by inhibiting the activity of phosphorylated-MKK7
- (2011) S Takahashi et al. CELL DEATH AND DIFFERENTIATION
- 7,3′,4′-Trihydroxyisoflavone, a Metabolite of the Soy Isoflavone Daidzein, Suppresses Ultraviolet B-induced Skin Cancer by Targeting Cot and MKK4
- (2011) Dong Eun Lee et al. JOURNAL OF BIOLOGICAL CHEMISTRY
- The Loss of c-Jun N-Terminal Protein Kinase Activity Prevents the Amyloidogenic Cleavage of Amyloid Precursor Protein and the Formation of Amyloid Plaques In Vivo
- (2011) S. Mazzitelli et al. JOURNAL OF NEUROSCIENCE
- Stress-Activated Protein Kinase MKK7 Regulates Axon Elongation in the Developing Cerebral Cortex
- (2011) T. Yamasaki et al. JOURNAL OF NEUROSCIENCE
- The stress kinase MKK7 couples oncogenic stress to p53 stability and tumor suppression
- (2011) Daniel Schramek et al. NATURE GENETICS
- Crystal structures of MKK4 kinase domain reveal that substrate peptide binds to an allosteric site and induces an auto-inhibition state
- (2010) Takashi Matsumoto et al. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
- Cyanidin suppresses ultraviolet B-induced COX-2 expression in epidermal cells by targeting MKK4, MEK1, and Raf-1
- (2010) Jong-Eun Kim et al. BIOCHEMICAL PHARMACOLOGY
- The Mitogen-Activated Protein Kinase Kinase 4 Has a Pro-Oncogenic Role in Skin Cancer
- (2010) K. G. Finegan et al. CANCER RESEARCH
- A functional variant (−1304T>G) in the MKK4 promoter contributes to a decreased risk of lung cancer by increasing the promoter activity
- (2010) Bin Liu et al. CARCINOGENESIS
- The Rac1/MKK7/JNK pathway signals upregulation of Atg5 and subsequent autophagic cell death in response to oncogenic Ras
- (2009) Joo-Yun Byun et al. CARCINOGENESIS
- Therapeutic peptides for cancer therapy. Part I – peptide inhibitors of signal transduction cascades
- (2009) Gene L Bidwell et al. Expert Opinion on Drug Delivery
- The association between −1304T>G polymorphism in the promoter ofMKK4gene and the risk of sporadic colorectal cancer in southern Chinese population
- (2009) Yisheng Wei et al. INTERNATIONAL JOURNAL OF CANCER
- c-Jun NH2-Terminal Kinase Activating Kinase 1/Mitogen-Activated Protein Kinase Kinase 4-Mediated Inhibition of SKOV3ip.1 Ovarian Cancer Metastasis Involves Growth Arrest and p21 Up-regulation
- (2008) T. Lotan et al. CANCER RESEARCH
- Proliferation of human HCC cells and chemically induced mouse liver cancers requires JNK1-dependent p21 downregulation
- (2008) Lijian Hui et al. JOURNAL OF CLINICAL INVESTIGATION
- Mitogen-Activated Protein Kinase Kinase 4/c-Jun NH2-Terminal Kinase Kinase 1 Protein Expression Is Subject to Translational Regulation in Prostate Cancer Cell Lines
- (2008) V. L. Robinson et al. MOLECULAR CANCER RESEARCH
Create your own webinar
Interested in hosting your own webinar? Check the schedule and propose your idea to the Peeref Content Team.
Create NowAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started