Literature DB >> 17538955

The functional contrariety of JNK.

Ann M Bode1, Zigang Dong.   

Abstract

The JNK proteins are activated by multiple and diverse stimuli, leading to varied and seemingly contradictory cellular responses. In particular, JNKs have been reported to have a role in the induction of apoptosis, but have also been implicated in enhancing cell survival and proliferation. Thus the JNK proteins seem to represent an archetype of contrariety of intracellular signaling. The opposing roles of JNKs have been attributed to the observation that JNKs activate different substrates based on specific stimulus, cell type or temporal aspects. Because of their analogous expression in apparently almost every tissue, JNK1 and JNK2 have most often been considered to have overlapping or redundant functions. In spite of this assessment, research evidence suggests that the functions of JNKs should be addressed in a manner that differentiates between their precise contributions. Specifically in this review, we examine evidence regarding whether the JNKs proteins might play distinctive roles in cellular processes associated with carcinogenesis.

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Year:  2007        PMID: 17538955      PMCID: PMC2832829          DOI: 10.1002/mc.20348

Source DB:  PubMed          Journal:  Mol Carcinog        ISSN: 0899-1987            Impact factor:   4.784


  66 in total

1.  A nuclear tyrosine phosphorylation circuit: c-Jun as an activator and substrate of c-Abl and JNK.

Authors:  D Barilá; R Mangano; S Gonfloni; J Kretzschmar; M Moro; D Bohmann; G Superti-Furga
Journal:  EMBO J       Date:  2000-01-17       Impact factor: 11.598

2.  Selective interaction of JNK protein kinase isoforms with transcription factors.

Authors:  S Gupta; T Barrett; A J Whitmarsh; J Cavanagh; H K Sluss; B Dérijard; R J Davis
Journal:  EMBO J       Date:  1996-06-03       Impact factor: 11.598

3.  Cell apoptosis: requirement of H2AX in DNA ladder formation, but not for the activation of caspase-3.

Authors:  Chengrong Lu; Feng Zhu; Yong-Yeon Cho; Faqing Tang; Tatyana Zykova; Wei-ya Ma; Ann M Bode; Zigang Dong
Journal:  Mol Cell       Date:  2006-07-07       Impact factor: 17.970

4.  Regulation of c-Myc through phosphorylation at Ser-62 and Ser-71 by c-Jun N-terminal kinase.

Authors:  K Noguchi; C Kitanaka; H Yamana; A Kokubu; T Mochizuki; Y Kuchino
Journal:  J Biol Chem       Date:  1999-11-12       Impact factor: 5.157

5.  A dominant role for the c-Jun NH2-terminal kinase in oncogenic ras-induced morphologic transformation of human lung carcinoma cells.

Authors:  L Xiao; W Lang
Journal:  Cancer Res       Date:  2000-01-15       Impact factor: 12.701

6.  Inhibition of c-Jun N-terminal kinase 2 expression suppresses growth and induces apoptosis of human tumor cells in a p53-dependent manner.

Authors:  O Potapova; M Gorospe; R H Dougherty; N M Dean; W A Gaarde; N J Holbrook
Journal:  Mol Cell Biol       Date:  2000-03       Impact factor: 4.272

7.  Blocking of tumor promoter-induced AP-1 activity inhibits induced transformation in JB6 mouse epidermal cells.

Authors:  Z Dong; M J Birrer; R G Watts; L M Matrisian; N H Colburn
Journal:  Proc Natl Acad Sci U S A       Date:  1994-01-18       Impact factor: 11.205

8.  JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins.

Authors:  Fuminori Tsuruta; Jun Sunayama; Yasunori Mori; Seisuke Hattori; Shigeomi Shimizu; Yoshihide Tsujimoto; Katsuji Yoshioka; Norihisa Masuyama; Yukiko Gotoh
Journal:  EMBO J       Date:  2004-04-08       Impact factor: 11.598

9.  Inhibition of cell proliferation and cell cycle progression by specific inhibition of basal JNK activity: evidence that mitotic Bcl-2 phosphorylation is JNK-independent.

Authors:  Lihua Du; Christopher S Lyle; Toria B Obey; William A Gaarde; Jeffrey A Muir; Brydon L Bennett; Timothy C Chambers
Journal:  J Biol Chem       Date:  2004-01-02       Impact factor: 5.157

10.  JNK2 is a positive regulator of the cJun transcription factor.

Authors:  Anja Jaeschke; Maria Karasarides; Juan-Jose Ventura; Anka Ehrhardt; Chao Zhang; Richard A Flavell; Kevan M Shokat; Roger J Davis
Journal:  Mol Cell       Date:  2006-09-15       Impact factor: 17.970

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  106 in total

1.  2-Phenyl-5-(pyrrolidin-1-yl)-1-(3,4,5-trimethoxybenzyl)-1H-benzimidazole, a benzimidazole derivative, inhibits growth of human prostate cancer cells by affecting tubulin and c-Jun N-terminal kinase.

Authors:  Wei-Ling Chang; Chih-Shiang Chang; Po-Cheng Chiang; Yunn-Fang Ho; Ju-Fang Liu; Kai-Wei Chang; Jih-Hwa Guh
Journal:  Br J Pharmacol       Date:  2010-08       Impact factor: 8.739

2.  Measuring the constitutive activation of c-Jun N-terminal kinase isoforms.

Authors:  Ryan T Nitta; Shawn S Badal; Albert J Wong
Journal:  Methods Enzymol       Date:  2010       Impact factor: 1.600

3.  The role of the c-Jun N-terminal kinase 2-α-isoform in non-small cell lung carcinoma tumorigenesis.

Authors:  R T Nitta; C A Del Vecchio; A H Chu; S S Mitra; A K Godwin; A J Wong
Journal:  Oncogene       Date:  2010-09-27       Impact factor: 9.867

4.  Reversibility of regorafenib effects in hepatocellular carcinoma cells.

Authors:  Rosalba D'Alessandro; Maria G Refolo; Catia Lippolis; Caterina Messa; Aldo Cavallini; Roberta Rossi; Leonardo Resta; Antonio Di Carlo; Brian I Carr
Journal:  Cancer Chemother Pharmacol       Date:  2013-10       Impact factor: 3.333

5.  ACh receptors link two signaling pathways to neuroprotection against glutamate-induced excitotoxicity in isolated RGCs.

Authors:  Chinwe O Asomugha; David M Linn; Cindy L Linn
Journal:  J Neurochem       Date:  2009-10-21       Impact factor: 5.372

6.  New insights into oncogenic stress.

Authors:  Kevin M Haigis; Alejandro Sweet-Cordero
Journal:  Nat Genet       Date:  2011-03       Impact factor: 38.330

7.  c-Jun N-terminal kinase is required for thermotherapy-induced apoptosis in human gastric cancer cells.

Authors:  Feng Xiao; Bin Liu; Qing-Xian Zhu
Journal:  World J Gastroenterol       Date:  2012-12-28       Impact factor: 5.742

8.  JNK-mediated phosphorylation of paxillin in adhesion assembly and tension-induced cell death by the adenovirus death factor E4orf4.

Authors:  Nicolas Smadja-Lamère; Marie-Chloé Boulanger; Claudia Champagne; Philip E Branton; Josée N Lavoie
Journal:  J Biol Chem       Date:  2008-09-25       Impact factor: 5.157

9.  10-formyltetrahydrofolate dehydrogenase-induced c-Jun-NH2-kinase pathways diverge at the c-Jun-NH2-kinase substrate level in cells with different p53 status.

Authors:  Sampa Ghose; Natalia V Oleinik; Natalia I Krupenko; Sergey A Krupenko
Journal:  Mol Cancer Res       Date:  2009-01       Impact factor: 5.852

10.  Interactions between cells with distinct mutations in c-MYC and Pten in prostate cancer.

Authors:  Jongchan Kim; Isam-Eldin A Eltoum; Meejeon Roh; Jie Wang; Sarki A Abdulkadir
Journal:  PLoS Genet       Date:  2009-07-03       Impact factor: 5.917

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