Specific regulation of JNK signalling by the novel rat MKK7gamma1 isoform

Cellular Signalling
Wiebke HaeusgenVicki Waetzig

Abstract

The c-Jun N-terminal kinases (JNKs) mediate a diversity of physiological and pathophysiological effects. Apart from isoform-specific JNK activation, upstream kinases are supposed to be the relevant regulators, which are involved in the context- and signalosome-depending functions. In the present study we report the cloning and characterization of the novel rat MKK7gamma1, a splice variant of MKK7 with an additional exon in the N-terminal region, in the neuronal pheochromocytoma cell line PC12. Transfected MKK7gamma1 increased basal JNK activity, in particular phosphorylation of JNK2. Consequently, JNK signalling was changed in mRNA-, protein- and activation-levels of JNK targets, such as transcription factors (c-Jun, p53, c-Myc), cell cycle regulators (p21, CyclinD1) and apoptotic proteins (Fas, Bim, Bcl-2, Bcl-xl). These alterations promote the sensitivity of MKK7gamma1-transfected cells towards cell death and repress cell proliferation under normal cell growth conditions. Complexes of JIP-1, MKK7 and JNK2 were the major JNK signalosomes under basal conditions. After stimulation with taxol (5muM) and tunicamycin (1.4mug/ml), MKK7gamma1- but not MKK7beta1-transfection, reduced cell death and even increased cell proliferation. C...Continue Reading

References

May 1, 1996·European Journal of Immunology·D J WilsonR C Budd
Mar 4, 1997·Proceedings of the National Academy of Sciences of the United States of America·V AdlerZ Ronai
Jul 8, 1997·Proceedings of the National Academy of Sciences of the United States of America·C TournierR J Davis
Oct 6, 1997·The Journal of Biological Chemistry·P M HollandJ A Cooper
Jan 31, 1998·The EMBO Journal·T MoriguchiE Nishida
Apr 30, 1998·Current Opinion in Cell Biology·Y T Ip, R J Davis
Jan 16, 1999·Current Biology : CB·S LawlerP Cohen
Jan 16, 1999·Molecular and Cellular Biology·C TournierR J Davis
Jan 5, 2000·The Journal of Biological Chemistry·S KharbandaD Kufe
Jan 29, 2000·Brain Research. Molecular Brain Research·K MielkeT Herdegen
Apr 27, 2001·The Journal of Biological Chemistry·X DengW S May
Jun 12, 2002·The Journal of Biological Chemistry·Geum-Yi KimEileen Friedman
Oct 29, 2002·The Journal of Biological Chemistry·Vicki Waetzig, Thomas Herdegen
Feb 20, 2003·Proceedings of the National Academy of Sciences of the United States of America·Kui Lei, Roger J Davis
Jun 24, 2003·Neuron·Girish V PutchaEugene M Johnson
Aug 2, 2003·Genes & Development·Deborah BranchoRoger J Davis
Mar 25, 2004·Nature Cell Biology·Teiji WadaJosef M Penninger
Sep 18, 2004·Proceedings of the National Academy of Sciences of the United States of America·Claire R WestonRoger J Davis
May 19, 2005·Cancer Research·Andrei L Gartel, Senthil K Radhakrishnan
Jan 31, 2006·Biochemical and Biophysical Research Communications·Laura MichaelMegan J Robinson

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Citations

Feb 23, 2013·Behavioural Brain Research·Kirstin ReineckeThomas Schiffelholz
Mar 20, 2012·PloS One·Kirstin ReineckeChristian Sina
Mar 6, 2012·Journal of Cardiac Failure·Olena AndrukhovaSeyedhossein Aharinejad
Feb 9, 2018·Cell Biology International·Xiao-Xi GuoTian-Rui Xu

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