scholarly journals Stress kinases in the regulation of inter-organ communication in obesity comorbidities

2021 ◽  
Author(s):  
Leticia Herrera-Melle
Keyword(s):  
Stress Kinases

scholarly journals Activation of stress kinases in the brain of mucopolysaccharidosis IIIB mice

2011 ◽  
Vol 89 (9) ◽  
pp. 1431-1438 ◽  
Author(s):  
Francesca Cecere ◽  
Carmela Di Domenico ◽  
Daniele Di Napoli ◽  
Francesca Boscia ◽  
Paola Di Natale
Keyword(s):  
Stress Kinases ◽  
The Brain

Stress kinases p38 and ERK play an important role in acinar cell IL-1 and TNF production

2005 ◽  
Vol 201 (3) ◽  
pp. S13-S14
Author(s):  
Isaac Samuel ◽  
Smita Zaheer ◽  
Rory Fisher ◽  
Asgar Zaheer
Keyword(s):  
Acinar Cell ◽  
Stress Kinases

scholarly journals Proteasome Inhibitors Activate Stress Kinases and Induce Hsp72

1998 ◽  
Vol 273 (11) ◽  
pp. 6373-6379 ◽  
Author(s):  
Anatoli B. Meriin ◽  
Vladimir L. Gabai ◽  
Julia Yaglom ◽  
Victor I. Shifrin ◽  
Michael Y. Sherman
Keyword(s):  
Proteasome Inhibitors ◽  
Stress Kinases

scholarly journals Chfr acts with the p38 stress kinases to block entry to mitosis in mammalian cells

2004 ◽  
Vol 166 (4) ◽  
pp. 507-516 ◽  
Author(s):  
Takahiro Matsusaka ◽  
Jonathon Pines
Keyword(s):  
Cell Lines ◽  
Mammalian Cells ◽  
Proteasome Activity ◽  
Chromosomal Damage ◽  
Stress Kinases ◽  
Curr Biol ◽  
G2 Phase ◽  
Transformed Cell Lines ◽  
Recent Demonstration ◽  
Microtubule Poisons

Entry into mitosis in vertebrate cells is guarded by a checkpoint that can be activated by a variety of insults, including chromosomal damage and disrupting microtubules (Rieder, C.L., and R.W. Cole. 1998. J. Cell Biol. 142:1013–1022; Rieder, C.L., and R.W. Cole. 2000. Curr. Biol. 10:1067–1070). This checkpoint acts at the end of interphase to delay cells from entering mitosis, causing cells in prophase to decondense their chromosomes and return to G2 phase. Here, we show that in response to microtubule poisons this “antephase” checkpoint is primarily mediated by the p38 stress kinases and requires the Chfr protein that is absent or inactive in several transformed cell lines (Scolnick, D.M., and T.D. Halazonetis. 2000. Nature. 406:430–435) and lung tumors (Mizuno, K., H. Osada, H. Konishi, Y. Tatematsu, Y. Yatabe, T. Mitsudomi, Y. Fujii, and T. Takahashi. 2002. Oncogene. 21:2328–2333). Furthermore, in contrast to previous reports, we find that the checkpoint requires ubiquitylation but not proteasome activity, which is in agreement with the recent demonstration that Chfr conjugates ubiquitin through lysine 63 and not lysine 48 (Bothos, J., M.K. Summers, M. Venere, D.M. Scolnick, and T.D. Halazonetis. 2003. Oncogene. 22:7101–7107).

scholarly journals Hsp70 Prevents Activation of Stress Kinases

1997 ◽  
Vol 272 (29) ◽  
pp. 18033-18037 ◽  
Author(s):  
Vladimir L. Gabai ◽  
Anatoli B. Meriin ◽  
Dick D. Mosser ◽  
A. W. Caron ◽  
Sophia Rits ◽  
...  
Keyword(s):  
Stress Kinases

scholarly journals Influence of proteasome and redox state on heat shock-induced activation of stress kinases, AP-1 and HSF

2001 ◽  
Vol 1538 (1) ◽  
pp. 76-89 ◽  
Author(s):  
Lorenza Tacchini ◽  
Paola Dansi ◽  
Emanuela Matteucci ◽  
Aldo Bernelli-Zazzera ◽  
Maria Alfonsina Desiderio
Keyword(s):  
Heat Shock ◽  
Redox State ◽  
Stress Kinases
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