scholarly journals A Mitogen-Activated Protein Kinase Signals to Programmed Cell Death Induced by Self-Incompatibility in Papaver Pollen

2007 ◽  
Vol 145 (1) ◽  
pp. 236-245 ◽  
Author(s):  
Shutian Li ◽  
Jozef Šamaj ◽  
Vernonica E. Franklin-Tong
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
Mitogen Activated Protein Kinase ◽  
Self Incompatibility ◽  
Mitogen Activated Protein

Die Systemtherapie des fortgeschrittenen Melanoms im Jahr 2016

2017 ◽  
Vol 5 (3) ◽  
pp. 126-133
Author(s):  
Markus Vincent Heppt ◽  
Cecilia Dietrich ◽  
Saskia Graf ◽  
Thomas Ruzicka ◽  
Julia Tietze ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Programmed Cell Death ◽  
T Lymphocyte ◽  
Checkpoint Blockade ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Cell Death Protein

Das Melanom ist eine häufige Form von Hautkrebs mit hoher Tendenz zur Metastasenbildung. Tyrosinkinase-Inhibitoren, die zielgerichtet in den MAPK (mitogen-activated protein kinase)-Signaltransduktionsweg eingreifen, sowie die Immun-Checkpoint-Blockade haben in jüngster Zeit die Behandlung des nicht-resezierbaren und des metastasierten Melanoms revolutioniert. Doch erworbene Resistenzen und primäres Nichtansprechen auf diese Therapien machen neuartige Behandlungsstrategien und Kombinationsansätze erforderlich. Das Ziel dieser Übersichtsarbeit ist es, einen kurzen und aktuellen Überblick über das klinische Management des Melanoms und die gegenwärtige Studiensituation zu geben. Die Arbeit enthält Zusammenfassungen der relevantesten Studien zu BRAF- und MEK-Inhibitoren sowie zu Antikörpern gegen CTLA-4 (T-lymphocyte-associated protein 4) und PD-1 (programmed cell death protein 1). Während die meisten Wirkstoffe schon in Monotherapie eine gute antitumorale Wirksamkeit zeigen, sind durch Kombinationstherapien mit zugelassenen und in der Entwicklung befindlichen Wirkstoffen weitere Verbesserungen erzielt worden. Wir besprechen hier laufende Studien und evaluieren Ansätze, die künftig eine noch höhere Wirksamkeit bei geringerer Toxizität gewährleisten könnten. Übersetzung aus Oncol Res Treat 2016;39:635-642 (DOI:10.1159/000448904)

scholarly journals Targeted Inhibition of p38 Mitogen-activated Protein Kinase Antagonizes Cardiac Injury and Cell Death Following Ischemia-Reperfusionin Vivo

2004 ◽  
Vol 279 (15) ◽  
pp. 15524-15530 ◽  
Author(s):  
Robert A. Kaiser ◽  
Orlando F. Bueno ◽  
Daniel J. Lips ◽  
Pieter A. Doevendans ◽  
Fred Jones ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Cardiac Injury ◽  
Mitogen Activated Protein Kinase ◽  
Mitogen Activated Protein ◽  
Targeted Inhibition

scholarly journals Violacein induces p44/42 mitogen-activated protein kinase-mediated solid tumor cell death and inhibits tumor cell migration

2015 ◽  
Vol 12 (1) ◽  
pp. 1443-1448 ◽  
Author(s):  
TORAL MEHTA ◽  
KOEN VERCRUYSSE ◽  
TERRANCE JOHNSON ◽  
ANTHONY OKECHUKWU EJIOFOR ◽  
ELBERT MYLES ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Migration ◽  
Protein Kinase ◽  
Tumor Cell ◽  
Solid Tumor ◽  
Mitogen Activated Protein Kinase ◽  
Tumor Cell Death ◽  
Tumor Cell Migration ◽  
Mitogen Activated Protein

scholarly journals Role of Mitogen- and Stress-Activated Kinases in Ischemic Injury

2002 ◽  
Vol 22 (6) ◽  
pp. 631-647 ◽  
Author(s):  
Elaine A. Irving ◽  
Mark Bamford
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Protein Kinase ◽  
Signaling Pathways ◽  
Focal Cerebral Ischemia ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Amino Terminal ◽  
Biological Responses ◽  
Mitogen Activated Protein

Protein kinase-mediated signaling cascades constitute the major route by which cells respond to their extracellular environment. Of these, three well-characterized mitogen-activated protein kinase (MAPK) signaling pathways are those that use the extracellular signal-regulated kinase (ERK1/2) or the stress-activated protein kinase (p38/SAPK2 or JNK/SAPK) pathways. Mitogenic stimulation of the MAPK-ERK1/2 pathway modulates the activity of many transcription factors, leading to biological responses such as proliferation and differentiation. In contrast, the p38/SAPK2 and JNK/SAPK (c-Jun amino-terminal kinase/stress-activated protein kinase) pathways are only weakly, if at all, activated by mitogens, but are strongly activated by stress stimuli. There is now a growing body of evidence showing that these kinase signaling pathways become activated following a variety of injury stimuli including focal cerebral ischemia. Whether their activation, however, is merely an epiphenomenon of the process of cell death, or is actually involved in the mechanisms underlying ischemia-induced degeneration, remains to be fully understood. This review provides an overview of the current understanding of kinase pathway activation following cerebral ischemia and discusses the evidence supporting a role for these kinases in the mechanisms underlying ischemia-induced cell death.

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