JNK Signaling in Apoptosis

By DN Dhanasekaran, E. Reddy. Oncogene, 2008

1,532 citations recorded by the source corpus.

Jun N-terminal kinases or JNKs play a critical role in death receptor-initiated extrinsic as well as mitochondrial intrinsic apoptotic pathways. JNKs activate apoptotic signaling by the upregulation of pro-apoptotic genes through the transactivation of specific transcription factors or by directly modulating the activities of mitochondrial pro- and antiapoptotic proteins through distinct phosphorylation events. This review analyses our present understanding of the role of JNK in apoptotic signaling and the various mechanisms by which JNK promotes apoptosis.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/1350e9f390d81d00110d4809eecc92fb8711e2a6

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. José M. López
2. R. Seger
3. M. Circu
4. Jicheng Yue
5. T. Aw

In Pathology and Forensic Medicine

1. R. Seger
2. M. Circu
3. T. Aw

Citations in the corpus

• REACTIVE OXYGEN SPECIES, CELLULAR REDOX SYSTEMS AND APOPTOSIS (2010, positive): “ROS activation of JNK can induce extrinsic or intrinsic apoptotic signaling [129].”
• Understanding MAPK Signaling Pathways in Apoptosis (2020, background): “A variety of transcription factors have been reported to be regulated by JNK and p38, which result in increased expression of pro-apoptotic proteins and decreased expression of anti-apoptotic proteins [14,16].”
• Apoptosis, autophagy, necroptosis, and cancer metastasis (2015, background): “Activated JNK translocates to the nucleus and transactivates c-Jun and other transcription factors (e.g., p53), which further transactivate various pro-apoptotic genes, such as Fas-L, Bak, and p53-upregulated modulator of apoptosis (PUMA) [67].”
• Drug-Induced Oxidative Stress and Toxicity (2012, background): “, Bid, Bim), or suppress/antagonize the activity of antiapoptotic Bcl-2 and Bcl-xL proteins (reviewed in [51]).”
• The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. (2011, background): “These phosphorylated targets further regulate the transcription of many genes, which in turn, mediate cellular processes such as apoptosis [37], immunological effects [38], neuronal activity [39], insulin signaling [39], and more [8].”