Topic
c-jun
About: c-jun is a research topic. Over the lifetime, 3267 publications have been published within this topic receiving 186910 citations. The topic is also known as: JUN & activator protein 1.
Papers published on a yearly basis
Papers
TL;DR: JNK1 is a component of a novel signal transduction pathway that is activated by oncoproteins and UV irradiation and its properties indicate that JNK1 activation may play an important role in tumor promotion.
3,355 citations
TL;DR: This work has identified a serine/threonine kinase whose activity is stimulated by the same signals that stimulate the amino-terminal phosphorylation of c-Jun, and suggests a mechanism through which protein kinase cascades can specifically modulate the activity of distinct nuclear targets.
Abstract: The activity of c-Jun is regulated by phosphorylation. Various stimuli including transforming oncogenes and UV light, induce phosphorylation of serines 63 and 73 in the amino-terminal activation domain of c-Jun and thereby potentiate its trans-activation function. We identified a serine/threonine kinase whose activity is stimulated by the same signals that stimulate the amino-terminal phosphorylation of c-Jun. This novel c-Jun amino-terminal kinase (JNK), whose major form is 46 kD, binds to a specific region within the c-Jun trans-activation domain and phosphorylates serines 63 and 73. Phosphorylation results in dissociation of the c-Jun-JNK complex. Mutations that disrupt the kinase-binding site attenuate the response of c-Jun to Ha-Ras and UV. Therefore the binding of JNK to c-Jun is of regulatory importance and suggests a mechanism through which protein kinase cascades can specifically modulate the activity of distinct nuclear targets.
2,001 citations
TL;DR: The c-Jun amino-terminal kinase (JNK) group of MAP kinases has been identified in mammals and insects as discussed by the authors, indicating that this signaling pathway may contribute to inflammatory responses.
1,632 citations
TL;DR: Findings reveal a cross talk between two major signal transduction systems used to control gene transcription in response to extracellular stimuli, and a novel mechanism for transcriptional repression.
1,630 citations
TL;DR: Evidence is presented that the glucocorticoid receptor (GR) and transcription factor Jun/AP-1 can reciprocally repress one another's transcriptional activation by a novel mechanism that is independent of DNA binding.
1,310 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2025 | 8 |
| 2024 | 21 |
| 2023 | 55 |
| 2022 | 28 |
| 2021 | 70 |
| 2020 | 82 |