Uses for JNK: the Many and Varied Substrates of the c-Jun N-Terminal Kinases
By M. Bogoyevitch, Bostjan Kobe. Microbiology and Molecular Biology Reviews, 2006
602 citations recorded by the source corpus.
SUMMARY The c-Jun N-terminal kinases (JNKs) are members of a larger group of serine/threonine (Ser/Thr) protein kinases from the mitogen-activated protein kinase family. JNKs were originally identified as stress-activated protein kinases in the livers of cycloheximide-challenged rats. Their subsequent purification, cloning, and naming as JNKs have emphasized their ability to phosphorylate and activate the transcription factor c-Jun. Studies of c-Jun and related transcription factor substrates have provided clues about both the preferred substrate phosphorylation sequences and additional docking domains recognized by JNK. There are now more than 50 proteins shown to be substrates for JNK. These include a range of nuclear substrates, including transcription factors and nuclear hormone receptors, heterogeneous nuclear ribonucleoprotein K, and the Pol I-specific transcription factor TIF-IA, which regulates ribosome synthesis. Many nonnuclear substrates have also been characterized, and these are involved in protein degradation (e.g., the E3 ligase Itch), signal transduction (e.g., adaptor and scaffold proteins and protein kinases), apoptotic cell death (e.g., mitochondrial Bcl2 family members), and cell movement (e.g., paxillin, DCX, microtubule-associated proteins, the stathmin family member SCG10, and the intermediate filament protein keratin 8). The range of JNK actions in the cell is therefore likely to be complex. Further characterization of the substrates of JNK should provide clearer explanations of the intracellular actions of the JNKs and may allow new avenues for targeting the JNK pathways with therapeutic agents downstream of JNK itself.
Subfields: Molecular Biology, Oncology
View Paper: https://www.semanticscholar.org/paper/7656f3f631900795c9b92437053ec3ba9fe60f13
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Citations in the corpus
- THP-1 and U937 Cells (2015, background): “…mechanism of JNK activation under each of these circumstances remains not fully clear, but there may be involvement of Toll-like receptors, direct pathway modulation through interaction with upstream protein regulators or the activation following an ER stress response (Bogoyevitch and Kobe 2006 ).”
- The MAPK cascades: signaling components, nuclear roles and mechanisms of nuclear translocation. (2011, background): “Some of the main transcription factors regulated by JNKs are: c-Jun, JunB, JunD, ATF2, p53, JDP2, and c-Myc [152], and by p38s: ATF-1/2/6, Sap1, CHOP, p53, C/EBP, MEF2C, MEF2A, and HBP1 [44].”
- Mitogen-activated protein kinase signaling in the heart: angels versus demons in a heart-breaking tale. (2010, background): “Like ERK, JNK plays a role in a number of different biological processes including cell proliferation, differentiation, apoptosis, cell survival, actin reorganization, cell mobility, metabolism, and cytokine production (43, 93, 332).”