JNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective.
c-Jun N-terminal kinases (JNKs) are intracellular stress-activated signalling molecules, which are controlled by a highly evolutionarily conserved signalling cascade. In mammalian cells, JNKs are regulated by a wide variety of cellular stresses and growth factors and have been implicated in the regu...
| Main Authors: | , |
|---|---|
| Format: | Journal article |
| Language: | English |
| Published: |
1998
|
| _version_ | 1826304141913227264 |
|---|---|
| author | Goberdhan, D Wilson, C |
| author_facet | Goberdhan, D Wilson, C |
| author_sort | Goberdhan, D |
| collection | OXFORD |
| description | c-Jun N-terminal kinases (JNKs) are intracellular stress-activated signalling molecules, which are controlled by a highly evolutionarily conserved signalling cascade. In mammalian cells, JNKs are regulated by a wide variety of cellular stresses and growth factors and have been implicated in the regulation of remarkably diverse biological processes, such as cell shape changes, immune responses and apoptosis. How can such different stimuli activate the JNK pathway and what roles does JNK play in vivo? Molecular genetic analysis of the Drosophila JNK gene has started to provide answers to these questions, confirming the role of this molecule in development and stress responses and suggesting a conserved function for JNK signalling in processes such as wound healing. Here, we review this work and discuss how future experiments in Drosophila should reveal the cell type-specific mechanisms by which JNKs perform their diverse functions. |
| first_indexed | 2024-03-07T06:13:18Z |
| format | Journal article |
| id | oxford-uuid:f043cd0e-505d-4a5a-b3eb-80472f177985 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T06:13:18Z |
| publishDate | 1998 |
| record_format | dspace |
| spelling | oxford-uuid:f043cd0e-505d-4a5a-b3eb-80472f1779852022-03-27T11:46:28ZJNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:f043cd0e-505d-4a5a-b3eb-80472f177985EnglishSymplectic Elements at Oxford1998Goberdhan, DWilson, Cc-Jun N-terminal kinases (JNKs) are intracellular stress-activated signalling molecules, which are controlled by a highly evolutionarily conserved signalling cascade. In mammalian cells, JNKs are regulated by a wide variety of cellular stresses and growth factors and have been implicated in the regulation of remarkably diverse biological processes, such as cell shape changes, immune responses and apoptosis. How can such different stimuli activate the JNK pathway and what roles does JNK play in vivo? Molecular genetic analysis of the Drosophila JNK gene has started to provide answers to these questions, confirming the role of this molecule in development and stress responses and suggesting a conserved function for JNK signalling in processes such as wound healing. Here, we review this work and discuss how future experiments in Drosophila should reveal the cell type-specific mechanisms by which JNKs perform their diverse functions. |
| spellingShingle | Goberdhan, D Wilson, C JNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective. |
| title | JNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective. |
| title_full | JNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective. |
| title_fullStr | JNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective. |
| title_full_unstemmed | JNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective. |
| title_short | JNK, cytoskeletal regulator and stress response kinase? A Drosophila perspective. |
| title_sort | jnk cytoskeletal regulator and stress response kinase a drosophila perspective |
| work_keys_str_mv | AT goberdhand jnkcytoskeletalregulatorandstressresponsekinaseadrosophilaperspective AT wilsonc jnkcytoskeletalregulatorandstressresponsekinaseadrosophilaperspective |