Literature DB >> 9414114

Selective activation of JNK/SAPK by interleukin-1 in rabbit liver is mediated by MKK7.

A Finch1, P Holland, J Cooper, J Saklatvala, M Kracht.   

Abstract

Activation of jun N-terminal kinase (JNK)/stress-activated protein kinase (SAPK) by interleukin-1 (IL-1) has been reported in many cells and in rabbit liver. Here we report selective activation of JNK/SAPK, without activation of p38 or p42 mitogen-activated protein kinases (MAPKs), by IL-1 in rabbit liver. We identified an IL-1 regulated JNK/SAPK activator present in rabbit liver using S Sepharose chromatography. It was purified and immunoprecipitated by two antisera to MAP kinase kinase 7 (MKK7). It was not recognised by an antibody to MKK4. We conclude that MKK7 is the activator of JNK/SAPK activated by IL-1 in liver and that JNK/SAPK is the only MAPK activated by IL-1 in liver.

Entities:  

Mesh:

Substances:

Year:  1997        PMID: 9414114     DOI: 10.1016/s0014-5793(97)01364-1

Source DB:  PubMed          Journal:  FEBS Lett        ISSN: 0014-5793            Impact factor:   4.124


  14 in total

1.  Analysis of mitogen-activated protein kinase pathways used by interleukin 1 in tissues in vivo: activation of hepatic c-Jun N-terminal kinases 1 and 2, and mitogen-activated protein kinase kinases 4 and 7.

Authors:  A Finch; W Davis; W G Carter; J Saklatvala
Journal:  Biochem J       Date:  2001-01-15       Impact factor: 3.857

2.  Synergistic activation of JNK/SAPK by interleukin-1 and platelet-derived growth factor is independent of Rac and Cdc42.

Authors:  W Davis; L R Stephens; P T Hawkins; J Saklatvala
Journal:  Biochem J       Date:  1999-03-01       Impact factor: 3.857

3.  Induction of interleukin-8 synthesis integrates effects on transcription and mRNA degradation from at least three different cytokine- or stress-activated signal transduction pathways.

Authors:  H Holtmann; R Winzen; P Holland; S Eickemeier; E Hoffmann; D Wallach; N L Malinin; J A Cooper; K Resch; M Kracht
Journal:  Mol Cell Biol       Date:  1999-10       Impact factor: 4.272

4.  Protein-damaging stresses activate c-Jun N-terminal kinase via inhibition of its dephosphorylation: a novel pathway controlled by HSP72.

Authors:  A B Meriin; J A Yaglom; V L Gabai; L Zon; S Ganiatsas; D D Mosser; L Zon; M Y Sherman
Journal:  Mol Cell Biol       Date:  1999-04       Impact factor: 4.272

Review 5.  Lineage-specific and ubiquitous biological roles of the mammalian transcription factor LSF.

Authors:  Jelena Veljkovic; Ulla Hansen
Journal:  Gene       Date:  2004-12-08       Impact factor: 3.688

6.  Synergistic activation of stress-activated protein kinase 1/c-Jun N-terminal kinase (SAPK1/JNK) isoforms by mitogen-activated protein kinase kinase 4 (MKK4) and MKK7.

Authors:  Y Fleming; C G Armstrong; N Morrice; A Paterson; M Goedert; P Cohen
Journal:  Biochem J       Date:  2000-11-15       Impact factor: 3.857

7.  Differential activation of stress-activated protein kinase kinases SKK4/MKK7 and SKK1/MKK4 by the mixed-lineage kinase-2 and mitogen-activated protein kinase kinase (MKK) kinase-1.

Authors:  A Cuenda; D S Dorow
Journal:  Biochem J       Date:  1998-07-01       Impact factor: 3.857

8.  The role of MKK4 in T-cell development and immunity to viral infections.

Authors:  Simon P Preston; Marcel Doerflinger; Hamish W Scott; Cody C Allison; Miles Horton; James Cooney; Marc Pellegrini
Journal:  Immunol Cell Biol       Date:  2020-12-08       Impact factor: 5.126

9.  Alpinetin suppresses proliferation of human hepatoma cells by the activation of MKK7 and elevates sensitization to cis-diammined dichloridoplatium.

Authors:  Bo Tang; Jian Du; Jingwen Wang; Guang Tan; Zhenming Gao; Zhongyu Wang; Liming Wang
Journal:  Oncol Rep       Date:  2011-12-06       Impact factor: 3.906

10.  Activation of SAPK/JNK by camptothecin sensitizes androgen-independent prostate cancer cells to Fas-induced apoptosis.

Authors:  A P Costa-Pereira; S L McKenna; T G Cotter
Journal:  Br J Cancer       Date:  2000-06       Impact factor: 7.640

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.