| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| NA |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| 0.56715847 |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.86312222 |
| Here we show that GCs induce the disassembly of JNK from mitogen activated protein kinase kinase 7 ( MKK 7 ) by promoting its association with GR . 0.86312222^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Expression of NF kappaB and , interestingly , also JNK 1 and p 38 inhibited the activity of the GR . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Overexpression of GR mimicked the effect of flow to inhibit JNK activation . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Present studies show that lethal doses of gamma radiation ( GR ) induced JNK activities at the early phase of apoptosis in Jurkat T cells . ^^^ We demonstrate that JNK 1 was activated by either the T cell activation signals , anti CD 28 monoclonal antibody plus phorbol 12 myristate 13 acetate ( PMA ) , or the apoptosis inducing treatment , GR ; however , the induction patterns were different . ^^^ In contrast to the rapid and transient JNK 1 activation caused by CD 28 signaling plus PMA , GR induced a delayed and persistent JNK 1 activation . ^^^ The abilities of GR to induce JNK 1 activation and DNA fragmentation were correlated . ^^^ Peripheral blood lymphocytes were more sensitive to GR than Jurkat cells in JNK 1 induction . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| The mitogen activated protein kinases ERK ( extracellular signal regulated kinase ) , JNK ( c Jun N terminal kinase ) , and p 38 phosphorylate and activate transcription factors that promote proliferative and inflammatory responses , whereas glucocorticoid receptor ( GR ) activation inhibits cell growth and inflammation . ^^^ We demonstrate that JNK and ERK but not p 38 phosphorylate GR in vitro primarily at Ser 246 . ^^^ Selective activation of either ERK or JNK in vivo inhibits GR mediated transcriptional activation , which depends on receptor phosphorylation at Ser 246 by JNK but not ERK . ^^^ Thus , JNK inhibits GR transcriptional activation by direct receptor phosphorylation , whereas ERK does so indirectly . ^^^ We propose that phosphorylation of GR by JNK or of a GR cofactor by ERK provides mechanisms to ensure the rapid inhibition of GR dependent gene expression when it conflicts with mitogenic or proinflammatory signals . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Our results suggest that the anti inflammatory effect of glucocorticoids on the inflammatory pathways induced by TNF alpha can be explained , at least in part , by modulating JNK activity through a direct protein protein interaction ; the JNK phosphorylation and tyrosine phosphorylation state of GR may be regulatory steps also involved in that effect . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Consistently with previous findings , a glucocorticoid receptor mutant ( GRdim ) , which is deficient in dimerization , DNA binding , and transactivation , but retains AP 1 transrepressing activity , was as efficient as wild type GR in mediating the same effects of dexamethasone on JNK in transfected Cos 7 cells . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| In addition , we performed experiments with a mutant of the glucocorticoid receptor in which the JNK phosphorylation target Ser 246 had been mutated to Ala . ^^^ Our results demonstrate that the phosphorylation of the glucocorticoid receptor on Ser 246 is not responsible for the JNK repression of glucocorticoid stimulated PF2K / Fru 2 , 6 BPase gene expression . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Src potentiates activation functions in CREB binding protein ( CBP ) and glucocorticoid receptor interacting protein 1 ( GRIP 1 ) , and we discuss the possibility that the Src / JNK pathway enhances the activity of these coactivators , which are known to mediate AF 1 action . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| The c Jun N terminal kinase ( JNK ) phosphorylates the glucocorticoid receptor ( GR ) and inhibits GR mediated transcription . ^^^ Here we demonstrate that activated JNK phosphorylates human GR at Ser 226 and enhances its nuclear export after withdrawal of a ligand for GR , dexamethasone . ^^^ JNK overexpression alone mimics UV exposure and enhanced GR export accompanied by inhibition of GR mediated transcription . ^^^ However , mutation of the Ser 226 JNK phosphorylation site in GR abrogated UV mediated enhancement of GR nuclear export . ^^^ Taken together , these findings suggest that JNK mediated phosphorylation of the GR Ser 226 enhances GR nuclear export and may contribute to termination of GR mediated transcription . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Surprisingly , mitogen activated protein kinase phosphatase 1 ( MKP 1 ) , a GR induced gene in other cell types , was repressed 3 fold and correlated with an induction of JNK activity . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| In a cell free system , the phosphorylation of glutathione S transferase fused c Jun by recombinant JNK was not inhibited by dexamethasone but was inhibited by the addition of recombinant glucocorticoid receptor ( GR ) . ^^^ These findings suggest that the inhibition of antigen induced IL 13 production by dexamethasone is due to the GR mediated inhibition of c Jun phosphorylation induced by JNK . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| MIAs activate c Jun N terminal kinase ( JNK ) , which phosphorylates and inactivates GR , whereas proinflammatory cytokines , such as IL 6 or IL1beta , induce AP 1 or NF kB activation , respectively , leading to GR inhibition . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| The mitogen activated protein ( MAP ) kinases , p 38 and c Jun N terminal kinase ( JNK ) , are important mediators of target gene activation by TNF , and JNK activation was earlier shown to inhibit GR mediated transcriptional activation by direct phosphorylation of GR at Ser 246 . ^^^ Data from `` domain swap ' ' experiments using GR chimeras indicated that the main target of the p 38 mediated ( but not JNK mediated ) inhibition is the ligand binding domain of GR ( spanning amino acids 525 795 ) , whereas the constitutively active N terminal AF 1 region ( spanning amino acids 106 237 ) is dispensable for the inhibitory effect of p 38 . ^^^ Suppression of GR function by activated p 38 and JNK MAP kinases may be physiologically important as a mechanism of resistance to glucocorticoids seen in many patients with chronic inflammatory conditions . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| Inhibition of Jun N terminal kinase ( JNK ) enhances glucocorticoid receptor mediated function in mouse hippocampal HT 22 cells . ^^^ Relevant to negative regulation of inflammatory pathways by glucocorticoids and the development of glucocorticoid resistance ( observed in inflammatory disorders as well as certain neuropsychiatric disorders such as major depression ) , activation of JNK has been reported to inhibit glucocorticoid receptor ( GR ) function . ^^^ In this study , the role of JNK pathways in modulating GR function was further investigated . ^^^ Treatment of mouse hippocampal ( HT 22 ) cells with the selective JNK inhibitor , SP 600125 ( 0 . 1 10 microM ) , resulted in dose dependent induction of GR mediated MMTV luciferase activity . ^^^ Taken together , the data indicate that constitutive expression of JNK plays a tonic inhibitory role in GR function , which is consistent with findings that activation of JNK pathways inhibits GR . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| The glucocorticoid receptor ( GR ) , activator protein 1 ( AP 1 ) , nuclear factor kappa B ( NF kappaB ) and c jun N terminal kinase ( JNK ) regulate the above mentioned processes ; we therefore assessed their role in BD . ^^^ Whole cell and nuclear extracts from lymphocytes were immunoblotted for GR , c fos , JNK and NF kappaB and nuclear aliquots were submitted to electrophoretic mobility shift assay for GR , AP 1 and NF kappaB . ^^^ Concluding , intracellular signaling of GR , AP 1 and JNK are altered in BD and may underly disease aetiopathogenesis and / or reflect the effect of the anti depressants . . ^^^ |
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| Interacting proteins: P45983 and P04150 |
Pubmed |
SVM Score :0.0 |
| These include PCNA , GR , BMP 1 , BMP3b , Chk 1 , Caspase 6 , E2F1 , c Raf , ERK1 / 2 and JNK 1 , as well as several others of lesser importance . ^^^ |
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