JIP1 binding to RBP-Jk mediates cross-talk between the Notch1 and JIP1-JNK signaling pathway

Kim, M. Y.; Ann, Eun-Jung; Mo, Jung-Soon; Dajas-Bailador, Federico; Seo, Mi Sun; Hong, Ji-Ae; Jung, Ji‐Yeon; Choi, Yun Hee; Yoon, Ji-Hye; Kim, S. M.; Choi, Eui Ju; Hoe, Hyang‐Sook; Whitmarsh, Alan J.; Park, H. S.

doi:10.1038/cdd.2010.50

Cited by 16 publications

(13 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notch-IC interacts with CBF1 and translocates to the nucleus, resulting in the elevated expression of target genes (38). Our recent finding suggests that RBP-Jk has an antiapoptotic function by suppressing JIP1-mediated JNK signaling (39). Our data now indicate that activation of the transcription factor RBP-Jk is not required for inhibition of the ASK1-p38 MAPK pathway by Notch1-IC or by itself.…”

Section: Discussionmentioning

confidence: 51%

Notch1 modulates oxidative stress induced cell death through suppression of apoptosis signal-regulating kinase 1

Yoon

Ann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Notch1 genes encode receptors for a signaling pathway that regulates various aspects of cell growth and differentiation; however, the role of Notch1 signaling in p38 mitogen-activated protein kinase (MAPK) signaling pathway is still not well defined. In this study, we found that Notch1 intracellular domain (Notch1-IC) prevents oxidative stress-induced cell death through the suppression of the Apoptosis signal-regulating kinase (ASK) 1 signaling pathway. Notch1-IC inhibited H 2 O 2 -induced activation of ASK1 and the activation of downstream kinases in the p38 MAPK signaling cascade. The results of both in vivo binding and kinase studies have revealed that ASK1 is the direct target of Notch1-IC, whereas it produced no effect on either MAP kinase kinase (MKK) 3 or p38 MAPK. Notch1-IC blocked both the homooligomerization of ASK1 and inhibited ASK1 activity. Furthermore, Notch1-IC facilitated the translocation of activated ASK1 toward the nucleus. Notch1 knockdown was determined to be highly susceptible to oxidative stress-induced activation of ASK1-MKK3/MKK6-p38 MAPK signaling cascade and cell death. Taken together, our findings suggest that Notch1-IC may act as a negative regulator in ASK1 signaling cascades.

show abstract

Section: Discussionmentioning

confidence: 51%

Notch1 modulates oxidative stress induced cell death through suppression of apoptosis signal-regulating kinase 1

Yoon

Ann

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

show abstract

“…The phosphorylated substrates were separated by SDS-PAGE and quantified using a Fuji FLA7000 PhosphorImager. The GST fusion proteins that were used as substrates were expressed in E. coli using pGEX-4T (Pharmacia) and purified using glutathione-Sepharose, as described previously (66,67). The protein concentrations were determined by the Bradford method (Shimadzu).…”

Section: Methodsmentioning

confidence: 99%

Wnt5a Controls Notch1 Signaling through CaMKII-mediated Degradation of the SMRT Corepressor Protein

Ann¹,

Kim²,

Seo³

et al. 2012

Journal of Biological Chemistry

View full text Add to dashboard Cite

“…In the Cytoplasm region, we included total 35 molecules, out of which 5 molecules are metabolic compounds such as O-linked glucose, Xylose, O-linked Fucose, GALACTOSE, N-acetylglucosamine [62][63][64][65]. The "Oval" shaped and deep blue colored entities were chosen to represent the metabolites in the pathway map.…”

Section: Pathway Drawing and Annotationmentioning

confidence: 99%

“…During this travel through cytoplasmic region, NICD encounters with various activator (RAS, GSK_3BETA, WDR12) and inhibitor (DVL, JIP1) proteins [62,63,73,74]. RAS pathway proteins activate NICD1 through some intermediate proteins which were not included in the pathway map for the sake of simplicity.…”

Section: Reactions In Cytoplasmmentioning

confidence: 99%

“…After encountering with several modifications and interactions by nuclear proteins, the activated NICD1/2/3/4 enters and starts the transcription process in the nucleus [6,62,63,73,74]. NICD initiates its transcription by binding with another transcription factor CSL, which in general forms a transcription repressor complex with another transcription Co-repressor complex (COR).…”

Section: Reactions In Nucleusmentioning

confidence: 99%

See 1 more Smart Citation

Drug Targets and Biomarker Identification from Computational Study of Human Notch Signaling Pathway

Chowdhury¹,

Sarkar²

2013

Clin Exp Pharmacol

View full text Add to dashboard Cite

Notch signaling pathway is widely implicated in controlling various cellular functions, cell fate determination, and stem cell renewal in human but aberrant activity in cancer stem cells may cause different types of cancers. Understanding the complexity of this pathway to identify important targets for cancer therapy and to suppress the pathway activity without affecting the normal functions is of utmost importance to clinical and experimental pharmacologists. For developing therapeutic strategy, non availability of detailed molecular interactions, complex regulations and cross talks with other pathways pose a serious challenge to get a coherent understanding of this pathway. This motivated us to reconstruct the largest human cell specific Notch pathway with more number of molecules and interactions available from literatures and databases. To identify probable drug targets and biomarkers for cancer prognosis, we also performed computational study of the pathway using structural and logical analysis and identified important hub proteins, cross talks and feedback mechanisms. The model simulation is validated using reported mRNA expression profile in Glioblastoma cell line and the predictions not only show significant accuracy but also able to identify the undetermined expressions. From our simulation, to identify novel combinations of drug targetable proteins and better substitute for GAMMA SECRETASE inhibition, we proposed two alternative scenarios: partial suppression of Notch target proteins by NICD1 & HIF1A; and complete suppression by NICD1 & MAML, in Glioblastoma cell line. This reconstructed Notch signaling pathway and the computational analysis for identifying new biomarkers and combinatory drug targets will be useful for future in-vitro and in-vivo analysis to control different cancers.

show abstract

JIP1 binding to RBP-Jk mediates cross-talk between the Notch1 and JIP1-JNK signaling pathway

Cited by 16 publications

References 32 publications

Notch1 modulates oxidative stress induced cell death through suppression of apoptosis signal-regulating kinase 1

Notch1 modulates oxidative stress induced cell death through suppression of apoptosis signal-regulating kinase 1

Wnt5a Controls Notch1 Signaling through CaMKII-mediated Degradation of the SMRT Corepressor Protein

Drug Targets and Biomarker Identification from Computational Study of Human Notch Signaling Pathway

Contact Info

Product

Resources

About