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Ada Girnita

Researcher at Karolinska University Hospital

Publications -  51
Citations -  2783

Ada Girnita is an academic researcher from Karolinska University Hospital. The author has contributed to research in topics: Receptor & Insulin-like growth factor. The author has an hindex of 25, co-authored 45 publications receiving 2580 citations. Previous affiliations of Ada Girnita include Karolinska Institutet.

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Cyclolignans as inhibitors of the insulin-like growth factor-1 receptor and malignant cell growth

TL;DR: It is reported that certain cyclolignans are potent and selective inhibitors of tyrosine phosphorylation of the IGF-1R, and the possibility to use PPP or related compounds with inhibitory effects on IGF- 1R as lead compounds in development of anticancer agents is opened.
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Role of insulin-like growth factor 1 receptor signalling in cancer.

TL;DR: The insulin-like growth factor (IGF-1) signalling is highly implicated in cancer and a close interplay with the p53/MDM2 pathway may cause IGF-1R upregulation and growth advantage for the cancer cell.
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Mdm2-dependent ubiquitination and degradation of the insulin-like growth factor 1 receptor.

TL;DR: It is shown that inhibition of p53 causes ubiquitination and down-regulation, through increased degradation, of the IGF-1R in human malignant melanoma cells, and evidence is provided that Mdm2 serves as a ligase in ubiquitinations of the insulin-like growth factor 1 receptor and thereby causes its degradation by the proteasome system.
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The cyclolignan PPP induces activation loop-specific inhibition of tyrosine phosphorylation of the insulin-like growth factor-1 receptor. Link to the phosphatidyl inositol-3 kinase/Akt apoptotic pathway.

TL;DR: The data suggest that the preferential inhibition of phosphorylated Akt, after PPP treatment, may be due to specific inhibition of Y1136, and PPP was proven not to interfere directly with Akt or any of its downstream molecules in the apoptotic pathway.
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β-Arrestin Is Crucial for Ubiquitination and Down-regulation of the Insulin-like Growth Factor-1 Receptor by Acting as Adaptor for the MDM2 E3 Ligase

TL;DR: Evidence is provided that β-arrestin, otherwise known to be involved in the regulation of G protein-coupled receptors, serves as an adaptor to bring the oncoprotein E3 ubiquitin ligase MDM2 to the IGF-1R, which acts as a crucial component in the ubiquitination and down-regulation of the receptor.