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These experiments demonstrate an important role of Nischarin in regulating cell attachment, which adds to our understanding of the early events of the metastatic process in breast cancer.
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In the prefrontal cortex of long-term opiate/cocaine abusers, IRAS content was increased when compared to matched controls.
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IRAS is a new mu opioid receptor interacting protein that regulates agonist-induced trafficking of mu opioid receptor.
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The present data confirmed that Nishcharin might be a novel tumor suppressor and plays an important role in breast cancer cell apoptosis and metastasis, which can be used as a potential therapeutic target for breast cancer treatment.
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Data found that NISCH was significantly downregulated in ovarian neoplasm through its promotor silencing with hypermethylation and its expression was correlated with poor prognosis.
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Nischarin expression may therefore be used as a marker to predict the invasiveness and metastasis of primary breast cancer
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Tobacco smoke induces methylation changes in the NISCH gene promoter before any detectable cancer.
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unctional interaction between LKB1 and Nischarin to inhibit cell migration and breast tumor progression
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Imidazoline receptor 1 gene plays a role in the development of cardiac hypertrophy and ventirular remodeling.
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Nischarin reduces alpha5 integrin expression leading to reduction of FAK phosphorylation and Rac GTP loading, which in turn reduces tumor growth. NISCH also regulates PAK and LIMK signaling.
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Insulin receptor substrate 4 associates with the protein IRAS (IRAS protein)
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The heart possesses imidazoline I1-receptors that are up-regulated in the presence of hypertension or heart failure, which suggests their involvement in cardiovascular regulation.
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I(1)-receptors can abrogate the primary signaling cascade activated by NGF, most likely by increasing levels of a specific phosphatase to return dually phosphorylated ERK to its unphosphorylated state.
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hIRAS expression in PC12 cells resulted in protection against apoptosis
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Results suggest that IRAS may represent a previously unknown anti-apoptotic protein involved in the regulation of cell survival.
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Results describe three alternatively spliced transcripts of the human I(1)-imidazoline receptor candidate gene, IRAS.
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Results suggest that imidazoline-1 receptors (I(1)R) and alpha(2)-noradrenergic receptors (alpha(2)AR) may interact with each other.
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platelets lacked the 170-kD form of IRAS, but 33-kD and 85-kD bands were detectable and seemed to be possible fragments of full-length IRAS
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PX domain of imidazoline receptor antisera-selected protein(IRAS) is essential for association with phosphatidylinositol 3-phosphate-enriched endosomal membranes but is insufficient without coiled-coil domain
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The signaling pathway of IRAS in response to I1R agonists coupled with the activation of PC-PLC and its downstream signal transduction molecule, ERK. These findings are similar to those in the signaling pathways of native I1R.