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A pleckstrin homology domain in PIKE-L directly binds alpha-synuclein and antagonizes its aggregation. Accordingly, PIKE-L overexpression decreases dopaminergic cell death elicited by MPP(+), whereas PIKE-L knockdown elevates alpha-synuclein oligomerization and cell death.
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these findings support that PIKE amplification or overexpression coordinately acts with CDK4 to drive glioblastoma tumorigenesis.
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Studies showed that overexpression or mutation of PIKE has been observed in a variety of tumors, promoting cancer cell growth, transformation and invasion through AKT signaling or other signaling pathways, such as focal adhesion kinase. [review]
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Mutation of Fyn phosphorylation sites on PIKE-A, depletion of Fyn, or pharmacological inhibition of Fyn blunts the association between PIKE-A and AMPK, resulting in loss of its inhibitory effect on AMPK.
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expression of PLC-gamma1 and PIKE positively correlated with the tumor differentiation of oral squamous cell carcinoma.
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PIKE reduction rescued PI3K-dependent and -independent neuronal defects in fragile X syndrome.
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In this review the CENTG1 gene is amplified in a variety of human cancers which lead to the enhancement of tumor invasion.
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AGAP2 plays a role in the signalling and recycling of beta2-adrenergic receptors.
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Fyn regulates the activity of the adipogenic transcription factor signal transducer and activator of transcription 5a (STAT5a) through enhancing its interaction with the GTPase phosphoinositide 3-kinase enhancer A (PIKE-A).
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PIKE is highly expressed in human squamous cell carcinoma and has a critical role in EGF-induced squamous cell carcinoma proliferation.
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The presence of heterogeneous missense mutations of GGAP2 in prostate cancer was associated with aggressive clinical behavior.
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PIKE is a critical factor in controlling synaptic AMPA receptor insertion.
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Akt-phosphorylated PIKE-A inhibits UNC5B-induced apoptosis in cancer cell lines in a p53-dependent manner. [PIKE-A]
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regulates retrograde protein transport between early endosomes and the Golgi complex
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This study have identified, cloned and characterized PIKE-L, which localizes to both the cytoplasm and the nucleus, activates mGlur1 enhances formation of an mGluRI-Homer-PIKE-L complex, then activates PI3 kinase activity and prevents neuronal apoptosis.
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a physiologic regulator of Akt and an oncogenic effector of cell invasion
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PIKE binds PI 3-kinase & stimulates its lipid kinase activity. There are 3 isoforms which function throught the cell and meadiate processes from invasiveness to apoptosis. Review.
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The AGAP2 colocalized with AP-1, transferrin receptor and Rab4 on endosomes. Overexpression of AGAP2 changed the intracellular distribution of AP-1 and promoted Rab4-dependent fast recycling of transferrin.
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an important role of PIKE gene aberrations in the molecular pathogenesis of primary glioblastomas
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Fyn is essential for phosphorylating PIKE-A and protects it from apoptotic cleavage.