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data demonstrate that miR-515-5p dramatically inhibits cell migration by directly down-regulating MARK4 expression in two different cancer types
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Our results show that MARK4 acts as a negative regulator of the Hippo kinase cassette to promote YAP/TAZ activity and that loss of MARK4 restrains the tumorigenic properties of breast cancer cells.
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Atypical PKC phosphorylates serine-threonine residues of MARK4.
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Suggest role for polypyrimidine-tract binding protein in regulating alternative splicing of MARK4 in gliomas.
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MARK4 is a key component in the regulation of microtubule dynamics and has major role in cell cycle progression, particularly at the G1/S transition.
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Molecular dynamic simulation data predicted the three dimensional structure for the kinase domain of MARK4 and its structural properties.
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A strong and significant elevation of MARK4 expression and MARK4-tau interactions in AD brains correlates with the Braak stages of the disease, suggesting that the MARK4-tau interactions are of functional importance in the progression of AD.
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MARK4 is a critical positive regulator of early steps in ciliogenesis.
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MARK4 is a new negative regulator of mTORC1
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The balance between the MARK4 isoforms is carefully guarded during neural differentiation but may be subverted in gliomagenesis.
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Even though an association of the polymorphisms rs2850328 and rs2395 and breast cancer was not detected in our case-control study population, other variants within the PPP3CA and MARK4 genes may still be associated with breast cancer.
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demonstrated that the endogenous MARK4L colocalizes with centrosomes at all mitotic stages and resides in centrosome-enriched fractions.
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Normally expressed in neural progenitors, re-expressed in gliomas and may become a target of amplification upon chr. 19 rearrangement.
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MARK4 is likely to be directly involved in microtubule organization in neuronal cells
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NUAK1 and MARK4 are substrates of USP9X