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Kwok-Ming Yao

Researcher at University of Hong Kong

Publications -  59
Citations -  3239

Kwok-Ming Yao is an academic researcher from University of Hong Kong. The author has contributed to research in topics: Cell growth & Transcription factor. The author has an hindex of 29, co-authored 58 publications receiving 2979 citations. Previous affiliations of Kwok-Ming Yao include University of Texas at Dallas & Li Ka Shing Faculty of Medicine, University of Hong Kong.

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The elav gene product of Drosophila, required in neurons, has three RNP consensus motifs

TL;DR: DNA sequence data presented in this report suggest that the elav gene product is an RNA binding protein, based on the presence of RNP (ribonucleoprotein) consensus sequences, which leads to the proposal that this protein is involved in the RNA metabolism of neurons.
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Raf/MEK/MAPK signaling stimulates the nuclear translocation and transactivating activity of FOXM1c

TL;DR: The hTERT-BJ1 fibroblasts study provides the first evidence that Raf/MEK/MAPK signaling exerts its G2/M regulatory effect via FOXM1c, and Mutations of two ERK1/2 target sequences within FOXm1c completely abolish the MEK1 enhancing effect, suggesting a direct link between Raf/ MEK/ MAPK signaling and FOXM 1 function.
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Loss of MKP3 mediated by oxidative stress enhances tumorigenicity and chemoresistance of ovarian cancer cells

TL;DR: A molecular mechanism by which the accumulation of ROS during ovarian cancer progression may cause the degradation of MKP3, which in turn leads to aberrant ERK1/2 activation and contributes to tumorigenicity and chemoresistance of human ovarian cancer cells is suggested.
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Neural specificity of elav expression: defining a Drosophila promoter for directing expression to the nervous system.

TL;DR: To understand the molecular basis of this neural‐specific expression of ELAV, a defined and analyzed the structure of the elav promoter was defined and a 3.5‐kb promoter fragment encompassing this region was designed for targeting gene expression specifically to the nervous system and would be a useful tool for the analysis of nervous system function.
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Over-expression of FoxM1 stimulates cyclin B1 expression.

TL;DR: Quantitation of cyclin B1 and D1 levels using flow cytometric, Western and Northern analyses reveals that elevated FoxM1 levels lead to stimulation of cyclIn B1 but not cyclin D1 expression, while transient reporter assays in the dox‐inducible lines and upon co‐transfection with a constitutive FoxM 1 expression plasmid suggest that FoxM2 can activate the cyclinB1 promoter.