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Mong Hong Lee

Researcher at University of Texas MD Anderson Cancer Center

Publications -  107
Citations -  10292

Mong Hong Lee is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Cancer & Cell cycle. The author has an hindex of 46, co-authored 99 publications receiving 9533 citations. Previous affiliations of Mong Hong Lee include University of Texas at Austin & University of Texas Health Science Center at Houston.

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New use of BCG for recombinant vaccines.

TL;DR: Extrachromosomal and integrative expression vectors carrying the regulatory sequences for major BCG heat-shock proteins have been developed and can elicit long-lasting humoral and cellular immune responses to foreign antigens in mice.
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Cytoplasmic localization of p21Cip1/WAF1 by Akt-induced phosphorylation in HER-2/neu-overexpressing cells.

TL;DR: It is shown that HER-2/neu-mediated cell growth requires the activation of Akt, which associates with p 21Cip1/WAF1 and phosphorylates it at threonine 145, resulting in cytoplasmic localization of p21Cip 1/Waf1.
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Interleukin-2-mediated elimination of the p27Kip1 cyclin-dependent kinase inhibitor prevented by rapamycin.

TL;DR: The results show that p27Kipl governs Cdk activity during the transition from quiescence to S phase in T lymphocytes and that p21 function may be restricted to cycling cells.
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Ablation of the CDK inhibitor p57Kip2 results in increased apoptosis and delayed differentiation during mouse development.

TL;DR: Findings indicate that p57(Kip2) has an important role during mouse development that cannot be compensated by other Cdk inhibitors and is an upstream regulator of these Rb-related proteins.
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Roles of p53, Myc and HIF-1 in Regulating Glycolysis — the Seventh Hallmark of Cancer

TL;DR: The underlying mechanisms leading to the Warburg phenomenon include mitochondrial changes, upregulation of rate-limiting enzymes/proteins in glycolysis and intracellular pH regulation, hypoxia-induced switch to anaerobic metabolism, and metabolic reprogramming after loss of p53 function.