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ISOLATION AND STRUCTURE DETERMINATION OF NEW MACROLIDE ANTIBIOTICS
HATFIELD, GEORGE M.,WOODARD, RONALD W.,SON, JONG-KEUN 영남대학교 약품개발연구소 1992 영남대학교 약품개발연구소 연구업적집 Vol.2 No.-
Three new bafilomycin-like compounds PD 118, 576-A1[1], PD 118, 576-A2 [2], and PD 118, 576-A3 [3] were isolated from a new soil Streptomyces species (WP 3913). The structures of PD 118, 576-A1, PD 118, 576-A2, and PD 118, 576-A3 were elucidated on the basis of spectroscopic studies including 2D nmr.
The Cancer Stem Cell Theory: Is It Correct?
유민혁,Dolph L. Hatfield 한국분자세포생물학회 2008 Molecules and cells Vol.26 No.5
The cancer stem cell hypothesis posits that tumor growth is driven by a rare subpopulation of cells, designated cancer stem cells (CSC). Studies supporting this theory are based in large part on xenotransplantation experiments wherein human cancer cells are grown in immunocompromised mice and only CSC, often constituting less than 1% of the malignancy, generate tumors. Herein, we show that all colonies derived from randomly chosen single cells in mouse lung and breast cancer cell lines form tumors following allografting histocompatible mice. Our study suggests that the majority of malignant cells rather than CSC can sustain tumors and that the cancer stem cell theory must be reevaluated.
CONTROLLED LYSIS OF ESCHERICHIA COLI DOUBLE - LYSOGEN OF BACTERIOPHAGES λHL1 AND φ434
Koo, Yoon Mo,Parekh, Bhavin S,Hatfield, G Wesley,Lim, Henry C 한국화학공학회 1996 Korean Journal of Chemical Engineering Vol.13 No.2
A novel phage double-lysogen was developed to produce an intracellular protein and disrupt the host cell in the same reactor. Using this double-lysogen, we could simplify the recovering processes without cell harvest and disruption. Construction of the double-lysogen is based on the fact that a lysogen of a phage can be superinfected by another phage with different immunity. The single-lysogen of Escherichia coli, P90c/λHL1, was superinfected with bacteriophage Φ434 to produce a double-lysogen, in which phage genomes from each phage coexisted in the host chromosome. Two different inducers were used to induice the double-lysogen to produce a protein and to lyse the host cell. The first phage genome, λHL1, the prophage of the original lysogen, containing the temperature sensitive cI_(857), lacZ and defective Q genes was induced by increasing temperature to produce β-galactosidase, an intracellular reporter protein. The overproduction of β-galactosidase was carried out without experiencing the cell lysis due to the defective Q gene. After the temperature shift, the second prophage from the lysogen MS21/Φ434 was induced by mitomycin C or ultra-violet light to lyse the cell. The lysis of the cell releases the intracellular protein to the outer space. The cell lysis was confirmed by the decrease of cell density and the increase of the extracellular activity of β-galactosidase at the same time.
Salvador Naranjo-Suarez,Dolph L. Hatfield,Bradley A. Carlson,Ryuta Tobe,유민혁,Petra A. Tsuji,Vadim N. Gladyshev 한국분자세포생물학회 2013 Molecules and cells Vol.36 No.2
Under hypoxic conditions, cells activate a transcriptional response mainly driven by hypoxia-inducible factors (HIFs). HIF-1 stabilization and activity are known to be regulated by thioredoxin 1 (Txn1), but how the thioredoxin system regulates the hypoxic response is unknown. By examining the effects of Txn1 overexpression on HIF-1 function in HeLa, HT-29, MCF-7 and EMT6 cell lines, we found that this oxidoreductase did not stabilize HIF-1, yet could increase its activity. These effects were dependent on the redox function of Txn1. However, Txn1 deficiency did not affect HIF-1 hypoxic-stabilization and activity, and overexpression of thioredoxin reductase 1 (TR1), the natural Txn1 reductase, had no influence on HIF-1 activity. Moreover, overexpression of Txn1 in TR1 deficient HeLa and EMT6 cells was still able to increase HIF-1 hypoxic activity. These results indicate that Txn1 is not essential for HIF-1 hypoxic stabilization or activity, that its overex-pression can increase HIF-1 hypoxic activity, and that this effect is observed regardless of TR1 status. Thus, regulation of HIF-1 by the thioredoxin system depends on the specific levels of this system’s major components.