D. M. Klotz

发表

Inhibition of progesterone receptor activity in yeast by synthetic chemicals.

J. McLachlan, S. F. Arnold, D. Q. Tran, 1996, Biochemical and biophysical research communications.

Identification of environmental chemicals with estrogenic activity using a combination of in vitro assays.

S. Hill, J. McLachlan, S. F. Arnold, 1996, Environmental health perspectives.

Expression of a constitutively active estrogen receptor variant in the estrogen receptor-negative BT-20 human breast cancer cell line.

S. Hill, S. Fuqua, D. M. Klotz, 1993, Cancer research.

E2-induced degradation of uterine insulin receptor substrate-2: requirement for an IGF-I-stimulated, proteasome-dependent pathway.

M. Bush, D. Walmer, R. Richards, 2001, Endocrinology.

o,p′-DDT and its metabolites inhibit progesterone-dependent responses in yeast and human cells

J. McLachlan, S. F. Arnold, D. M. Klotz, 1997, Molecular and Cellular Endocrinology.

Mammary gland branching morphogenesis is diminished in mice with a deficiency of insulin-like growth factor-I (IGF-I), but not in mice with a liver-specific deletion of IGF-I.

M. P. Walker, R. Richards, D. M. Klotz, 2004, Endocrinology.

Printed in U.S.A. Copyright © 2000 by The Endocrine Society Activation of a Uterine Insulin-Like Growth Factor I Signaling Pathway by Clinical and Environmental

K. Korach, S. Hewitt, D. M. Klotz, 2000 .

Synergism in estrogen-regulated gene expression

J. McLachlan, S. F. Arnold, D. M. Klotz, 1996, Molecular and Cellular Endocrinology.

Inhibition of 17 beta-estradiol and progesterone activity in human breast and endometrial cancer cells by carbamate insecticides.

J. McLachlan, S. F. Arnold, D. M. Klotz, 1997, Life sciences.

Identification ofEnvironmental Chemicals withEstrogenic Activity Using a Combination ofInVitro Assays

B. Beckman, D. M. Klotz, 1996 .

Dexniguldipine hydrochloride, a protein-kinase-C-specific inhibitor, affects the cell cycle, differentiation, P-glycoprotein levels, and nuclear protein phosphorylation in friend erythroleukemia cells

B. Beckman, J. R. Jeter, D. M. Klotz, 2005, Journal of Cancer Research and Clinical Oncology.

Hormonal Activation of the Gab-1 Docking Protein in Uterine Cells

D. Walmer, R. Richards, D. M. Klotz, 2005 .

Differential responsiveness of MCF‐7 human breast cancer cell line stocks to the pineal hormone, melatonin

P. Ram, S. Hill, Lin Yuan, 2000, Journal of pineal research.

Requirement of Estrogen Receptor-α in Insulin-like Growth Factor-1 (IGF-1)-induced Uterine Responses and in Vivo Evidence for IGF-1/Estrogen Receptor Cross-talk*

K. Korach, J. Foley, A. Maggi, 2002, The Journal of Biological Chemistry.

Activation of a uterine insulin-like growth factor I signaling pathway by clinical and environmental estrogens: requirement of estrogen receptor-alpha.

K. Korach, S. Hewitt, D. M. Klotz, 2000, Endocrinology.

Genetics of Breast Cancer

S. Hill, D. M. Klotz, C. S. Cohn, 1996 .

Coexpression of wild-type and variant oestrogen receptor mRNAs in a panel of human breast cancer cell lines.

S. Fuqua, S. Hill, D. M. Klotz, 1995, British Journal of Cancer.

Synergistic Activation of Estrogen Receptor with Combinations of Environmental Chemicals

Steven F. Arnold, J. McLachlan, L. Guillette, 1996, Science.

Essiac® and Flor-Essence® herbal tonics stimulate the in vitro growth of human breast cancer cells

D. Nelson, L. Bennett, K. Kulp, 2005, Breast Cancer Research and Treatment.

In vitro synergistic interaction of alligator and human estrogen receptors with combinations of environmental chemicals.

J. McLachlan, L. Guillette, S. F. Arnold, 1997, Environmental health perspectives.

Differential expression of wild-type and variant ER mRNAs by stocks of MCF-7 breast cancer cells may account for differences in estrogen responsiveness.

S. Fuqua, S. Hill, D. M. Klotz, 1995, Biochemical and biophysical research communications.

Activation of a uterine insulin-like growth factor I signaling pathway by clinical and environmental estrogens: requirement of estrogen receptor-alpha.

K. Korach, S. Hewitt, D. M. Klotz, 2000, Endocrinology.