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26 results on '"Goldstein, Marsha"'

1. Comparative PRKAR1A Genotype-Phenotype Analyses in Humans with Carney Complex and prkar1a Haploinsufficient Mice

Author

Veugelers, Mark, Wilkes, David, Burton, Kimberly, McDermott, Deborah A., Song, Yan, Goldstein, Marsha M., La Perle, Krista, Vaughan, Carl J., O'Hagan, Art, Bennett, Kenneth R., Meyer, Beat J., Legius, Eric, Karttunen, Mervi, Norio, Reijo, Kaariainen, Helena, Lavyne, Michael, Neau, Jean-Philippe, Richter, Gert, Kirali, Kaan, Farnsworth, Alan, Stapleton, Karen, Morelli, Peter, Takanashi, Yoshinori, Bamforth, John-Steven, Eitelberger, Franz, Noszian, Irene, Manfroi, Waldimiro, Powers, James, Mochizuki, Yoshihiko, Imai, Tsuneo, Driscoll, Deborah A., Goldmuntz, Elizabeth, Edelberg, Jay M., Collins, Amanda, Eccles, Diana, Irvine, Alan D., McKnight, G. Stanley, Basson, Craig T., and Taylor, Susan S.

Published
2004

6. TBX5 regulates cardiac cell behavior during cardiogenesis

Author

Artman, Michael, Benson, D. Woodrow, Srivastava, Deepak, Nakazawa, Makoto, Hatcher, Cathy J., Kim, Min-Su, Pennisi, David J., Song, Yan, Diman, Nata, Goldstein, Marsha M., Mikawa, Takashi, Basson, Craig T., Artman, Michael, Benson, D. Woodrow, Srivastava, Deepak, Nakazawa, Makoto, Hatcher, Cathy J., Kim, Min-Su, Pennisi, David J., Song, Yan, Diman, Nata, Goldstein, Marsha M., Mikawa, Takashi, and Basson, Craig T.

Abstract

Mutations in human TBX5 cause congenital structural abnormalities of the heart and limb in autosomal dominant Holt–Oram syndrome.1–3 Holt–Oram syndrome presents as congenital heart disease in the setting of preaxial radial ray limb deformity. Our previous analyses have shown that TBX5 haploinsufficiency causes human atrial and ventricular defects as well as abnormalities of my- ocardial and trabecular structure that reflect cardiac isomerism.2,4...

Published
2005

7. A role for Tbx5 in proepicardial cell migration during cardiogenesis

Author

Hatcher, Cathy J., Diman, Nata Y.S.-G., Kim, Min-Su, Pennisi, David J., Song, Yan, Goldstein, Marsha M., Mikawa, Takashi, Basson, Craig T., Hatcher, Cathy J., Diman, Nata Y.S.-G., Kim, Min-Su, Pennisi, David J., Song, Yan, Goldstein, Marsha M., Mikawa, Takashi, and Basson, Craig T.

Abstract

Transcriptional regulatory cascades during epicardial and coronary vascular development from proepicardial progenitor cells remain to be defined. We have used immunohistochemistry of human embryonic tissues to demonstrate that the TBX5 transcription factor is expressed not only in the myocardium, but also throughout the embryonic epicardium and coronary vasculature. TBX5 is not expressed in other human fetal vascular beds. Furthermore, immunohistochemical analyses of human embryonic tissues reveals that unlike their epicardial counterparts, delaminating epicardial-derived cells do not express TBX5 as they migrate through the subepicardium before undergoing epithelial-mesenchymal transformation required for coronary vasculogenesis. In the chick, Tbx5 is expressed in the embryonic proepicardial organ (PEO), which is composed of the epicardial and coronary vascular progenitor cells. Retrovirus-mediated overexpression of human TBX5 inhibits cell incorporation of infected proepicardial cells into the nascent chick epicardium and coronary vasculature. TBX5 overexpression as well as antisense-mediated knockdown of chick Tbx5 produce a cell-autonomous defect in the PEO that prevents proepicardial cell migration. Thus, both increasing and decreasing Tbx5 dosage impairs development of the proepicardium. Culture of explanted PEOs demonstrates that untreated chick proepicardial cells downregulate Tbx5 expression during cell migration. Therefore, we propose that Tbx5 participates in regulation of proepicardial cell migration, a critical event in the establishment of the epicardium and coronary vasculature.

Published
2004

12. A t(2;19)(p13;p13.2) in a giant invasive cardiac lipoma from a patient with multiple lipomatosis

Author

Vaughan, Carl J., primary, Weremowicz, Stanislawa, additional, Goldstein, Marsha M., additional, Casey, Mairead, additional, Hart, Matt, additional, Hahn, Rebecca T., additional, Devereux, Richard B., additional, Girardi, Leonard, additional, Schoen, Frederick J., additional, Fletcher, Jonathan A., additional, Morton, Cynthia C., additional, and Basson, Craig T., additional

Published
2000
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15. Mice Transgenic for Monocyte-Tropic HIV Type 1 Produce Infectious Virus and Display Plasma Viremia: A Newin VivoSystem for Studying the Postintegration Phase of HIV Replication

Author

Paul, Jessie Browning, primary, Wang, Emilie-Jeanne, additional, Pettoello-Mantovani, Massimo, additional, Raker, Christina, additional, Yurasov, Sergey, additional, Goldstein, Marsha M., additional, Horner, James W., additional, Chan, John, additional, and Goldstein, Harris, additional

Published
2000
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21. Comparative PRKAR1A genotype -- phenotype analyses in humans with Carney complex and prkar1a haploinsufficient mice.

Author

Veugeler, Mark, Wilkes, David, Burton, Kimberly, McDermott, Deborah A., Song, Van, Goldstein, Marsha M., Perle, Krista La, Vaughan, Carl J., O'hagan, Art, Bennett, Kenneth R., Meyer, Beat J., Legius, Eric, Karttunen, Mervi, Norio, Reijo, Kaariainen, Helena, Lavyne, Michael, Neau, Jean-philippe, Richter, Gert, Kirali, Kaan, and Farnsworth, Alan

Subjects
TUMORS, PHENOTYPES, RODENTS, GENETIC polymorphisms, GENETIC research, CARCINOGENESIS, PROTEIN kinases
Abstract

Carney complex (CNC) is a familial multiple neoplasia syndrome characterized by cardiac and extracardiac myxomas in the setting of spotty skin pigmentation and endocrinopathy. We previously identified PRKAR1A (regulatory subunit 1α of protein kinase A) mutations in CNC. Mutational analyses of the PRKAR1A gene in 51 unrelated CNC probands now detect mutations in 65%. All mutations, except for one unique missense mutation, lead to PRKAR1A haploinsufficiency. Therefore, we studied the consequences of prkar1a haploinsufficiency in mice. Although we did not observe cardiac myxomas or altered pigmentation in prkar1a+/- mice, we did observe some phenotypes similar to CNC, including altered heart rate variability. Moreover, prkar1a+/- mice exhibited a marked propensity for extracardiac tumorigenesis. They developed sarcomas and hepatocellular carcinomas. Sarcomas were frequently associated with myxomatous differentiation. Tumors from prkar1a+/- mice did not exhibit prkar1a loss of heterozygosity. Thus, we conclude that although PRKAR1A haploinsufficiency does predispose to tumorigenesis, distinct secondary genetic events are required for tumor formation. [ABSTRACT FROM AUTHOR]

Published
2004
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22. Feast from the Mideast

Author

Goldstein, Marsha

Subjects
Cookery, Middle Eastern, General interest, Home and garden
Published
1992

23. Mice Transgenic for Monocyte-Tropic HIV Type 1 Produce Infectious Virus and Display Plasma Viremia: A New in Vivo System for Studying the Postintegration Phase of HIV Replication

Author

Paul, Jessie Browning, Wang, Emilie-Jeanne, Pettoello-Mantovani, Massimo, Raker, Christina, Yurasov, Sergey, Goldstein, Marsha M., Horner, James W., Chan, John, and Goldstein, Harris

Abstract

To generate an in vivo system for investigating the postintegration phase of HIV-1 replication, mouse lines transgenic for a full-length infectious proviral clone of a monocyte-tropic HIV-1 isolate, HIV-1JR-C SF, were constructed. Leukocytes from two independent JR-CSF transgenic mouse lines produced HIV-1 that infected human PBMCs. Plasma viremia was detected in these mice at levels (mean, >60,000 HIV RNA copies/ml) comparable to those reported for HIV-1-infected individuals. The levels of HIV RNA in these mice increased several-fold after either treatment with the superantigen Staphylococcus enterotoxin B or infection with Mycobacterium tuberculosis. Thus, a provirus encoding a monocyte-tropic HIV-1 strain under the control of its LTR expressed as a transgene in mice can proceed through the postintegration replication phase and produce infectious virus. In addition, the presence of plasma viremia that can be monitored by measuring plasma HIV1 RNA levels permits these mice to be used to study the impact of different interventions on modulating in vivo HIV-1 production. Therefore, these mice provide a novel manipulable system to investigate the in vivo regulation of HIV-1 production by factors that activate the immune system. Furthermore, this murine system should be useful in delineating the role of human-specific factors in modulating HIV-1 replication and investigating the in vivo therapeutic efficacy of agents that target the postintegration stages of HIV-1 replication.

Published
2000
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24. VIGNETTES The Carney Complex: Unusual Skin Findings and Recurrent Cardiac Myxoma.

Author

Bennett, Kenneth R., Heath, Bobby J., Creswell, Lawrence L., Veugelers, Mark A., McDermott, Deborah A., Barksdale, Sarah, Goldstein, Marsha, and Basson, Craig T.

Subjects
SKIN inflammation, LETTERS to the editor
Abstract

Presents a letter to the editor about the clinical course of an African-American woman with Carney complex and a hypopigmented skin lesion.

Published
2005
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