Michael P. Rosenberg

Research Triangle Park Foundation

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Friedrich Propst

Max Perutz Labs

Miriam H. Meisler

University of Michigan–Ann Arbor

Donna M. Bortner

Research Triangle Park Foundation

George F. Vande Woude

Van Andel Institute

Scott A. Keller

Coleman University

Robert M. Kovatch

National Center for Toxicological Research

Karen Lundgren

Immunome (United States)

L Osborn

Harvard University

Nancy A. Jenkins

The University of Texas MD Anderson Cancer Center

Robert P. Erickson

University of Arizona

Cooperative Institutions

National Cancer Institute

National Institutes of Health

Cancer Research Center

University of Michigan–Ann Arbor

The University of Texas MD Anderson Cancer Center

Research Triangle Park Foundation

Harvard University

Frederick National Laboratory for Cancer Research

Center for Cancer Research

Howard Hughes Medical Institute

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

Neuropathological changes in transgenic mice carrying copies of a transcriptionally activated Mos protooncogene.

Proceedings of the National Academy of Sciences (1990)

Friedrich Propst Michael P. Rosenberg Linda C. Cork Robert M. Kovatch Steven D. Rauch

Independent transgenic mouse lines carrying the mouse Mos protooncogene linked to a retroviral transcriptional control sequence display behavioral abnormalities including circling, head tilting, and head bobbing. This dominant phenotype shows various degrees of penetrance in different transgenic founder animals and lines. Neuronal and axonal degeneration, gliosis, and inflammatory infiltrates are found in all transgenic mouse lines in which behavioral traits are present. Recordings of auditory-evoked potentials in mice of one of these lines demonstrate that transgenic mice are deaf; in these mice spiral ganglia degenerate and most of the cochlear hair cells are absent. By using an S1 nuclease protection assay, we have detected RNA expression of the transgene in all tissues examined and, in particular, at high levels in brain. In situ hybridization experiments show that Mos expression can be detected in specific areas of the central nervous system. Lesions are present in areas with demonstrable overexpression of Mos.

Gliosis

10.1073/pnas.87.24.9703

Cite

Citations (33)

Deregulated cyclin E promotes p53 loss of heterozygosity and tumorigenesis in the mouse mammary gland

Oncogene (2006)

Adrian Smith Martha Henze J A Lee Kent G. Osborn Jakob Keck

Cyclin D

Cyclin A2

Cyclin E

Mammary tumor

Cyclin B

10.1038/sj.onc.1209713

Cite

Citations (32)

Male sterility caused byp6H andqk mutations is not corrected in chimeric mice

Journal of Experimental Zoology (1987)

Mary Ann Handel Linda L. Washburn Michael P. Rosenberg Eva M. Eicher

Abstract It is not known if the male sterility caused by the pleiotropic mutations p 6H (pink‐eyed 6H) and qk (quaking) is intrinsic or extrinsic to spermatogenic cells. This question was addressed by juxtaposing mutant and normal cells in the testes of chimeric mice and determining whether the mutant germ cells could form functional sperm. Twenty‐one male chimeras consisting of normal cells and p 6H / p 6H or qk / qk cells were analyzed. For each, breeding productivity and testicular and sperm morphology were determined. Karyotypes and isozyme analyses were performed to identify the two cellular components of each chimera. All male chimeras that contained p 6H / p 6H , XY cells were sterile. Although some chimeras with a qk / qk , XY mutant component were fertile, none produced offspring from the homozygous qk component. Spermatids of the sterile chimeras showed abnormalities characteristic of the mutations. We conclude from this study that the presence of normal XY germ and somatic cells in the testis did not rescue the male sterile phenotype of homozygous p 6H or qk XY germ cells. Therefore, the action of these mutant genes in causing sperm abnormalities and sterility is autonomous to the germ cells.

Chimera (genetics)

10.1002/jez.1402430111

Cite

Citations (11)

Pheochromocytomas and C-cell thyroid neoplasms in transgenic c-mos mice: a model for the human multiple endocrine neoplasia type 2 syndrome.

PubMed (1992)

N Schulz Friedrich Propst Michael P. Rosenberg R. Ilona Linnoila Richard S. Paules

Transgenic mice carrying and expressing a mos protooncogene, linked to the Moloney murine sarcoma virus long terminal repeat, develop severe neurological defects and lens abnormalities. Here we report that after long latent periods, mice in three of four of these mos transgenic lines develop a high frequency of multicentric pheochromocytomas and/or medullary thyroid neoplasms. The pattern of tumor formation is remarkably similar to the human autosomal dominantly inherited neoplastic syndrome, multiple endocrine neoplasia type 2 (MEN 2), and tumors from these transgenic animals display the same neuroendocrine marker staining pattern as seen in MEN 2. The similarity between the tumor pathologies and presentation patterns of MEN 2 patients and mos transgenic mice suggests that they may arise through related pathways. The type of tumor presentation varies in a line-dependent manner indicating that there is interaction between the transgene and the genetic background. Moreover, when the non-tumor-bearing mos transgenic line is crossed to a different mouse background, the F1 offspring display the MEN 2 phenotype. These studies indicate that penetrance of the autosomal dominant mos transgenic phenotype is dependent on both integration site and background.

Penetrance

Source

Cite

Citations (44)

Genomic instability in Gadd45a-deficient mice

Nature Genetics (1999)

M. Christine Hollander M. Saeed Sheikh Dmitry V. Bulavin Karen Lundgren Laura Augeri-Henmueller

Chromosome instability

10.1038/13802

Cite

Citations (501)

Carbon dioxide efflux accompanies release of fertilization acid from sea urchin eggs

Journal of Cellular Physiology (1981)

Robert J. Gillies Michael P. Rosenberg David W. Deamer

"Fertilization acid" is released from sea urchin eggs upon fertilization and decreases the pH of the surrounding seawater. In bicarbonate-free artificial seawater flushed with nitrogen gas, the pH shift still occurs but returns to the original value in a few minutes, suggesting that the released acid volatile. A likely candidate for a volatile acid is carbon dioxide released from the eggs. Therefore, the total CO2 content of seawater was measured pre- and post-fertilization and was found to be correlated stoichiometrically with released proton equivalents, leading to the conclusion that fertilization acid is largely carbon dioxide. Manometric analysis of cell extracts and ashed eggs suggest that the carbon dioxide may be stored in the unfertilized egg as an inorganic carbonate.

Efflux

10.1002/jcp.1041080202

Cite

Citations (10)

The Vascular Endothelial Growth Factor (VEGF) Receptor Flt-1 (VEGFR-1) Modulates Flk-1 (VEGFR-2) Signaling During Blood Vessel Formation

American Journal Of Pathology (2004)

David M. Roberts Joseph B. Kearney Jennifer H. Johnson Michael P. Rosenberg Rakesh Kumar

10.1016/s0002-9440(10)63711-x

Cite

Citations (186)

An insulin-responsive element in the pancreatic enhancer of the amylase gene.

Journal of Biological Chemistry (1993)

Thomas M. Johnson Michael P. Rosenberg Miriam H. Meisler

We have identified a distinct insulin-responsive element (IRE) located within the pancreatic enhancer of the mouse amylase gene Amy-2.2. A 30-base pair (bp) fragment was previously shown to be sufficient to transfer insulin response to a heterologous promoter. The 30-bp fragment overlaps the tissue-specific pancreatic enhancer that binds the putative transcriptional activator PTF1. To determine whether enhancer and IRE activities could be separated, we introduced three 10-base pair substitutions into the 30-bp region. The mutated regulatory regions were cloned upstream of a heterologous promoter and transferred to transgenic mice. Mutants 1 and 2 retained PTF1 binding activity and insulin response. Mutant 3 retained PTF1 binding, but was defective in insulin response. The results indicate that the IRE is functionally distinct from the PTF1-binding site, although the two overlap physically. In contrast to the wild-type gene, mutant 3 is characterized by constitutive expression in diabetic animals, suggesting that a binding site for a repressor has been destroyed. A nuclear protein with affinity for the IRE was detected in normal and diabetic pancreas. This protein does not bind mutant 3, suggesting that it may be involved in negative regulation of amylase in diabetic pancreas.

10.1016/s0021-9258(18)54174-0

Cite

Citations (43)

Overexpression of anAgouticDNA in the Skin of Transgenic Mice Recapitulates Dominant Coat Color Phenotypes of Spontaneous Mutants

Developmental Biology (1996)

Gary Kucera Donna M. Bortner Michael P. Rosenberg

Coat

Ectopic expression

Wild type

10.1006/dbio.1996.0014

Cite

Citations (73)

c-mos proto-oncogene RNA transcripts in mouse tissues: structural features, developmental regulation, and localization in specific cell types.

Molecular and Cellular Biology (1987)

Friedrich Propst Michael P. Rosenberg Anuradha R. Iyer Karen L. Kaul George F. Vande Woude

c-mos RNA transcripts have been previously detected in mouse gonadal tissue and in late-term embryos. Here, we show that they are also present at low levels in placenta and in adult mouse brain, kidney, mammary gland, and epididymis. Marked differences are observed in the size of the mos RNA transcripts detected in different tissues. All transcripts appear to end at the same 3' position, and the tissue-specific size variations appear to be due to the use of different promoters. For example, the testicular and ovarian RNA transcripts initiate approximately 280 and approximately 70 base pairs, respectively, upstream from the first initiation codon, but both end at a common site downstream from the mos open reading frame. The expression of mos is developmentally regulated in gonadal tissue. Thus, the level of mos transcripts in testes is low for the first 3 weeks after birth, increases at least 10-fold around day 25, and reaches adult levels by day 30. In contrast, ovaries from preweaning mice contain a higher level of mos mRNA compared to ovaries from adult mice. In cell fractionation experiments we show that mos transcripts are present in haploid germ cells. We find that these transcripts are associated with monosomes and polysomes. The peculiar pattern of mos expression in mouse gonadal tissue suggests a role for the c-mos proto-oncogene in germ cell differentiation.

Polysome

10.1128/mcb.7.5.1629

Cite

Citations (157)