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Your search keyword '"Pattengale, Paul K."' showing total 145 results
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145 results on '"Pattengale, Paul K."'

7. Multiple factors determine the selection of the ectodomain cleavage site of human cell surface macrophage colony-stimulating factor

Author

Deng, Ping, Wang, Ying-Lin, Haga, Yoichi, and Pattengale, Paul K.

Subjects
Scission (Chemistry) -- Research, Plasma membranes -- Research, Macrophage colony stimulating factor -- Research, Proteins -- Analysis, Biological sciences, Chemistry
Abstract

The ectodomain cleavage of cell surface transmembrane proteins was carried out using the human cell surface macrophage colony-stimulating factor (CSF-1 (super 256), M-CSFalpha) as a model system. CSF-1(super 256), M-CSFalpha was converted to a soluble growth factor using a regulated proteolytic cleavage process at amino acid residues 157-159. Experimental results showed that the amino acid sequence of the juxtamembrane region, the steric accessibility of the protease and the distance of the cleavage selection site from the transmembrane domain determine the cleavage selection site.

Published
1998

10. Bethesda proposals for classification of nonlymphoid hematopoietic neoplasms in mice

Author

Kogan, Scott C., Ward, Jerrold M., Anver, Miriam R., Berman, Jules J., Brayton, Cory, Cardiff, Robert D., Carter, John S., de Coronado, Sherri, Downing, James R., Fredrickson, Torgny N., Haines, Diana C., Harris, Alan W., Harris, Nancy Lee, Hiai, Hiroshi, Jaffe, Elaine S., MacLennan, Ian C.M., Pandolfi, Pier Paolo, Pattengale, Paul K., Perkins, Archibald S., Simpson, R. Mark, Tuttle, Mark S., Wong, Joanne F., and Morse, Herbert C., III

Published
2002
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17. Acute leukemia in bcr/abl transgenic mice

Author

Heisterkamp, Nora, Jenster, Guido, ten Hoeve, Joanne, Zovich, Daniel, Pattengale, Paul K., and Groffen, John

Subjects
Translocation (Genetics) -- Research, Genetically modified mice -- Research, Acute leukemia -- Models, Human chromosome abnormalities -- Research, Myeloblastic leukemia -- Causes of, Lymphocytic leukemia -- Causes of, Oncogenes -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

The Philadelphia chromosome is a chromosomal abnormality where a part of chromosome 9 is translocated, or moved, to chromosome 22 and a part of chromosome 22 is translocated to chromosome 9. The Philadelphia chromosome is seen in patients with certain leukemias such as chronic myelocytic leukemia and acute lymphoblastic leukemia. The oncogene (gene which can cause cancer), known as 'abl', and located on chromosome 9, is moved next to another oncogene, known as 'bcr', on chromosome 22. In patients with acute lymphoblastic leukemia, there are two areas of the chromosomes where the deoxyribose nucleic acid (DNA) breaks and the genes join with the other genes. One area is in a cluster of breakpoints, the other is in a part of the bcr gene. When the DNA breaks in the part of the bcr gene, two genes (bcr and abl) code for a protein which is a combination of two proteins, known as the bcr/abl fusion protein, p190. The fusion protein has abnormal functions, including the addition of phosphate molecules to other molecules and to itself. Transgenic mice were injected with a gene that codes for the bcr/abl p190 fusion protein. The progeny of the mice were either born dead, or died within 10 to 58 days after birth, after developing acute myeloid or lymphoid leukemia. These findings support the theory that the Philadelphia chromosome is involved in the development of leukemia. This animal model for human leukemia, containing the Philadelphia chromosome, will result in a better understanding of the disease and provide further opportunities for testing treatments. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1990

22. A human immunoglobulin gene reduces the incidence of lymphomas in c-Myc-bearing transgenic mice

Author

Nussenzweig, Michel C., Schmidt, Emmett V., Shaw, Albert C., Sinn, Eric, Campos-Torres, Juanita, Mathey-Provot, Bernard, Pattengale, Paul K., and Leder, Philip

Subjects
Genetic research -- Reports, Immunoglobulins -- Genetic aspects, Lymphomas -- Research, Cancer -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Published
1988

25. Assessment of the morphology and significance of the lymph nodal and hepatic lesions produced in rats by the feeding of certain mineral oils and waxes

Author

Carlton, William W., primary, Boitnott, John K., additional, Dungworth, Donald L., additional, Ernst, Heinrich, additional, Hayashi, Yuzo, additional, Mohr, Ulrich, additional, Parodi, André Laurent, additional, Pattengale, Paul K., additional, Rittinghausen, Susanne, additional, and Ward, Jerrold M., additional

Published
2001
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28. Thymic lymphoproliferative disease after successful correction of CD40 ligand deficiency by gene transfer in mice

Author

Brown, Michael P., primary, Topham, David J., additional, Sangster, Mark Y., additional, Zhao, Jingfeng, additional, Flynn, Kirsten J., additional, Surman, Sherri L., additional, Woodland, David L., additional, Doherty, Peter C., additional, Farr, Andrew G., additional, Pattengale, Paul K., additional, and Brenner, Malcolm K., additional

Published
1998
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33. Subcutaneous Panniculitis-Like T-Cell Lymphoma in Two Pediatric Patients: An HIV-Positive Adolescent and a 4-Month-Old Infant.

Author

Acree, Sara C., Tovar, Jason P., Pattengale, Paul K., Wang, Larry L., Church, Joseph A., Gaynon, Paul S., and Cassarino, David S.

Subjects
LYMPHOMAS in children, T cells, HIV-positive persons, PEDIATRIC hematology, IMMUNOSUPPRESSIVE agents, CANCER treatment
Abstract

Subcutaneous Panniculitis-like T-cell lymphoma (SPTCL) is a rare subtype of childhood non-Hodgkin lymphoma. Subcutaneous Panniculitis-like T-cell lymphoma has an aggressive variant associated with the hemophagocytic syndrome (HPS). Patients without HPS show resolution of the disease with prednisone or immunosuppressive therapy unlike other T-cell lymphomas. One HIV-positive adolescent and one infant with multiple subcutaneous masses are presented and the literature is reviewed. Lesional cells were consistent with SPTCL alpha-beta type. Our cases, without HPS, showed complete resolution of their lesions when treated with non-aggressive therapies. Patients with SPTCL alpha-beta should be treated conservatively. [ABSTRACT FROM AUTHOR]

Published
2013
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37. Virus-Induced Immunosuppression

Author

Pattengale, Paul K.

Subjects
Virus-Induced Immunosuppression (Book) -- Book reviews, Books -- Book reviews
Published
1990

48. BCR/ABL P210 and P190 Cause Distinct Leukemia in Transgenic Mice

Author

Voncken, Jan Willem, Kaartinen, Vesa, Pattengale, Paul K., Germeraad, Wilfred T.V., Groffen, John, and Heisterkamp, Nora

Abstract

DNA constructs encoding BCR/ABLP210 have been introduced into the mouse germ line using microinjection of one-cell fertilized eggs. Kinetics of BCR/ABLP210 expression in transgenic mice were very similar to those of BCR/ABLP190 constructs in transgenic mice. mRNA transcripts were detectable early in embryonic development and also in hematopoietic tissue of adult animals. Expression of BCR/ABLin peripheral blood preceded development of overt disease. P210 founder and progeny transgenic animals, when becoming ill, developed leukemia of B, T-lymphoid, or myeloid origin after a relatively long latency period. In contrast, P190-transgenic mice exclusively developed leukemia of B-cell origin, with a relatively short period of latency. The observed dissimilarities are most likely due to intrinsically different properties of the P190 and P210 oncoproteins and may also involve sequences that control transgene expression. The delayed progression of BCR/ABLP210-associated disease in the transgenic mice is consistent with the apparent indolence of human chronic myeloid leukemia during the chronic phase. We conclude that, in transgenic models, comparable expression of BCR/ABLP210 and BCR/ABLP190 results in clinically distinct conditions.

Published
1995
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49. Specificity of Disease Induced by M-MuLV Chimeric Retroviruses Containing v-mycor v-srcIs Not Determined by the LTR

Author

Feuer, Gerold, Lee, William T., Pattengale, Paul K., and Fan, Hung

Abstract

The long terminal repeats (LTRs) of defective Moloney Murine Leukemia Virus (M-MuLV) containing the avian v-mycand v-srconcogenes were exchanged for LTRs from murine retroviruses inducing myeloid and erythroid disease, in an attempt to retarget disease specificity. Chimeric MuLVs containing either the Myeloproliferative sarcoma virus or the Rauscher mink cell focus-inducing virus LTRs induced the same disease as the parental viruses, suggesting that for these viruses the v-mycand v-srconcogenes are the major determinants in the disease specificity. However, substitution of the LTRs did affect the efficiency of tumorigenesis.

Published
1993
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