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Articles 1 - 11 of 11
Full-Text Articles in Entire DC Network
A Defect In Interleukin 12-Induced Activation And Interferon Gamma Secretion Of Peripheral Natural Killer T Cells In Nonobese Diabetic Mice Suggests New Pathogenic Mechanisms For Insulin-Dependent Diabetes Mellitus., Marika Falcone, Brian Yeung, Lee Tucker, Enrique Rodriguez, Nora Sarvetnick
A Defect In Interleukin 12-Induced Activation And Interferon Gamma Secretion Of Peripheral Natural Killer T Cells In Nonobese Diabetic Mice Suggests New Pathogenic Mechanisms For Insulin-Dependent Diabetes Mellitus., Marika Falcone, Brian Yeung, Lee Tucker, Enrique Rodriguez, Nora Sarvetnick
Journal Articles: Regenerative Medicine
The function of natural killer T (NKT) cells in the immune system has yet to be determined. There is some evidence that their defect is associated with autoimmunity, but it is still unclear how they play a role in regulating the pathogenesis of T cell-mediated autoimmune diseases. It was originally proposed that NKT cells could control autoimmunity by shifting the cytokine profile of autoimmune T cells toward a protective T helper 2 cell (Th2) type. However, it is now clear that the major function of NKT cells in the immune system is not related to their interleukin (IL)-4 secretion. In …
Insulin-Like Growth Factor Ii Signaling In Neoplastic Proliferation Is Blocked By Transgenic Expression Of The Metalloproteinase Inhibitor Timp-1, David C. Martin, John L. Fowlkes, Bojana Babic, Rama Khokha
Insulin-Like Growth Factor Ii Signaling In Neoplastic Proliferation Is Blocked By Transgenic Expression Of The Metalloproteinase Inhibitor Timp-1, David C. Martin, John L. Fowlkes, Bojana Babic, Rama Khokha
Pediatrics Faculty Publications
Insulin-like growth factor (IGF) II is overexpressed in many human cancers and is reactivated by, and crucial for viral oncogene (SV40 T antigen, [TAg])-induced tumorigenesis in several tumor models. Using a double transgenic murine hepatic tumor model, we demonstrate that tissue inhibitor of metalloproteinase 1 (TIMP-1) blocks liver hyperplasia during tumor development, despite TAg-mediated reactivation of IGF-II. Because the activity of IGFs is controlled by IGF-binding proteins (IGFBPs), we investigated whether TIMP-1 overexpression altered the IGFBP status in the transgenic liver. Ligand blotting showed that IGFBP-3 protein levels were increased in TIMP-1-overexpressing double transgenic littermates, whereas IGFBP-3 mRNA levels were …
Phosphoinositide-Ap-2 Interactions Required For Targeting To Plasma Membrane Clathrin-Coated Pits., I Gaidarov, James H. Keen
Phosphoinositide-Ap-2 Interactions Required For Targeting To Plasma Membrane Clathrin-Coated Pits., I Gaidarov, James H. Keen
Department of Microbiology and Immunology Faculty Papers
The clathrin-associated AP-2 adaptor protein is a major polyphosphoinositide-binding protein in mammalian cells. A high affinity binding site has previously been localized to the NH(2)-terminal region of the AP-2 alpha subunit (Gaidarov et al. 1996. J. Biol. Chem. 271:20922-20929). Here we used deletion and site- directed mutagenesis to determine that alpha residues 21-80 comprise a discrete folding and inositide-binding domain. Further, positively charged residues located within this region are involved in binding, with a lysine triad at positions 55-57 particularly critical. Mutant peptides and protein in which these residues were changed to glutamine retained wild-type structural and functional characteristics by …
Interaction Between Fgf And Bmp Signaling Pathways Regulates Development Of Metanephric Mesenchyme., Andrew T. Dudley, R. E. Godin, E. J. Robertson
Interaction Between Fgf And Bmp Signaling Pathways Regulates Development Of Metanephric Mesenchyme., Andrew T. Dudley, R. E. Godin, E. J. Robertson
Journal Articles: Genetics, Cell Biology & Anatomy
Nephrogenesis in the mouse kidney begins at embryonic day 11 and ends approximately 10 days postpartum. During this period, new nephrons are continually being generated from a stem-cell population-the nephrogenic mesenchyme-in response to signals emanating from the tips of the branching ureter. Relatively little is known about the mechanism by which the nephrogenic mesenchyme cell population is maintained at the tips of the ureter in the presence of signals promoting tubulogenesis. Previous studies have shown that a loss of Bmp7 function leads to kidney defects that are a likely result of progressive loss of nephrogenic mesenchyme by apoptosis. The studies …
Signal Transducer And Activator Of Transcription (Stat)5 Activation By Bcr/Abl Is Dependent On Intact Src Homology (Sh)3 And Sh2 Domains Of Bcr/Abl And Is Required For Leukemogenesis., M Nieborowska-Skorska, M A Wasik, A Slupianek, P Salomoni, T Kitamura, B Calabretta, T Skorski
Signal Transducer And Activator Of Transcription (Stat)5 Activation By Bcr/Abl Is Dependent On Intact Src Homology (Sh)3 And Sh2 Domains Of Bcr/Abl And Is Required For Leukemogenesis., M Nieborowska-Skorska, M A Wasik, A Slupianek, P Salomoni, T Kitamura, B Calabretta, T Skorski
Department of Microbiology and Immunology Faculty Papers
Signal transducer and activator of transcription (STAT)5 is constitutively activated in BCR/ ABL-expressing cells, but the mechanisms and functional consequences of such activation are unknown. We show here that BCR/ABL induces phosphorylation and activation of STAT5 by a mechanism that requires the BCR/ABL Src homology (SH)2 domain and the proline-rich binding site of the SH3 domain. Upon expression in 32Dcl3 growth factor-dependent myeloid precursor cells, STAT5 activation-deficient BCR/ABL SH3+SH2 domain mutants functioned as tyrosine kinase and activated Ras, but failed to protect from apoptosis induced by withdrawal of interleukin 3 and/or serum and did not induce leukemia in severe combined …
A Cbfa1-Dependent Genetic Pathway Controls Bone Formation Beyond Embryonic Development, P Ducy, M Starbuck, M Priemel, J Shen, G Pinero, V Geoffroy, M Amling, G Karsenty
A Cbfa1-Dependent Genetic Pathway Controls Bone Formation Beyond Embryonic Development, P Ducy, M Starbuck, M Priemel, J Shen, G Pinero, V Geoffroy, M Amling, G Karsenty
Journal Articles
The molecular mechanisms controlling bone extracellular matrix (ECM) deposition by differentiated osteoblasts in postnatal life, called hereafter bone formation, are unknown. This contrasts with the growing knowledge about the genetic control of osteoblast differentiation during embryonic development. Cbfa1, a transcriptional activator of osteoblast differentiation during embryonic development, is also expressed in differentiated osteoblasts postnatally. The perinatal lethality occurring in Cbfa1-deficient mice has prevented so far the study of its function after birth. To determine if Cbfa1 plays a role during bone formation we generated transgenic mice overexpressing Cbfa1 DNA-binding domain (DeltaCbfa1) in differentiated osteoblasts only postnatally. DeltaCbfa1 has a higher …
Induction Of Integral Membrane Pam Expression In Att-20 Cells Alters The Storage And Trafficking Of Pomc And Pc1, Giuseppe D. Ciccotosto, Martin R. Schiller, Betty A. Eipper, Richard E. Mains
Induction Of Integral Membrane Pam Expression In Att-20 Cells Alters The Storage And Trafficking Of Pomc And Pc1, Giuseppe D. Ciccotosto, Martin R. Schiller, Betty A. Eipper, Richard E. Mains
Life Sciences Faculty Research
Peptidylglycine alpha-amidating monooxygenase (PAM) is an essential enzyme that catalyzes the COOH-terminal amidation of many neuroendocrine peptides. The bifunctional PAM protein contains an NH2-terminal monooxygenase (PHM) domain followed by a lyase (PAL) domain and a transmembrane domain. The cytosolic tail of PAM interacts with proteins that can affect cytoskeletal organization. A reverse tetracycline-regulated inducible expression system was used to construct an AtT-20 corticotrope cell line capable of inducible PAM-1 expression. Upon induction, cells displayed a time- and dose-dependent increase in enzyme activity, PAM mRNA, and protein. Induction of increased PAM-1 expression produced graded changes in PAM-1 metabolism. Increased expression of …
Mechanisms Of Immunotherapeutic Intervention By Anti-Cd40l (Cd154) Antibody In An Animal Model Of Multiple Sclerosis, Laurence M. Howard, Amy J. Miga, Carol L. Vanderlugt, Mauro C. Dal Canto, John D. Laman, Randolph J. Noelle, Stephen D. Miller
Mechanisms Of Immunotherapeutic Intervention By Anti-Cd40l (Cd154) Antibody In An Animal Model Of Multiple Sclerosis, Laurence M. Howard, Amy J. Miga, Carol L. Vanderlugt, Mauro C. Dal Canto, John D. Laman, Randolph J. Noelle, Stephen D. Miller
Dartmouth Scholarship
Relapsing experimental autoimmune encephalomyelitis (R-EAE) in the SJL mouse is a Th1-mediated autoimmune demyelinating disease model for human multiple sclerosis and is characterized by infiltration of the central nervous system (CNS) by Th1 cells and macrophages. Disease relapses are mediated by T cells specific for endogenous myelin epitopes released during acute disease, reflecting a critical role for epitope spreading in the perpetuation of chronic central CNS pathology. We asked whether blockade of the CD40–CD154 (CD40L) costimulatory pathway could suppress relapses in mice with established R-EAE. Anti-CD154 antibody treatment at either the peak of acute disease or during remission effectively blocked …
Transgenic Mice Which Overexpress Neurotrophin-3 (Nt-3) And Method Of Use, Kathryn M. Albers, Brian M. Davis
Transgenic Mice Which Overexpress Neurotrophin-3 (Nt-3) And Method Of Use, Kathryn M. Albers, Brian M. Davis
Neuroscience Faculty Patents
Transgenic mice express increased levels of neurotrophin-3 (NT-3) in epithelium when their ancestors are microinjected with the NT-3 gene. The NT-3 growth factor expressing transgenic mice are useful in the study of neurodegenerative disorders of the brain such as Parkinson's syndrome and Alzheimer's disease, of the spinal cord motor neurons such as amyotrophic lateral sclerosis, and for testing drug candidates for the treatment of these diseases.
Supraspinal Neurotensin-Induced Antianalgesia In Mice Is Mediated By Spinal Cholecystokinin., Blythe B. Holmes, Jodie J. Rady, David J. Smith, James M. Fujimoto
Supraspinal Neurotensin-Induced Antianalgesia In Mice Is Mediated By Spinal Cholecystokinin., Blythe B. Holmes, Jodie J. Rady, David J. Smith, James M. Fujimoto
Faculty & Staff Scholarship
No abstract provided.
Osteopathy And Resistance To Vitamin D Toxicity In Mice Null For Vitamin D Binding Protein, Fayez F. Safadi, Paul Thornton, Holly Magiera, Bruce W. Hollis, Michael Gentile, John G. Haddad, Stephen A. Liebhaber, Nancy E. Cooke
Osteopathy And Resistance To Vitamin D Toxicity In Mice Null For Vitamin D Binding Protein, Fayez F. Safadi, Paul Thornton, Holly Magiera, Bruce W. Hollis, Michael Gentile, John G. Haddad, Stephen A. Liebhaber, Nancy E. Cooke
MUSC Faculty Journal Articles
A line of mice deficient in vitamin D binding protein (DBP) was generated by targeted mutagenesis to establish a model for analysis of DBP's biological functions in vitamin D metabolism and action. On vitamin D-replete diets, DBP-/-mice had low levels of total serum vitamin D metabolites but were otherwise normal. When maintained on vitamin D-deficient diets for a brief period, the DBP-/- but not DBP+/+, mice developed secondary hyperparathyroidism and the accompanying bone changes associated with vitamin D deficiency. DBP markedly prolonged the serum half-life of 25(OH)D and less dramatically prolonged the half-life of vitamin D by slowing its hepatic …