Signaling through MHC class II molecules blocks CD95-induced apoptosis.
AuthorsCatlett IM,Xie P,Hostager BS,Bishop GA
JournalJournal of immunology (Baltimore, Md. : 1950)
PubMed ID11342618
Cutting edge: cellular Fas-associated death domain-like IL-1-converting enzyme-inhibitory protein protects germinal center B cells from apoptosis during germinal center reactions.
Authorsvan Eijk M, Medema JP, de Groot C
JournalJ Immunol
PubMed ID11359796
'During germinal center (GC) reactions, follicular dendritic cells are believed to select memory B lymphocytes by switching off apoptosis in the successfully binding B cells. The cellular signals involved in this process are largely unknown. Here, we show that GC B lymphocytes have a long isoform of the cellular homologue ... More
Huntingtin's neuroprotective activity occurs via inhibition of procaspase-9 processing.
AuthorsRigamonti D, Sipione S, Goffredo D, Zuccato C, Fossale E, Cattaneo E
JournalJ Biol Chem
PubMed ID11278258
Huntington's Disease is an inherited neurodegenerative disease that affects the medium spiny neurons in the striatum. The disease is caused by the expansion of a polyglutamine sequence in the N terminus of Huntingtin (Htt), a widely expressed protein. Recently, we have found that Htt is an antiapoptotic protein in striatal ... More
A combinatorial approach defines specificities of members of the caspase family and granzyme B. Functional relationships established for key mediators of apoptosis.
AuthorsThornberry NA, Rano TA, Peterson EP, Rasper DM, Timkey T, Garcia-Calvo M, Houtzager VM, Nordstrom PA, Roy S, Vaillancourt JP, Chapman KT, Nicholson DW
JournalJ Biol Chem
PubMed ID9218414
There is compelling evidence that members of the caspase (interleukin-1beta converting enzyme/CED-3) family of cysteine proteases and the cytotoxic lymphocyte-derived serine protease granzyme B play essential roles in mammalian apoptosis. Here we use a novel method employing a positional scanning substrate combinatorial library to rigorously define their individual specificities. The ... More
Kep1 interacts genetically with dredd/caspase-8, and kep1 mutants alter the balance of dredd isoforms.
AuthorsDi Fruscio M, Styhler S, Wikholm E, Boulanger MC, Lasko P, Richard S
JournalProc Natl Acad Sci U S A
PubMed ID12563030
The Drosophila kep1 gene encodes an RNA binding protein related to the murine QUAKING apoptotic inducer. We have previously shown that kep1 can induce apoptosis when transfected into different cell lines. To better define the role of Kep1 in apoptosis, we generated kep1 null flies. These flies were viable, but ... More
Pivotal role of oligomerization in expanded polyglutamine neurodegenerative disorders.
AuthorsSánchez I, Mahlke C, Yuan J
JournalNature
PubMed ID12540902
The expansion of a CAG repeat coding for polyglutamine in otherwise unrelated gene products is central to eight neurodegenerative disorders including Huntington's disease. It has been well documented that expanded polyglutamine fragments, cleaved from their respective full-length proteins, form microscopically visible aggregates in affected individuals and in transgenic mice. The ... More
DEDD regulates degradation of intermediate filaments during apoptosis.
AuthorsLee JC, Schickling O, Stegh AH, Oshima RG, Dinsdale D, Cohen GM, Peter ME
JournalJ Cell Biol
PubMed ID12235123
Apoptosis depends critically on regulated cytoskeletal reorganization events in a cell. We demonstrate that death effector domain containing DNA binding protein (DEDD), a highly conserved and ubiquitous death effector domain containing protein, exists predominantly as mono- or diubiquitinated, and that diubiquitinated DEDD interacts with both the K8/18 intermediate filament network ... More
Activation of pro-death Bcl-2 family proteins and mitochondria apoptosis pathway in tumor necrosis factor-alpha-induced liver injury.
AuthorsZhao Y, Li S, Childs EE, Kuharsky DK, Yin XM
JournalJ Biol Chem
PubMed ID11369777
Tumor necrosis factor-alpha (TNFalpha)-induced cytotoxicity contributes to the pathogenesis in inflammatory and immune responses. Here, we studied the role of pro-death Bcl-2 family proteins and the mitochondria apoptosis pathway in the development of TNFalpha-induced hepatic injury during endotoxemia. After treating mice with lipopolysaccharide or TNFalpha in the presence of d-galactosamine, ... More
Effects of interferon beta on transcobalamin II-receptor expression and antitumor activity of nitrosylcobalamin.
AuthorsBauer JA, Morrison BH, Grane RW, Jacobs BS, Dabney S, Gamero AM, Carnevale KA, Smith DJ, Drazba J, Seetharam B, Lindner DJ
JournalJ Natl Cancer Inst
PubMed ID12096086
BACKGROUND: The ubiquitous plasma membrane transcobalamin II receptor (TC II-R) mediates uptake of cobalamin (Cbl; vitamin B12), an essential micronutrient. Tumors often require more Cbl than normal tissue, and increased Cbl uptake may result from increased TC II-R expression. To examine whether Cbl could therefore be used as a carrier ... More
Changes of caspase activities involved in apoptosis of a macrophage-like cell line J774.1/JA-4 treated with lipopolysaccharide (LPS) and cycloheximide.
AuthorsKarahashi H, Amano F
JournalBiol Pharm Bull
PubMed ID10706374
The addition of lipopolysaccharide (LPS) together with cycloheximide (CHX) induced apoptosis in a subline of a J774.1 macrophage-like cell line, JA-4, as judged by terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL)-staining and poly(adenosine 5'-diphosphate (ADP)-ribose) polymerase (PARP)-cleavage. Caspase activities were examined in these macrophages in vitro ... More
The mitochondrial permeability transition augments Fas-induced apoptosis in mouse hepatocytes.
AuthorsHatano E, Bradham CA, Stark A, Iimuro Y, Lemasters JJ, Brenner DA
JournalJ Biol Chem
PubMed ID10766806
Tumor necrosis factor-alpha receptor 1 and Fas recruit overlapping signaling pathways. To clarify the differences between tumor necrosis factor alpha (TNFalpha) and Fas pathways in hepatocyte apoptosis, primary mouse hepatocytes were treated with TNFalpha or an agonist anti-Fas antibody after infection with an adenovirus expressing an IkappaB superrepressor (Ad5IkappaB). Treatment ... More