184,305 research outputs found
The CD69 receptor: a multipurpose cell-surface trigger for hematopoietic cells.
No full textCD69 was initially described as being restricted to recently activated lymphoid cells, brat is now known to be expressed on the surface of all hematopoietically derived leukocytes. Crosslinking of CD69 generates intracellular signals in all cell lineages studied, both mouse and human, and results in a variety of cellular end I responses. Since a specific ligand has not yet been identified, a definite functional identity for CD69 is still missing. However, as discussed here by Roberto Testi and colleagues, the broad expression of CD69 and its conserved ability to generate intracellular signals suggests a general role for the CD69 receptor in the biology of hematopoietic cells
Acidic sphingomyelinase (ASM) is necessary for fas-induced GD3 ganglioside accumulation and efficient apoptosis of lymphoid cells
No full textCeramides deriving from sphingomyelin hydrolysis are important mediators of apoptotic signals originating from Fas (APO-1/CD95). However, definitive evidence for the role played by individual sphingomyelinases is still lacking. We have analyzed lymphoblastoid cell lines derived from patients affected by Niemann Pick disease (NPD), an autosomal recessive disorder caused by loss-of-function mutations within the acidic sphingomyelinase (ASM) gene. NPD lymphoblasts, which display normal neutral sphingomyelinase activity, fail to activate ASM in response to Fas cross-linking, unlike normal lymphoblasts. NPD lymphoblasts also fail to accumulate GD3 ganglioside, a downstream mediator of ceramide-induced cell death (De Maria, R., L. Lenti, F. Malisan, F. D'Agostino, B. Tomassini, A. Zeuner, M.R. Rippo, R. Testi. 1997. Science. 277:1652-1655), and display a substantially inefficient apoptosis after Fas cross-linking. Inefficient apoptosis is due to lack of ASM activity, because proximal signaling from Fas in NPD lymphoblasts is not impaired and apoptosis can be efficiently triggered by passing the ASM defect with exogenous ceramides. Moreover, mannose receptor- mediated transfer of ASM into NPD lymphoblasts rescues their ability to transiently activate ASM, accumulate GD3, and rapidly undergo apoptosis after Fas cross-linking. These results provide definitive genetic evidence for the role of ASM in the progression of apoptotic signals originating from Fas
Studi e testi per la Storia della musica
No full textEdizioni criticamente accurate e commentate di testi importanti per la storia della musica, segnatamente italiana: trattati, partiture, libretti, poesia per musica, ecc
Intracellular mediators of programmed cell death initiated at the cell surface receptor Fas
No full textApoptosis is a programmed cell death process, which plays a pivotal role in development, in tissue homeostasis and in several human diseases. Fas (CD95/Apo-1) is a member of the "death receptors" family, a group of cell surface proteins that trigger apoptosis upon binding with their natural ligands. In the immune system, intracellular signal transduction triggered from Fas splits into two different pathways. The proteolytic pathway is mediated by a family of cysteine proteases, the caspases, responsible for the morphological changes occurring in the apoptotic process. To complete this death program, another series of events, involving a lipid pathway, is necessary. Upon Fas stimulation, a sequential activation of specific enzymes results in the accumulation of ceramides and GD3 ganglioside. GD3 directly induces mitochondrial damage and triggers the release of apoptogenic factors, allowing efficient execution of Fas-mediated apoptosis
Mitochondria as sensors of sphingolipids
No full textMuch of the action in the mammalian apoptotic program takes place at the mitochondrial level. Physicochemical characteristics and integrity of mitochondrial membranes may play a crucial role in the recruitment and multimerization of pro-apoptotic Bcl-2 family members, opening of the permeability transition pore complex (PTPC) and the release of mitochondrial components which trigger the 'intrinsic' pathways of cellular apoptosis and activate executioner caspases. Recent evidence has accumulated pointing toward the mitochondrial membranes as the key targets for lipid and glycolipid mediators of stress-induced apoptosis. Mitochondrial membranes may thus act as 'sensors' of cellular stress by quantitating the local accumulation of specific lipids and glycolipids. Acute accumulation of ceramides, directly or indirectly, profoundly affects mitochondrial functions. GD3 ganglioside, a glycolipid which is actively synthesized and transiently accumulates in the early stages of apoptosis, relocates to the mitochondrial membranes causing the opening of the PTPC and the release of apoptogenic factors. Mitochondrial membranes appear to represent a common destination where protein and glycolipid mediators of stress converge and where crucial decisions about cellular adaptation or apoptotic cell death are taken
A Keplerian Gaseous Disk around the B0 Star R Monocerotis
No full textWe present high angular resolution observations of the circumstellar disk around the massive Herbig Be star R Mon (M*~8 Msolar) in the continuum at 2.7 and 1.3 mm and the 12CO 1-->0 and 2-->1 rotational lines. On the basis of the new 1.3 mm continuum image, we estimate a disk mass (gas+dust) of 0.007 Msolar and an outer radius of <150 AU. Our CO images are consistent with the existence of a Keplerian rotating gaseous disk around this star. Up to our knowledge, this is the most clear evidence for the existence of Keplerian disks around massive stars reported thus far. The mass and physical characteristics of this disk are similar to those of the more evolved T Tauri stars and indicate a shorter timescale for the evolution and dispersal of circumstellar disks around massive stars which lose most of their mass before the star becomes visible
GD3 in cellular ageing and apoptosis
No full textLipid and glycolipid mediators are important components of the adaptive responses to stress, including apoptosis. In mammalian cells, the intracellular accumulation of ganglioside GD3, an acidic glycosphingolipid, contributes to mitochondrial damage, a crucial event during the apoptotic program. GD3 is a minor ganglioside in most normal tissues. Its expression increases during development and in pathological conditions such as cancer and neurodegenerative disorders. Interestingly, GD3 expression also increases with the normal ageing process. Moreover, GD3 can also mediate biological events like proliferation and differentiation. Since organism integrity requires a tight balance between cell proliferation, apoptosis and senescence, controlling the intracellular level of GD3 appears of particular importance for cell fate determination
GD3 ganglioside and apoptosis
No full textLipid and glycolipid mediators are important messengers of the adaptive responses to stress, including apoptosis. In mammalian cells, the intracellular accumulation of ganglioside GD3, an acidic glycosphingolipid, contributes to mitochondrial damage, a crucial event during the apoptopic program. GD3 is a minor ganglioside in most normal tissues. Its expression increases during development and in pathological conditions such as cancer and neurodegenerative disorders. Intriguingly, GD3 can mediate additional biological events such as cell proliferation and differentiation. These diverse and opposing effects indicate that tightly regulated mechanisms, including 9-O-acetylation, control GD3 function, by affecting intracellular levels, localization and structure of GD3, and eventually dictate biological outcomes and cell fate decisions. © 2002 Elsevier Science B.V. All rights reserved
The ganglioside GD3 as the greek goddess Hecate: Several faces turned towards as many directions
No full textThe disialoganglioside GD3 can mediate biological functions as diverse as proliferation, differentiation, and apoptosis. Since intracellular level of GD3 is crucial for the cell, understanding the mechanisms by which GD3 metabolism is tightly regulated seems of particular importance. GD3 can be enlisted among the most potent natural inducers of mitochondrial damage and apoptosis. However, some cell types resist GD3-mediated mitochondrial damage through complex mechanisms which are beginning to be unveiled. © 2005 IUBMB
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