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Showing papers by "Andrea Cossarizza published in 1994"


Journal ArticleDOI
TL;DR: This method studied alterations of mitochondrial membrane potential in a classical model of apoptosis, i.e., dexamethasone-treated rat thymocytes, where the involvement of mitochondria is apparently not a primary event.

199 citations


Journal ArticleDOI
TL;DR: Evidence that normal human keratinocytes in culture express the low- and the high-affinity NGF-R both at the mRNA level, as determined by reverse-transcription polymerase chain reaction and at the protein level, and results suggest that NGF could act as a cytokine in human skin and take part in disorders of keratinocyte proliferation.

191 citations


Journal ArticleDOI
TL;DR: It is demonstrated that D(-)-ribose and 2-deoxy-D-ribose can be useful tools to study the cellular and molecular events of apoptosis in human quiescent lymphocytes.

70 citations


Journal ArticleDOI
TL;DR: Results indicate that fLC do not express B7 protein on their surface, but acquire B7 during culture, 2) surface B7 is not sensitive to trypsin, 3) B7 expression is regulated primarily at the mRNA level, and 4) membrane B7 can be internalized within cLC.

48 citations


Journal ArticleDOI
TL;DR: Direct evidence of competition between CRF and IL‐2 was revealed by immunocytochemical and cytofluorimetric analysis, and the data are compatible with the presence of a unique (ancestral?) receptor on molluscan hemocytes, capable of binding bothCRF andIL‐2, two key molecules of the neuroendocrine and immune system, respectively.

44 citations


Journal ArticleDOI
TL;DR: Data indicate that PADPRP is involved in the death of target cells, and the different sensitivity of NK and LAK activities to P ADPRP inhibitors suggests that the molecular mechanisms underlying these two types of cytotoxicity are at least partially different.

29 citations


Journal ArticleDOI
TL;DR: It is suggested that cytoskeleton is an important target of 3-ABA, which appears to be due to a specific effect of the drug on some cytoskeletal elements and could be associated with its differentiating capability.

10 citations



Journal ArticleDOI
TL;DR: The mechanism by which the drug can exert its protective effects on target cell killing by NK effectors can also be due to its ability to impair cell-to-cell conjugate formation (binding), without affecting either the expression of cell adhesion molecules nor the features of effector-target cell contact.

7 citations