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0025916387
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The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosis
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The TNF receptor superfamily of cellular and viral proteins: Activation, costimulation, and death
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Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis
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Watanabe-Fukunaga R, Brannan CI, Copeland NG, Jenkins NA, Nagata S. Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosis. Nature. 356:1992;314-317.
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Watanabe-Fukunaga, R.1
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4
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Molecular cloning and expression of the Fas ligand, a novel member of the tumor necrosis factor family
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Suda, T.1
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5
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0028223847
-
Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand
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of outstanding interest. The defect in gld/gld mice, which leads to autoimmune disease, is shown to be a point mutation in the gene for FasL (see also [6]]). The same group had shown previously that lpr/lpr mice carry a mutant Fas gene (see [3]).
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Takahashi T, Tanaka M, Brannan CI, Jenkins NA, Copeland NG, Suda T, Nagata S. Generalized lymphoproliferative disease in mice, caused by a point mutation in the Fas ligand. of outstanding interest Cell. 76:1994;969-976 The defect in gld/gld mice, which leads to autoimmune disease, is shown to be a point mutation in the gene for FasL (see also [6]]). The same group had shown previously that lpr/lpr mice carry a mutant Fas gene (see [3]).
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Takahashi, T.1
Tanaka, M.2
Brannan, C.I.3
Jenkins, N.A.4
Copeland, N.G.5
Suda, T.6
Nagata, S.7
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6
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0028429962
-
The mouse Fas-ligand gene is mutated in gld mice and is part of the TNF family gene cluster
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of outstanding interest. See annotation [5].
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Lynch DH, Watson M, Alderson MR, Baum PR, Miller RE, Tough T, Gibson M, Davis-Smith T, Smith CA, Hunter K, et al. The mouse Fas-ligand gene is mutated in gld mice and is part of the TNF family gene cluster. of outstanding interest Immunity. 1:1994;131-136 See annotation [5].
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Lynch, D.H.1
Watson, M.2
Alderson, M.R.3
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Miller, R.E.5
Tough, T.6
Gibson, M.7
Davis-Smith, T.8
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The Fas death factor
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Nagata S, Golstein P. The Fas death factor. Science. 267:1995;1449-1456.
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Nagata, S.1
Golstein, P.2
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8
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0029036650
-
Expression and function of mouse Fas antigen on immature and mature T cells
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Nishimura Y, Ishii A, Kobayashi Y, Yamasaki Y, Yonehara S. Expression and function of mouse Fas antigen on immature and mature T cells. J Immunol. 154:1995;4395-4403.
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Nishimura, Y.1
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Kobayashi, Y.3
Yamasaki, Y.4
Yonehara, S.5
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9
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0028888832
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Characterization of human Fas gene. Exon/intron and promoter region
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Cheng J, Liu C, Koopman WJ, Mountz JD. Characterization of human Fas gene. Exon/intron and promoter region. J Immunol. 154:1995;1239-1245.
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Cheng, J.1
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0028839250
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A naturally occuring soluble isoform of murine Fas generated by alternative splicing
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Hughes, D.P.M.1
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0028963667
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Three functional soluble forms of the human apoptosis-inducing Fas molecule are produced by alternative splicing
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Cascino, I.1
Fucci, G.2
Papoff, G.3
Ruberti, G.4
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0028919473
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Expression of the functional soluble form of human Fas ligand in activated lymphocytes
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Tanaka M, Suda T, Takahashi T, Nagata S. Expression of the functional soluble form of human Fas ligand in activated lymphocytes. EMBO J. 14:1995;1129-1135.
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Tanaka, M.1
Suda, T.2
Takahashi, T.3
Nagata, S.4
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13
-
-
14844345988
-
Expression of the Fas ligand in cells of the T cell lineage
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Suda T, Okazaki T, Naito Y, Yokoto T, Arai N, Ozaki S, Nakao K, Nagata S. Expression of the Fas ligand in cells of the T cell lineage. J Immunol. 154:1995;3806-3813.
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Suda, T.1
Okazaki, T.2
Naito, Y.3
Yokoto, T.4
Arai, N.5
Ozaki, S.6
Nakao, K.7
Nagata, S.8
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14
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0028835952
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Constitutive activation of the Fas ligand gene in mouse lymphoproliferative disorders
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Watanabe D, Suda T, Hashimoto H, Nagata S. Constitutive activation of the Fas ligand gene in mouse lymphoproliferative disorders. EMBO J. 14:1995;12-18.
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Watanabe, D.1
Suda, T.2
Hashimoto, H.3
Nagata, S.4
-
15
-
-
0028928654
-
Massive upregulation of the Fas ligand in Ipr and gId mice: Implications for Fas regulation and the graft-versus-host disease-like wasting syndrome
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Chu JL, Ramos P, Rosendorff A, Nikolic-Zugic J, Lacy E, Matsuzawa A. Massive upregulation of the Fas ligand in Ipr and gId mice: implications for Fas regulation and the graft-versus-host disease-like wasting syndrome. J Exp Med. 181:1995;393-398.
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Chu, J.L.1
Ramos, P.2
Rosendorff, A.3
Nikolic-Zugic, J.4
Lacy, E.5
Matsuzawa, A.6
-
16
-
-
0028485743
-
The Fas antigen is involved in peripheral but not thymic deletion of T lymphocytes in T cell receptor transgenic mice
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+ T cells in peripheral lymphoid organs, but plays no role in thymic deletion of developing thymocytes.
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+ T cells in peripheral lymphoid organs, but plays no role in thymic deletion of developing thymocytes.
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(1994)
Immunity
, vol.1
, pp. 365-371
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Singer, G.G.1
Abbas, A.K.2
-
17
-
-
0028983657
-
Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T cell hybridomas
-
of special interest. Describes that Fas and FasL are co-expressed following activation of T-cell hybridomas, and that subsequent engagement of Fas by FasL is responsible for the induction of AICD in these cells. On the basis of limiting dilution analysis, the argument is made that AICD may occur in a cell-autonomous fashion (see also [18] and [19]).
-
Brunner T, Mogil RJ, LaFace D, Yoo NJ, Mahboubi A, Echeverri F, Martin SJ, Force WR, Lynch DH, Ware CF, Green DR. Cell-autonomous Fas (CD95)/Fas-ligand interaction mediates activation-induced apoptosis in T cell hybridomas. of special interest Nature. 373:1995;441-444 Describes that Fas and FasL are co-expressed following activation of T-cell hybridomas, and that subsequent engagement of Fas by FasL is responsible for the induction of AICD in these cells. On the basis of limiting dilution analysis, the argument is made that AICD may occur in a cell-autonomous fashion (see also [18] and [19]).
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(1995)
Nature
, vol.373
, pp. 441-444
-
-
Brunner, T.1
Mogil, R.J.2
LaFace, D.3
Yoo, N.J.4
Mahboubi, A.5
Echeverri, F.6
Martin, S.J.7
Force, W.R.8
Lynch, D.H.9
Ware, C.F.10
Green, D.R.11
-
18
-
-
0028795758
-
Autocrine T-cell suicide mediated by APO-1/(Fas/CD95)
-
of special interest. See annotation [17].
-
Dhein J, Walczak H, Baumler C, Debatin K-M, Krammer PH. Autocrine T-cell suicide mediated by APO-1/(Fas/CD95). of special interest Nature. 373:1995;438-441 See annotation [17].
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(1995)
Nature
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-
Dhein, J.1
Walczak, H.2
Baumler, C.3
Debatin, K.-M.4
Krammer, P.H.5
-
19
-
-
0028893078
-
Fas (CD95)/ FasL interactions required for programmed cell death after T-cell activation
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of special interest. See annotation [17].
-
Ju S-T, Panka DJ, Cui H, Ettinger R, El-Kharib ML, Sherr DH, Stanger BZ. Fas (CD95)/ FasL interactions required for programmed cell death after T-cell activation. of special interest Nature. 373:1995;441-448 See annotation [17].
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(1995)
Nature
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, pp. 441-448
-
-
Ju, S.-T.1
Panka, D.J.2
Cui, H.3
Ettinger, R.4
El-Kharib, M.L.5
Sherr, D.H.6
Stanger, B.Z.7
-
20
-
-
0029939945
-
The roles of costimulation and Fas in T cell apoptosis and peripheral tolerance
-
L, play a crucial role in protecting T cells from PCD, but not from AICD.
-
L, play a crucial role in protecting T cells from PCD, but not from AICD.
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(1996)
Immunity
, vol.4
, pp. 321-328
-
-
Van Parijs, L.1
Ibraghimov, A.2
Abbas, A.K.3
-
21
-
-
0029609086
-
Bcl-2 and Fas/APO-1 regulate distinct pathways to lymphocyte apoptosis
-
of special interest. See annotation [20].
-
Strasser A, Harris AW, Huang DCS, Krammer PH, Cory S. Bcl-2 and Fas/APO-1 regulate distinct pathways to lymphocyte apoptosis. of special interest EMBO J. 14:1996;6136-6147 See annotation [20].
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(1996)
EMBO J
, vol.14
, pp. 6136-6147
-
-
Strasser, A.1
Harris, A.W.2
Huang, D.C.S.3
Krammer, P.H.4
Cory, S.5
-
23
-
-
0028790829
-
Bcl-2 blocks glucocorticoid- but not Fas- or activation-induced apoptosis in a T cell hybridoma
-
of special interest. See annotation [20].
-
Memon SA, Moreno MB, Petrak D, Zacharchuk CM. Bcl-2 blocks glucocorticoid- but not Fas- or activation-induced apoptosis in a T cell hybridoma. of special interest J Immunol. 155:1995;4644-4652 See annotation [20].
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, pp. 4644-4652
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-
Memon, S.A.1
Moreno, M.B.2
Petrak, D.3
Zacharchuk, C.M.4
-
24
-
-
0029912189
-
Molecular ordering of the cell death pathway: Bcl-2 and Bcl-xL function upstream of the CED-3 like apoptotic proteases
-
of special interest. See annotation [20].
-
Chinnaiyan AM, Orth K, O'Rourke K, Duan H, Poinier GG, Dixit VM. Molecular ordering of the cell death pathway: Bcl-2 and Bcl-xL function upstream of the CED-3 like apoptotic proteases. of special interest J Biol Chem. 271:1996;4573-4576 See annotation [20].
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-
Chinnaiyan, A.M.1
Orth, K.2
O'Rourke, K.3
Duan, H.4
Poinier, G.G.5
Dixit, V.M.6
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25
-
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0028912626
-
Selective apoptosis of CD4+CD8+ thymocytes by the anti-Fas antibody
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Ogasawara J, Suda T, Nagata S. Selective apoptosis of CD4+CD8+ thymocytes by the anti-Fas antibody. J Exp Med. 181:1995;485-491.
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Ogasawara, J.1
Suda, T.2
Nagata, S.3
-
27
-
-
0028110928
-
Fas and perforin pathways as major mechanisms of T cell-mediated cytotoxicity
-
+ T cells can lead to the induction of apoptosis in target cells by interacting with Fas. This pathway of CTL-mediated cytotoxicity complements perforin-mediated cell lysis (see also [28]).
-
+ T cells can lead to the induction of apoptosis in target cells by interacting with Fas. This pathway of CTL-mediated cytotoxicity complements perforin-mediated cell lysis (see also [28]).
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(1994)
Science
, vol.265
, pp. 528-530
-
-
Kagi, D.1
Vignaux, F.2
Lederman, B.3
Burki, K.4
Depraetere, V.5
Nagata, S.6
Hengartner, H.7
Golstein, P.8
-
28
-
-
0027937745
-
Cytolytic T-cell cytotoxicity is mediated through perforin and Fas lytic pathways
-
of outstanding interest. of outstanding interest. See annotation [27].
-
of outstanding interest Lowin B, Hahne M, Mattman C, Tschopp J. Cytolytic T-cell cytotoxicity is mediated through perforin and Fas lytic pathways. of outstanding interest Nature. 370:1994;650-652 See annotation [27].
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(1994)
Nature
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, pp. 650-652
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Lowin, B.1
Hahne, M.2
Mattman, C.3
Tschopp, J.4
-
29
-
-
0028257947
-
Participation of target Fas protein in apoptosis pathway induced by CD4+ Th1 and CD8+ cytotoxic T cells
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of outstanding interest
-
of outstanding interest Ju S-T, Cui H, Panka DJ, Ettinger R, Marshak-Rothstein A. Participation of target Fas protein in apoptosis pathway induced by CD4+ Th1 and CD8+ cytotoxic T cells. Proc Natl Acad Sci USA. 91:1994;4185-4189.
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Ju, S.-T.1
Cui, H.2
Panka, D.J.3
Ettinger, R.4
Marshak-Rothstein, A.5
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30
-
-
0028920079
-
Protection against Fas-dependent Th1-mediated apoptosis by antigen receptor engagement in B cells
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Rothstein TL, Wang JK, Panka DJ, Foote LC, Wang Z, Stanger B, Cui H, Ju ST, Marshak-Rothstein A. Protection against Fas-dependent Th1-mediated apoptosis by antigen receptor engagement in B cells. Nature. 374:1995;163-165.
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Nature
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, pp. 163-165
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-
Rothstein, T.L.1
Wang, J.K.2
Panka, D.J.3
Foote, L.C.4
Wang, Z.5
Stanger, B.6
Cui, H.7
Ju, S.T.8
Marshak-Rothstein, A.9
-
31
-
-
0028799935
-
Fas ligation induces apoptosis of CD40-activated human B lymphocytes
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Garrone P, Neidhardt E-M, Garcia E, Galibert L, Van Kooten C, Banchereau J. Fas ligation induces apoptosis of CD40-activated human B lymphocytes. J Exp Med. 182:1995;1265-1273.
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J Exp Med.
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Garrone, P.1
Neidhardt, E.-M.2
Garcia, E.3
Galibert, L.4
Van Kooten, C.5
Banchereau, J.6
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32
-
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0028865583
-
CD40 ligation induces Apo-1/Fas expression on human B lymphocytes and facilitates apoptosis through the Apo-1/Fas pathway
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Schattner EJ, Elkon KB, Yoo D-H, Tumang J, Krammer PH, Crow MK, Friedman SM. CD40 ligation induces Apo-1/Fas expression on human B lymphocytes and facilitates apoptosis through the Apo-1/Fas pathway. J Exp Med. 182:1995;1557-1565.
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Schattner, E.J.1
Elkon, K.B.2
Yoo, D.-H.3
Tumang, J.4
Krammer, P.H.5
Crow, M.K.6
Friedman, S.M.7
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33
-
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0029062080
-
Regulation of germinal center B cell differentiation. Role of the human APO-1/Fas (CD95) molecule
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Legresle C, Bella C, Daniel PT, Krammer PH, Defrance T. Regulation of germinal center B cell differentiation. Role of the human APO-1/Fas (CD95) molecule. J Immunol. 154:1995;5746-5756.
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Legresle, C.1
Bella, C.2
Daniel, P.T.3
Krammer, P.H.4
Defrance, T.5
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34
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0028931042
-
Breakdown of B cell tolerance in a mouse model of systemic lupus erythematosus
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Roark JH, Kuntz CL, Nguyen KA, Caton AJ, Erikson J. Breakdown of B cell tolerance in a mouse model of systemic lupus erythematosus. J Exp Med. 181:1995;1157-1167.
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Roark, J.H.1
Kuntz, C.L.2
Nguyen, K.A.3
Caton, A.J.4
Erikson, J.5
-
35
-
-
0029076561
-
CD95 (Fas)-dependent elimination of self-reative B cells upon interaction with CD4+ T cells
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Rathmell JC, Cooke MP, Ho WY, Grein J, Townsend SE, Davis MM, Goodnow CC. CD95 (Fas)-dependent elimination of self-reative B cells upon interaction with CD4+ T cells. Nature. 376:1995;181-184.
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Nature
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, pp. 181-184
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Rathmell, J.C.1
Cooke, M.P.2
Ho, W.Y.3
Grein, J.4
Townsend, S.E.5
Davis, M.M.6
Goodnow, C.C.7
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36
-
-
0028789148
-
Anatomy of autoantibody production: Dominant localization of antibody-producing cells to cell zones in Fas-deficient mice
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Jacobson BA, Panka DJ, Nguyen K-A, Erikson J, Abbas AK, Marshak-Rothstein A. Anatomy of autoantibody production: dominant localization of antibody-producing cells to cell zones in Fas-deficient mice. Immunity. 3:1995;509-519.
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(1995)
Immunity
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, pp. 509-519
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Jacobson, B.A.1
Panka, D.J.2
Nguyen, K.-A.3
Erikson, J.4
Abbas, A.K.5
Marshak-Rothstein, A.6
-
37
-
-
0029022365
-
Involvement of an ICE-like protease in Fas-mediated apoptosis
-
of outstanding interest. A variety of ICE antagonists are used to formally demonstrate that an ICE-like protease is involved in Fas-mediated apoptosis (see also [38] and [39]).
-
Enari M, Hug H, Nagata S. Involvement of an ICE-like protease in Fas-mediated apoptosis. of outstanding interest Nature. 375:1995;78-81 A variety of ICE antagonists are used to formally demonstrate that an ICE-like protease is involved in Fas-mediated apoptosis (see also [38] and [39]).
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(1995)
Nature
, vol.375
, pp. 78-81
-
-
Enari, M.1
Hug, H.2
Nagata, S.3
-
38
-
-
0029005805
-
Requirement of an ICE/CED-3 protease for Fas/APO-1-mediated apoptosis
-
of outstanding interest. See annotation [37].
-
Los M, Van De Craen M, Penning LC, Schenk H, Westendrop M, Baeuerle PA, Droge W, Krammer PH, Fiers W, Schulze-Osthoff K. Requirement of an ICE/CED-3 protease for Fas/APO-1-mediated apoptosis. of outstanding interest Nature. 375:1995;81-83 See annotation [37].
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(1995)
Nature
, vol.375
, pp. 81-83
-
-
Los, M.1
Van De Craen, M.2
Penning, L.C.3
Schenk, H.4
Westendrop, M.5
Baeuerle, P.A.6
Droge, W.7
Krammer, P.H.8
Fiers, W.9
Schulze-Osthoff, K.10
-
39
-
-
0028873964
-
Fas- and tumor necrosis factor-induced apoptosis is inhibited by the poxvirus crmA gene product
-
of outstanding interest. See annotation [37].
-
Tewari M, Dixit VM. Fas- and tumor necrosis factor-induced apoptosis is inhibited by the poxvirus crmA gene product. of outstanding interest J Biol Chem. 270:1995;3255-3260 See annotation [37].
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(1995)
J Biol Chem.
, vol.270
, pp. 3255-3260
-
-
Tewari, M.1
Dixit, V.M.2
-
40
-
-
0028920863
-
Altered cytokine export and apoptosis in mice deficient in interleukin-1β converting enzyme
-
of outstanding interest. This report on the ICE knockout mouse shows that thymocytes derived from this mouse are resistant to Fas-mediated apoptosis. As no autoimmune pathology is observed, however, it is suggested that other ICE homologs may play a significant role in Fas-mediated deletion of auto-reactive T cells.
-
Kuida K, Lippke JA, Ku G, Harding MW, Livingston DJ, Su MS, Flavell RA. Altered cytokine export and apoptosis in mice deficient in interleukin-1β converting enzyme. of outstanding interest Science. 267:1995;2000-2003 This report on the ICE knockout mouse shows that thymocytes derived from this mouse are resistant to Fas-mediated apoptosis. As no autoimmune pathology is observed, however, it is suggested that other ICE homologs may play a significant role in Fas-mediated deletion of auto-reactive T cells.
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(1995)
Science
, vol.267
, pp. 2000-2003
-
-
Kuida, K.1
Lippke, J.A.2
Ku, G.3
Harding, M.W.4
Livingston, D.J.5
Su, M.S.6
Flavell, R.A.7
-
41
-
-
0028913550
-
A novel protein that interacts with the death domain of Fas/APO-1 contains a sequence motif related to the death domain
-
of outstanding interest. This paper reports the identification of FADD/MORT-1, an intracellular protein that interacts with the cytoplasmic tail of Fas and mediates Fas-induced apoptotic signaling (see also [42]).
-
Boldin MP, Varfolomeev EE, Pancer Z, Mett IL, Camonis JH, Wallach D. A novel protein that interacts with the death domain of Fas/APO-1 contains a sequence motif related to the death domain. of outstanding interest J Biol Chem. 270:1995;7795-7798 This paper reports the identification of FADD/MORT-1, an intracellular protein that interacts with the cytoplasmic tail of Fas and mediates Fas-induced apoptotic signaling (see also [42]).
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(1995)
J Biol Chem.
, vol.270
, pp. 7795-7798
-
-
Boldin, M.P.1
Varfolomeev, E.E.2
Pancer, Z.3
Mett, I.L.4
Camonis, J.H.5
Wallach, D.6
-
42
-
-
0029026548
-
FADD, a novel death domain-containing protein, interacts with the death domain of fas and initiates apoptosis
-
of outstanding interest. See annotation [41].
-
Chinnaiyan AM, O'Rourke K, Tewari M, Dixit VM. FADD, a novel death domain-containing protein, interacts with the death domain of fas and initiates apoptosis. of outstanding interest Cell. 81:1995;505-512 See annotation [41].
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(1995)
Cell.
, vol.81
, pp. 505-512
-
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Chinnaiyan, A.M.1
O'Rourke, K.2
Tewari, M.3
Dixit, V.M.4
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43
-
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0027275490
-
A novel domain within the 55kd TNF receptor signals cell death
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Tartaglia LA, Ayres TM, Wong GHW, Goeddel DV. A novel domain within the 55kd TNF receptor signals cell death. Cell. 74:1993;845-853.
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Cell.
, vol.74
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Tartaglia, L.A.1
Ayres, T.M.2
Wong, G.H.W.3
Goeddel, D.V.4
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44
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0027281373
-
A novel protein domain required for apoptosis. Mutational analysis of the human fas antigen
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Itoh N, Nagata S. A novel protein domain required for apoptosis. Mutational analysis of the human fas antigen. J Biol Chem. 268:1993;10932-10937.
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J Biol Chem.
, vol.268
, pp. 10932-10937
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Itoh, N.1
Nagata, S.2
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45
-
-
0028985261
-
Self-association of the "death domains" of the p55 tumor necrosis factor (TNF) receptor and Fas/APO-1 prompts signalling for TNF and Fas/APO-1 effects
-
of special interest. Regions of homology, so called 'death domains', found in many proteins involved in apoptosis, including Fas and FADD/MORT-1, may be involved in regulating homeotypic and heterotypic interactions between these proteins.
-
Boldin MP, Mett IL, Varfolomeev EE, Chumakov I, Shemer-Avni Y, Camonis JH, Wallach D. Self-association of the "death domains" of the p55 tumor necrosis factor (TNF) receptor and Fas/APO-1 prompts signalling for TNF and Fas/APO-1 effects. of special interest J Biol Chem. 270:1995;387-391 Regions of homology, so called 'death domains', found in many proteins involved in apoptosis, including Fas and FADD/MORT-1, may be involved in regulating homeotypic and heterotypic interactions between these proteins.
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(1995)
J Biol Chem.
, vol.270
, pp. 387-391
-
-
Boldin, M.P.1
Mett, I.L.2
Varfolomeev, E.E.3
Chumakov, I.4
Shemer-Avni, Y.5
Camonis, J.H.6
Wallach, D.7
-
46
-
-
0029054725
-
RIP: A novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death
-
of outstanding interest. Using the same technology as that of [41,42] this report describes the identification and characterization of a distinct cytoplasmic molecule, RIP, which may be involved in Fas-mediated apoptotic signaling.
-
Stanger BZ, Leder P, Lee TH, Kim E, Seed B. RIP: a novel protein containing a death domain that interacts with Fas/APO-1 (CD95) in yeast and causes cell death. of outstanding interest Cell. 81:1995;513-523 Using the same technology as that of [41,42] this report describes the identification and characterization of a distinct cytoplasmic molecule, RIP, which may be involved in Fas-mediated apoptotic signaling.
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(1995)
Cell.
, vol.81
, pp. 513-523
-
-
Stanger, B.Z.1
Leder, P.2
Lee, T.H.3
Kim, E.4
Seed, B.5
-
47
-
-
0028964917
-
Fas-induced apoptosis is mediated via a ceramide-initiated RAS signaling pathway
-
of special interest. A ceramide-mediated signaling pathway plays a role in Fas-induced apoptosis (see also [48]).
-
of special interest Gulbins E, Bissonnette R, Mahboubi A, Martin S, Nishioka W, Bruner T. Fas-induced apoptosis is mediated via a ceramide-initiated RAS signaling pathway. Immunity. 2:1995;341-351 A ceramide-mediated signaling pathway plays a role in Fas-induced apoptosis (see also [48]).
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(1995)
Immunity
, vol.2
, pp. 341-351
-
-
Gulbins, E.1
Bissonnette, R.2
Mahboubi, A.3
Martin, S.4
Nishioka, W.5
Bruner, T.6
-
48
-
-
0028095477
-
Apoptotic signaling through CD95 (Fas/APO-1) activates an acidic sphingomyelinase
-
of special interest. of special interest. See annotation [47].
-
of special interest Cifone MG, De Maria R, Roncaioli P, Rippo MR, Azuma M, Lanier LL, Santoni A, Testi R. Apoptotic signaling through CD95 (Fas/APO-1) activates an acidic sphingomyelinase. of special interest J Exp Med. 180:1995;1547-1552 See annotation [47].
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(1995)
J Exp Med.
, vol.180
, pp. 1547-1552
-
-
Cifone, M.G.1
De Maria, R.2
Roncaioli, P.3
Rippo, M.R.4
Azuma, M.5
Lanier, L.L.6
Santoni, A.7
Testi, R.8
-
49
-
-
0028990125
-
Yama/CPP32β, a mammalian homolog of CED-3, is a crmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase
-
One of the substrates of the ICE homolog, Yama/CPP32 is an enzyme previously implicated in the induction of apoptosis (see also [50]).
-
Tewari M, Quan LT, O'Rourke K, Desnoyers S, Zeng Z, Beidler DR, Poirier GG, Salvesen GS, Dixit VM. Yama/CPP32β, a mammalian homolog of CED-3, is a crmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase. Cell. 81:1995;801-809 One of the substrates of the ICE homolog, Yama/CPP32 is an enzyme previously implicated in the induction of apoptosis (see also [50]).
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(1995)
Cell.
, vol.81
, pp. 801-809
-
-
Tewari, M.1
Quan, L.T.2
O'Rourke, K.3
Desnoyers, S.4
Zeng, Z.5
Beidler, D.R.6
Poirier, G.G.7
Salvesen, G.S.8
Dixit, V.M.9
-
50
-
-
0029068871
-
Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis
-
of special interest. of special interest. See annotation [49].
-
of special interest Nicholson DW, Ali A, Thornberry NA, Vaillancourt JP, Ding CK, Gallant M, Gareau Y, Griffin PR, Labelle M, Lazebnik YA, et al. Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis. of special interest Nature. 376:1995;37-43 See annotation [49].
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(1995)
Nature
, vol.376
, pp. 37-43
-
-
Nicholson, D.W.1
Ali, A.2
Thornberry, N.A.3
Vaillancourt, J.P.4
Ding, C.K.5
Gallant, M.6
Gareau, Y.7
Griffin, P.R.8
Labelle, M.9
Lazebnik, Y.A.10
-
51
-
-
0029066512
-
FAP-1: A protein tyrosine phosphatase that associates with Fas
-
of outstanding interest. This paper reports the identification of a phosphatase that associates with Fas, and negatively regulates the Fas signaling pathway.
-
Sato T, Irie S, Kitada S, Reed JC. FAP-1: a protein tyrosine phosphatase that associates with Fas. of outstanding interest Science. 268:1995;411-415 This paper reports the identification of a phosphatase that associates with Fas, and negatively regulates the Fas signaling pathway.
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(1995)
Science
, vol.268
, pp. 411-415
-
-
Sato, T.1
Irie, S.2
Kitada, S.3
Reed, J.C.4
-
52
-
-
0028856130
-
Targeted mutation in the fas gene causes hyperplasia in peripheral lymphoid organs and liver
-
of special interest. This study describes the fas knockout mouse, and together with [53] confirms that the Ipr phenotype arises from a defect in a single gene, fas.
-
Adachi M, Suematsu S, Kondo T, Ogasawara J, Tanaka T, Yoshida N, Nagata S. Targeted mutation in the fas gene causes hyperplasia in peripheral lymphoid organs and liver. of special interest Nat Genet. 11:1995;294-300 This study describes the fas knockout mouse, and together with [53] confirms that the Ipr phenotype arises from a defect in a single gene, fas.
-
(1995)
Nat Genet
, vol.11
, pp. 294-300
-
-
Adachi, M.1
Suematsu, S.2
Kondo, T.3
Ogasawara, J.4
Tanaka, T.5
Yoshida, N.6
Nagata, S.7
-
53
-
-
0028206729
-
Correction of accelerated autoimmune disease by early replacement of the mutated Ipr gene with the normal fas apoptosis gene in the T cells of transgenic MRL-Ipr/Ipr mice
-
The Ipr defect is rescued by a functional fas transgene, confirming, together with [52], that the Ipr phenotype results from a single gene defect in fas.
-
Wu J, Zhou T, Zhang J, He J, Gause WC, Mountz JD. Correction of accelerated autoimmune disease by early replacement of the mutated Ipr gene with the normal fas apoptosis gene in the T cells of transgenic MRL-Ipr/Ipr mice. Proc Natl Acad Sci USA. 91:1994;2344-2348 The Ipr defect is rescued by a functional fas transgene, confirming, together with [52], that the Ipr phenotype results from a single gene defect in fas.
-
(1994)
Proc Natl Acad Sci USA
, vol.91
, pp. 2344-2348
-
-
Wu, J.1
Zhou, T.2
Zhang, J.3
He, J.4
Gause, W.C.5
Mountz, J.D.6
-
54
-
-
0028326095
-
Prevention of nephritis in major histocompatibility complex class-II-deficient MRL-Ipr mice
-
of special interest
-
of special interest Jevnikar AM, Grusby MJ, Glimcher LH. Prevention of nephritis in major histocompatibility complex class-II-deficient MRL-Ipr mice. J Exp Med. 179:1994;1137-1143.
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(1994)
J Exp Med.
, vol.179
, pp. 1137-1143
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-
Jevnikar, A.M.1
Grusby, M.J.2
Glimcher, L.H.3
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55
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0028898599
-
Greatly reduced lymphoproliferation in Ipr mice lacking major histocompatibility complex class I
-
Maldonado MA, Eisenberg RA, Roper E, Cohen PL, Kotzin BL. Greatly reduced lymphoproliferation in Ipr mice lacking major histocompatibility complex class I. J Exp Med. 181:1995;641-648.
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(1995)
J Exp Med.
, vol.181
, pp. 641-648
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-
Maldonado, M.A.1
Eisenberg, R.A.2
Roper, E.3
Cohen, P.L.4
Kotzin, B.L.5
-
56
-
-
0028985378
-
Reduced development of CD4-8-B220+ T cells but normal autoantibody production in Ipr/Ipr mice lacking major histocompatibility complex class I molecules
-
Ohteki T, Iwamoto M, Izui S, MacDonald HR. Reduced development of CD4-8-B220+ T cells but normal autoantibody production in Ipr/Ipr mice lacking major histocompatibility complex class I molecules. Eur J Immunol. 25:1995;37-41.
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(1995)
Eur J Immunol.
, vol.25
, pp. 37-41
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Ohteki, T.1
Iwamoto, M.2
Izui, S.3
MacDonald, H.R.4
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57
-
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0027141228
-
Lack of connectivity between the induced and autoimmune repertoires of Ipr/Ipr mice
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Very DLJ, Panka DJ, Weissman D, Wysocki L, Manser T. Lack of connectivity between the induced and autoimmune repertoires of Ipr/Ipr mice. Immunology. 80:1993;518-526.
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(1993)
Immunology
, vol.80
, pp. 518-526
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Very, D.L.J.1
Panka, D.J.2
Weissman, D.3
Wysocki, L.4
Manser, T.5
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58
-
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0029076413
-
Lymphocyte apoptosis during the silencing of the immune response to acute viral infection in normal, Ipr, and Bcl-2 transgenic mice
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Razvi ES, Jiang Z, Woda BA, Welsh RM. Lymphocyte apoptosis during the silencing of the immune response to acute viral infection in normal, Ipr, and Bcl-2 transgenic mice. Am J Path. 147:1995;79-91.
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(1995)
Am J Path.
, vol.147
, pp. 79-91
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Razvi, E.S.1
Jiang, Z.2
Woda, B.A.3
Welsh, R.M.4
-
59
-
-
0029025441
-
Dominant interfering fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome
-
of special interest. Describes that defects in Fas-mediated T-cell apoptosis in five children with lymphoproliferative disorders and autoimmune manifestations arise from mutations in the Fas gene. The mutations result either in a loss of function, or impart a dominant negative phenotype on the gene product (see also [60]).
-
Fisher GH, Rosenberg FJ, Straus SE, Dale JK, Midleton LA, Lin AY, Strober W, Lenardo MJ, Puck JM. Dominant interfering fas gene mutations impair apoptosis in a human autoimmune lymphoproliferative syndrome. of special interest Cell. 81:1995;935-946 Describes that defects in Fas-mediated T-cell apoptosis in five children with lymphoproliferative disorders and autoimmune manifestations arise from mutations in the Fas gene. The mutations result either in a loss of function, or impart a dominant negative phenotype on the gene product (see also [60]).
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(1995)
Cell.
, vol.81
, pp. 935-946
-
-
Fisher, G.H.1
Rosenberg, F.J.2
Straus, S.E.3
Dale, J.K.4
Midleton, L.A.5
Lin, A.Y.6
Strober, W.7
Lenardo, M.J.8
Puck, J.M.9
-
60
-
-
0029006893
-
Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity
-
of outstanding interest. Three children with lymphadenopathy and autoimmune phenomena exhibit defects in Fas-mediated apoptosis, and are shown to carry deletions within the Fas gene leading to depressed surface expression and signaling defects (see also [59]).
-
Rieux-Laucat F, Le Deist F, Hivroz C, Roberts IAG, Debatin KM, Fischer A, De Villartay JP. Mutations in Fas associated with human lymphoproliferative syndrome and autoimmunity. of outstanding interest Science. 268:1995;1347-1349 Three children with lymphadenopathy and autoimmune phenomena exhibit defects in Fas-mediated apoptosis, and are shown to carry deletions within the Fas gene leading to depressed surface expression and signaling defects (see also [59]).
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(1995)
Science
, vol.268
, pp. 1347-1349
-
-
Rieux-Laucat, F.1
Le Deist, F.2
Hivroz, C.3
Roberts, I.A.G.4
Debatin, K.M.5
Fischer, A.6
De Villartay, J.P.7
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61
-
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0028274042
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Protection from Fas-mediated apoptosis by a soluble form of the fas molecule
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Cheng J, Zhou T, Liu C, Shapiro JP, Brauer MJ, Kiefer MC, Barr PJ, Mountz JD. Protection from Fas-mediated apoptosis by a soluble form of the fas molecule. Science. 263:1995;1759-1762.
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(1995)
Science
, vol.263
, pp. 1759-1762
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-
Cheng, J.1
Zhou, T.2
Liu, C.3
Shapiro, J.P.4
Brauer, M.J.5
Kiefer, M.C.6
Barr, P.J.7
Mountz, J.D.8
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62
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0028329009
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The apoptosis-1/Fas protein in human systemic lupus erythematosus
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Mysler E, Bini P, Drappa J, Ramos P, Friedman SM, Krammer PH, Elkon KB. The apoptosis-1/Fas protein in human systemic lupus erythematosus. J Clin Invest. 93:1995;1029-1034.
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J Clin Invest.
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Mysler, E.1
Bini, P.2
Drappa, J.3
Ramos, P.4
Friedman, S.M.5
Krammer, P.H.6
Elkon, K.B.7
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63
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0026017971
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Interleukin-2 programs mouse α β T lymphocytes for apoptosis
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Lenardo MJ. Interleukin-2 programs mouse α β T lymphocytes for apoptosis. Nature. 353:1991;858-861.
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(1991)
Nature
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, pp. 858-861
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Lenardo, M.J.1
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64
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0027369395
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Ulcerative colitis-like disease in mice with disrupted interleukin-2 gene
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Sadlack B, Merz H, Schorle H, Schimpl A, Feller AC, Horak I. Ulcerative colitis-like disease in mice with disrupted interleukin-2 gene. Cell. 75:1993;253-261.
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(1993)
Cell.
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Sadlack, B.1
Merz, H.2
Schorle, H.3
Schimpl, A.4
Feller, A.C.5
Horak, I.6
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65
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0028784289
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Interleukin-2 receptor α chain regulates the size and content of the peripheral lymphoid compartment
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Willerford DM, Chen J, Ferry JA, Davidson L, Ma A, Alt FW. Interleukin-2 receptor α chain regulates the size and content of the peripheral lymphoid compartment. Immunity. 3:1995;521-530.
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(1995)
Immunity
, vol.3
, pp. 521-530
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Willerford, D.M.1
Chen, J.2
Ferry, J.A.3
Davidson, L.4
Ma, A.5
Alt, F.W.6
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66
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0029028363
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Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor β
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Suzuki H, Kundig TM, Furlonger C, Wakeham A, Timms E, Matsuyama T, Schmits R, Simard JJL, Ohasi PS, Griesser H, et al. Deregulated T cell activation and autoimmunity in mice lacking interleukin-2 receptor β Science. 268:1995;1472-1476.
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(1995)
Science
, vol.268
, pp. 1472-1476
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Suzuki, H.1
Kundig, T.M.2
Furlonger, C.3
Wakeham, A.4
Timms, E.5
Matsuyama, T.6
Schmits, R.7
Simard, J.J.L.8
Ohasi, P.S.9
Griesser, H.10
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67
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0029118133
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Normal clonal expansion but impaired Fas-mediated cell death and anergy in IL-2 deficient mice
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Kneitz B, Herman T, Yonehara S, Schimpl A. Normal clonal expansion but impaired Fas-mediated cell death and anergy in IL-2 deficient mice. Eur J Immunol. 25:1995;2572-2577.
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(1995)
Eur J Immunol.
, vol.25
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Kneitz, B.1
Herman, T.2
Yonehara, S.3
Schimpl, A.4
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68
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0028864778
-
A role for CD95 ligand in preventing graft rejection
-
of outstanding interest. The survival of testis grafts in the mouse is shown to be due to constitutive expression of FasL, providing a molecular explanation for the 'immune-priveleged' status of this organ (see also [69]).
-
Bellgrau D, Gold D, Selawry H, Moore J, Franzusoff A, Duke RC. A role for CD95 ligand in preventing graft rejection. of outstanding interest Nature. 377:1995;630-632 The survival of testis grafts in the mouse is shown to be due to constitutive expression of FasL, providing a molecular explanation for the 'immune-priveleged' status of this organ (see also [69]).
-
(1995)
Nature
, vol.377
, pp. 630-632
-
-
Bellgrau, D.1
Gold, D.2
Selawry, H.3
Moore, J.4
Franzusoff, A.5
Duke, R.C.6
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69
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0028879109
-
Fas ligand-induced apoptosis is a mechanism of immune privilege
-
of outstanding interest. Constitutive expression of FasL limits immune responses to virus in the eye, and contributes to the 'immune-priveleged' nature of this organ. Uncontrolled responses to viral infection in FasL-deficient gld mice result in significant tissue destruction (also see [68]).
-
Griffith TS, Brunner T, Fletcher SM, Green DR, Ferguson TA. Fas ligand-induced apoptosis is a mechanism of immune privilege. of outstanding interest Science. 270:1995;1189-1192 Constitutive expression of FasL limits immune responses to virus in the eye, and contributes to the 'immune-priveleged' nature of this organ. Uncontrolled responses to viral infection in FasL-deficient gld mice result in significant tissue destruction (also see [68]).
-
(1995)
Science
, vol.270
, pp. 1189-1192
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-
Griffith, T.S.1
Brunner, T.2
Fletcher, S.M.3
Green, D.R.4
Ferguson, T.A.5
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70
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0028883850
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Cytotoxicity-dependent APO-1(Fas/CD95)-associated proteins from a death-inducing signaling complex (DISC) with the recerptor
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Kischkel FC, Hellbardt S, Behrmann I, Germer M, Pawlita M, Krammer PH, Peter ME. Cytotoxicity-dependent APO-1(Fas/CD95)-associated proteins from a death-inducing signaling complex (DISC) with the recerptor. EMBO J. 14:1995;5579-5588.
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(1995)
EMBO J
, vol.14
, pp. 5579-5588
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Kischkel, F.C.1
Hellbardt, S.2
Behrmann, I.3
Germer, M.4
Pawlita, M.5
Krammer, P.H.6
Peter, M.E.7
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