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0029808295
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Frequent provirus insertional mutagenesis of Notch1 in thymomas of MMTVD/myc transgenic mice suggests a collaboration of c-myc and Notch1 for oncogenesis
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of outstanding interest. Activating mutations of Notch can collaborate with an oncogenic form of myc to generate T-cell leukemias. These results confirm the oncogenic potential of Notch and indicate that the Notch and myc signaling pathways can collaborate to generate T-cell leukemias.
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Girard L, Hanna Z, Beu N, Hoemann N, Hoemann C, Simard C, Kozak C, Jolicoeur P. Frequent provirus insertional mutagenesis of Notch1 in thymomas of MMTVD/myc transgenic mice suggests a collaboration of c-myc and Notch1 for oncogenesis. of outstanding interest Genes Dev. 10:1996;1930-1944 Activating mutations of Notch can collaborate with an oncogenic form of myc to generate T-cell leukemias. These results confirm the oncogenic potential of Notch and indicate that the Notch and myc signaling pathways can collaborate to generate T-cell leukemias.
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Girard, L.1
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Kozak, C.7
Jolicoeur, P.8
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31
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0030297895
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An activated form of Notch influences the choice between CD4 and CD8 T cell lineages
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of outstanding interest. An activated form of Notch overrides the developmental cues that normally guide the CD4 versus CD8 lineage choice and causes T-cell precursors to choose the CD8 lineage over the CD4 lineage.
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Robey E, Chang D, Itano A, Cado D, Alexander H, Lans D, Weinmaster G, Salmon P. An activated form of Notch influences the choice between CD4 and CD8 T cell lineages. of outstanding interest Cell. 87:1996;483-492 An activated form of Notch overrides the developmental cues that normally guide the CD4 versus CD8 lineage choice and causes T-cell precursors to choose the CD8 lineage over the CD4 lineage.
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of outstanding interest. Gene disruptions of Notch1 and CBF1 (RBF-Jk) in the mouse lead to down-regulation of the enhancer of split homolog. HES5 and the Delta homolog, DII1 and upregulation of the Ac/Su homolog, Mash1. These results provide further evidence for the conservation of several members of the Notch signaling pathway between invertebrates and vertebrates.
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De La Poma J, Wakeman A, Correla K, Samper E, Brown S, Aguilera R, Nakano T, Honjo T, Mak T, Rossant J, Conlon R. Conservation of the Notch signaling pathway in mammalian neurogenesis. of outstanding interest Development. 124:1997;1139-1148 Gene disruptions of Notch1 and CBF1 (RBF-Jk) in the mouse lead to down-regulation of the enhancer of split homolog. HES5 and the Delta homolog, DII1 and upregulation of the Ac/Su homolog, Mash1. These results provide further evidence for the conservation of several members of the Notch signaling pathway between invertebrates and vertebrates.
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De La Poma, J.1
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Dorsky, R.1
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Mutations in T-cell antigen receptor genes α and β block thymocyte development at different stages
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0031001247
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Notch activity influences the αβ vs. γ delta T cell lineage decision
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of outstanding interest. An activated form of Notch overrides the developmental cues that normally guide the αβ versus γδ lineage choice and drives αβ T-cell development in the absence of the TCR β chain.
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Washburn T, Schweighoffer E, Gridley T, Chang D, Fowlkes B, Cado D, Salmon P, Robey E. Notch activity influences the αβ vs. γ delta T cell lineage decision. of outstanding interest Cell. 88:1997;833-843 An activated form of Notch overrides the developmental cues that normally guide the αβ versus γδ lineage choice and drives αβ T-cell development in the absence of the TCR β chain.
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TAN-1, the human homolog of the Drosophila Notch gene, is broken by chromosomal translocations in T lymphoblastic neoplasms
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Ellisen LW, Bird J, West DC, Soreng AL, Reynolds TC, Smith SD, Sklar J. TAN-1, the human homolog of the Drosophila Notch gene, is broken by chromosomal translocations in T lymphoblastic neoplasms. Cell. 66:1991;649-661.
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Mouse mammary tumor gene int-3: A member of the notch gene family transforms mammary epithelial cells
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Robbins J, Blondel B, Gallahan D, Callahan R. Mouse mammary tumor gene int-3: a member of the notch gene family transforms mammary epithelial cells. J Virol. 66:1992;2594-2599.
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Struhl G, Fitzgerald K, Greenwald I. Intrinsic activity of the Lin-12 and Notch intracellular domains in vivo. Cell. 74:1993;331-345.
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0027386233
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Antineurogenic phenotypes induced by truncated Notch proteins indicate a role in signal transduction and may point to a novel function for Notch in nuclei
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Lieber T, Kidd S, Alcamo E, Corbin V, Young M. Antineurogenic phenotypes induced by truncated Notch proteins indicate a role in signal transduction and may point to a novel function for Notch in nuclei. Genes Dev. 7:1993;1949-1965.
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Serrate signals through Notch to establish a Wingless-dependent organizer at the dorsal/vental compartment boundary of the Drosophila wing
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Diaz-Benjumea F, Cohen SM. Serrate signals through Notch to establish a Wingless-dependent organizer at the dorsal/vental compartment boundary of the Drosophila wing. Development. 121:1995;4215-4255.
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The intracellular domain of mouse Notch: A constitutively activated repressor of myogenesis directed at the basic helix-loop-helix region of MyoD
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Kopan R, Nye J, Weintraub H. The intracellular domain of mouse Notch: a constitutively activated repressor of myogenesis directed at the basic helix-loop-helix region of MyoD. Development. 120:1994;2385-2396.
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48
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An activated Notch suppresses neurogenesis and myogenesis but not gliogenesis in mammalian cells
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Nye J, Kopan R, Axel R. An activated Notch suppresses neurogenesis and myogenesis but not gliogenesis in mammalian cells. Development. 120:1994;2421-2430.
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Inhibition of granulocytic differentiation by mNotch1
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Milner L, Bigas A, Kopan R, Brashem-Stein C, Bernstein I, Martin D. Inhibition of granulocytic differentiation by mNotch1. Proc Natl Acad Sci. 93:1996;13014-13019.
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Milner, L.1
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Bernstein, I.5
Martin, D.6
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50
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Specific truncations of Drosophila Notch define dominant activated and dominant negative forms of the receptor
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Rebay I, Fehon R, Artavanis-Tsakonas S. Specific truncations of Drosophila Notch define dominant activated and dominant negative forms of the receptor. Cell. 74:1993;319-329.
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Rebay, I.1
Fehon, R.2
Artavanis-Tsakonas, S.3
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51
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0026647098
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Suppressor of Hairless, the Drosophila homolog of the mouse recombination signal-binding protein gene, controls sensory organ cell fates
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Schweisguth F, Posakony J. Suppressor of Hairless, the Drosophila homolog of the mouse recombination signal-binding protein gene, controls sensory organ cell fates. Cell. 69:1992;1199-1212.
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Schweisguth, F.1
Posakony, J.2
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52
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0028171718
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The suppressor of Hairless protein participates in Notch receptor signaling
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Fortini ME, Artavanis-Tsakonas S. The suppressor of Hairless protein participates in Notch receptor signaling. Cell. 79:1994;273-282.
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Fortini, M.E.1
Artavanis-Tsakonas, S.2
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53
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0030014642
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Lag-1, a gene required for lin-12 and glp-1 signaling in C. elegans, is homologous to human CBF1 and Drosophila Su(H)
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Christensen S, Kodoyianni V, Bosenberg M, Friedman L, Kimble J. lag-1, a gene required for lin-12 and glp-1 signaling in C. elegans, is homologous to human CBF1 and Drosophila Su(H). Development. 122:1996;1373-1383.
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Christensen, S.1
Kodoyianni, V.2
Bosenberg, M.3
Friedman, L.4
Kimble, J.5
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54
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0029583607
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Physical interaction between a novel domain of the receptor Notch and the transcription factor RBP-Jk/Su(H)
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Tamura K, Taniguchi Y, Minoguchi S, Sakai T, Tun T, Furukawa T, Honjo T. Physical interaction between a novel domain of the receptor Notch and the transcription factor RBP-Jk/Su(H). Curr Biol. 5:1995;1416-1423.
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Tamura, K.1
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Honjo, T.7
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55
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0030063909
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Truncated mammalian Notch1 activates CBF1/RBPJk repressed genes by a mechanism resembling that of Epbstein-Barr virus EBNA2
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of special interest. This paper demonstrates an interaction between CBF1 (RBP-Jk) and the intracellular domain of Notch. Together with [56], these data provide evidence that the intracellular domain of Notch can act as a transcriptional co-activator and suggest that Notch could act directly in the nucleus.
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Hsieh JJD, Henkel T, Salmon P, Robey E, Peterson MG, Hayward D. Truncated mammalian Notch1 activates CBF1/RBPJk repressed genes by a mechanism resembling that of Epbstein-Barr virus EBNA2. of special interest Mol Cell Biol. 16:1996;952-959 This paper demonstrates an interaction between CBF1 (RBP-Jk) and the intracellular domain of Notch. Together with [56], these data provide evidence that the intracellular domain of Notch can act as a transcriptional co-activator and suggest that Notch could act directly in the nucleus.
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(1996)
Mol Cell Biol
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Hsieh, J.J.D.1
Henkel, T.2
Salmon, P.3
Robey, E.4
Peterson, M.G.5
Hayward, D.6
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56
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Signalling downstream of activated mammalian Notch
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Jarriault S, Brou C, Logeat F, Schroeter E, Kopan R, Israel A. Signalling downstream of activated mammalian Notch. Nature. 377:1995;355-358.
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Jarriault, S.1
Brou, C.2
Logeat, F.3
Schroeter, E.4
Kopan, R.5
Israel, A.6
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57
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0028973381
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The neurogenic Suppressor of Hairless DNA-binding protein mediates the transcriptional activation of Enhancer of split complex genes triggered by Notch signaling
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Lecourtois M, Schweisguth F. The neurogenic Suppressor of Hairless DNA-binding protein mediates the transcriptional activation of Enhancer of split complex genes triggered by Notch signaling. Genes Dev. 9:1995;2598-2608.
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Lecourtois, M.1
Schweisguth, F.2
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58
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0028973380
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Suppressor of Hairless directly activates transcription of Enhancer of split complex genes in response to Notch receptor activity
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Bailey A, Posakony J. Suppressor of Hairless directly activates transcription of Enhancer of split complex genes in response to Notch receptor activity. Genes Dev. 9:1995;2609-2622.
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Genes Dev
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Bailey, A.1
Posakony, J.2
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59
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0029819667
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Functional relationships between Notch, Su(H) and the bHLH genes of the E(spl) complex: The E(spl) genes mediate only a subset of Notch activities during imaginal development
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De Celis JF, de Celis J, Ligoxygakis P, Priess A, Delidakis C, Bray S. Functional relationships between Notch, Su(H) and the bHLH genes of the E(spl) complex: the E(spl) genes mediate only a subset of Notch activities during imaginal development. Development. 122:1996;2719-2728.
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De Celis, J.F.1
De Celis, J.2
Ligoxygakis, P.3
Priess, A.4
Delidakis, C.5
Bray, S.6
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60
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0029188455
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Targeted disruption of mammalian hairy and enhancer of split homolog-1 (HES-1) leads to up-regulation of neural helix-loop-helix factors, premature neurogenesis and severe neural tube defects
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Ishibashi M, Ang S, Shiota K, Nakanishi S, Kageyama R, Guillemot F. Targeted disruption of mammalian hairy and enhancer of split homolog-1 (HES-1) leads to up-regulation of neural helix-loop-helix factors, premature neurogenesis and severe neural tube defects. Genes Dev. 9:1995;3136-3148.
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Genes Dev
, vol.9
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Ishibashi, M.1
Ang, S.2
Shiota, K.3
Nakanishi, S.4
Kageyama, R.5
Guillemot, F.6
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61
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0030010697
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The WRPW motif of the Hairy-related basic HLH repressor proteins acts as a 4 amino acid transcription repression and protein - protein interaction domain
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Fisher A, Ohsako S, Caudy M. The WRPW motif of the Hairy-related basic HLH repressor proteins acts as a 4 amino acid transcription repression and protein - protein interaction domain. Mol Cell Biol. 16:1996;2670-2677.
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Mol Cell Biol
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Fisher, A.1
Ohsako, S.2
Caudy, M.3
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62
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0031043087
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The Xenopus homolog of Drosophila Suppressor of Hairless mediates Notch signaling during primary neurogenesis
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of special interest. Changes in activity of the Xenopus homolog of Suppressor of Hairless alter expression of the enhancer of split homolog ESR1 and affect Notch signaling during neurogenesia. These results provide further evidence for the conservation of the Notch signaling pathway between invertebrates and vertebrates
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Wettstein D, Turner D, Kinter C. The Xenopus homolog of Drosophila Suppressor of Hairless mediates Notch signaling during primary neurogenesis. of special interest Development. 124:1997;693-702 Changes in activity of the Xenopus homolog of Suppressor of Hairless alter expression of the enhancer of split homolog ESR1 and affect Notch signaling during neurogenesia. These results provide further evidence for the conservation of the Notch signaling pathway between invertebrates and vertebrates.
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(1997)
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, vol.124
, pp. 693-702
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Wettstein, D.1
Turner, D.2
Kinter, C.3
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63
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0003073157
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Identification of neurogenin, a vertebrate neuronal determination gene
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of outstanding interest. This paper describes the identification of a bHLH protein, neurogenin, that is both structurally and functionally homologous to Drosophila Ac/Sc proteins, providing further evidence for the conservation of the Notch signaling pathway between invertebrates and vertebrates.
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Ma Q, Kintner C, Anderson D. Identification of neurogenin, a vertebrate neuronal determination gene. of outstanding interest Cell. 87:1996;43-52 This paper describes the identification of a bHLH protein, neurogenin, that is both structurally and functionally homologous to Drosophila Ac/Sc proteins, providing further evidence for the conservation of the Notch signaling pathway between invertebrates and vertebrates.
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(1996)
Cell
, vol.87
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Ma, Q.1
Kintner, C.2
Anderson, D.3
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64
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0030453171
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Notch signaling inhibits muscle cell differentiation through a CBF1-independent pathway
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Shawber C, Nofziger D, Hsieh J, Lindsell C, Bogler O, Hayward D, Weinmaster G. Notch signaling inhibits muscle cell differentiation through a CBF1-independent pathway. Development. 122:1996;3765-3773.
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Development
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Shawber, C.1
Nofziger, D.2
Hsieh, J.3
Lindsell, C.4
Bogler, O.5
Hayward, D.6
Weinmaster, G.7
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65
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0029078323
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Alterations in Notch signaling in neoplastic lesions of the human cervix
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Zagouras P, Stifani S, Blaumueller CM, Carcangiu ML, Artavanis-Tsakonas S. Alterations in Notch signaling in neoplastic lesions of the human cervix. Proc Natl Acad Sci USA. 92:1995;6414-6418.
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Proc Natl Acad Sci USA
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Zagouras, P.1
Stifani, S.2
Blaumueller, C.M.3
Carcangiu, M.L.4
Artavanis-Tsakonas, S.5
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66
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0029942842
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Exclusive development of T cell neoplasms in mice transplanted with bone marrow expressing activated Notch alleles
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Pear W, Aster J, Scott M, Hasserjian R, Soffer B, Sklar J, Baltimore D. Exclusive development of T cell neoplasms in mice transplanted with bone marrow expressing activated Notch alleles. J Exp Med. 183:1996;2283-2291.
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J Exp Med
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Pear, W.1
Aster, J.2
Scott, M.3
Hasserjian, R.4
Soffer, B.5
Sklar, J.6
Baltimore, D.7
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67
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0029819876
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Transduction of Notch2 in feline leukemia virus-induced thymic lymphoma
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Rohn JL, Lauring AS, Linenberger ML, Overbaugh J. Transduction of Notch2 in feline leukemia virus-induced thymic lymphoma. J Virol. 70:1996;8071-8080.
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(1996)
J Virol
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Rohn, J.L.1
Lauring, A.S.2
Linenberger, M.L.3
Overbaugh, J.4
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68
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0029116848
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Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimers disease gene
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Levitan D, Greenwald I. Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimers disease gene. Nature. 377:1995;351-354.
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Nature
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Levitan, D.1
Greenwald, I.2
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69
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0029906585
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Assessment of normal and mutant human presenilin function in Caenorhabditis elegans
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of outstanding interest. Human presenilins can functionally substitute for sel-12 in C. elegans. In addition, mutant versions of presenilin that are associated with Alzheimer's disease have reduced activity compared to wild-type presenilins in this assay.
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Levitan D, Doyle TG, Brousseau D, Lee MK, Thinakaran G, Slunt HH, Sisodia SS, Greenwald I. Assessment of normal and mutant human presenilin function in Caenorhabditis elegans. of outstanding interest Proc Natl Acad Sci USA. 93:1996;14940-14944 Human presenilins can functionally substitute for sel-12 in C. elegans. In addition, mutant versions of presenilin that are associated with Alzheimer's disease have reduced activity compared to wild-type presenilins in this assay.
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(1996)
Proc Natl Acad Sci USA
, vol.93
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Levitan, D.1
Doyle, T.G.2
Brousseau, D.3
Lee, M.K.4
Thinakaran, G.5
Slunt, H.H.6
Sisodia, S.S.7
Greenwald, I.8
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70
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16044362074
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Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia
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of outstanding interest. Human patients with CADASIL - a genetic syndrome that leads to smooth muscle defects, stroke, and dementia - carry missense mutations in the Notch3 gene. These results suggest that alterations in Notch function in humans may be responsible for this disease.
-
Joutel A, Corpechot C, Ducros A, Vahedi K, Chabriat H, Mouton P, Alamowitch S, Domenga V, Cecillion M, Marechal E, et al. Notch3 mutations in CADASIL, a hereditary adult-onset condition causing stroke and dementia. of outstanding interest Nature. 383:1997;707-710 Human patients with CADASIL - a genetic syndrome that leads to smooth muscle defects, stroke, and dementia - carry missense mutations in the Notch3 gene. These results suggest that alterations in Notch function in humans may be responsible for this disease.
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(1997)
Nature
, vol.383
, pp. 707-710
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-
Joutel, A.1
Corpechot, C.2
Ducros, A.3
Vahedi, K.4
Chabriat, H.5
Mouton, P.6
Alamowitch, S.7
Domenga, V.8
Cecillion, M.9
Marechal, E.10
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71
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Depletion of CD4+ T cells in major histocompatibility complex class II-deficient mice
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Grusby MJ, Johnson RS, Papaioannou VE, Glimcher LH. Depletion of CD4+ T cells in major histocompatibility complex class II-deficient mice. Science. 253:1991;1417-1420.
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(1991)
Science
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Grusby, M.J.1
Johnson, R.S.2
Papaioannou, V.E.3
Glimcher, L.H.4
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