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Volumn 6, Issue 5, 1996, Pages 587-596

Roles of the JAK STAT system in signal transduction via cytokine receptors

Author keywords

[No Author keywords available]

Indexed keywords

CYTOKINE RECEPTOR; INTERFERON;

EID: 0030272581     PISSN: 0959437X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0959-437X(96)80088-8     Document Type: Article
Times cited : (70)

References (54)
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    • Differential regulation of the alpha/beta interferon-stimulated Jak/Stat pathway by the SH2 domain-containing tyrosine phosphatase SHPTP1
    • of special interest. Complementation of SHP-1 to cells derived from an SHP-1 null mouse here shows that SHP-1 increases just the tyrosine phosphorylation of JAK1 and STAT1α but does not affect the activation of TYK2 and STAT2 as induced by IFNα. It appears that SHP-1 regulates the member of JAK and STAT differentially.
    • David M, Chen H, Goelz S, Larner AC, Neel BG. Differential regulation of the alpha/beta interferon-stimulated Jak/Stat pathway by the SH2 domain-containing tyrosine phosphatase SHPTP1. of special interest Mol Cell Biol. 15:1995;7050-7058 Complementation of SHP-1 to cells derived from an SHP-1 null mouse here shows that SHP-1 increases just the tyrosine phosphorylation of JAK1 and STAT1α but does not affect the activation of TYK2 and STAT2 as induced by IFNα. It appears that SHP-1 regulates the member of JAK and STAT differentially.
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    • of special interest. Experiments using dominant negative JAK2 show that all the known activities centering on c-fos gene activation and cell proliferation as induced by hGM - CSF are mediated by JAK2. JAK2 is also shown to mediate phosphorylation of tyrosine residues of the receptor.
    • Watanabe S, Itoh T, Arai K. JAK2 is essential for activation of c-fos and c-myc promoters and cell proliferation through the human granulocyte - macrophage colony-stimulating factor receptor in BA/F3 cells. of special interest J Biol Chem. 271:1996;12681-12686 Experiments using dominant negative JAK2 show that all the known activities centering on c-fos gene activation and cell proliferation as induced by hGM - CSF are mediated by JAK2. JAK2 is also shown to mediate phosphorylation of tyrosine residues of the receptor.
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    • Kinase-negative mutants of JAK1 can sustain interferon-γ-inducible gene expression but not an antiviral state
    • of outstanding interest. By complementing kinase negative JAK1 or JAK2 to cells lacking either JAK1 or JAK2, the authors show that the kinase activity of JAK1 is dispensable for IFNγ activity, even though JAK1 protein is essential for IFNγ signaling. This indicates that JAK1 plays a structural role in the correct assembly and function of receptors. This work provides an insight in the analysis of other cytokines which activate multiple JAKs.
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    • of special interest. Involvement of the JAK-STAT pathway in the differentiation of hematopoietic cells is an interesting issue. This report indicates that the increase in JAK-STAT activity is coincident with monocytic U937 differentiation. The authors also report that phosphorylation of the serine rather than tyrosine residue is responsible for augmentation of STAT activity.
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    • Erythropoietin induces activation of Stat5 through association with specific tyrosines on the receptor that are not required for a mitogenic response
    • of outstanding interest. The authors describe the tyrosine residue of Epo receptor, which is required for activation of STAT5 by erythropoietin. As mutation of the tyrosine does not affect cell proliferation induced by Epo, the authors speculate that proliferation and STAT5 activation are separated in Epo signaling.
    • Quelle FW, Wang D, Nosaka T, Thierfelder WE, Stravopodis D, Weinstein Y, Ihle JN. Erythropoietin induces activation of Stat5 through association with specific tyrosines on the receptor that are not required for a mitogenic response. of outstanding interest Mol Cell Biol. 16:1996;1622-1631 The authors describe the tyrosine residue of Epo receptor, which is required for activation of STAT5 by erythropoietin. As mutation of the tyrosine does not affect cell proliferation induced by Epo, the authors speculate that proliferation and STAT5 activation are separated in Epo signaling.
    • (1996) Mol Cell Biol , vol.16 , pp. 1622-1631
    • Quelle, F.W.1    Wang, D.2    Nosaka, T.3    Thierfelder, W.E.4    Stravopodis, D.5    Weinstein, Y.6    Ihle, J.N.7
  • 43
    • 0029923780 scopus 로고    scopus 로고
    • Cell growth arrest and induction of cyclin-dependent kinase inhibitor p21WAF1/CIP1 mediated by STAT1
    • of outstanding interest. This paper describes a relationship between STAT1 activation and the inhibition of cell growth by EGF and IFNγ. Inhibition is caused by recognition of the STAT binding site in the promoter region of cyclin-dependent kinase inhibitor p21 by activated STAT1. This is the first report describing both negative regulation via the JAK - STAT pathway and the relationship between cell cycle machinery and JAK - STAT signaling.
    • Chin YE, Kitagawa M, Su W-CS, You A-H, Iwamoto Y, Fu X-Y. Cell growth arrest and induction of cyclin-dependent kinase inhibitor p21WAF1/CIP1 mediated by STAT1. of outstanding interest Science. 272:1996;719-721 This paper describes a relationship between STAT1 activation and the inhibition of cell growth by EGF and IFNγ. Inhibition is caused by recognition of the STAT binding site in the promoter region of cyclin-dependent kinase inhibitor p21 by activated STAT1. This is the first report describing both negative regulation via the JAK - STAT pathway and the relationship between cell cycle machinery and JAK - STAT signaling.
    • (1996) Science , vol.272 , pp. 719-721
    • Chin, Y.E.1    Kitagawa, M.2    Su W-CS3    You A-H4    Iwamoto, Y.5    Fu X-Y6
  • 44
    • 13344282731 scopus 로고    scopus 로고
    • Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the Jak-Stat signaling pathway
    • of special interest. The authors here and in [45] arrive at the same conclusion that STAT1 is essential for IFNα/b and IFNγ signaling but not for other cytokines, such as IL-10, GH and EGF, which are known to activate STAT1.
    • Meraz MA, White JM, Sheehan KCF, Bach EA, Rodig SJ, Dighe AS, Kaplan DH, Riley JK, Greenlund AC, Campbell. Targeted disruption of the Stat1 gene in mice reveals unexpected physiologic specificity in the Jak-Stat signaling pathway. of special interest Cell. 84:1996;431-442 The authors here and in [45] arrive at the same conclusion that STAT1 is essential for IFNα/b and IFNγ signaling but not for other cytokines, such as IL-10, GH and EGF, which are known to activate STAT1.
    • (1996) Cell , vol.84 , pp. 431-442
    • Meraz, M.A.1    White, J.M.2    Sheehan, K.C.F.3    Bach, E.A.4    Rodig, S.J.5    Dighe, A.S.6    Kaplan, D.H.7    Riley, J.K.8    Greenlund, A.C.9    Campbell10
  • 45
    • 0030024563 scopus 로고    scopus 로고
    • Targeted disruption of the mouse Stat1 gene results in compromised innate immunity to viral disease
    • of special interest. The specific requirement of STAT1 for IFN activities but not for other cytokines is unexpected. It is of interest to examine whether or not other STATs, such as STAT3, can substitute STAT1 or has redundant activity of STAT1 in other cytokine signals.
    • Durbin JE, Hackenmiller R, Simon MC, Levy DE. Targeted disruption of the mouse Stat1 gene results in compromised innate immunity to viral disease. of special interest Cell. 84:1996;443-450 The specific requirement of STAT1 for IFN activities but not for other cytokines is unexpected. It is of interest to examine whether or not other STATs, such as STAT3, can substitute STAT1 or has redundant activity of STAT1 in other cytokine signals.
    • (1996) Cell , vol.84 , pp. 443-450
    • Durbin, J.E.1    Hackenmiller, R.2    Simon, M.C.3    Levy, D.E.4
  • 46
    • 0029937270 scopus 로고    scopus 로고
    • Impaired IL-12 responses and enhanced development of Th2 cells in Stat4-deficient mice
    • of special interest. IL-12 promotes Th1 development but the molecular mechanisms that regulate differentiation of Th1 and Th2 cells are largely unknown. IL - 12 is known to activate STAT4; this study and [47] reconfirms this at various levels. STAT4 knockout mice have an impaired development of Th1 cells in response to IL-12. This report provides an important clue regarding differentiation of Th1 cells.
    • Kaplan MH, Sun Y-L, Hoey T, Grusby MJ. Impaired IL-12 responses and enhanced development of Th2 cells in Stat4-deficient mice. of special interest Nature. 382:1996;174-177 IL-12 promotes Th1 development but the molecular mechanisms that regulate differentiation of Th1 and Th2 cells are largely unknown. IL - 12 is known to activate STAT4; this study and [47] reconfirms this at various levels. STAT4 knockout mice have an impaired development of Th1 cells in response to IL-12. This report provides an important clue regarding differentiation of Th1 cells.
    • (1996) Nature , vol.382 , pp. 174-177
    • Kaplan, M.H.1    Sun Y-L2    Hoey, T.3    Grusby, M.J.4
  • 47
    • 15844396183 scopus 로고    scopus 로고
    • Requirement for Stat4 in interleukin-12 mediated responses of natural killer and T cells
    • of special interest. The conclusion of this paper is the same as that of [46] and also describes natural killer cell activity induced by IL-12. These reports show the primary and specific roles of STAT4 in all the known IL-12 activities tested. In addition, knockout of STAT1 and STAT6 implicate STAT protein specificity for particular cytokines.
    • Thierfelder WE, Van Deursen JM, Yamamoto K, Tripp RA, Sarawar SR, Carson RT, Sangster MY, Vignali DAA, Doherty PC, Grosveld GC, Ihle JN. Requirement for Stat4 in interleukin-12 mediated responses of natural killer and T cells. of special interest Nature. 382:1996;171-174 The conclusion of this paper is the same as that of [46] and also describes natural killer cell activity induced by IL-12. These reports show the primary and specific roles of STAT4 in all the known IL-12 activities tested. In addition, knockout of STAT1 and STAT6 implicate STAT protein specificity for particular cytokines.
    • (1996) Nature , vol.382 , pp. 171-174
    • Thierfelder, W.E.1    Van Deursen, J.M.2    Yamamoto, K.3    Tripp, R.A.4    Sarawar, S.R.5    Carson, R.T.6    Sangster, M.Y.7    Vignali, D.A.A.8    Doherty, P.C.9    Grosveld, G.C.10    Ihle, J.N.11
  • 48
    • 15844404509 scopus 로고    scopus 로고
    • Essential role of Stat6 in IL-4 signalling
    • of special interest. Mice lacking STAT6 show defects in the IL-4 mediated response, such as expression of cell surface markers and B-cell proliferation co-stimulated by anti-IgM. These phenotypes were indistinguishable from those of IL-4 deficient mice. The authors conclude that - between two distinct signaling pathways mediated by STAT6 and 4PS described thus far - STAT6 plays a central role in exerting biological responses mediated by IL-4.
    • Takeda K, Tanaka T, Shi W, Matsumoto M, Minami M, Kashiwamura S, Nakanishi K, Yoshida N, Kishimoto T, Akira S. Essential role of Stat6 in IL-4 signalling. of special interest Nature. 380:1996;627-630 Mice lacking STAT6 show defects in the IL-4 mediated response, such as expression of cell surface markers and B-cell proliferation co-stimulated by anti-IgM. These phenotypes were indistinguishable from those of IL-4 deficient mice. The authors conclude that - between two distinct signaling pathways mediated by STAT6 and 4PS described thus far - STAT6 plays a central role in exerting biological responses mediated by IL-4.
    • (1996) Nature , vol.380 , pp. 627-630
    • Takeda, K.1    Tanaka, T.2    Shi, W.3    Matsumoto, M.4    Minami, M.5    Kashiwamura, S.6    Nakanishi, K.7    Yoshida, N.8    Kishimoto, T.9    Akira, S.10
  • 49
    • 15844374279 scopus 로고    scopus 로고
    • Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene
    • of special interest. This report also demonstrates impairment of various IL-4-mediated activities in STAT6 knockout mice. Interestingly, IL-4-mediated proliferation is only partially affected and this observation should be discussed in terms of involvement of STAT in cell proliferation.
    • Shimoda K, Van Deursen J, Sangster MY, Sarawar SR, Carson RT, Tripp RA, Chu C, Quelle FW, Nosaka T, Vignali DAA, et al. Lack of IL-4-induced Th2 response and IgE class switching in mice with disrupted Stat6 gene. of special interest Nature. 380:1996;630-633 This report also demonstrates impairment of various IL-4-mediated activities in STAT6 knockout mice. Interestingly, IL-4-mediated proliferation is only partially affected and this observation should be discussed in terms of involvement of STAT in cell proliferation.
    • (1996) Nature , vol.380 , pp. 630-633
    • Shimoda, K.1    Van Deursen, J.2    Sangster, M.Y.3    Sarawar, S.R.4    Carson, R.T.5    Tripp, R.A.6    Chu, C.7    Quelle, F.W.8    Nosaka, T.9    Vignali, D.A.A.10
  • 50
    • 0029876629 scopus 로고    scopus 로고
    • Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells
    • of special interest. This paper describes an impairment of IL-13-induced cytokine production in T cells differentiated in vitro in addition to impairment of IL-4 activities in STAT6 knockout mice.
    • Kaplan MH, Schindler U, Smiley ST, Grusby MJ. Stat6 is required for mediating responses to IL-4 and for the development of Th2 cells. of special interest Immunity. 4:1996;313-319 This paper describes an impairment of IL-13-induced cytokine production in T cells differentiated in vitro in addition to impairment of IL-4 activities in STAT6 knockout mice.
    • (1996) Immunity , vol.4 , pp. 313-319
    • Kaplan, M.H.1    Schindler, U.2    Smiley, S.T.3    Grusby, M.J.4
  • 51
    • 0029005549 scopus 로고
    • Constitutively activated Jak - STAT pathway in T cells transformed with HTLV-1
    • of special interest. The mechanism of HTLV-1 transformation has long been studied and the role of Tax and other proteins encoded by the pX region is discussed. This report adds a new dimension to the study of the roles of the JAK-STAT pathway in cell transformation and proliferation.
    • Migone TS, Lin J-X, Cereseto A, Mulloy JC, O'Shea JJ, Franchini G, Leonard WJ. Constitutively activated Jak - STAT pathway in T cells transformed with HTLV-1. of special interest Science. 269:1995;79-81 The mechanism of HTLV-1 transformation has long been studied and the role of Tax and other proteins encoded by the pX region is discussed. This report adds a new dimension to the study of the roles of the JAK-STAT pathway in cell transformation and proliferation.
    • (1995) Science , vol.269 , pp. 79-81
    • Migone, T.S.1    Lin J-X2    Cereseto, A.3    Mulloy, J.C.4    O'Shea, J.J.5    Franchini, G.6    Leonard, W.J.7
  • 53
    • 0029863169 scopus 로고    scopus 로고
    • Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl
    • Carlesso N, Frank DA, Griffin JD. Tyrosyl phosphorylation and DNA binding activity of signal transducers and activators of transcription (STAT) proteins in hematopoietic cell lines transformed by Bcr/Abl. J Exp Med. 183:1996;811-820.
    • (1996) J Exp Med , vol.183 , pp. 811-820
    • Carlesso, N.1    Frank, D.A.2    Griffin, J.D.3
  • 54
    • 0030003920 scopus 로고    scopus 로고
    • Lack of constitutive activation of Janus kinases and signal transduction and activation of transcription factors in philadelphia chromosome-positive acute lymphoblastic leukemia
    • Kanwar VS, Witthuhn B, Campana D, Ihle JN. Lack of constitutive activation of Janus kinases and signal transduction and activation of transcription factors in philadelphia chromosome-positive acute lymphoblastic leukemia. Blood. 87:1996;4911-4912.
    • (1996) Blood , vol.87 , pp. 4911-4912
    • Kanwar, V.S.1    Witthuhn, B.2    Campana, D.3    Ihle, J.N.4


* 이 정보는 Elsevier사의 SCOPUS DB에서 KISTI가 분석하여 추출한 것입니다.