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Functional characterization of the ‘PBX interacting protein’ (HPIP) in normal and malignant human haematopoiesis.

von Dr. Pak

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[1.] Pak/Fragment 022 01 - Diskussion
Zuletzt bearbeitet: 2014-04-06 06:49:03 Hindemith
Ahmed 2007, Fragment, Gesichtet, Pak, SMWFragment, Schutzlevel sysop, Verschleierung

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Some other factors appear to be more lineage-specific in action such as GATA-3, Ikaros, PU.1, GATA-1, CBP, Atf4, c-myb, and E2A, and their absence affects specific haematopoietic lineages. 73-77 The genetic factors involved in regulating fetal liver HSC are: Meis1, which is highly expressed in fetal liver Sca-1 +Lin- cells that are enriched for HSC activity78 and Hoxb4, which causes in vivo and ex vivo expansion of HSC when constitutively expressed. 79,80 Hox proteins interact with another transcription factor Pbx1, which itself interacts with Meis1 and forms a trimeric nuclear complex which is involved in target gene regulation81,82 (Fig.1.3.4a).

HSC self- renewal maintenance in adult BM is regulated by a different set of genes. A number of recent studies point out to nuclear factors such as the Polycomb (PcG) genes Bmi-1 and Rae-28, GATA-2 and TEL for potentially regulating this process. It has been observed that Bmi-1 levels decline during haematopoietic development, and that Bmi-1 deficient mice develop hypocellular BM and die at less than 2 months of age. This led to the speculation that Bmi-1 is involved in maintenance of the HSC pool.83 Rae-28, a known nuclear partner of Bmi-1, also plays a crucial role in maintaining the activity of HSCs during fetal haematopoiesis. 84

The zinc-finger transcription factor GATA-2, a member of GATA family, plays a critical role in maintaining the pool of multipotent progenitors and HSCs, both during embryogenesis and in the adult.85 The zinc-finger transcription factors GATA-1 and its transcriptional cofactor called Friend of GATA-1 (FOG-1), have been found to be essential for erythroid and megakaryocytic differentiation.86,87 PU.1 is a member of the Ets family of transcription factors and is essential in the development of cells of the monocytic, granulocytic and lymphoid lineages.88


73.Bain G, Maandag EC, Izon DJ, et al. E2A proteins are required for proper B cell development and initiation of immunoglobulin gene rearrangements. Cell. 1994;79:885-892.

74.Wang H, Xie Z, Scott RE. JunD phosphorylation, and expression of AP-1 DNA binding activity modulated by serum growth factors in quiescent murine 3T3T cells. Oncogene. 1996;13:2639-2647.

75.Scott G, Ewing J, Ryan D, Abboud C. Stem cell factor regulates human melanocyte-matrix interactions. Pigment Cell Res. 1994;7:44-51.

76.Emambokus N, Vegiopoulos A, Harman B, Jenkinson E, Anderson G, Frampton J. Progression through key stages of haemopoiesis is dependent on distinct threshold levels of c-Myb. EMBO J. 2003;22:4478-4488.

77.Lessard J, Faubert A, Sauvageau G. Genetic programs regulating HSC specification, maintenance and expansion. Oncogene. 2004;23:7199-7209.

78.Pineault N, Helgason CD, Lawrence HJ, Humphries RK. Differential expression of Hox, Meis1, and Pbx1 genes in primitive cells throughout murine hematopoietic ontogeny. Exp Hematol. 2002;30:49-57.

79.Antonchuk J, Sauvageau G, Humphries RK. HOXB4-induced expansion of adult hematopoietic stem cells ex vivo. Cell. 2002;109:39-45.

80.Buske C, Feuring-Buske M, Antonchuk J, et al. Overexpression of HOXA10 perturbs human lymphomyelopoiesis in vitro and in vivo. Blood. 2001;97:2286-2292.

81.Liu JP, Laufer E, Jessell TM. Assigning the positional identity of spinal motor neurons: rostrocaudal patterning of Hox-c expression by FGFs, Gdf11, and retinoids. Neuron. 2001;32:997-1012.

82. Mann RS, Affolter M. Hox proteins meet more partners. Curr Opin Genet Dev. 1998;8:423-429.

83.Lessard J, Schumacher A, Thorsteinsdottir U, van Lohuizen M, Magnuson T, Sauvageau G. Functional antagonism of the Polycomb-Group genes eed and Bmi1 in hemopoietic cell proliferation. Genes Dev. 1999;13:2691-2703.

84.Ohta H, Sawada A, Kim JY, et al. Polycomb group gene rae28 is required for sustaining activity of hematopoietic stem cells. J Exp Med. 2002;195:759-770.

85.Tsai FY, Orkin SH. Transcription factor GATA-2 is required for proliferation/survival of early hematopoietic cells and mast cell formation, but not for erythroid and myeloid terminal differentiation. Blood. 1997;89:3636-3643.

86.Pevny L, Simon MC, Robertson E, et al. Erythroid differentiation in chimaeric mice blocked by a targeted mutation in the gene for transcription factor GATA-1. Nature. 1991;349:257-260.

87.Vyas P, McDevitt MA, Cantor AB, Katz SG, Fujiwara Y, Orkin SH. Different sequence requirements for expression in erythroid and megakaryocytic cells within a regulatory element upstream of the GATA- 1 gene. Development. 1999;126:2799-2811.

88.Scott EW, Simon MC, Anastasi J, Singh H. Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages. Science. 1994;265:1573-1577.

Some other factors appear to be more lineage-specific in action such as GATA-3, Ikaros, PU.1, GATA-1, CBP, Atf4, c-myb, and E2A, and their absence affects specific haematopoietic lineages (Bain et al 1994, Scott 1994, Wang et al 1996 Mauoka 2002, Wang 1997, Emambokus 2003). [...] The genetic factors involved in regulating fetal liver HSC are: Meis1, which is highly expressed in fetal liver Sca-1 + Lin- cells that are enriched for HSC activity (Pineault et al., 2002) and Hoxb4, the overexpression of which causes in vivo and ex vivo expansion of HSC (Antonchuk et al., 2001; Buske et al., 2002). Hox proteins interact with another transcription factor Pbx which itself interacts with Meis1 and forms a trimeric nuclear complex which is involved in target gene regulation (Liu et al., 2001; Swift et al., 1998). HSC self-renewal maintenance in adult BM is regulated by a different set of genes. A number of recent studies point out to nuclear factors such as the Polycomb-Group (PcG) genes Bmi-1 and Rae-28, GATA-2 and TEL for potentially regulating this process. It has been observed that Bmi-1 levels decline during haematopoietic development, and that Bmi-1 deficient mice develop hypocellular BM and die at less than 2 months of age. This led to the speculation that Bmi-1 is involved in maintenance of the HSC pool (Lessard et al., 2004). Rae-28, a known nuclear partner of Bmi-1 also plays a crucial role in maintaining the activity of HSC during fetal haematopoiesis (Ohta et al., 2002). The zinc-finger transcription factor GATA-2, a member of GATA family, plays a critical role in

[page 8]

maintaining the pool of multipotent progenitors and HSC, both during embryogenesis and in the adult (Tsai et al., 1994).

[...] The zinc-finger transcription factor GATA-1 and its transcriptional cofactor called Friend of GATA-1 (FOG-1), have been found to be essential for erythroid and megakaryocytic differentiation (Pevny et al., 1991; Tsang et al., 1998; Vyas et al., 1999). PU.1 is a member of the Ets family of transcription factors and is essential in the development of cells of the monocytic, granulocytic and lymphoid lineages (Scott et al., 1994).


Antonchuk,J., Sauvageau,G., and Humphries,R.K. (2001). HOXB4 overexpression mediates very rapid stem cell regeneration and competitive haematopoietic repopulation. Exp. Hematol. 29, 1125-1134.

Buske,C., Feuring-Buske,M., Abramovich,C., Spiekermann,K., Eaves,C.J., Coulombel,L., Sauvageau,G., Hogge,D.E., and Humphries,R.K. (2002). Deregulated expression of HOXB4 enhances the primitive growth activity of human hematopoietic cells. Blood 100, 862-868.

Lessard,J., Faubert,A., and Sauvageau,G. (2004). Genetic programs regulating HSC specification, maintenance and expansion. Oncogene 23, 7199-7209.

Liu,Y., MacDonald,R.J., and Swift,G.H. (2001). DNA binding and transcriptional activation by a PDX1.PBX1b.MEIS2b trimer and cooperation with a pancreas-specific basic helix-loop-helix complex. J Biol. Chem. 276, 17985-17993.

Ohta,H., Sawada,A., Kim,J.Y., Tokimasa,S., Nishiguchi,S., Humphries,R.K., Hara,J., and Takihara,Y. (2002). Polycomb group gene rae28 is required for sustaining activity of hematopoietic stem cells. J Exp. Med. 195, 759-770.

Pevny,L., Simon,M.C., Robertson,E., Klein,W.H., Tsai,S.F., D'Agati,V., Orkin,S.H., and Costantini,F. (1991). Erythroid differentiation in chimaeric mice blocked by a targeted mutation in the gene for transcription factor GATA-1. Nature 349, 257-260.

Pineault,N., Helgason,C.D., Lawrence,H.J., and Humphries,R.K. (2002). Differential expression of Hox, Meis1, and Pbx1 genes in primitive cells throughout murine hematopoietic ontogeny. Exp. Hematol. 30, 49-57.

Scott,E.W., Simon,M.C., Anastasi,J., and Singh,H. (1994). Requirement of transcription factor PU.1 in the development of multiple hematopoietic lineages. Science 265, 1573-1577.

Swift,G.H., Liu,Y., Rose,S.D., Bischof,L.J., Steelman,S., Buchberg,A.M., Wright,C.V., and MacDonald,R.J. (1998). An endocrine-exocrine switch in the activity of the pancreatic homeodomain protein PDX1 through formation of a trimeric complex with PBX1b and MRG1 (MEIS2). Mol. Cell Biol. 18, 5109-5120.

Tsai,F.Y., Keller,G., Kuo,F.C., Weiss,M., Chen,J., Rosenblatt,M., Alt,F.W., and Orkin,S.H. (1994). An early haematopoietic defect in mice lacking the transcription factor GATA-2. Nature 371, 221-226.

Tsang,A.P., Fujiwara,Y., Hom,D.B., and Orkin,S.H. (1998). Failure of megakaryopoiesis and arrested erythropoiesis in mice lacking the GATA-1 transcriptional cofactor FOG. Genes Dev. 12, 1176-1188.

Vyas,P., Ault,K., Jackson,C.W., Orkin,S.H., and Shivdasani,R.A. (1999). Consequences of GATA-1 deficiency in megakaryocytes and platelets. Blood 93, 2867-2875.

Wang,J.C., Doedens,M., and Dick,J.E. (1997). Primitive human hematopoietic cells are enriched in cord blood compared with adult bone marrow or mobilized peripheral blood as measured by the quantitative in vivo SCID-repopulating cell assay. Blood 89, 3919-3924.

Anmerkungen

The source is not given.

Note: Bain et al (1994) is not listed in the list of references of the source, neither is Wang et al. (1996), Mauoka (2002) and Emambokus (2003).

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(Hindemith), SleepyHollow02

[2.] Pak/Fragment 022 26 - Diskussion
Zuletzt bearbeitet: 2014-04-06 07:31:19 Hindemith
Fragment, Gesichtet, KomplettPlagiat, Pak, SMWFragment, Schutzlevel sysop, Wikipedia cell signaling 2008

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Many growth factors (CSF, GCSF, GMCSF, FLT3, TPO,IL-6, IL-3, IL-11 etc.) bind to receptors at the cell surface and stimulate cells to progress through the cell cycle and divide. Several of these receptors are kinases that start to phosphorylate themselves and other proteins when binding to a ligand. This phosphorylation can generate a binding site for a different protein and thus induce protein-protein interaction. Many growth factors bind to receptors at the cell surface and stimulate cells to progress through the cell cycle and divide. Several of these receptors are kinases that start to phosphorylate themselves and other proteins when binding to a ligand. This phosphorylation can generate a binding site for a different protein and thus induce protein-protein interaction.
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Note that the internal links that appear in the Wikipedia are directly translated into underlined words in the thesis.

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