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Ectopic expression of the homeobox gene Cdx2 is the key transforming event in a mouse model of t(12;13)(p13;q12) acute myeloid leukemia; a novel mechanism in AML

von Dr. Vpr

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[1.] Vpr/Fragment 020 01 - Diskussion
Zuletzt bearbeitet: 2014-03-17 12:28:08 Graf Isolan
Fontanari Krause 2006, Fragment, Gesichtet, KomplettPlagiat, SMWFragment, Schutzlevel sysop, Vpr

Typus
KomplettPlagiat
Bearbeiter
SleepyHollow02, Hindemith
Gesichtet
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Untersuchte Arbeit:
Seite: 20, Zeilen: 1-21
Quelle: Fontanari Krause 2006
Seite(n): 21, 22, Zeilen: 21: 12-21; 22: 1-9
20a diss Vpr.png

Figure 10. ETV6 protein structure.

1.6.1 Role of ETV6 in hematopoiesis

ETV6 is widely expressed throughout embryonic development and in the adult. Embryos with a conventional knockout (KO) of the Etv6 gene die by day 11 of embryonic development (E11) due to vascular abnormalities. Blood formation in the embryo is largely unperturbed (Wang et. al., 1997). Yet, studies using chimeric mice from Etv6-deficient embryonic stem (ES) cells suggested a requirement of Etv6 in bone marrow hematopoiesis. Inducible and lineagespecific gene disruption of Etv6 in adult hematopoiesis in mice suggests that it plays two important roles in hematopoietic differentiation. First, Etv6 controls the survival of HSCs so that its disruption indirectly affects the majority of all hematopoietic cells which have limited clonal life spans and eventually will extinguish without constant regeneration from HSCs. Secondly, Etv6 is required late in the development of the megakaryocyte lineage, where it presumably acts in concert with transcriptional regulators previously implicated in megakaryopoiesis (Hock et. al., 2004).

1.6.2 ETV6 fusion partners

Translocations involving the ETV6 gene contribute to leukemogenesis through at least 3 different mechanisms. One mechanism is the activation of kinases. The second mechanism is the loss of function of critical transcription factors and/or the formation of aberrant transcription factors and the third mechanism is the induction of ectopic and aberrant expression of the proto-oncogene by the [chromosomal translocation.]


Hock, H., Meade, E., Medeiros, S., Schindler, J. W., Valk, P. J., Fujiwara, Y., and Orkin, S. H. (2004). Tel/Etv6 is an essential and selective regulator of adult hematopoietic stem cell survival. Genes Dev.

Wang, L. C., Kuo, F., Fujiwara, Y., Gilliland, D. G., Golub, T. R., and Orkin, S. H. (1997). Yolk sac angiogenic defect and intra-embryonic apoptosis in mice lacking the Ets-related factor TEL. Embo J 16, 4374-4383.

[page 21]

20a source Vpr.png

Figure 4.7: ETV6 protein structure. The pointed domain is represented between Nt 38 and Nt 123; ETS domain is between Nt 338 and Nt 422 (modified from Slupsky, 1998).

4.3.1. Role of ETV6 in hematopoiesis

ETV6 is widely expressed throughout embryonic development and in the adult. Embryos with a conventional knockout (KO) of the Etv6 gene die by day 11 of embryonic development (E11) due to vascular abnormalities. Blood formation in the embryo is largely unperturbed (Wang, 1997). Yet, studies using chimeric mice from Etv6-deficient embryonic stem (ES) cells suggested a requirement of Etv6 in bone marrow hematopoiesis. Inducible and lineagespecific gene disruption of Etv6 in adult hematopoiesis in mice suggests that it plays two important roles in hematopoietic differentiation. First, Etv6 controls the survival of HSCs so that its disruption indirectly affects the majority of all hematopoietic cells which have limited clonal life spans and eventually will extinguish without constant regeneration from HSCs.

[page 22]

Secondly, Etv6 is required late in the development of the megakaryocyte lineage, where it presumably acts in concert with transcriptional regulators previously implicated in megakaryopoiesis (Hock, 2004).

4.3.2. ETV6 fusion partners

Translocations involving the ETV6 gene contribute to leukemogenesis through at least 3 different mechanisms. One mechanism is the activation of kinases. The second mechanism is the loss of function of critical transcription factors and/or the formation of aberrant transcription factors and the third mechanism is the induction of ectopic and aberrant expression of the proto-oncogene by the chromosomal translocation.


Hock H., Meade E., Medeiros S., Schindler J. W., Valk P. J., Fujiwara Y., Orkin S. H. (2004). Tel/Etv6 is an essential and selective regulator of adult hematopoietic stem cell survival. Genes Dev. 18 (19), 2336-41.

Wang L. C., Kuo F., Fujiwara Y., Gilliland D. G., Golub T. R., Orkin S. H. (1997). Yolk sac angiogenic defect and intra-embryonic apoptosis in mice lacking the Ets-related factor TEL. EMBO J. 16, 4374-83.

Anmerkungen

The source is not mentioned. For the figure neither the original source Slupsky (1998) is mentioned.

Note that much of section 1.6.1 can also be found verbatim in Hock et al. (2004). This includes the reference to Wang (1997).

Sichter
(SleepyHollow02) Schumann, Hindemith


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