ライフサイエンスコーパス: v-erbA

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1 ceptor beta1 and inactive in the oncoprotein v-ErbA.

2 s contributes to the oncogenic properties of v-ErbA.

3 The oncoprotein v-ErbA, a member of the zinc finger transcription factor

4 ing and provide a mechanistic explanation of v-ErbA activity in AEV-induced erythroleukemia.

5 erbA, as well as genes that are regulated by v-erbA alone.

6 Furthermore, v-ErbA, an oncogenic derivative of cT3R, also activates

7 v-ErbA, an oncogenic derivative of the thyroid hormone r

8 ulture (AML12 cells) stably transfected with v-erbA and exposed to RA for 3 h or 24 h.

9 v-ErbA and other members of this family can bind as homo

10 inal domain, the I box (10 and 11 helices in v-ErbA and thyroid hormone receptors) and the 20-amino a

11 We find that both v-ErbA and TR can recruit the corepressor N-CoR, but, in

12 ied RA-responsive genes that are affected by v-erbA, as well as genes that are regulated by v-erbA al

13 gulation of TGF-beta signaling required that v-ErbA associate with the Smad4 which sequesters Smad4 i

14 v-erbA belongs to a superfamily of transcription factors

15 faces in the mechanism of action not only of v-ErbA but also of other members of the superfamily.

16 We have found that v-erbA can affect gene expression in the presence of RA

17 he thyroid hormone receptor-derived oncogene v-ErbA can arrest the differentiation of avian erythrobl

18 To determine which amino acid changes in v-ErbA confer CRM1-dependent nuclear export, we expresse

19 Heterokaryon experiments revealed that v-ErbA did not undergo nucleocytoplasmic shuttling when

20 a sensitivity could be recovered by reducing v-ErbA expression.

21 fferent dimerization interfaces are used for v-ErbA homodimerization and heterodimerization with reti

22 oteins were tested for their ability to form v-ErbA homodimers and heterodimers with retinoid X recep

23 a panel of ligand-binding domain mutants of v-ErbA lacking the Gag sequence exhibited greater nuclea

24 ermine the dominant negative activity of the v-ErbA mutants.

25 Nuclear export of v-ErbA occurs through a CRM1-mediated pathway.

26 In order to study the effect of v-erbA on RA-responsive genes, we used microarray analys

27 TR) and its mutated version, the oncoprotein v-ErbA, on partly and fully chromatinized TR-responsive

28 The v-erbA oncogene is known to exert a dominant-negative ef

29 t C-terminal sequence that is deleted in the v-ErbA oncoprotein and conserved in members of the nucle

30 ctivation in cancer, we stably expressed the v-ErbA oncoprotein in TGF-beta responsive cells.

31 planation for the mechanism of action of the v-erbA oncoprotein, a retroviral homolog of chicken T3R

32 v-ErbA participates in erythroleukemic transformation of

33 ticularly broad DNA specificity, whereas the v-ErbA protein is comparatively quite specific.

34 in) and that of an oncogenic derivative, the v-ErbA protein.

35 e (HDAC) inhibitor treatment and, unlike TR, v-ErbA required mature chromatin to effect repression.

36 We have also identified a number of v-erbA-responsive genes that are known to be involved in

37 ation and apoptosis in a variety of tissues, v-erbA seems to play a role in oncogenesis, namely in th

38 In support of this notion, we find v-ErbA to be less competent than TR for binding to TFIIB

39 repression and suggest that the inability of v-ErbA to silence on partly chromatinized templates may

40 Repression by v-ErbA was not as efficient as that mediated by TR, was

41 Here we demonstrate that expression of v-ErbA was sufficient to antagonize TGF-beta-induced cel

42 and point mutations within these regions of v-ErbA were made by site-directed mutagenesis.

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