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1 s, are not required for Friend virus-induced erythroblastosis.
2 v-erbB tyrosine kinase, which induces avian erythroblastosis.
3 rations must be selected during induction of erythroblastosis.
4 erythropoietin receptors (EpoR) to stimulate erythroblastosis.
5 -erbB intron 14 integrations associated with erythroblastosis.
6 erythropoietin receptors (EpoR) to stimulate erythroblastosis.
7 oncoviruses by demonstrating that the avian erythroblastosis (a form of chicken leukaemia) could be
8 within the c-myc proto-oncogene and induces erythroblastosis after integration within the c-erbB pro
11 lastosis may be distinct from F-gp55-induced erythroblastosis and possibly not involve the EPO-R.
12 e splenomegaly, with splenic and bone marrow erythroblastosis and reduced apoptosis in vivo during er
13 thogenic helper virus developed long-latency erythroblastosis, and subsequent viral passages resulted
14 R itself was required for the development of erythroblastosis but not for gp55-mediated erythroid pro
16 to increased hemolysis in conditions such as erythroblastosis fetalis, septicemia, biliary atresia, a
17 tly reduced anti-erythrocyte autoantibodies, erythroblastosis, hemolytic anemia, anti-DNA autoantibod
18 t described in the 1960s and causes an acute erythroblastosis in chickens, more reminiscent of the di
20 ia, jaundice, hepatosplenomegaly, and marked erythroblastosis is more severe than that present in con
21 Rauscher virus envelope glycoprotein-induced erythroblastosis may be distinct from F-gp55-induced ery
23 inase A), or the neuregulin receptor, ErbB3 (erythroblastosis oncogene B3), with a peptide ligand for
24 A is the transforming component of S13 Avian Erythroblastosis Retrovirus that causes erythroblastosis
28 enotype, biochemical recurrence, v-ets avian erythroblastosis virus E26 oncogene homolog (ERG) status
31 2 production by several TFs, including v-ets erythroblastosis virus E26 oncogene homolog 1 (avian) (E
32 nd Western blot analysis revealed that v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets-1), a
33 ogenic responses by directly targeting v-ets erythroblastosis virus E26 oncogene homolog 1 (Ets-1).
34 r contains binding sites of the ETS-1 (v-ets erythroblastosis virus E26 oncogene homolog 1) transcrip
36 n that CDK10 silencing increases ETS2 (v-ets erythroblastosis virus E26 oncogene homolog 2)-driven ac
37 tease isoform 2, and ERG, encoding the v-ets erythroblastosis virus E26 oncogene homolog, are among t
38 pecificity protein 3 (Sp1/Sp3) and two v-ets erythroblastosis virus E26 oncogene homologue (Ets) bind
39 spective activator protein 1 (AP1) and v-ets erythroblastosis virus E26 oncogene homologue (Ets) site
40 e yeast one-hybrid selection including avian erythroblastosis virus E26 oncogene homologue 2, Ets-lik
41 Although recurrent gene fusions involving erythroblastosis virus E26 transformation-specific (ETS)
42 tions including fusion of a portion of avian erythroblastosis virus Gag to its N terminus, N- and C-t
44 ), Friend leukemia integration 1 (Fli1), and erythroblastosis virus oncogene homolog E twenty-six-1 (
45 ryotic transcription factor Ets-1 (E26 avian erythroblastosis virus oncogene-E twenty-six) is negativ
46 sitol 3-kinase/mammalian target of rapamycin/erythroblastosis virus transcription factor 2 pathway.
47 ve IL10 production, in retention of an avian erythroblastosis virus transcription factor recognition
48 eceptor alpha (TRalpha) carried by the avian erythroblastosis virus, contains several alterations inc
49 e transforming gene product of the S13 avian erythroblastosis virus, the env-sea protein, is a member
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